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).
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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

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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.

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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.

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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

Lupus Nephritis

Alternative Names: Nephritis – lupus; Lupus glomerular disease

Definition:
Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system. Apart from the kidneys, SLE can also damage the skin, joints, nervous system and virtually any organ or system in the body.

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Symptoms:
General symptoms of lupus include malar rash, discoid rash, photosensitivity, oral ulcers, nonerosive arthritis, pleuropericarditis, renal disease, neurological manifestations, and haematological disorders.

Clinically, SLE usually presents with fever, weight loss (100%), arthralgias, synovitis, arthritis (95%), pleuritis, pericarditis (80%), malar facial rash, photodermatosis, alopecia (75%), anaemia, leukopaenia, thrombocytopaenia, and thromboses (50%).

About half of cases of SLE demonstrate signs of lupus nephritis at one time or another. Renal-specific signs include proteinuria (100%), nephrotic syndrome (55%), granular casts (30%), red cell casts (10%), microhematuria (80%), macrohematuria (2%), reduced renal function (60%), RPGN (30%), ARF (2%), hypertension (35%), hyperkalemia (15%) and tubular abnormalities (70%).

The World Health Organization (WHO) developed a system to classify the six different stages of lupus nephritis:

Stage 1: no evidence of lupus nephritis:
In histology, Stage I (minimal mesangial) disease has a normal appearance under light microscopy, but mesangial deposits are visible under electron microscopy. At this stage urinalysis is typically normal.
Stage 2: mildest form, easily treated with corticosteroids:
Stage 2 disease (mesangial proliferative) is noted by mesangial hypercellularity and matrix expansion. Microscopic haematuria with or without proteinuria may be seen. Hypertension, nephrotic syndrome, and acute renal insufficiency are rare at this stage.
Stage 3: earliest stage of advanced lupus. Treatment requires high amounts of corticosteroids. The outlook remains favorable.

Stage 3 disease (focal lupus nephritis) is indicated by sclerotic lesions involving less than 50% of the glomeruli, which can be segmental or global, and active or chronic, with endocapillary or extracapillary proliferative lesions. Under electron microscopy, subendothelial deposits are noted, and some mesangial changes may be present. Immunofluorescence reveals the so-called “Full House” stain, staining positively for IgG, IgA, IgM, C3, and C1q. Clinically, haematuria and proteinuria is present, with or without nephrotic syndrome, hypertension, and elevated serum creatinine.
Diffuse proliferative lupus nephritis; photo shows the classic “flea-bitten” appearance of the cortical surface in the diffuse proliferative glomerulonephritides

Stage 4: advanced stage of lupus.

Stage 4 lupus nephritis (diffuse proliferative) is both the most severe, and the most common subtype. More than 50% of glomeruli are involved. Lesions can be segmental or global, and active or chronic, with endocapillary or extracapillary proliferative lesions. Under electron microscopy, subendothelial deposits are noted, and some mesangial changes may be present. Immunofluorescence reveals the so-called “Full House” stain, staining positively for IgG, IgA, IgM, C3, and C1q. Clinically, haematuria and proteinuria are present, frequently with nephrotic syndrome, hypertension, hypocomplementemia, elevated anti-dsDNA titres and elevated serum creatinine. There is the risk of kidney failure. Patients require high amounts of corticosteroids and immune suppression medications.
A wire-loop lesion may be present in stage III and IV. This is a glomerular capillary loop with subendothelial immune complex deposition that is circumferential around the loop. Stage V is denoted by a uniformly thickened, eosinophilic basement membrane. Stage III and IV are differentiated only by the number of glomeruli involved (which is subject to inherent sample bias), but clinically the presentation and prognosis are both expected to be more severe in stage 4 versus stage 3.
Stage 5:
Stage 5 (membranous lupus nephritis) is characterized by diffuse thickening of the glomerular capillary wall (segmentally or globally), with diffuse membrane thickening, and subepithelial deposits seen under electron microscopy. Clinically, stage V presents with signs of nephrotic syndrome. Microscopic haematuria and hypertension may also been seen. Plasma creatinine is usually normal or slightly elevated, and stage V may not present with any other clinical/serological manifestations of SLE (complement levels may be normal; anti-DNA Ab may not be detectable). Stage 5 also predisposes the affected individual to thrombotic complications such as renal vein thromboses or pulmonary emboli.Excessive protein loss and swelling. Doctors will treat with high amounts of corticosteroids. Doctors may or may not give immune-suppressing drugs.
A final stage is usually included by most practitioners, stage VI, or advanced sclerosing lupus nephritis. It is represented by Global sclerosis involving more than 90% of glomeruli, and represents healing of prior inflammatory injury. Active glomerulonephritis is usually not present. This stage is characterised by slowly progressive renal dysfunction, with relatively bland urine sediment. Response to immunotherapy is usually poor.

