Alagille Syndrome


Description:
Alagille syndrome is a genetic disorder that affects the liver, heart, kidney, and other systems of the body. Problems associated with the disorder generally become evident in infancy or early childhood. The disorder is inherited in an autosomal dominant pattern, and the estimated prevalence of Alagille syndrome is 1 in every 100,000 live births.It is named after Daniel Alagille.

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A person with Alagille syndrome has fewer than the normal number of small bile ducts inside the liver. The liver is the organ in the abdomen—the area between the chest and hips—that makes blood proteins and bile, stores energy and nutrients, fights infection, and removes harmful chemicals from the blood.

Bile ducts are tubes that carry bile from the liver cells to the gallbladder for storage and to the small intestine for use in digestion. Bile is fluid made by the liver that carries toxins and waste products out of the body and helps the body digest fats and the fat-soluble vitamins A, D, E, and K. In people with Alagille syndrome, the decreased number of bile ducts causes bile to build up in the liver, a condition also called cholestasis, leading to liver damage and liver disease.

The digestive system:
The digestive system is made up of the gastrointestinal (GI) tract—also called the digestive tract—and the liver, pancreas, and gallbladder. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The hollow organs that make up the GI tract are the mouth, esophagus, stomach, small intestine, large intestine—which includes the colon and rectum—and anus. Food enters the mouth and passes to the anus through the hollow organs of the digestive system. The liver, pancreas, and gallbladder are the solid organs of the digestive system. The digestive system helps the body digest food.
Symptoms:
The symptoms of Alagille syndrome and their severity vary, even among people in the same family sharing the same gene mutation.

Liver:  In some people, problems in the liver may be the first signs and symptoms of the disorder. These symptoms can occur in children and adults and in infants as early as the first 3 months of life.
Jaundice. Jaundice—when the skin and whites of the eyes turn yellow—is a result of the liver not removing bilirubin from the blood. Bilirubin is a reddish-yellow substance formed when hemoglobin breaks down. Hemoglobin is an iron-rich protein that gives blood its red color. Bilirubin is absorbed by the liver, processed, and released into bile. Blockage of the bile ducts forces bilirubin and other elements of bile to build up in the blood.
Jaundice may be difficult for parents and even health care providers to detect. Many healthy newborns have mild jaundice during the first 1 to 2 weeks of life due to an immature liver. This normal type of jaundice disappears by the second or third week of life, whereas the jaundice of Alagille syndrome deepens. Newborns with jaundice after 2 weeks of life should be seen by a health care provider to check for a possible liver problem.
Dark urine and gray or white stools. High levels of bilirubin in the blood that pass into the urine can make the urine darker, while stool lightens from a lack of bilirubin reaching the intestines. Gray or white bowel movements after 2 weeks of age are very reliable signs of a liver problem.
Pruritus. The buildup of bilirubin in the blood may cause itching, also called pruritus. Pruritus usually starts after 3 months of age and can be severe.
Xanthomas. Xanthomas are fatty deposits that appear as yellow bumps on the skin. They are caused by abnormally high cholesterol levels in the blood, common in people with liver disease. Xanthomas may appear anywhere on the body. However, xanthomas are usually found on the elbows, joints, tendons, knees, hands, feet, or buttocks.
Other Symptoms of Alagille Syndrome are:
Certain signs of Alagille syndrome are unique to the disorder, including those that affect the vertebrae and facial features.

Face.  Many children with Alagille syndrome have deep-set eyes, a straight nose, a small and pointed chin, large ears, and a prominent, wide forehead. These features are not usually recognized until after infancy. By adulthood, the chin is more prominent.

Eyes. Posterior embryotoxon is a condition in which an opaque ring is present in the cornea, the transparent covering of the eyeball. The abnormality is common in people with Alagille syndrome, though it usually does not affect vision.

Skeleton. The most common skeletal defect in a person with Alagille syndrome is when the shape of the vertebrae—bones of the spine—gives the appearance of flying butterflies. This defect, known as “butterfly” vertebrae, rarely causes medical problems or requires treatment.

Heart and blood vessels. People with Alagille syndrome may have the following signs and symptoms having to do with the heart and blood vessels:

heart murmur—an extra or unusual sound heard during a heartbeat. A heart murmur is the most common sign of Alagille syndrome other than the general symptoms of liver disease.1 Most people with Alagille syndrome have a narrowing of the blood vessels that carry blood from the heart to the lungs.1 This narrowing causes a murmur that can be heard with a stethoscope. Heart murmurs usually do not cause problems.

heart walls and valve problems. A small number of people with Alagille syndrome have serious problems with the walls or valves of the heart. These conditions may need treatment with medications or corrective surgery.

blood vessel problems. People with Alagille syndrome may have abnormalities of the blood vessels in the head and neck. This serious complication can lead to internal bleeding or stroke. Alagille syndrome can also cause narrowing or bulging of other blood vessels in the body.
Kidney disease. A wide range of kidney diseases can occur in Alagille syndrome. The kidneys are two bean-shaped organs, each about the size of a fist, that filter wastes and extra fluid from the blood. Some people have small kidneys or have cysts—fluid-filled sacs—in the kidneys. Kidney function can also decrease.
Causes:
Alagille syndrome is caused by a gene mutation, or defect. Genes provide instructions for making proteins in the body. A gene mutation is a permanent change in the DNA sequence that makes up a gene. DNA, or deoxyribonucleic acid, is the material inside cells that carries genetic information and passes genes from parent to child. Approximately 30 to 50 percent of people with Alagille syndrome have an inherited gene mutation, meaning it has been passed on by a parent. In the remaining cases, the gene mutation develops spontaneously.1 In spontaneous cases, neither parent carries a copy of the mutated gene.

Most cases of Alagille syndrome are caused by a mutation in the JAGGED1 (JAG1) gene. In less than 1 percent of cases, a mutation in the NOTCH2 gene is the cause.2

1Spinner NB, Leonard LD, Krantz ID. Alagille syndrome. GeneReviews website. www.ncbi.nlm.nih.gov/books/NBK1273/External NIH Link. Updated February 28, 2013. Accessed July 16, 2014.

2Kamath BM, Bauer RC, Loomes KM, et al. NOTCH2 mutations in Alagille syndrome. Journal of Medical Genetics. 2012;49(2):138–144.
Genetic Disorders: 
Each cell contains thousands of genes that provide the instructions for making proteins for growth and repair of the body. If a gene has a mutation, the protein made by that gene may not function properly, which sometimes creates a genetic disorder. Not all gene mutations cause a disorder.

People have two copies of most genes; one copy is inherited from each parent. A genetic disorder occurs when one or both parents pass a mutated gene to a child at conception. A genetic disorder can also occur through a spontaneous gene mutation, meaning neither parent carries a copy of the mutated gene. Once a spontaneous gene mutation has occurred in a person, it can be passed to the person’s children.
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Complications:
The complications of Alagille syndrome include liver failure, portal hypertension, and growth problems. People with Alagille syndrome usually have a combination of complications, and may not have every complication listed below.:-

Liver failure. Over time, the decreased number of bile ducts may lead to chronic liver failure, also called end-stage liver disease. This condition progresses over months, years, or even decades. The liver can no longer perform important functions or effectively replace damaged cells. A person may need a liver transplant. A liver transplant is surgery to remove a diseased or an injured liver and replace it with a healthy whole liver or a segment of a liver from another person, called a donor.

Portal hypertension. The spleen is the organ that cleans blood and makes white blood cells. White blood cells attack bacteria and other foreign cells. Blood flow from the spleen drains directly into the liver. When a person with Alagille syndrome has advanced liver disease, the blood flow backs up into the spleen and other blood vessels. This condition is called portal hypertension. The spleen may become larger in the later stages of liver disease. A person with an enlarged spleen should avoid contact sports to protect the organ from injury. Advanced portal hypertension can lead to serious bleeding problems.

Growth problems. Alagille syndrome can lead to poor growth in infants and children, as well as delayed puberty in older children. Liver disease can cause malabsorption, which can result in growth problems. Malabsorption is the inability of the small intestine to absorb nutrients from foods, which results in protein, calorie, and vitamin deficiencies. Serious heart problems, if present in Alagille syndrome, can also affect growth.

Malabsorption. People with Alagille syndrome may have diarrhea—loose, watery stools—due to malabsorption. The condition occurs because bile is necessary for the digestion of food. Malabsorption can lead to bone fractures, eye problems, blood-clotting problems, and learning delays.

Long-term Outlook:
The long-term outlook for people with Alagille syndrome depends on several factors, including the severity of liver damage and heart problems. Predicting who will experience improved bile flow and who will progress to chronic liver failure is difficult. Ten to 30 percent of people with Alagille syndrome will eventually need a liver transplant.

Many adults with Alagille syndrome whose symptoms improve with treatment lead normal, productive lives. Deaths in people with Alagille syndrome are most often caused by chronic liver failure, heart problems, and blood vessel problems.

Diagnosis:
The Doctor diagnoses Alagille syndrome by performing a thorough physical examination of the patient and ordering one or more of the following tests and exams:

Blood test. A blood test involves drawing blood at a health care provider’s office or a commercial facility and sending the sample to a lab for analysis. The blood test can show nutritional status and the presence of liver disease and kidney function.

Urinalysis. Urinalysis is the testing of a urine sample. The urine sample is collected in a special container in a health care provider’s office or a commercial facility and can be tested in the same location or sent to a lab for analysis. Urinalysis can show many problems of the urinary tract and other body systems. The sample may be observed for color, cloudiness, or concentration; signs of drug use; chemical composition, including glucose; the presence of protein, blood cells, or bacteria; or other signs of disease.

X ray. An x ray is a picture created by using radiation and recorded on film or on a computer. The amount of radiation used is small. An x-ray technician performs the x ray at a hospital or an outpatient center, and a radiologist—a doctor who specializes in medical imaging—interprets the images. Anesthesia is not needed. The patient will lie on a table or stand during the x ray. The technician positions the x-ray machine over the spine area to look for “butterfly” vertebrae. The patient will hold his or her breath as the picture is taken so that the picture will not be blurry. The patient may be asked to change position for additional pictures.

Abdominal ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. The transducer can be moved to different angles to make it possible to examine different organs. In abdominal ultrasound, the health care provider applies a gel to the patient’s abdomen and moves a handheld transducer over the skin. The gel allows the transducer to glide easily, and it improves the transmission of the signals. A specially trained technician performs the procedure in a health care provider’s office, an outpatient center, or a hospital, and a radiologist interprets the images; anesthesia is not needed. The images can show an enlarged liver or rule out other conditions.

Cardiology exam. A cardiologist—a doctor who treats people who have heart problems—performs a cardiology exam in a health care provider’s office, an outpatient center, or a hospital. During a full exam, a cardiologist may inspect the patient’s physical appearance, measure pulse rate and blood pressure, observe the jugular vein, check for rapid or skipped heartbeats, listen for variations in heart sounds, and listen to the lungs.

Slit-lamp exam. An ophthalmologist—a doctor who diagnoses and treats all eye diseases and eye disorders—performs a slit-lamp exam to diagnose posterior embryotoxon. The ophthalmologist examines the eye with a slit lamp, a microscope combined with a high-intensity light that shines a thin beam on the eye. While sitting in a chair, the patient will rest his or her head on the slit lamp. A yellow dye may be used to examine the cornea and tear layer. The dye is applied as a drop, or the specialist may touch a strip of paper stained with the dye to the white of the patient’s eye. The specialist will also use drops in the patient’s eye to dilate the pupil.

Liver biopsy. A liver biopsy is a procedure that involves taking a piece of liver tissue for examination with a microscope for signs of damage or disease. The health care provider may ask the patient to stop taking certain medications temporarily before the liver biopsy. The patient may be asked to fast for 8 hours before the procedure.

During the procedure, the patient lies on a table, right hand resting above the head. A local anesthetic is applied to the area where the biopsy needle will be inserted. If needed, sedatives and pain medication are also given. The health care provider uses a needle to take a small piece of liver tissue. The health care provider may use ultrasound, computerized tomography scans, or other imaging techniques to guide the needle. After the biopsy, the patient should lie on the right side for up to 2 hours and is monitored an additional 2 to 4 hours before being sent home.