A tubuloreticular inclusion is also characteristic of lupus nephritis, and can be seen under electron microscopy in all stages. It is not diagnostic however, as it exists in other conditions. It is thought to be due to chronic interferon exposure.
Causes:
Systemic lupus erythematosus (SLE, or lupus) is an autoimmune disease. This means there is a problem with the body’s immune system.

Normally, the immune system helps protect the body from infection or harmful substances. But in patients with an autoimmune disease, the immune system cannot tell the difference between harmful substances and healthy ones. As a result, the immune system attacks otherwise healthy cells and tissue.

SLE may damage different parts of the kidney, leading to interstitial nephritis, nephrotic syndrome, and membranous GN. It may rapidly worsen to kidney failure.

Lupus nephritis affects approximately 3 out of every 10,000 people. In children with SLE, about half will have some form or degree of kidney involvement.

More than half of patients have not had other symptoms of SLE when they are diagnosed with lupus nephritis.

SLE is most common in women ages 20 – 40.
Diagnosis:
The diagnosis of lupus nephritis depends on blood tests, urinalysis, X-rays, ultrasound scans of the kidneys, and a kidney biopsy. On urinalysis, a nephritic picture is found and RBC casts, RBCs and proteinuria is found.

The World Health Organization has divided lupus nephritis into five stages based on the biopsy. This classification was defined in 1982 and revised in 1995.

* Class I is minimal mesangial glomerulonephritis which is histologically normal on light microscopy but with mesangial deposits on electron microscopy. It constitutes about 5% of cases of lupus nephritis. Renal failure is very rare in this form.[2]

*Class II is based on a finding of mesangial proliferative lupus nephritis. This form typically responds completely to treatment with corticosteroids. It constitutes about 20% of cases.[2] Renal failure is rare in this form.[2]

* Class III is focal proliferative nephritis and often successfully responds to treatment with high doses of corticosteroids. It constitutes about 25% of cases. Renal failure is uncommon in this form.

*Class IV is diffuse proliferative nephritis. This form is mainly treated with corticosteroids and immunosuppressant drugs. It constitutes about 40% of cases. Renal failure is common in this form.

* Class V is membranous nephritis and is characterized by extreme edema and protein loss. It constitutes about 10% of cases.[2] Renal failure is uncommon in this form.

Medicines are prescribed that decrease swelling, lower blood pressure, and decrease inflammation by suppressing the immune system: Patients may need to monitor intake of protein, sodium, and potassium. Patients with severe disease should restrict their sodium intake to 2 grams per day and limit fluid as well. Depending on the histology, renal function and degree of proteinuria, patients may require steroid therapy or chemotherapy regimens such as cyclophosphamide, azathioprine, mycophenolate mofetil, or cyclosporine.
Possible Complications:

*Acute renal failure
*Chronic renal failure
*End-stage renal disease
*Nephrotic syndrome
Treatment:

There is no cure for lupus nephritis. The goal of treatment is to keep the problem from getting worse. Stopping kidney damage early can prevent the need for a kidney transplant.

Treatment can also provide relief from lupus symptoms.

Common treatments include:

*minimizing intake of protein and salt
*taking blood pressure medication
*using steroids to reduce swelling and inflammation
*taking immune-suppression medicines like prednisone to reduce immune system damage to the kidneys

Extensive kidney damage may require additional treatment.