Genetic testing. The health care provider may refer a person suspected of having Alagille syndrome to a geneticist—a doctor who specializes in genetic disorders. For a genetic test, the geneticist takes a blood or saliva sample and analyzes the DNA for the JAG1 gene mutation. The geneticist tests for the JAG1 gene mutation first, since it is more common in Alagille syndrome than NOTCH2. Genetic testing is often done only by specialized labs. The results may not be available for several months because of the complexity of the testing.

The usefulness of genetic testing for Alagille syndrome is limited by two factors:

*Detection of a mutated gene cannot predict the onset of symptoms or how serious the disorder will be.

*Even if a mutated gene is found, no specific cure for the disorder exists.

When to Consider Genetic Counseling:
People who are considering genetic testing may want to consult a genetics counselor. Genetic counseling can help family members understand how test results may affect them individually and as a family. Genetic counseling is provided by genetics professionals—health care professionals with specialized degrees and experience in medical genetics and counseling. Genetics professionals include geneticists, genetics counselors, and genetics nurses.

Genetics professionals work as members of health care teams, providing information and support to individuals or families who have genetic disorders or a higher chance of having an inherited condition. Genetics professionals

*assess the likelihood of a genetic disorder by researching a family’s history, evaluating medical records, and conducting a physical exam of the patient and
*other family members

*weigh the medical, social, and ethical decisions surrounding genetic testing

*provide support and information to help a person make a decision about testing

*interpret the results of genetic tests and medical data

*provide counseling or refer individuals and families to support services

*serve as patient advocates

*explain possible treatments or preventive measures

*discuss reproductive options

Genetic counseling may be useful when a family member is deciding whether to have genetic testing and again later when test results are available.

Treatment:
Treatment for Alagille syndrome includes medications and therapies that increase the flow of bile from the liver, promote growth and development in infants’ and children’s bodies, correct nutritional deficiencies, and reduce the person’s discomfort. Ursodiol (Actigall, Urso) is a medication that increases bile flow. Other treatments address specific symptoms of the disorder.

Liver failure. People with Alagille syndrome who develop end-stage liver failure need a liver transplant with a whole liver from a deceased donor or a segment of a liver from a living donor. People with Alagille syndrome who also have heart problems may not be candidates for a transplant because they could be more likely to have complications during and after the procedure. A liver transplant surgical team performs the transplant in a hospital.

Pruritus. Itching may decrease when the flow of bile from the liver is increased. Medications such as cholestyramine (Prevalite), rifampin (Rifadin, Rimactane), naltrexone (Vivitrol), or antihistamines may be prescribed to relieve pruritus. People should hydrate their skin with moisturizers and keep their fingernails trimmed to prevent skin damage from scratching. People with Alagille syndrome should avoid baths and take short showers to prevent the skin from drying out.

If severe pruritus does not improve with medication, a procedure called partial external biliary diversion may provide relief from itching. The procedure involves surgery to connect one end of the small intestine to the gallbladder and the other end to an opening in the abdomen—called a stoma—through which bile leaves the body and is collected in a pouch. A surgeon performs partial external biliary diversion in a hospital. The patient will need general anesthesia.

Malabsorption and growth problems. Infants with Alagille syndrome are given a special formula that helps the small intestine absorb much-needed fat. Infants, children, and adults can benefit from a high-calorie diet, calcium, and vitamins A, D, E, and K. They may also need additional zinc. If someone with Alagille syndrome does not tolerate oral doses of vitamins, a health care provider may give the person injections for a period of time. A child may receive additional calories through a tiny tube that is passed through the nose into the stomach. If extra calories are needed for a long time, a health care provider may place a tube, called a gastrostomy tube, directly into the stomach through a small opening made in the abdomen. A child’s growth may improve with increased nutrition and flow of bile from the liver.

Xanthomas. For someone who has Alagille syndrome, these fatty deposits typically worsen over the first few years of life and then improve over time. They may eventually disappear in response to partial external biliary diversion or the medications used to increase bile fl

Prevention:
Scientists have not yet found a way to prevent Alagille syndrome. However, complications of the disorder can be managed with the help of Doctors. Routine visits with Doctor are needed to prevent complications from becoming worse.

Hope through Research:The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and other Institutes of the National Institutes of Health (NIH) conduct and support research in digestive disorders, including Alagille syndrome. For example, the NIDDK is sponsoring a study called Evaluating the Genetic Causes and Progression of Cholestatic Liver Diseases (LOGIC). Funded under NIH clinical trial number NCT00571272, LOGIC will investigate the progression of cholestatic liver diseases, which can sometimes be caused by Alagille syndrome. The study will work to provide a better understanding of the causes and effects of these liver diseases, which will promote the development of prevention tactics and treatment strategies.

Clinical trials are research studies involving people. Clinical trials look at safe and effective new ways to prevent, detect, or treat disease. Researchers also use clinical trials to look at other aspects of care, such as improving the quality of life for people with chronic illnesses. To learn more about clinical trials, why they matter, and how to participate, visit the NIH Clinical Research Trials and You website at www.nih.gov/health/clinicaltrialsExternal NIH Link. For information about current studies,…click & see

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
Resources:

http://en.wikipedia.org/wiki/Alagille_syndrome

http://www.niddk.nih.gov/health-information/health-topics/liver-disease/Alagille-Syndrome/Pages/facts.aspx

 

Photodynamic therapy

Description:
Photodynamic therapy (PDT), sometimes called photochemotherapy, is a form of phototherapy using nontoxic light-sensitive compounds that are exposed selectively to light, whereupon they become toxic to targeted malignant and other diseased cells (phototoxicity). PDT has proven ability to kill microbial cells, including bacteria, fungi and viruses. PDT is popularly used in treating acne. It is used clinically to treat a wide range of medical conditions, including wet age-related macular degeneration and malignant cancers, and is recognised as a treatment strategy which is both minimally invasive and minimally toxic.

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Most modern PDT applications involve three key components: a photosensitizer, a light source and tissue oxygen. The combination of these three components leads to the chemical destruction of any tissues which have either selectively taken up the photosensitizer or have been locally exposed to light. The wavelength of the light source needs to be appropriate for exciting the photosensitizer to produce reactive oxygen species. These reactive oxygen species generated through PDT are free radicals (Type I PDT) generated through electron abstraction or transfer from a substrate molecule and highly reactive state of oxygen known as singlet oxygen (Type II PDT). In understanding the mechanism of PDT it is important to distinguish it from other light-based and laser therapies such as laser wound healing and rejuvenation, or intense pulsed light hair removal, which do not require a photosensitizer.

Why it is done:
Photodynamic therapy (PDT) was first used in 1905 for the treatment of skin cancers. Since then, it has been further developed and used for the treatment of many kinds of cancers (lung, colon, etc.) as well as certain kinds of blindness. PDT combines a drug (called a photosensitizer) that is preferentially absorbed by certain kinds of cells and a special light source. When used together, the photosensitizer and the light destroy the targeted cells. More recently, however, PDT has been used for photorejuvenation, wrinkles, discoloration, visible veins, and acne. When used for these conditions, the photosensitizer is applied to the face and then the skin is exposed to a light source. Rapidly growing cells, oil glands, and other structures in the skin absorb the photosensitizer and are destroyed by a reaction caused by the light. Cosmetic improvement in wrinkling, age spots, and visible veins has been documented after PDT treatment.

It is a new advance in facial rejuvenation and there are currently different methods in use. For example some physicians use blue light, red light, or intense pulse light. The photosensitizer is applied to the skin and is left on for a variable period of time. The skin is then exposed to the light source and the photosensitizer is then removed. Reported side effects include transient burning, stinging, swelling, and redness. Side effects are variable depending on what is being treated, how long the photosensitizer is left on, and which light source is used. No long-term studies have been performed to evaluate long term side effects.
Procedure:
In order to achieve the selective destruction of the target area using PDT while leaving normal tissues untouched, either the photosensitizer can be applied locally to the target area, or photosensitive targets can be locally excited with light. For instance, in the treatment of skin conditions, including acne, psoriasis, and also skin cancers, the photosensitizer can be applied topically and locally excited by a light source. In the local treatment of internal tissues and cancers, after photosensitizers have been administered intravenously, light can be delivered to the target area using endoscopes and fiber optic catheters....CLICK & SEE

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Photosensitizers can also target many viral and microbial species, including HIV and MRSA. Using PDT, pathogens present in samples of blood and bone marrow can be decontaminated before the samples are used further for transfusions or transplants. PDT can also eradicate a wide variety of pathogens of the skin and of the oral cavities. Given the seriousness that drug resistant pathogens have now become, there is increasing research into PDT as a new antimicrobial therapy.

Photosensitizers:
In air and tissue, molecular oxygen occurs in a triplet state, whereas almost all other molecules are in a singlet state. Reactions between these are forbidden by quantum mechanics, thus oxygen is relatively non-reactive at physiological conditions. A photosensitizer is a chemical compound that can be promoted to an excited state upon absorption light and undergo intersystem crossing with oxygen to produce singlet oxygen. This species rapidly attacks any organic compounds it encounters, thus being highly cytotoxic. It is rapidly eliminated: in cells, the average lifetime is 3 µs.[5]

A wide array of photosensitizers for PDT exist. They can be divided into porphyrins, chlorophylls and dyes. Some examples include aminolevulinic acid (ALA), Silicon Phthalocyanine Pc 4, m-tetrahydroxyphenylchlorin (mTHPC), and mono-L-aspartyl chlorin e6 (NPe6).

Several photosensitizers are commercially available for clinical use, such as Allumera, Photofrin, Visudyne, Levulan, Foscan, Metvix, Hexvix, Cysview, and Laserphyrin, with others in development, e.g. Antrin, Photochlor, Photosens, Photrex, Lumacan, Cevira, Visonac, BF-200 ALA. Amphinex. Also Azadipyrromethenes.

Although these photosensitizers can be used for wildly different treatments, they all aim to achieve certain characteristics:

*High absorption at long wavelengths

*Tissue is much more transparent at longer wavelengths (~700–850 nm). Absorbing at longer wavelengths would allow the light to penetrate deeper,[8] and allow the treatment of larger tumors.

*High singlet oxygen quantum yield

*Low photobleaching to prevent degradation of the photosensitizer

*Natural fluorescence

*Many optical dosimetry techniques, such as fluorescence spectroscopy, depend on the drug being naturally fluorescent[10]

*High chemical stability

*Low dark toxicity

*The photosensitizer should not be harmful to the target tissue until the treatment beam is applied.

*Preferential uptake in target tissue

The major difference between different types of photosensitizers is in the parts of the cell that they target. Unlike in radiation therapy, where damage is done by targeting cell DNA, most photosensitizers target other cell structures. For example, mTHPC has been shown to localize in the nuclear envelope and do its damage there. In contrast, ALA has been found to localize in the mitochondria and Methylene Blue in the lysosomes.

To allow treatment of deeper tumours some researchers are using internal chemiluminescence to activate the photosensitiser.

PUVA therapy is using psoralen as photosensitiser and UVA ultraviolet as light source, but this form of therapy is usually classified as a separate form of therapy from photodynamic therapy.

Targeted PDT:
Some photosensitisers naturally accumulate in the endothelial cells of vascular tissue allowing ‘vascular targeted’ PDT, but there is also research to target the photosensitiser to the tumour (usually by linking it to antibodies or antibody fragments). It is currently only in pre-clinical studies.

Applications:
Compared to normal tissues, most types of cancers are especially active in both the uptake and accumulation of photosensitizers agents, which makes cancers especially vulnerable to PDT. Since photosensitizers can also have a high affinity for vascular endothelial cells.