Drug regimens prescribed for lupus nephritis include mycophenolate mofetil (MMF), intravenous cyclophosphamide with corticosteroids, and the immune suppressant azathioprine with corticosteroids. MMF and cyclophosphamide with corticosteroids are equally effective in achieving remission of the disease. MMF is safer than cyclophosphamide with corticosteroids, with less chance of causing ovarian failure, immune problems or hair loss. It also works better than azathioprine with corticosteroids for maintenance therapy.

Prognosis:  How well you do depends on the specific form of lupus nephritis. You may have flare-ups, and then times when you do not have any symptoms.

Some people with this condition develop chronic kidney failure.

Although lupus nephritis may return in a transplanted kidney, it rarely leads to end-stage kidney disease.
Prevention: There is no known prevention for lupus nephritis.

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/Lupus_nephritis

http://www.nlm.nih.gov/medlineplus/ency/article/000481.htm

http://www.healthline.com/health/lupus-nephritis#Diagnosis3

Bone Broth Is A Most Nourishing Food And good For Any Ailment

Bone broth has a long history of medicinal use. It’s known to be warm, soothing, and nourishing for body, mind, and soul.

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Physicians harkening as far back as Hippocrates have associated bone broth with gut healing. And while the importance of gut health is just now starting to fill our medical journals, this knowledge is far from new.

In fact, you could say modern medicine is just now rediscovering how the gut influences health and disease.

Many of our modern diseases appear to be rooted in an unbalanced mix of microorganisms in your digestive system, courtesy of a diet that is too high in sugars and too low in healthful fats and beneficial bacteria.

Digestive problems and joint problems, in particular, can be successfully addressed using bone broth. But as noted by Dr. Kaayla Daniel, vice president of the Weston A. Price Foundation and coauthor (with Sally Fallon Morell) of the book, Nourishing Broth, bone broth is a foundational component of a healing diet regardless of what ails you.

BENEFITS OF BONE BROTH :

Leaky gut is the root of many health problems, especially allergies, autoimmune disorders, and many neurological disorders. The collagen found in bone broth acts like a soothing balm to heal and seal your gut lining, and broth is a foundational component of the Gut and Psychology Syndrome (GAPS) diet, developed by Russian neurologist Dr. Natasha Campbell-McBride.

The GAPS diet is often used to treat children with autism and other disorders rooted in gut dysfunction, but just about anyone with suboptimal gut health can benefit from it.

Bone broth is also a staple remedy for acute illnesses such as cold and flu. While there aren’t many studies done on soup, one study did find that chicken soup opened up the airways better than hot water.

Processed, canned soups  may not work as well as the homemade version made from slow-cooked bone broth. If combating a cold, make the soup hot and spicy with plenty of pepper.

The spices will trigger a sudden release of watery fluids in your mouth, throat, and lungs, which will help thin down the respiratory mucus so it’s easier to expel. Bone broth contains a variety of valuable nutrients in a form your body can easily absorb and use. And these are:

1. Calcium, phosphorus, and other minerals……Components of collagen and cartilage

2.Silicon and other trace minerals………….Components of bone and bone marrow

3.Glucosamine and chondroitin sulfate……….The “conditionally essential” amino acids proline, glycine, and glutamine

These nutrients account for many of the healing benefits of bone broth, which include the following:

1.Reduces joint pain and inflammation, courtesy of chondroitin sulfate, glucosamine, and other compounds extracted from the boiled down cartilage and collagen.

2.Inhibits infection caused by cold and flu viruses etc.
Indeed, Dr. Daniel reports2 chicken soup — known as “Jewish penicillin“—has been revered for its medicinal qualities at least since Moses Maimonides in the 12th century. Recent studies on cartilage, which is found abundantly in homemade broth, show it supports the immune system in a variety of ways; it’s a potent normalizer, true biological response modifier, activator of macrophages, activator of Natural Killer (NK) cells, rouser of B lymphocytes and releaser of Colony Stimulating Factor.

3.Fights inflammation: Amino acids such as glycine, proline, and arginine all have anti-inflammatory effects. Arginine, for example, has been found to be particularly beneficial for the treatment of sepsis3 (whole-body inflammation). Glycine also has calming effects, which may help you sleep better.