Usage in acne:
PDT is currently in clinical trials to be used as a treatment for severe acne. Initial results have shown for it to be effective as a treatment only for severe acne, though some question whether it is better than existing acne treatments. The treatment causes severe redness and moderate to severe pain and burning sensation. A phase II trial, while it showed improvement occurred, failed to show improved response compared to the blue/violet light alone
Advantages:
There are several advantages of photodynamic therapy over other forms of facial rejuvenation. For example, PDT is less destructive (and therefore less painful) than many of the deeper peels and lasers. There is also minimal recovery time. It is also a proven technique for the treatment of precancerous lesions. Thus, depending on the technique used, there may be an additional benefit of preventing skin cancer.

Disadvantages:
The disadvantage of photodynamic therapy is that it is new. Long-term side effects are unknown, and the benefits are not as well studied. For example, PDT is not known how long the benefits last.

Although PDT is a promising new therapy, you need to discuss the risks, benefits, and alternatives with your physician to decide if PDT is right for you.
Modern development of PDT in Russia:
Of all the nations beginning to use PDT in the late 20th century, the Russians were the quickest to advance its use clinically and to make many developments. One early Russian development was a new photosensitizer called Photogem which, like HpD, was derived from haematoporphyrin in 1990 by Professor Andrey F. Mironov and coworkers in Moscow. Photogem was approved by the Ministry of Health of Russia and tested clinically from February 1992 to 1996. A pronounced therapeutic effect was observed in 91 percent of the 1500 patients that underwent PDT using Photogem, with 62 percent having a total tumor resolution. Of the remaining patients, a further 29 percent had a partial tumor resolution, where the tumour at least halved in size. In those patients that had been diagnosed early, 92 percent of the patients showed complete resolution of the tumour.

Around this time, Russian scientists also collaborated with NASA medical scientists who were looking at the use of LEDs as more suitable light sources, compared to lasers, for PDT applications.

Modern development of PDT in Asia:
PDT has also seen considerably development in Asia. Since 1990, the Chinese have been developing specialist clinical expertise with PDT using their own domestically produced photosensitizers, derived from Haematoporphyrin, and light sources. PDT in China is especially notable for the technical skill of specialists in effecting resolution of difficult to reach tumours
Resources:

http://en.wikipedia.org/wiki/Photodynamic_therapy

http://www.dermanetwork.org/information/pdt.asp

Gastroenteritis

Description:
Gastroenteritis or infectious diarrhea is a medical condition from inflammation  of the gastrointestinal tract that involves both the stomach (“gastro”-) and the small intestine (“entero”-). It causes some combination of diarrhea, vomiting, and abdominal pain and cramping. Dehydration may occur as a result.

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Gastroenteritis has been referred to as gastro, stomach bug, and stomach virus. Although unrelated to influenza, it has also been called stomach flu and gastric flu.

Globally, most cases in children are caused by rotavirus. In adults, norovirus and Campylobacter are more common. Less common causes include other bacteria (or their toxins) and parasites. Transmission may occur due to consumption of improperly prepared foods or contaminated water or via close contact with  individuals who are infectious. Prevention includes the use of fresh water, regular hand washing, and breast feeding especially in areas where sanitation is less good. The rotavirus vaccine is recommended for all children.

The key treatment is enough fluids. For mild or moderate cases, this can typically be achieved via oral rehydration solution (a combination of water, salts, and sugar). In those who are breast fed, continued breast feeding is recommended. For more severe cases, intravenous fluids from a healthcare centre may be needed. Antibiotics are generally not recommended. Gastroenteritis primarily affects children and those in the developing world. It results in about three to five billion cases and causes 1.4 million deaths a year.

Symptoms:
Gastroenteritis typically involves both diarrhea and vomiting, or less commonly, presents with only one or the other. Abdominal cramping may also be present. Symptoms usually starts 12–72 hours after contracting the infectious agent. If due to a viral agent, the condition usually resolves within one week.Some viral causes may also be associated with fever, fatigue, headache, and muscle pain. If the stool is bloody, the cause is less likely to be viral and more likely to be bacterial. Some bacterial infections may be associated with severe abdominal pain and may persist for several weeks.

Children infected with rotavirus usually make a full recovery within three to eight days. However, in poor countries treatment for severe infections is often out of reach and persistent diarrhea is common. Dehydration is a common complication of diarrhea, and a child with a significant degree of dehydration may have a prolonged capillary refill, poor skin turgor, and abnormal breathing. Repeat infections are typically seen in areas with poor sanitation, and malnutrition, stunted growth, and long-term cognitive delays can result.

Reactive arthritis occurs in 1% of people following infections with Campylobacter species, and Guillain-Barre syndrome occurs in 0.1%. Hemolytic uremic syndrome (HUS) may occur due to infection with Shiga toxin-producing Escherichia coli or Shigella species, causing low platelet counts, poor kidney function, and low red blood cell count (due to their breakdown). Children are more predisposed to getting HUS than adults. Some viral infections may produce benign  infantile seizures.

Causes:
Viruses (particularly rotavirus) and the bacteria Escherichia coli and Campylobacter species are the primary causes of gastroenteritis. There are, however, many other infectious agents that can cause this syndrome. Non-infectious causes are seen on occasion, but they are less likely than a viral or bacterial cause. Risk of infection is higher in children due to their lack of immunity and relatively poor hygiene.

Viral:-
Rotavirus, norovirus, adenovirus, and astrovirus are known to cause viral gastroenteritis. Rotavirus is the most common cause of gastroenteritis in children, and produces similar rates in both the developed and developing world. Viruses cause about 70% of episodes of infectious diarrhea in the pediatric age group.

Rotavirus is a less common cause in adults due to acquired immunity. Norovirus is the cause in about 18% of all cases. Norovirus is the leading cause of gastroenteritis among adults in America, causing greater than 90% of outbreaks. These localized epidemics typically occur when groups of people spend time in close physical proximity to each other, such as on cruise ships, in hospitals, or in restaurants. People may remain infectious even after their diarrhea has ended. Norovirus is the cause of about 10% of cases in children.

Bacterial:-
In the developed world Campylobacter jejuni is the primary cause of bacterial gastroenteritis, with half of these cases associated with exposure to poultry. In children, bacteria are the cause in about 15% of cases, with the most common types being Escherichia coli, Salmonella, Shigella, and Campylobacter  species. If food becomes contaminated with bacteria and remains at room temperature for a period of several hours, the bacteria multiply and increase the  risk of infection in those who consume the food. Some foods commonly associated with illness include raw or undercooked meat, poultry, seafood, and eggs; raw sprouts; unpasteurized milk and soft cheeses; and fruit and vegetable juices. In the developing world, especially sub-Saharan Africa and Asia, cholera is a common cause of gastroenteritis. This infection is usually transmitted by contaminated water or food.

Toxigenic Clostridium difficile is an important cause of diarrhea that occurs more often in the elderly. Infants can carry these bacteria without developing  symptoms. It is a common cause of diarrhea in those who are hospitalized and is frequently associated with antibiotic use. Staphylococcus aureus infectious  diarrhea may also occur in those who have used antibiotics. “Traveler’s diarrhea” is usually a type of bacterial gastroenteritis. Acid-suppressing medication  appears to increase the risk of significant infection after exposure to a number of organisms, including Clostridium difficile, Salmonella, and Campylobacter  species. The risk is greater in those taking proton pump inhibitors than with H2 antagonists.

Parasitic:
A number of protozoans can cause gastroenteritis – most commonly Giardia lamblia – but Entamoeba histolytica and Cryptosporidium species have also been implicated. As a group, these agents comprise about 10% of cases in children. Giardia occurs more commonly in the developing world, but this etiologic agent causes this type of illness to some degree nearly everywhere. It occurs more commonly in persons who have traveled to areas with high prevalence, children who attend day care, men who have sex with men, and following disasters.

Non-infectious:
There are a number of non-infectious causes of inflammation of the gastrointestinal tract. Some of the more common include medications (like NSAIDs), certain foods such as lactose (in those who are intolerant), and gluten (in those with celiac disease). Crohn’s disease is also a non-infection source of (often severe) gastroenteritis. Disease secondary to toxins may also occur. Some food related conditions associated with nausea, vomiting, and diarrhea include: ciguatera poisoning due to consumption of contaminated predatory fish, scombroid associated with the consumption of certain types of spoiled fish, tetrodotoxin poisoning from the consumption of puffer fish among others, and botulism typically due to improperly preserved food.

There are also some other unusual ways to get gastroenteritis:-

1.Heavy metals (arsenic, cadmium, lead, or mercury) in drinking water
2.Eating a lot of acidic foods, like citrus fruit and tomatoes
3.Toxins that might be found in certain seafood
4.Medications such as antibiotics, antacids, laxatives, and chemotherapy drugs

Transmission:
Transmission may occur via consumption of contaminated water, or when people share personal objects. In places with wet and dry seasons, water quality typically worsens during the wet season, and this correlates with the time of outbreaks. In areas of the world with four seasons, infections are more common in the winter. Bottle-feeding of babies with improperly sanitized bottles is a significant cause on a global scale.Transmission rates are also related to poor hygiene, especially among children, in crowded households, and in those with pre-existing poor nutritional status. After developing tolerance, adults may carry certain organisms without exhibiting signs or symptoms, and thus act as natural reservoirs of contagion. While some agents (such as Shigella) only occur in primates, others may occur in a wide variety of animals (such as Giardia)

Diagnosis:
Gastroenteritis is typically diagnosed clinically, based on a person’s signs and symptoms. Determining the exact cause is usually not needed as it does not alter management of the condition. However, stool cultures should be performed in those with blood in the stool, those who might have been exposed to food poisoning, and those who have recently traveled to the developing world. Diagnostic testing may also be done for surveillance. As hypoglycemia occurs in approximately 10% of infants and young children, measuring serum glucose in this population is recommended. Electrolytes and kidney function should also be checked when there is a concern about severe dehydration.

A determination of whether or not the person has dehydration is an important part of the assessment, with dehydration typically divided into mild (3–5%), moderate (6–9%), and severe (?10%) cases. In children, the most accurate signs of moderate or severe dehydration are a prolonged capillary refill, poor skin turgor, and abnormal breathing. Other useful findings (when used in combination) include sunken eyes, decreased activity, a lack of tears, and a dry mouth. A normal urinary output and oral fluid intake is reassuring. Laboratory testing is of little clinical benefit in determining the degree of dehydration.

Other potential causes of signs and symptoms that mimic those seen in gastroenteritis that need to be ruled out include appendicitis, volvulus, inflammatory bowel disease, urinary tract infections, and diabetes mellitus. Pancreatic insufficiency, short bowel syndrome, Whipple’s disease, coeliac disease, and  laxative abuse should also be considered.  The differential diagnosis can be complicated somewhat if the person exhibits only vomiting or diarrhea (rather  than both).

Appendicitis may present with vomiting, abdominal pain, and a small amount of diarrhea in up to 33% of cases.  This is in contrast to the large amount of  diarrhea that is typical of gastroenteritis. Infections of the lungs or urinary tract in children may also cause vomiting or diarrhea.  Classical diabetic  ketoacidosis (DKA) presents with abdominal pain, nausea, and vomiting, but without diarrhea.  One study found that 17% of children with DKA were initially diagnosed as having gastroenteritis.

Treatment:
Gastroenteritis is usually an acute and self-limiting disease that does not require medication in most cases.The preferred treatment in those with mild to  moderate dehydration is oral rehydration therapy (ORT). Metoclopramide and/or ondansetron, however, may be helpful in some children, and butylscopolamine is  useful in treating abdominal pain.

The primary treatment of gastroenteritis in both children and adults is rehydration. This is preferably achieved by oral rehydration therapy, although  intravenous delivery may be required if there is a decreased level of consciousness or if dehydration is severe. Oral replacement therapy products made with  complex carbohydrates (i.e. those made from wheat or rice) may be superior to those based on simple sugars. Drinks especially high in simple sugars, such as  soft drinks and fruit juices, are not recommended in children under 5 years of age as they may increase diarrhea. Plain water may be used if more specific  and effective ORT preparations are unavailable or are not palatable. A nasogastric tube can be used in young children to administer fluids if warranted.