4.Promotes strong, healthy bones: Dr. Daniel reports bone broth contains surprisingly low amounts of calcium, magnesium and other trace minerals, but she says “it plays an important role in healthy bone formation because of its abundant collagen. Collagen fibrils provide the latticework for mineral deposition and are the keys to the building of strong and flexible bones.”

5.Promotes healthy hair and nail growth, thanks to the gelatin in the broth. Dr. Daniel reports that by feeding collagen fibrils, broth can even eliminate cellulite too.

In the conclution it can be said :Bone Broth—A Medicinal ‘Soul Food

Slow-simmering bones for a day will create one of the most nutritious and healing foods there is. You can use this broth for soups, stews, or drink it straight. The broth can also be frozen for future use. Making bone broth also allows you to make use of a wide variety of leftovers, making it very economical. Bone broth used to be a dietary staple, as were fermented foods, and the elimination of these foods from our modern diet is largely to blame for our increasingly poor health, and the need for dietary supplements.

“I would like to urge people to make as much broth as possible,” Dr. Daniel says in closing. “Keep that crockpot going; eat a variety of soups, and enjoy them thoroughly.”

Resources: Mercola.com

Lumbar Spondylosis

Definition:
Lumbar Spondylosis is a condition associated with degenerative changes in the intervertebral discs and facet joints. Spondylosis, also known as spinal osteoarthritis, can affect the lumbar, thoracic, and/or the cervical regions of the spine. Although aging is the primary cause, the location and rate of degeneration is individual. As the lumbar discs and associated ligaments undergo aging, the disc spaces frequently narrow. Thickening of the ligaments that surround the disc and those that surround the facet joints develops. These ligamentous thickening may eventually become calcified. Compromise of the spinal canal or of the openings through which the spinal nerves leave the spinal canal can occur.

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Lumbar spondylosis encompasses lumbar disc bulges, herniations, facet joint degeneration, and vertebral bony overgrowths (osteophytes). Degenerative changes, including osteophyte formation, increase with age but are often asymptomatic. Disc herniation is symptomatic when it causes nerve root compression and spinal stenosis. Common symptoms include low back pain, sciatica, and restriction in back movement. Treatment is usually conservative, although surgery is indicated for spinal cord compression or intractable pain. Relapse is common, with patients experiencing episodic back pain.

Symptoms:
Symptoms of lumbar spondylosis follow those associated with each of the various aspects of the disorder: disc herniation, sciatica, spinal stenosis, degenerative spondylolisthesis, and degenerative scoliosis. Pain associated with disc degeneration may be felt locally in the back or at a distance away. This is called referred pain, as the pain is not felt at its site of origin. Lower back arthritis may be felt as pain in the buttock, hips, groin, and thighs. As with spinal stenosis or disc herniation in the lumbar region, it is important to be aware of any bowel or bladder incontinence, or numbness in the perianal area. These signs and symptoms could represent an important massive nerve compression needing surgical intervention (cauda equina syndrome).

Causes:
Spondylosis is mainly caused by ageing. As people age, certain biological and chemical changes cause tissues throughout the body to degenerate. In the spine, the vertebrae (spinal bones) and intervertebral discs degenerate with ageing. the intervertebral discs are cushion like structures that act as shock absorbers between the vertebral bones.

One of the structures that form the discs is known as the annulus fibrosus. The annulus fibrosus is made up of the 60 or more tough circular bands of collagen fiber (called lamellae). Collagen is a type of inelastic fiber. Collagen fibers, along with water and proteoglycans (types of large molecules made of a protein and at least one carbohydrate chain) help to form the soft, gel-like center part of each disk. This soft, center part is known as the nucleus pulposus and is surrounded by the annulus fibrosus.

The degenerative effects of ageing can cause the fibers of the discs to weaken, causing wear and tear. Constant wear and tear and injury to the joints of the vertebrae causes inflammation in the joints. Degeneration of the discs leads to the formation of mineral deposits within the discs. The water content of the center of the disc decreases with age and as a result the discs become hard, stiff, and decreased in size. This, in turn, results in strain on all the surrounding joints and tissues, causing the sensation of stiffness. With less water in the center of the discs, they have decreased shock absorbing qualities. An increased risk of disc herniation also results, which is when the disc abnormally protrudes from its normal position.

Each vertebral body contains four joints that act as hinges. These hinges are known as facet joints or zygapophyseal joints. The job of the facet joins is to allow the spinal column to flex, extend, and rotate. The bones of the facet joints are covered with cartilage (a type of flexible tissue) known as end plates. The job of the end plates is to attach the disks to the vertebrae and to supply nutrients to the disc. When the facet joints degenerate, the size of the end plates can decrease and stiffen. Movement can stimulate pain fibers in the facet joints and annulus fibrosus. Furthermore, the vertebral bone underneath the end plates can become thick and hard.

Degenerative disease can cause ligaments to lose their strength. A ligament is a tough band of tissue that attaches to joint bones. In the spine, ligaments connect spinal structures such as vertebrae and prevent them from moving too much. In degenerative spondylosis, one of the main ligaments (known as the ligamentum flavum) can thicken or buckle, making it weaken.

Knobby, abnormal bone growths (known as bone spurs or osteophytes) can form in the vertebrae. These changes can also cause osteoarthritis. Osteoarthritis is a disease of the joints that is made worse by stress. In more severe cases, these bones spurs can compress nerves coming out of the spinal cord and/or decreased blood supply to the vertebrae. Areas of the body supplied by these nerves may become painful or develop loss of sensation and function.

Carrying around excessive weight can cause lumbar spondylosis. Spending much of the day seated can also be a contributing factor. An injury or trauma to the back can also contribute, as can genetic factors.

The main Risk Factors:
• Age: As a person ages the healing ability of the body decreases and developing arthritis at that time can make the disease progress much faster. Persons over 40 years of age are more prone to developing lumbar spondylosis.

• Obesity: Overweight puts excess load on the joints as the lumbar region carries most of the body’s weight, making a person prone to lumbar spondylosis.

• Sitting for prolonged periods: Sitting in one position for prolonged time which puts pressure on the lumbar vertebrae.

• Prior injury: Trauma makes a person more susceptible to developing lumbar spondylosis.

• Heredity or Family history
Diagnosis:
Physical Examination:
A thorough physical examination reveals much about the patient’s health and general fitness. The physical part of the exam includes a review of the patient’s medical and family history. Often laboratory tests such as complete blood count and urinalysis are ordered. The physical exam may include:

*Palpation (exam by touch) determines spinal abnormalities, areas of tenderness, and muscle spasm.

*Range of Motion measures the degree to which a patient can perform movement of flexion, extension, lateral bending, and spinal rotation.

*A neurologic evaluation assesses the patient’s symptoms including pain, numbness, paresthesias (e.g. tingling), extremity sensation and motor function, muscle spasm, weakness, and bowel/bladder changes. Particular attention may be given to the extremities. Either a CT Scan or MRI study may be required if there is evidence of neurologic dysfunction.

X-rays and Other Tests:
Radiographs (X-rays) may indicate loss of vertebral disc height and the presence of osteophytes, but is not as useful as a CT Scan or MRI. A CT Scan may help reveal bony changes sometimes associated with spondylosis. An MRI is a sensitive imaging tool capable of revealing disc, ligament, and nerve abnormalities. Discography seeks to reproduce the patient’s symptoms to identify the anatomical source of pain. Facet blocks work in a similar manner. Both are considered controversial.

The physician compares the patient’s symptoms to the findings to formulate a diagnosis and treatment plan. The results from the examination provide a baseline from which the physician can monitor and measure the patient’s progress.

Treatment:
Each patient is treated differently for arthritis depending on their individual condition. In the early stages lifestyle modifications or medicines are used for treatment and surgery is needed only if these measures are ineffective.