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HOMEOPATHIC TREATMENT

HOME REMEDIES

Dietary:
It is recommended that breast-fed infants continue to be nursed in the usual fashion, and that formula-fed infants continue their formula immediately after  rehydration with ORT. Lactose-free or lactose-reduced formulas usually are not necessary. Children should continue their usual diet during episodes of diarrhea with the exception that foods high in simple sugars should be avoided. The BRAT diet (bananas, rice, applesauce, toast and tea) is no longer  recommended, as it contains insufficient nutrients and has no benefit over normal feeding. Some probiotics have been shown to be beneficial in reducing both  the duration of illness and the frequency of stools. They may also be useful in preventing and treating antibiotic associated diarrhea.Fermented milk  products (such as yogurt) are similarly beneficial. Zinc supplementation appears to be effective in both treating and preventing diarrhea among children in  the developing world.

Antiemetics:
Antiemetic medications may be helpful for treating vomiting in children. Ondansetron has some utility, with a single dose being associated with less need for  intravenous fluids, fewer hospitalizations, and decreased vomiting.  Metoclopramide might also be helpful. However, the use of ondansetron might possibly be  linked to an increased rate of return to hospital in children. The intravenous preparation of ondansetron may be given orally if clinical judgment warrants.

Dimenhydrinate, while reducing vomiting, does not appear to have a significant clinical benefit.

Antibiotics:
Antibiotics are not usually used for gastroenteritis, although they are sometimes recommended if symptoms are particularly severe or if a susceptible bacterial cause is isolated or suspected. If antibiotics are to be employed, a macrolide (such as azithromycin) is preferred over a fluoroquinolone due to higher rates of resistance to the latter. Pseudomembranous colitis, usually caused by antibiotic use, is managed by discontinuing the causative agent and treating it with either metronidazole or vancomycin. Bacteria and protozoans that are amenable to treatment include Shigella Salmonella typhi,  and Giardia species. In those with Giardia species or Entamoeba histolytica, tinidazole treatment is recommended and superior to metronidazole. The World Health Organization (WHO) recommends the use of antibiotics in young children who have both bloody diarrhea and fever.

Antimotility agents:
Antimotility medication has a theoretical risk of causing complications, and although clinical experience has shown this to be unlikely, these drugs are bdiscouraged in people with bloody diarrhea or diarrhea that is complicated by fever. Loperamide, an opioid analogue, is commonly used for the symptomatic treatment of diarrhea. Loperamide is not recommended in children, however, as it may cross the immature blood–brain barrier and cause toxicity. Bismuth subsalicylate, an insoluble complex of trivalent bismuth and salicylate, can be used in mild to moderate cases, but salicylate toxicity is theoretically possible.

Prevention:
Lifestyle:
A supply of easily accessible uncontaminated water and good sanitation practices are important for reducing rates of infection and clinically significant gastroenteritis. Personal measures (such as hand washing) have been found to decrease incidence and prevalence rates of gastroenteritis in both the developing and developed world by as much as 30%. Alcohol-based gels may also be effective. Breastfeeding is important, especially in places with poor hygiene, as is improvement of hygiene generally. Breast milk reduces both the frequency of infections and their duration. Avoiding contaminated food or drink should also be effective.

Vaccination:
Due to both its effectiveness and safety, in 2009 the World Health Organization recommended that the rotavirus vaccine be offered to all children globally. Two commercial rotavirus vaccines exist and several more are in development. In Africa and Asia these vaccines reduced severe disease among infants  and countries that have put in place national immunization programs have seen a decline in the rates and severity of disease. This vaccine may also prevent illness in non-vaccinated children by reducing the number of circulating infections. Since 2000, the implementation of a rotavirus vaccination program in the United States has substantially decreased the number of cases of diarrhea by as much as 80 percent. The first dose of vaccine should be given to infants between 6 and 15 weeks of age. The oral cholera vaccine has been found to be 50–60% effective over 2 years.

Research:
There are a number of vaccines against gastroenteritis in development. For example, vaccines against Shigella and enterotoxigenic Escherichia coli (ETEC), two of the leading bacterial causes of gastroenteritis worldwide.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://en.wikipedia.org/wiki/Gastroenteritis

http://www.webmd.com/digestive-disorders/gastroenteritis?print=true

Epstein-Barr infection

Description: The Epstein-Barr virus, also called EBV, is an extremely common virus that infects most people at one time or another during their lifetimes. There are several forms of Epstein–Barr virus infection. Infectious mononucleosis, nasopharyngeal carcinoma, and Burkitt’s lymphoma can all be caused by the Epstein–Barr virus.

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It is best known as the cause of infectious mononucleosis (glandular fever). It is also associated with particular forms of cancer, such as Hodgkin’s lymphoma, Burkitt’s lymphoma, nasopharyngeal carcinoma, and conditions associated with human immunodeficiency virus (HIV), such as hairy leukoplakia and central nervous system lymphomas. There is evidence that infection with the virus is associated with a higher risk of certain autoimmune diseases, especially dermatomyositis, systemic lupus erythematosus, rheumatoid arthritis, Sjögren’s syndrome, and multiple sclerosis.

Infection with EBV occurs by the oral transfer of saliva and genital secretions.

Most people become infected with EBV and gain adaptive immunity. In the United States, about half of all five-year-old children and 90 to 95 percent of adults have evidence of previous infection. Infants become susceptible to EBV as soon as maternal antibody protection disappears. Many children become infected with EBV, and these infections usually cause no symptoms or are indistinguishable from the other mild, brief illnesses of childhood. In the United States and other developed countries, many people are not infected with EBV in their childhood years. When infection with EBV occurs during adolescence, it causes infectious mononucleosis 35 to 50 percent of the time.

EBV infects B cells of the immune system and epithelial cells. Once the virus’s initial lytic infection is brought under control, EBV latently persists in the individual’s B cells for the rest of the individual’s life.

Symptoms:
Epstein-Barr virus infection generally causes a minor cold-like or flu-like illness, but, in some cases, there may be no symptoms of infection.Initial symptoms of infectious mononucleosis are fever, sore throat, and swollen lymph glands. Sometimes, a swollen spleen or liver involvement may develop. Heart problems or involvement of the central nervous system occurs only rarely, and infectious mononucleosis is almost never fatal. There are no known associations between active EBV infection and problems during pregnancy, such as miscarriages or birth defects. Although the symptoms of infectious mononucleosis usually resolve in 1 or 2 months, EBV remains dormant or latent in a few cells in the throat and blood for the rest of the person’s life. Periodically, the virus can reactivate and is commonly found in the saliva of infected persons. Reactivated and post-latent virus may pass the placental barrier in (also seropositive) pregnant women via macrophages and therefore can infect the fetus. Also re-infection of prior seropositive individuals may occur. In contrast, reactivation in adults usually occurs without symptoms of illness.

EBV also establishes a lifelong dormant infection in some cells of the body’s immune system. A late event in a very few carriers of this virus is the emergence of Burkitt’s lymphoma and nasopharyngeal carcinoma, two rare cancers. EBV appears to play an important role in these malignancies, but is probably not the sole cause of disease.

Most individuals exposed to people with infectious mononucleosis have previously been infected with EBV and are not at risk for infectious mononucleosis. In addition, transmission of EBV requires intimate contact with the saliva (found in the mouth) of an infected person. Transmission of this virus through the air or blood does not normally occur. The incubation period, or the time from infection to appearance of symptoms, ranges from 4 to 6 weeks. Persons with infectious mononucleosis may be able to spread the infection to others for a period of weeks. However, no special precautions or isolation procedures are recommended, since the virus is also found frequently in the saliva of healthy people. In fact, many healthy people can carry and spread the virus intermittently for life. These people are usually the primary reservoir for person-to-person transmission. For this reason, transmission of the virus is almost impossible to prevent.

The clinical diagnosis of infectious mononucleosis is suggested on the basis of the symptoms of fever, sore throat, swollen lymph glands, and the age of the patient. Usually, laboratory tests are needed for confirmation. Serologic results for persons with infectious mononucleosis include an elevated white blood cell count, an increased percentage of certain atypical white blood cells, and a positive reaction to a “mono spot” test.
Causes:
Epstein–Barr can cause infectious mononucleosis, also known as ‘glandular fever’, ‘Mono‘ and ‘Pfeiffer’s disease’. Infectious mononucleosis is caused when a person is first exposed to the virus during or after adolescence. Though once deemed “The Kissing Disease,” recent research has shown that transmission of EBV not only occurs from exchanging saliva, but also from contact with the airborne virus. It is predominantly found in the developing world, and most children in the developing world are found to have already been infected by around 18 months of age. Infection of children can occur when adults mouth feed or pre-chew food before giving it to the child. EBV antibody tests turn up almost universally positive.

Treatment:
There is no specific treatment for infectious mononucleosis, other than treating the symptoms. No antiviral drugs or vaccines are available. Some physicians have prescribed a 5-day course of steroids to control the swelling of the throat and tonsils. The use of steroids has also been reported to decrease the overall length and severity of illness, but these reports have not been published.

It is important to note that symptoms related to infectious mononucleosis caused by EBV infection seldom last for more than 4 months. When such an illness lasts more than 6 months, it is frequently called chronic EBV infection. However, valid laboratory evidence for continued active EBV infection is seldom found in these patients. The illness should be investigated further to determine if it meets the criteria for chronic fatigue syndrome, or CFS. This process includes ruling out other causes of chronic illness or fatigue.

Prognosis:
There is currently no specific cure for an Epstein-Barr virus infection. Treatment includes measures to help relieve symptoms and keep the body as strong as possible until the disease runs its course. This includes rest, medications to ease body aches and fever, and drinking plenty of fluids. People who are in good health can generally recover from an Epstein-Barr virus infection at home with supportive care, such as rest, fluids and pain relievers.

Prevention:
Treatment of most viral diseases begins with preventing the spread of the disease with basic hygiene measures. However, controlling the spread of the Epstein-Barr virus is extremely difficult because it is so common and because it is possible to spread the Epstein-Barr virus even when a person does not appear sick. Many healthy people who have had an Epstein-Barr virus infection continue to carry the virus in their saliva, which means they can spread it to others throughout their lifetimes. However, avoiding contact with another person’s saliva by not sharing drinking glasses or toothbrushes is still a good general disease prevention measure.

Regular exercise with healthy food habits and healthy life style is the best way of prevention.

Research:
As a relatively complex virus, EBV is not yet fully understood. Laboratories around the world continue to study the virus and develop new ways to treat the diseases it causes. One popular way of studying EBV in vitro is to use bacterial artificial chromosomes.[33] Epstein–Barr virus and its sister virus KSHV can be maintained and manipulated in the laboratory in continual latency. Although many viruses are assumed to have this property during infection of their natural host, they do not have an easily managed system for studying this part of the viral lifecycle. Genomic studies of EBV have been able to explore lytic reactivation and regulation of the latent viral episome.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
Resources:

http://en.wikipedia.org/wiki/Epstein%E2%80%93Barr_virus

http://en.wikipedia.org/wiki/Epstein–Barr_virus_infection

http://www.healthgrades.com/conditions/epstein-barr-virus

Ficus benjamina

Botanical Name :Ficus benjamina
Family:    Moraceae
Tribe:    Ficeae
Genus:    Ficus
Subgenus:Conosycea
Species:F. benjamina
Kingdom:Plantae
Order:    Rosales

Common Names: Weeping Chinese Banyan, Weeping Fig, Benjamin’s fig, or ficus tree

Habitat :Ficus benjamina is native to south and southeast Asia and Australia.Occasionally found self-sown in Britain, especially in the south-west. It is the official tree of Bangkok.

Description:
Ficus carica is a deciduous Tree growing to 6 m (19ft) by 6 m (19ft) at a medium rate.It is a tree reaching 30 metres (98 ft) tall in natural conditions, with gracefully drooping branchlets and glossy leaves 6–13 cm (2–5 in), oval with an acuminate tip. In its native range, its small fruit are favored by some birds, such as the Superb Fruit Dove, Wompoo Fruit Dove, Pink-spotted Fruit Dove, Ornate Fruit Dove, orange-bellied Fruit Dove, Torresian Imperial Pigeon, Purple-tailed Imperial Pigeon

Growth Rate: 24 Inches per Season
Landscape Use: Screen, Espalier or Hedged
Longevity: 40 to 150 years
Leaves: Ovate Glossy Medium to Dark Green. Evergreen.
Flowers: Inconspicuous. Flowers in Summer. Has separate male and female flowers on the same tree (monoecious).
Bloom Color is Green, Yellow. Main Bloom Time: Early spring, Late spring, Mid spring. Form: Spreading or horizontal, Upright or erect.

Fruit: Red Follicle, Small (0.25 – 0.50 inches), fruiting in Summer or Fall…..click & see
Bark: Light Green or Light Gray, Smooth
Branch Strength: Rated as Medium

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It is in flower from Jun to September, and the seeds ripen from Aug to September. The flowers are monoecious (individual flowers are either male or female, but both sexes can be found on the same plant)The plant is self-fertile.

Cultivation:
Landscape Uses:Container, Specimen. Requires a well-drained medium to light loam and some lime rubble incorporated into the soil. Succeeds in dry soils. A heavy wet soil tends to encourage excessive plant growth at the expense of fruit production[1]. Prefers a very sunny position but tolerates part-day shade when grown on a warm wall. Plants are hardy to about -15°c. The top growth is susceptible to frost damage and can be killed back to the base in severe winters, though plants usually recover well. Trees require the protection of a south or west facing wall in most parts of Britain if they are to produce a worthwhile crop, though free standing trees can succeed in Cornwall. There is a small orchard of free-standing trees in Anthony garden near Plymouth. These were seen in July 1995 with a very heavy crop of ripening fruits that would have been ready by August. Figs are very widely cultivated in warmer climes than Britain for their edible fruit, there are many named varieties. ‘Brown Turkey’ is the cultivar most commonly grown in Britain and is probably the most suitable for this climate. ‘White Ischia’ is a dwarf cultivar (though it can still be 5 metres tall and wide) and is ideal for pot culture. It produces an abundance of green-white thin-skinned fruits. Up to three crops of fruit a year can be obtained in some countries[46]. When grown outdoors in Britain only one crop is usually obtained, though in exceptionally hot years two crops are sometimes produced. The fruit usually takes about 12 months to mature in Britain, baby fruits no larger than about 15mm long in the autumn usually overwinter to form the following years crop of fruit. If plants are grown in pots in a conservatory or cold greenhouse, two crops of fruit can be obtained, one in early summer and one in late summer to autumn. Pinch back the new shoots to about six leaves in order to encourage the second crop. It is a good idea to restrict the roots of fig trees on most soil types in order to discourage excessive vegetative growth at the expense of fruit production. This can be done by root pruning, but it is easier to place some kind of permanent restriction around the roots – planting into a large tub that is then buried into the ground is one method. It is important to make sure that the tree still gets ample moisture, especially when the fruits are ripening. Special Features: Attractive foliage, Not North American native, Invasive, Inconspicuous flowers or blooms.

Propagation:     
Seed – sow spring in a warm greenhouse. Prick out the seedlings as soon as they are large enough to handle and overwinter the young plants in a greenhouse for at least their first year. Plant out in late spring after the last expected frosts and give some protection for their first winter outdoors. Cuttings of mature wood 10 – 12cm with a heel, winter in a frame. Fairly easy, but the cuttings must be kept frost free. It is probably best if the cuttings are put in individual pots. Layering.

Edible Uses   :
Edible Parts: Fruit.
Edible Uses: Curdling agent.
Fruits are eaten raw or cooked. Sweet and succulent, a fully ripe specimen is an exquisite fruit that almost literally melts in the mouth. The fruit is often dried for later use[183] and this dried fruit is a major item of commerce. Figs are usually pear-shaped and up to 5cm in diameter. A nutritional analysis is available. The latex from the sap can be used to coagulate plant milks.

Medicinal Uses:
Cancer;  Demulcent;  Digestive;  Emollient;  Galactogogue;  Laxative;  Pectoral;  Stings;  Stomachic;  Tonic;  Warts.

A decoction of the leaves is stomachic. The leaves are also added to boiling water and used as a steam bath for painful or swollen piles. The latex from the stems is used to treat corns, warts and piles. It also has an analgesic effect against insect stings and bites. The fruit is mildly laxative, demulcent, digestive and pectoral. The unripe green fruits are cooked with other foods as a galactogogue and tonic. The roasted fruit is emollient and used as a poultice in the treatment of gumboils, dental abscesses etc. Syrup of figs, made from the fruit, is a well-known and effective gentle laxative that is also suitable for the young and very old. A decoction of the young branches is an excellent pectoral. The plant has anticancer properties.

Other Uses:
Wood – pliable but porous and of little value. It is used for hoops, garlands, ornaments etc. When saturated with oil and covered with emery is used as a substitute for a hone. This tree is very suitable for bonsai and can be used as a house plant.This plant is also used as a land scaping plant.

Known Hazards: The sap and the half-ripe fruits are said to be poisonous. The sap can be a serious eye irritant.

Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.

Resources:

http://selectree.calpoly.edu/treedetail.lasso?rid=603

http://www.pfaf.org/user/Plant.aspx?LatinName=Ficus+carica

http://en.wikipedia.org/wiki/Ficus_benjamina

Pain

Definition:
Pain is an unpleasant feeling often caused by intense or damaging stimuli, such as stubbing a toe, burning a finger, putting alcohol on a cut, and bumping the “funny bone”. The International Association for the Study of Pain‘s widely used definition states: “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”

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Everyone feels pain at some point in their lives. Unfortunately, there is no machine to objectively assess pain. Physicians have to rely on what the patient says. Sensitivity to pain varies – acute pain may make a person only grit her teeth and wince whereas the same injury can produce “severe, unbearable pain” with weeping and wailing in others.

Pain forces a person to take notice of a body part they had probably taken for granted. This is particularly true of acute pain such as a toothache, sinusitis, appendicitis or urinary tract infection.

Our bodies are plentifully supplied with “nociceptors” in the skin, bones, muscles and internal organs. Noxious stimuli, (either injury or infection) activates them. They release electrical currents and biochemical agents. These travel along the nerves, up the spinal cord and eventually reach certain areas in the brain. The reaction occurs in a flash and the perception of pain is instantaneous

Pain motivates the individual to withdraw from damaging situations, to protect a damaged body part while it heals, and to avoid similar experiences in the future. Most pain resolves promptly once the painful stimulus is removed and the body has healed, but sometimes pain persists despite removal of the stimulus and apparent healing of the body; and sometimes pain arises in the absence of any detectable stimulus, damage or disease.

Symptoms:
Pain may occur with other symptoms depending on the underlying disease, disorder or condition. For instance, if your pain is due to arthritis, you may experience pain in more than one joint. Pain due to a compressed nerve in the lower back can even lead to loss of bladder control. Pain is often a major symptom of fibromyalgia, which is also characterized by fatigue and sleep problems.

Symptoms that might occur along with pain:

The range of symptoms that may occur with pain include:

*Depression
*Flu-like symptoms (fever, chills, sore throat, fatigue, headache, cough)
*Inability to concentrate
*Loss of appetite
*Muscle spasms
*Numbness
*Sleep disturbances
*Unexpected weight loss

There are certain Serious symptoms that might indicate a life-threatening condition:
In some cases, pain may occur with other symptoms that might indicate a serious or life-threatening condition, such as a heart attack. Seek immediate medical care  if you, or someone you are with, have any of these serious symptoms, with or without pain, including:

*Bleeding symptoms, such as bloody urine or bloody stools
*Change in consciousness or alertness; confusion
*Chest pain radiating to the arm, shoulder, neck or jaw
*Difficulty breathing, wheezing, or shortness of breath
*High fever (higher than 101 degrees Fahrenheit)
*Increased or decreased urine output
*Loss of bladder or bowel control
*Progressive weakness and numbness
*Redness, warmth or swelling
*Seizures
*Stiff neck and headache, with or without nausea or vomiting
*Weakness or lethargy

Causes:
Hundreds of diseases, disorders and conditions can cause pain, such as inflammatory syndromes, malignancy, trauma, and infection. In some cases, pain may be a symptom of a serious or life-threatening condition, such as a heart attack or cancer.

The experience of pain is invariably tied to emotional, psychological, and cognitive factors.

Pain can be due to a wide variety of diseases, disorders and conditions that range from a mild injury to a debilitating disease. Pain can be categorized as acute, chronic, referred, cancer, neuropathic, and visceral.

Acute pain is experienced rapidly in response to disease or injury. Acute pain serves to alert the body that something is wrong and that action should be taken, such as pulling your arm away from a flame. Acute pain often resolves within a short time once the underlying condition is treated.

Chronic pain is defined as lasting more than three months. Chronic pain often begins as acute pain that lingers beyond the natural course of healing or after steps have been taken to address the cause of pain.

Referred pain is pain that originates in one part of the body but is felt in another part of the body.

Cancer pain is due to malignancy.

Neuropathic pain is caused by damage to the nervous system and is often perceived as tingling, burning, and pins-and-needles sensations called paresthesias.

Visceral pain is caused by a problem with the internal organs, such as the liver, gallbladder, kidney, heart or lungs.

Recent studies have found that some people with chronic pain may have low levels of endorphins in their spinal fluid. Endorphins are neurochemicals, similar to opiate drugs (like morphine), that are produced in the brain and released into the body in response to pain. Endorphins act as natural pain killers. Chronic pain most often affects older adults, but it can occur at any age. Chronic pain can persist for several months to years.

Complications:
Complications associated with pain depend on the underlying disease, disorder or condition. For example, pain resulting from a degenerative condition such as multiple sclerosis can lead to inactivity and its associated complications. Fortunately, pain can often be alleviated or minimized by physical therapy, basic self-help measures, and following the treatment plan outlined by your doctor.

However, in some cases the degree and duration of your pain may become overwhelming and affect your everyday living. Research into the diagnosis and treatment of chronic pain is ongoing, so contact your health care professional for the latest information.

Over time, pain can lead to complications including:

*Absenteeism from work or school
*Dependence on prescription pain medication
*Pain that does not respond to treatment (intractable pain)
*Permanent nerve damage (due to a pinched nerve) including paralysis
*Physiological and psychological response to chronic pain
*Poor quality of life

Diagnosis:
A person’s self-report is the most reliable measure of pain, with health care professionals tending to underestimate severity.A definition of pain widely employed in nursing, emphasizing its subjective nature and the importance of believing patient reports, was introduced by Margo McCaffery in 1968: “Pain is whatever the experiencing person says it is, existing whenever he says it does”. To assess intensity, the patient may be asked to locate their pain on a scale of 0 to 10, with 0 being no pain at all, and 10 the worst pain they have ever felt. Quality can be established by having the patient complete the McGill Pain Questionnaire indicating which words best describe their pain.

As an aid to diagnosis:
Pain is a symptom of many medical conditions. Knowing the time of onset, location, intensity, pattern of occurrence (continuous, intermittent, etc.), exacerbating and relieving factors, and quality (burning, sharp, etc.) of the pain will help the examining physician to accurately diagnose the problem. For example, chest pain described as extreme heaviness may indicate myocardial infarction, while chest pain described as tearing may indicate aortic dissection.

Physiological measurement of pain:
fMRI brain scanning has been used to measure pain, giving good correlations with self-reported pain.

Hedonic adaptation:
Hedonic adaptation means that actual long-term suffering due to physical illness is often much lower than expected.

Legal awards for pain and suffering:
One area where assessments of pain are effectively required to be made is in legal awards for pain and suffering. In the Western world these are typically discretionary awards made by juries and are regarded as difficult to predict, variable and subjective, for instance in the US, UK, Australia and New Zealand.

Treatment:
Inadequate treatment of pain is widespread throughout surgical wards, intensive care units, accident and emergency departments, in general practice, in the management of all forms of chronic pain including cancer pain, and in end of life care. This neglect is extended to all ages, from neonates to the frail elderly. African and Hispanic Americans are more likely than others to suffer needlessly in the hands of a physician; and women’s pain is more likely to be undertreated than men’s.