Yoga:
A few yoga poses and sequences can help lumbar spondylosis. Sun salutations, also known as Surya Namaskar A and B, are good for back strengthening and flexibility. The cobra pose, or Bhjangasana, stretches the lower back. The locust pose, or Shalabhasana, strengthens the lower back because it requires lifting one’s upper and lower body off the ground from a prone position on the floor. Meditation & pranayam 

Exercises:
Physical therapy is often prescribed to relieve problems caused by lumbar spondylosis. Back extensions are used on patients who can tolerate them. The patient lies face down on her stomach and then slowly lifts only her upper body off the floor. The arms may be placed palms down under her chest to take some strain off the back muscles. If lying down is too painful, this exercise can also be done against a wall. The patient puts her hands against a wall, standing about a foot away, and bends back, using a combination of lower back muscles and arms.

Stretches to Avoid:
Lying on the back and bringing the knees into the chest is an example of a common lower back stretch that flexes the spine. This is not recommended for people with lumbar spondylosis. Bending down to touch one’s toes from a standing position is also not recommended. Reaching for the toes while sitting can be problematic, too.

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.ehow.com/about_5039006_lumbar-spondylosis-exercises.html

http://www.physiotherapy-treatment.com/lumbar-spondylosis.html

 

Preventing Kidney Stones May Be Simple

Today, the rates of kidney stones are rising like any other diseas.In most cases, kidney stones pass without causing lasting damage, but the pain during passing can be excruciating. Kidney stones are also sometimes associated with lower back pain, stomach pain, nausea or vomiting, fever, and chills.

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Generally, the larger the stone, the more pain and symptoms it will cause. Sometimes aggressive treatments are needed to clear the stones, and each year, more & more people are going to emergency rooms due to kidney stones.

Once you’ve had them, your risk of recurrence increases. About 35 percent to 50 percent of people will have another bout with kidney stones within five years unless changes are made.Now, What type of changes? According to new guidelines issued by the American College of Physicians (ACP), one of the simplest strategies you can take is to drink more water.
If you Stay Hydrated you Lower Your Risk of Recurrent Kidney Stones:

The number one risk factor for kidney stones is not drinking enough water. If you aren’t drinking enough, your urine will have higher concentrations of substances that can precipitate out and form stones.

Specifically, stone-forming chemicals include calcium, oxalate, urate, cysteine, xanthine, and phosphate. These chemicals should be eliminated in your urine via your kidney, but if too little liquid is present, they can join together to form a stone. According to the National Kidney Foundation:

Urine has various wastes dissolved in it. When there is too much waste in too little liquid, crystals begin to form. The crystals attract other elements and join together to form a solid that will get larger unless it is passed out of the body with the urine… In most people, having enough liquid washes them out or other chemicals in urine stop a stone from forming.”

The new ACP guidelines call for people who have had a kidney stone in the past to increase their fluid intake so they have at least two liters of urine per day, which they say could decrease stone recurrence by at least half.And to achieve this, they recommend increased fluid intake spread throughout the day, pointing out that both water and mineral water are beneficial.

The National Kidney Foundation recommends drinking more than 12 glasses of water a day, but a simpler way to know if you are drinking enough water is to check the color of your urine; you want your urine to be a very light, pale yellow (darker urine is more concentrated).

Every person’s water requirement is different, depending on your particular metabolic requirements and activity level, but simply keeping your urine light yellow will go a long way toward preventing kidney stones.

Remember to increase your water intake whenever you increase your activity and when you’re in a warmer climate. If you happen to be taking any multivitamins or B supplements that contain vitamin B2 (riboflavin), the color of your urine will be a very bright, nearly fluorescent yellow and this will not allow you to use the color of your urine as a guide to how well you are hydrated.

By increasing water intake you will get rid of discomfort like, constipation,prostrate problems etc.

But if it in mind that Water Reduces Risk of kidney stone, but Soda wate or any othar areated water Increases It:

One important point: not just any fluid will do to increase your urine output. While water and mineral water were protective, drinking soda is associated with kidney stones, possibly because the phosphorus acid it contains acidifies your urine, which promotes stone formation.

In addition, one South African study found that drinking soda exacerbates conditions in your urine that lead to formation of calcium oxalate kidney stone problems.6 The sugar, including fructose (and high fructose corn syrup in soda), is also problematic.