The International Association for the Study of Pain advocates that the relief of pain should be recognized as a human right, that chronic pain should be considered a disease in its own right, and that pain medicine should have the full status of a specialty. It is a specialty only in China and Australia at this time. Elsewhere, pain medicine is a subspecialty under disciplines such as anesthesiology, physiatry, neurology, palliative medicine and psychiatry. In 2011, Human Rights Watch alerted that tens of millions of people worldwide are still denied access to inexpensive medications for severe pain.

A number of medications can be used to treat acute pain. Many of these are available OTC (over the counter). Commonly used medication is paracetemol (10 mg /kg/dose in children 500 mg per dose in adults). It can be repeated every four hours. Paracetemol helps with fever as well, so if the aches and pains are due to seasonal flu, there is rapid improvement. It also blocks the areas of the brain that recognise pain. NSAIDs (non steroidal anti inflammatory drugs) like ibuprofen (Brufen) and nalidixic acid relieve pain but do not have much effect on fever. They act by blocking prostaglandin, one of the chemicals responsible for feeling pain. Topical anti-inflammatory medications, particularly those containing capsaicin are very effective. They should be applied lightly over the painful area followed by an ice pack.

More often chronic pain is due to the various types of arthritis (rheumatoid, osteoarthritis), autoimmune diseases, gout and mechanical problems like a disc prolapse. It needs to be diagnosed correctly so that appropriate treatment can be started. The medications taken may be steroids, opiods or the coxib group of drugs.

Acute pain is usually managed with medications such as analgesics and anesthetics. Caffeine when added to pain medications provides some additional benefit. Management of chronic pain, however, is much more difficult and may require the coordinated efforts of a pain management team, which typically includes medical practitioners, clinical psychologists, physiotherapists, occupational therapists, physician assistants, and nurse practitioners.

Sugar taken orally reduces the total crying time but not the duration of the first cry in newborns undergoing a painful procedure (a single lancing of the heel). It does not moderate the effect of pain on heart rate and a recent single study found that sugar did not significantly affect pain-related electrical activity in the brains of newborns one second after the heel lance procedure. Sweet oral liquid moderately reduces the incidence and duration of crying caused by immunization injection in children between one and twelve months of age.

The brain has to be retrained in its perception and response to pain. This can be done with a combination of physiotherapy and aerobic exercise. Judiciously used, these interventions help to reduce long-term dependence on pain medication.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://www.healthgrades.com/right-care/bones-joints-and-muscles/pain–symptoms

http://www.telegraphindia.com/1141229/jsp/knowhow/story_5590.jsp

http://en.wikipedia.org/wiki/Pain

Ulcerative colitis

Definition:
Ulcerative colitis (Colitis ulcerosa, UC) is a form of inflammatory bowel disease (IBD). Ulcerative colitis is a form of colitis, a disease of the colon (the largest portion of the large intestine), that includes characteristic ulcers, or open sores. The main symptom of active disease is usually constant diarrhea mixed with blood, of gradual onset. IBD is often confused with irritable bowel syndrome (IBS).
CLICK & SEE THE PICTURES
It is a disease that causes inflammation and sores (ulcers) in the lining of the large intestine (colon ). It usually affects the lower section (sigmoid colon) and the rectum. But it can affect the entire colon. In general, the more of the colon that’s affected, the worse the symptoms will be.

CLICK & SEE THE PICTURE OF  CHRONIC ULCERARIVE COLITIS

Ulcerative colitis shares much in common with Crohn’s disease, another form of IBD, but Crohn’s disease can affect the whole gastrointestinal tract while ulcerative colitis only attacks the large intestine, and while ulcerative colitis can be treated by performing a total colectomy (i.e., removing the entire large intestine), surgery for Crohn’s disease involves removing the damaged parts of the intestine and reconnecting the healthy parts, which does not cure Crohn’s, as it can recur after surgery, mostly at the site of the intestinal anastomosis (connection) or in other areas. Ulcerative colitis is an intermittent disease, with periods of exacerbated symptoms, and periods that are relatively symptom-free. Although the symptoms of ulcerative colitis can sometimes diminish on their own, the disease usually requires treatment to go into remission. Ulcerative colitis has an incidence of 1 to 20 cases per 100,000 individuals per year, and a prevalence of 8 to 246 per 100,000 individuals.

The disease is more prevalent in northern countries of the world, as well as in northern areas of individual countries or other regions. Rates tend to be higher in more affluent countries, which may indicate the increased prevalence is due to increased rates of diagnosis. It may also indicate that an industrial or Western diet and lifestyle increases the prevalence of this disease, including symptoms which may or may not be related to ulcerative colitis. Although UC has no known cause, there is a presumed genetic component to susceptibility. The disease may be triggered in a susceptible person by environmental factors. Although dietary modification may reduce the discomfort of a person with the disease, ulcerative colitis is not thought to be caused by dietary factors.

Ulcerative colitis, like its sister condition Crohn’s disease, is treated as an autoimmune disease. Treatment is with anti-inflammatory drugs, immunosuppression, and biological therapy targeting specific components of the immune response. Colectomy (partial or total removal of the large bowel through surgery) is occasionally necessary if the disease is severe, does not respond to treatment, or if significant complications develop. A total proctocolectomy (removal of the entirety of the large bowel and rectum) can cure ulcerative colitis (extraintestinal symptoms will remain), as the disease only affects the large bowel and rectum. While extra intestinal symptoms will remain, complications may develop.

Symptoms:
As ulcerative colitis is believed to have a systemic (i.e., autoimmune) origin, patients may present with comorbidities leading to symptoms and complications outside the colon. The frequency of such extraintestinal manifestations has been reported as anywhere between 6 and 47 percent. These include the following:

*Aphthous ulcer of the mouth
*Ophthalmic (involving the eyes):
*Iritis or uveitis, which is inflammation of the iris Episcleritis

*Musculoskeletal:
#Seronegative arthritis, which can be a large-joint oligoarthritis (affecting one or two joints), or may affect many small joints of the hands and feet
#Ankylosing spondylitis, arthritis of the spine
#Sacroiliitis, arthritis of the lower spine

*Cutaneous (related to the skin):CLICK & SEE
#Erythema nodosum, which is a panniculitis, or inflammation of subcutaneous tissue involving the lower extremities
#Pyoderma gangrenosum, which is a painful ulcerating lesion involving the skin

*Deep venous thrombosis and pulmonary embolism
*Autoimmune hemolytic anemia
*Clubbing, a deformity of the ends of the fingers.
*Primary sclerosing cholangitis, a distinct disease that causes inflammation of the bile ducts

Gastrointestinal:
The clinical presentation of ulcerative colitis depends on the extent of the disease process. Patients usually present with diarrhea mixed with blood and mucus, of gradual onset that persists for an extended period (weeks). They may also have weight loss and blood on rectal examination. The inflammation caused by the disease along with chronic loss of blood from the GI tract leads to increased rates of anaemia. The disease may be accompanied with different degrees of abdominal pain, from mild discomfort to painful bowel movements or painful abdominal cramping with bowel movements.

Ulcerative colitis is associated with a general inflammatory process that affects many parts of the body. Sometimes these associated extra-intestinal symptoms are the initial signs of the disease, such as painful arthritic knees in a teenager and may be seen in adults also. The presence of the disease may not be confirmed immediately, however, until the onset of intestinal manifestations.

Extent of Involvement:
Ulcerative colitis is normally continuous from the rectum up the colon. The disease is classified by the extent of involvement, depending on how far up the colon the disease extends:

*Distal colitis, potentially treatable with enemas:
#Proctitis: Involvement limited to the rectum.
#Proctosigmoiditis: Involvement of the rectosigmoid colon, the portion of the colon adjacent to the rectum.
#Left-sided colitis: Involvement of the descending colon, which runs along the patient’s left side, up to the splenic flexure and the beginning of the transverse colon.

*Extensive colitis, inflammation extending beyond the reach of enemas:
#Pancolitis: Involvement of the entire colon, extending from the rectum to the cecum, beyond which the small intestine begins.

Severities of the diseases:..>...click & see   
In addition to the extent of involvement, people may also be characterized by the severity of their disease.

#Mild disease correlates with fewer than four stools daily, with or without blood, no systemic signs of toxicity, and a normal erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP). There may be mild abdominal pain or cramping. Patients may believe they are constipated when in fact they are experiencing tenesmus, which is a constant feeling of the need to empty the bowel accompanied by involuntary straining efforts, pain, and cramping with little or no fecal output. Rectal pain is uncommon.

#Moderate disease correlates with more than four stools daily, but with minimal signs of toxicity. Patients may display anemia (not requiring transfusions), moderate abdominal pain, and low grade fever, 38 to 39 °C (100 to 102 °F).
Severe disease, correlates with more than six bloody stools a day or observable massive and significant bloody bowel movement, and evidence of toxicity as demonstrated by fever, tachycardia, anemia or an elevated ESR or CRP.

#Fulminant disease correlates with more than ten bowel movements daily, continuous bleeding, toxicity, abdominal tenderness and distension, blood transfusion requirement and colonic dilation (expansion). Patients in this category may have inflammation extending beyond just the mucosal layer, causing impaired colonic motility and leading to toxic megacolon. If the serous membrane is involved, colonic perforation may ensue. Unless treated, fulminant disease will soon lead to death.
Causes:
Experts aren’t sure what causes it. They think it might be caused by the immune system overreacting to normal bacteria in the digestive tract. Or other kinds of bacteria and viruses may cause it.

Some factors are indicative:
Genetic factors:
*A genetic component to the etiology of ulcerative colitis can be hypothesized based on the following:

#Aggregation of ulcerative colitis in families.
#Identical twin concordance rate of 10% and dizygotic twin concordance rate of 3%
#Ethnic differences in incidence
#Genetic markers and linkages

There are 12 regions of the genome that may be linked to ulcerative colitis, including, in the order of their discovery, chromosomes 16, 12, 6, 14, 5, 19, 1, and 3, but none of these loci have been consistently shown to be at fault, suggesting that the disorder arises from the combination of multiple genes. For example, chromosome band 1p36 is one such region thought to be linked to inflammatory bowel disease.

Some of the putative regions encode transporter proteins such as OCTN1 and OCTN2. Other potential regions involve cell scaffolding proteins such as the MAGUK family. There may even be human leukocyte antigen associations at work. In fact, this linkage on chromosome 6 may be the most convincing and consistent of the genetic candidates.

Multiple autoimmune disorders have been recorded with the neurovisceral and cutaneous genetic porphyrias including ulcerative colitis, Crohn’s disease, celiac disease, dermatitis herpetiformis, diabetes, systemic and discoid lupus, rheumatoid arthritis, ankylosing spondylitis, scleroderma, Sjogren’s disease and scleritis. Physicians should be on high alert for porphyrias in families with autoimmune disorders and care must be taken with potential porphyrinogenic drugs, including sulfasalazine.

Environmental factors:
Many hypotheses have been raised for environmental contributants to the pathogenesis of ulcerative colitis. They include the following:

#Diet: as the colon is exposed to many dietary substances which may encourage inflammation, dietary factors have been hypothesized to play a role in the pathogenesis of both ulcerative colitis and Crohn’s disease. There have been few studies to investigate such an association, but one study showed no association of refined sugar on the prevalence of ulcerative colitis. High intake of unsaturated fat and vitamin B6 may enhance the risk of developing ulcerative colitis. Other identified dietary factors that may influence the development and/or relapse of the disease include meat protein and alcoholic beverages. Specifically, sulfur has been investigated as being involved in the etiology of ulcerative colitis, but this is controversial. Sulfur restricted diets have been investigated in patients with UC and animal models of the disease. The theory of sulfur as an etiological factor is related to the gut microbiota and mucosal sulfide detoxification in addition to the diet.

#Breastfeeding: There have been conflicting reports of the protection of breastfeeding in the development of inflammatory bowel disease. One Italian study showed a potential protective effect.

Several scientific studies have posited that Accutane is a possible trigger of Crohn’s disease and ulcerative colitis in some individuals. Three cases in the United States have gone to trial thus far, with all three resulting in multi-million dollar judgements against the makers of isotretinoin.

Autoimmune disease:
Ulcerative colitis is an autoimmune disease characterized by T-cells infiltrating the colon. In contrast to Crohn’s disease, which can affect areas of the gastrointestinal tract outside of the colon, ulcerative colitis usually involves the rectum and is confined to the colon, with occasional involvement of the ileum. This so-called “backwash ileitis” can occur in 10–20% of patients with pancolitis and is believed to be of little clinical significance. Ulcerative colitis can also be associated with comorbidities that produce symptoms in many areas of the body outside the digestive system. Surgical removal of the large intestine often cures the disease.

Alternative theories:
Levels of sulfate-reducing bacteria tend to be higher in persons with ulcerative colitis. This could mean that there are higher levels of hydrogen sulfide in the intestine. An alternative theory suggests that the symptoms of the disease may be caused by toxic effects of the hydrogen sulfide on the cells lining the intestine.

Pathophysiology:
An increased amount of colonic sulfate-reducing bacteria has been observed in some patients with ulcerative colitis, resulting in higher concentrations of the toxic gas hydrogen sulfide. Human colonic mucosa is maintained by the colonic epithelial barrier and immune cells in the lamina propria. N-butyrate, a short-chain fatty acid, gets oxidized through the beta oxidation pathway into carbon dioxide and ketone bodies. It has been shown that N-butyrate helps supply nutrients to this epithelial barrier. Studies have proposed that hydrogen sulfide plays a role in impairing this beta oxidation pathway by interrupting the short chain acetyl CoA dehydrogenase, an enzyme within the pathway. Furthermore, it has been suggested that the protective benefit of smoking in ulcerative colitis is due to the hydrogen cyanide from cigarette smoke reacting with hydrogen sulfide to produce the nontoxic isothiocyanate, thereby inhibiting sulfides from interrupting the pathway. An unrelated study suggested that the sulphur contained in red meats and alcohol may lead to an increased risk of relapse for patients in remission.

Diagnosis:
The doctor will likely diagnose ulcerative colitis after ruling out other possible causes for your signs and symptoms. To help confirm a diagnosis of ulcerative colitis, he or she may want to have one or more of the following tests and procedures:

*Blood tests.The doctor may suggest blood tests to check for anemia — a condition in which there aren’t enough red blood cells to carry adequate oxygen to the patient’s tissues — or to check for signs of infection.

*Stool sample. White blood cells in  stool can indicate ulcerative colitis. A stool sample can also help rule out other disorders, such as infections caused by bacteria, viruses and parasites.

*Colonoscopy. This exam allows the doctor to view the entire colon using a thin, flexible, lighted tube with an attached camera. During the procedure,the doctor can also take small samples of tissue (biopsy) for laboratory analysis. Sometimes a tissue sample can help confirm a diagnosis.

*Flexible sigmoidoscopy.The doctor uses a slender, flexible, lighted tube to examine the sigmoid, the last portion of the patient’s colon. If the colon is severely inflamed, the doctor may perform this test instead of a full colonoscopy.

*X-ray. If the patient have severe symptoms, the doctor may use a standard X-ray of the abdominal area to rule out serious complications, such as a perforated colon.

*CT scan. A CT scan of your abdomen or pelvis may be performed if the doctor suspects a complication from ulcerative colitis or inflammation of the small intestine. A CT scan may also reveal how much of the colon is inflamed.

Treatment:
Treatment for ulcerative colitis depends on the severity of the disease. Most people are treated with medication. If there is significant bleeding, infection, or complications, surgery may be required to remove the diseased colon. Surgery is the only cure for ulcerative colitis.

Ulcerative colitis may affect patients in different ways, and treatment is adjusted to meet the needs of the specific patient. Emotional and psychological support is also important.

The symptoms of ulcerative colitis come and go. Periods of remission, in which symptoms resolve, may last for months or years before relapsing. Patients and physicians need to decide together whether medications will be continued during remission times. In some patients, it may be the case that the medications keep the disease under control, and stopping them will cause a relapse.

Ulcerative colitis is a lifelong illness and cannot be ignored. Routine medical check-ups are necessary and scheduled colonoscopies are important to monitor the health of the patient and to make certain that the ulcerative colitis is under control and not spreading.

Modern medication:
Ulcerative colitis can be treated with a number of medications including 5-ASA drugs such as sulfasalazine and mesalazine. Corticosteroids such as prednisone can also be used due to their immunosuppressing and short term healing properties, but due to the risks outweighing the benefits, they are not used long term in treatment. Immunosuppressive medications such as azathioprine, and biological agents such as infliximab and adalimumab are given lastly, only if people cannot achieve remission with 5-ASA and corticosteroids, due to their possible risk factors, including, but not limited to increased risk of cancers in teenagers and adults, TB and new or worsening heart failure (these side effects are rare). A formulation of budesonide was approved by the FDA for treatment of active ulcerative colitis in January 2013.The evidence on methotrexate does not show a benefit in producing remission in those with ulcerative colitis.

Alternative medicine and experimental treatment avenues:
About 21% of inflammatory bowel disease patients use alternative treatments. A variety of dietary treatments show promise, but they require further research before they can be recommended.

In vitro research, animal evidence, and limited human study suggest that melatonin may be beneficial.

Dietary fiber, meaning indigestible plant matter, has been recommended for decades in the maintenance of bowel function. Of peculiar note is fiber from brassica, which seems to contain soluble constituents capable of reversing ulcers along the entire human digestive tract before it is cooked. Oatmeal is also commonly prescribed.

Fish oil, and eicosapentaenoic acid (EPA) derived from fish oil, inhibits leukotriene activity, the latter which may be a key factor of inflammation. As an IBD therapy, there are no conclusive studies in support and no recommended dosage. But dosages of EPA between 180 to 1500 mg/day are recommended for other conditions, most commonly cardiac.

Short chain fatty acid (butyrate) enema. The colon utilizes butyrate from the contents of the intestine as an energy source. The amount of butyrate available decreases toward the rectum. Inadequate butyrate levels in the lower intestine have been suggested as a contributing factor for the disease. This might be addressed through butyrate enemas. The results however are not conclusive.

Herbal medications are used by patients with ulcerative colitis. Compounds that contain sulfhydryl may have an effect in ulcerative colitis (under a similar hypothesis that the sulfa moiety of sulfasalazine may have activity in addition to the active 5-ASA component). One randomized control trial evaluated the over-the-counter medication S-methylmethionine and found a significant decreased rate of relapse when the medication was used in conjunction with oral sulfasalazine.

Boswellia is an Ayurvedic (Indian traditional medicine) herb. One study has found its effectiveness similar to sulfasalazine.
helminthic therapy is the use of intestinal parasitic nematodes to treat ulcerative colitis, and is based on the premises of the hygiene hypothesis. Studies have shown that helminths ameliorate and are more effective than daily corticosteroids at blocking chemically induced colitis in mice, and a trial of intentional helminth infection of rhesus monkeys with idiopathic chronic diarrhea (a condition similar to ulcerative colitis in humans) resulted in remission of symptoms in 4 out of 5 of the animals treated. A randomised controlled trial of Trichuris suis ova in humans found the therapy to be safe and effective, and further human trials are currently on going. Yoga and meditation may help a lot.

CLICK TO SEE : Homeopathic treatment of ulcerative colitis

Research:
Helminthic therapy using the whipworm Trichuris suis has been shown in a randomized control trial from Iowa to show benefit in patients with ulcerative colitis. The therapy tests the hygiene hypothesis which argues that the absence of helminths in the colons of patients in the developed world may lead to inflammation. Both helminthic therapy and fecal bacteriotherapy induce a characteristic Th2 white cell response in the diseased areas, which was unexpected given that ulcerative colitis was thought to involve Th2 overproduction.

Alicaforsen is a first generation antisense oligodeoxynucleotide designed to bind specifically to the human ICAM-1 messenger RNA through Watson-Crick base pair interactions in order to subdue expression of ICAM-1. ICAM-1 propagates an inflammatory response promoting the extravasation and activation of leukocytes (white blood cells) into inflamed tissue. Increased expression of ICAM-1 has been observed within the inflamed intestinal mucosa of ulcerative colitis sufferers, where ICAM-1 over production correlated with disease activity. This suggests that ICAM-1 is a potential therapeutic target in the treatment of ulcerative colitis

Prognosis:
Ulcerative colitis is a form of inflammatory bowel disease for which there is no cure. For the first 10 years after diagnosis, the prognosis for most people with ulcerative colitis is good — the rate of colectomy is low, and most patients achieve remission.

Patients with ulcerative colitis usually have an intermittent course, with periods of disease inactivity alternating with “flares” of disease. Patients with proctitis or left-sided colitis usually have a more benign course: only 15% progress proximally with their disease, and up to 20% can have sustained remission in the absence of any therapy. Patients with more extensive disease are less likely to sustain remission, but the rate of remission is independent of the severity of disease.

Other long-term features and Mortality:
Changes that can be seen in chronic ulcerative colitis include granularity, loss of the vascular pattern of the mucosa, loss of haustra, effacement of the ileocecal valve, mucosal bridging, strictures and pseudopolyps.

Research has not revealed any difference in overall risk of dying in patients with Ulcerative colitis from that of the background population. The cause-of-death distribution may be different from that of the background population. It is thought that the disease primarily affects quality of life, and not lifespan.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://www.webmd.com/ibd-crohns-disease/ulcerative-colitis/ulcerative-colitis-topic-overview

http://en.wikipedia.org/wiki/Ulcerative_colitis

http://www.emedicinehealth.com/ulcerative_colitis/page6_em.htm

http://www.mayoclinic.org/diseases-conditions/ulcerative-colitis/basics/treatment/con-20043763

http://ibdcrohns.about.com/od/ucbeyondbasics/f/ulcerative-colitis-prognosis.htm

Xanthoma

Other Names: Skin growths – fatty; Xanthelasma

Description:
A xanthoma, from Greek xanthos, “yellow”, is a deposition of yellowish cholesterol-rich material that can appear anywhere in the body in various disease states.It is a skin condition in which certain fats build up under the surface of the skin. They are cutaneous manifestations of lipidosis in which lipids accumulate in large foam cells within the skin. They are associated with hyperlipidemias, both primary and secondary types.

Tendon xanthomas are associated with type II hyperlipidemia, chronic biliary tract obstruction, and primary biliary cirrhosis. Palmar xanthomata and tuboeruptive xanthomata (over knees and elbows) occur in type III hyperlipidemia.

Types:
Xanthelasma:
A xanthelasma is a sharply demarcated yellowish collection of cholesterol underneath the skin, usually on or around the eyelids. Strictly, a xanthelasma is a distinct condition, only being called a xanthoma when becoming larger and nodular, assuming tumorous proportions. Still, it is often classified simply as a subtype of xanthoma.

Xanthoma tuberosum:
Xanthoma tuberosum (also known as tuberous xanthoma) is characterized by xanthomas located over the joints.

Xanthoma tendinosum:
Xanthoma tendinosum (also tendon xanthoma or tendinous xanthoma) is clinically characterized by papules and nodules found in the tendons of the hands, feet, and heel. Also associated with familial hypercholesterolemia (FH).

Eruptive xanthoma:
Eruptive xanthoma (ILDS E78.220) is clinically characterized by small, yellowish-orange to reddish-brown papules that appear all over the body. It tends to be associated with elevated triglycerides.

Xanthoma planum:
Xanthoma planum (ILDS D76.370), also known as plane xanthoma, is clinically characterized by macules and plaques spread diffusely over large areas of the body.

Palmar xanthoma:
Palmar xanthoma is clinically characterized by yellowish plaques that involve the palms and flexural surfaces of the fingers.[2]:531 Plane xanthomas are characterised by yellowish to orange, flat macules or slightly elevated plaques, often with a central white area which may be localised or generalised. They often arise in the skin folds, especially the palmar creases. They occur in hyperlipoproteinaemia type III and type IIA, and in association with biliary cirrhosis. The presence of palmar xanthomata, like the presence of tendinous xanthomata, is indicative of hypercholesterolaemia.

Tuberoeruptive xanthoma:
Tuberoeruptive xanthoma (ILDS E78.210) is clinically characterized by red papules and nodules that appear inflamed and tend to coalesce.[2]:532 Tuberous xanthomata are considered similar, and within the same disease spectrum as eruptive xanthomata.

Symptoms:
A xanthoma looks like a yellow to orange bump (papule) with defined borders.

Xanthomas are common, especially among older adults and people with high blood lipids.

Xanthomas vary in size. Some are very small. Others are bigger than 3 inches in diameter. They appear anywhere on the body, but are most often seen on the elbows, joints, tendons, knees, hands, feet, or buttocks.

Causes:
Xanthomas may be a sign of a medical condition that involves an increase in blood lipids. Such conditions include:

*Certain cancers
*Diabetes
*Hyperlipidemia
*Inherited metabolic disorders such as familial hypercholesterolemia
*Primary biliary cirrhosis
*Pancreatitis
*Hypothyroidism

Xanthelasma palpebra, a common type of xanthoma that appears on the eyelids and may occur without any underlying medical condition, is not necessarily associated with elevated cholesterol or lipids.

Diagnosis:
Your health care provider will examine the skin. Usually, a diagnosis of xanthoma can be made by looking at your skin. A biopsy of the growth will show a fatty deposit.

You may have blood tests done to check lipid levels, liver function, and for diabetes.

Treatment:
If you have a disease that causes increased blood lipids, treating the condition may help reduce the development of xanthomas.

If the growth bothers you, your doctor may remove it. But xanthomas may come back after surgery.

Prognosis:
The growth is non-cancerous and painless, but may be a sign of another medical condition.

Prevention:
Control of blood lipids, including triglycerides and cholesterol levels, may help reduce development of xanthomas.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://www.nlm.nih.gov/medlineplus/ency/article/001447.htm

http://en.wikipedia.org/wiki/Xanthoma

.

Takotsubo cardiomyopathy

Other Names: Broken-heart syndrome, Transient apical ballooning syndrome, Apical ballooning cardiomyopathy,Stress-induced cardiomyopathy, Gebrochenes-Herz-Syndrom, and Stress cardiomyopathy.
Definition:
Takotsubo cardiomyopathy is a type of non-ischaemic cardiomyopathy in which there is a sudden temporary weakening of the myocardium. Because this weakening can be triggered by emotional stress, It occurs as the response of the heart to sudden, intense emotional stress such as the death of a spouse; rejection at the workplace; acute fear; or uncontrolled anger. These intense emotions can cause immediate breathlessness or strokes. The broken heart can occur simultaneously or a few minutes later. Stress cardiomyopathy is a well-recognized cause of acute heart failure, lethal ventricular arrhythmias, and ventricular rupture.

CLICK & SEE

Around ten years ago, there were a few high profile deaths in young people. They were diagnosed as having died from a “broken heart”. Now, a broken heart or stunned myocardium syndrome is a documented condition.
Symptoms:
Takotsubo cardiomyopathy or Broken heart syndrome symptoms can mimic a heart attack.The symptoms are similar to a heart attack – chest pain, sweating, giddiness or dizziness, nausea, vomiting, weakness and palpitations. Blood pressure may drop. Heart failure may develop.

Any long-lasting or persistent chest pain could be a sign of a heart attack, so it’s important to take it seriously and call your doctor if you experience chest pain.

Causes:
The exact cause of Takotsubo cardiomyopathy is not very clear. It is thought that a surge of stress hormones, such as adrenaline, might temporarily damage the hearts of some people. How these hormones might hurt the heart or whether something else is responsible isn’t completely clear. A temporary constriction of the large or small arteries of the heart may play a role.

Takotsubo cardiomyopathy is often preceded by an intense physical or emotional event. Some potential triggers are:

*News of an unexpected death of a loved one
*A frightening medical diagnosis
*Domestic abuse
*Losing a lot of money
*Natural disasters
*A surprise party
*Having to perform publicly
*Job loss
*Divorce
*Physical stressors, such as an asthma attack, a car accident or major surgery

It’s also possible that some drugs, rarely, may cause broken heart syndrome by causing a surge of stress hormones. Drugs that may contribute to broken heart syndrome include:

*Epinephrine (EpiPen, EpiPen Jr), which is used to treat severe allergic reactions or a severe asthma attack
*Duloxetine (Cymbalta), a medication given to treat nerve problems in people with diabetes, or as a treatment for depression
*Venlafaxine (Effexor XR), which is a treatment for depression
*Levothyroxine (Synthroid, Levoxyl), a drug given to people whose thyroid glands don’t work properly
Differances between Takotsubo cardiomyopathy and hear attack are:

Heart attacks are generally caused by a complete or near complete blockage of a heart artery. This blockage is due to a blood clot forming at the site of narrowing from fatty buildup (atherosclerosis) in the wall of the artery. In Takotsubo cardiomyopathy, the heart arteries are not blocked, although blood flow in the arteries of the heart may be reduced.
Diagnosis:
Takotsubo cardiomyopathy or Transient apical ballooning syndrome is found in 1.7–2.2% of patients presenting with acute coronary syndrome. While the original case studies reported on individuals in Japan, Takotsubo cardiomyopathy has been noted more recently in the United States and Western Europe. It is likely that the syndrome went previously undiagnosed before it was described in detail in the Japanese literature.

The diagnosis of Takotsubo cardiomyopathy may be difficult upon presentation. The ECG findings are often confused with those found during an acute anterior wall myocardial infarction. It classically mimics ST-segment elevation myocardial infarction, and is characterised by acute onset of transient ventricular apical wall motion abnormalities (ballooning) accompanied by chest pain, dyspnea, ST-segment elevation, T-wave inversion or QT-interval prolongation on ECG. Elevation of myocardial enzymes is moderate at worst and there is absence of significant coronary artery disease.

The diagnosis is made by the pathognomonic wall motion abnormalities, in which the base of the left ventricle is contracting normally or is hyperkinetic while the remainder of the left ventricle is akinetic or dyskinetic. This is accompanied by the lack of significant coronary artery disease that would explain the wall motion abnormalities. Although apical ballooning has been classically described as the angiographic manifestation of takotsubo, it has been shown that left ventricular dysfunction in this syndrome includes not only the classic apical ballooning, but also different angiographic morphologies such as mid-ventricular ballooning and rarely local ballooning of other segments.

The ballooning patterns were classified by Shimizu et al. as takotsubo type for apical akinesia and basal hyperkinesia, reverse takotsubo for basal akinesia and apical hyperkinesia, mid-ventricular type for mid-ventricular ballooning accompanied by basal and apical hyperkinesia and localised type for any other segmental left ventricular ballooning with clinical characteristics of takotsubo-like left ventricular dysfunction.

The ECG changes are atypical, with imprecise changes in the ST segment and T waves. They are “suspicious of but non conclusive” of myocardial infraction. Blood tests for the enzyme creatine kinase and proteins troponin should be done. These are elevated in a heart attack. In a stunned heart, these results too are inconclusive. The echocardiogram is the clincher. The heart is ballooned out. This change occurs typically at the apex of the heart. It is important to make a distinction between heart attack and takotsubo as the medication is different.

Treatment:
The treatment for takotsubo is mainly supportive. Medication is given to remove fluid from the lungs and prevent clots. Recovery occurs within a few days.

About two per cent of people who were thought to have a heart attack actually had broken hearts. In the case of women, this increases to seven per cent. Women, mainly menopausal ones (60-75 years), have “broken hearts” eight to nine times more often than men. Some people are genetically prone to “broken hearts.” Depression plays a role in susceptibility to this condition. Recurrences can occur in 10 per cent of people.

People who are in poor physical condition do not need severe emotional stress to suffer a broken heart. An episode may be precipitated by a minor event like rejection, or even a lecture or talk before an audience.

In order to never develop this condition; it is important to develop metal and physical toughness. Walking for 40-60 minutes a day at a brisk pace exposes the heart to small doses of adrenaline and nor adrenaline in a controlled manner. The heart gets conditioned and is immune to sudden chemical surges. Meditation and yoga provide calmness and the mental strength to cope with good days and bad.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://en.wikipedia.org/wiki/Takotsubo_cardiomyopathy

http://www.mayoclinic.org/diseases-conditions/broken-heart-syndrome/basics/causes/con-20034635

http://www.telegraphindia.com/1141208/jsp/knowhow/story_2612.jsp

Nicotiana benthamiana

Botanical Name: Nicotiana benthamiana
Family: Solanaceae
Genus: Nicotiana
Species:N. benthamiana
Kingdom:Plantae
Order: Solanales

Synonyms: Nicotiana suaveolens var. cordifolia

Common indigenous names: Tjuntiwari and Muntju. Tangungnu, Ngkwerlp-pweter, Pinapitilypa, Tjiknga, Munju, Pirnki-warnu, Turlkamula

Habitat :Nicotiana benthamiana is native to Australia.It is found amongst rocks on hills and cliffs throughout the northern regions of Australia.

Description:
Nicotiana benthamiana is an erect, sometimes sprawling, annual herbaceous plant. This short-lived herb will reach from 0.65-5 feet (0.2-1.5 m) tall. Grown in containers, the plants rarely reach over 18 inches (0.45 m) tall by about half as wide. The dark green, broadly ovate leaves will reach up to 4 inches (10 cm) wide by 5 inches (12.7 cm) long. We selected this plant to use for TMV research because it is very susceptible to all kinds of viruses. Plants are easy to grow and we always keep several different ages of plants available at all times.

CLICK & SEE THE PICTURES

Blooming: In the greenhouse, plants flower all year round, but in nature, they normally bloom from May-September. The small, white flowers are 3/8 inch (1 cm) across by 1.5 inches (3.8 cm) long.

A vigorous plant with numerous erect leafy stems. Its alternate leaves are broadly egg-shaped, dull green and soft. Except at the top of the stems, where they are stalkless, its leaves have slender stalks. Flowers are whitish, with a long, slender tube and five blunt lobes; fruits are capsules containing many pitted seeds.

This plant is a close relative of tobacco and species of Nicotiana indigenous to Australia.The plant was used by peoples of Australia as a stimulant – it contains nicotine and other alkaloids – before the introduction of commercial tobacco (N.tabacum and N.rustica). It was first collected on the north coast of Australia by Benjamin Bynoe on a voyage of the H.M.S. Beagle in 1837.

Cultivation:
Nicotiana benthamiana need full sun to partial shade using a well-drained soil mix. In the greenhouse, we use a soil mix consisting of 2 parts peat moss to 1 part loam to 1 part coarse sand or perlite. Since we grow these plants for research, they are given water on a daily basis to keep them stress free. They are fertilized weekly with a balanced fertilizer diluted to 1/2 the strength recommended on the label. Since we have to have these plants for research, once they set seed, plants are discarded. During the winter months, we use supplemental lighting to keep the plants growing strong.

Propagation: Nicotiana benthamiana is best propagated from seed.
Medicinal Uses:
The scientists have shown that transgenic versions of a plant Nicotiana benthamiana, also known as ‘Tjuntiwari’ in the native language, may be able to produce large quantities of a protein griffithsin which can be used as an anti-HIV microbicide gel.The protein has shown capabilities of neutralizing HIV as it binds to the virus molecule in such a way that the virus could not disguise itself from the immune system of humans.

Anti-HIV microbicide gel directly targets entry of the virus and averts infection at the surfaces but at present they are being produced using biologicals like bacteria E.coli, an expensive process which is not cost-effective.

The researchers from USA and UK altered the genetic nature of the plant using a tobacco mosaic virus which produced the protein griffithsin.(Published in The Times Of India)

Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.

Resources:

http://en.wikipedia.org/wiki/Nicotiana_benthamiana

http://www.plantoftheweek.org/week425.shtml

http://biolinfo.org/cmkb/view.php?comname=cmkb_public&scid=412