A diet high in sugar can set you up for kidney stones, since sugar upsets the mineral relationships in your body by interfering with calcium and magnesium absorption. The consumption of unhealthy sugars and soda by children is a large factor in why children as young as age 5 are now developing kidney stones.

Sugar can also increase kidney size and produce pathological changes in your kidney, such as the formation of kidney stones. According to The National Kidney Foundation, you should pay particular attention to keeping your fructose levels under control:

“Eating too much fructose correlates with increasing risk of developing a kidney stone. Fructose can be found in table sugar and high fructose corn syrup. In some individuals, fructose can be metabolized into oxalate.”

So if you’re a soda drinker, cutting back is an important strategy to remember. In one study, those with kidney stones who eliminated soda from their diet lowered their risk of recurrence by about 15 percent.
Kidney Stones Associated with Increased Risk of Broken Bones:

As mentioned, kidney stones usually pass without any lasting complications, however there are some long-term associated risks. Kidney stones increase your risk of developing chronic kidney disease, for instance, and new research also shows they might be associated with more brittle bones.

Past research has suggested that people with kidney stones have lower bone mineral density. The new study used data from more than 52,000 people and showed that those with kidney stones were at a significantly higher risk of bone fractures. Specifically:

*Men with kidney stones were 10 percent more likely to suffer broken bones than men without

*Male teens with kidney stones had a 55 percent higher fracture risk than those without

*Women with kidneys stones had a 17 percent to 52 percent increased fracture risk depending on age (from their 20s to 60s); those aged 30-39 had the highest risk
Fluoride Also Linked to Kidney Stones:

If you live in area with fluoridated drinking water (such as most of the US), you might be interested to know that high levels of fluoride in water are associated with kidney stones.11 The condition was nearly five times more common in an area with high fluoride (3.5 to 4.9 parts per million, or ppm) than a similar area without high fluoride levels in the water.

Overall, the prevalence of kidney stones in the high-fluoride area was nearly double in those with fluorosis than those without. Dental fluorosis – a condition in which your tooth enamel becomes progressively discolored and mottled – is one of the first signs of over-exposure to fluoride.

Eventually, it can result in badly damaged teeth, and worse… It’s important to realize that dental fluorosis is NOT “just cosmetic.” It can also be an indication that the rest of your body, such as your bones and internal organs, including your brain, has been overexposed to fluoride as well. In other words, if fluoride is having a visually detrimental effect on the surface of your teeth, you can be virtually guaranteed that it’s also damaging other parts of your body, such as your bones. A reverse osmosis water filtration system can remove fluoride from your drinking water.

Exercise, Avoiding Overeating Are Two More Powerful Tools for Preventing Kidney Stones:

You’re more prone to kidney stones if you’re bedridden or very sedentary for a long period of time, partly because limited activity can cause your bones to release more calcium. Exercise will also help you to resolve high blood pressure, a condition that doubles your risk for kidney stones. Even low amounts of exercise may be beneficial to reducing your risk. In a study involving more than 84,000 postmenopausal women, it was found that those who exercised had up to a 31 percent lower risk of kidney stones.13 The link persisted even with only small amounts of physical activity.

Specifically, the research showed a lower risk from three hours a week of walking, four hours of light gardening or just one hour of moderate jogging. You can find my comprehensive exercise recommendations, including how to perform highly recommended high-intensity interval training (HIIT), here. Diet wise, women who ate more than 2,200 calories per day increased their risk of kidney stones by up to 42 percent, while obesity also raised the risk. It should be noted that even though obesity increases kidney stone risk, weight loss surgery that alters your digestive tract actually makes them more common. After weight loss surgery, levels of oxalate are typically much higher (oxalate is the most common type of kidney stone crystal).
Dietary Approaches for Avoiding Kidney Stones:-

1. Make Sure You’re Getting Enough Magnesium

Magnesium is responsible for more than 300 biochemical reactions in your body, and deficiency of this mineral has been linked to kidney stones. An estimated 80 percent of Americans are deficient, so this could be a major factor. Magnesium plays an important role in your body’s absorption and assimilation of calcium, as if you consume too much calcium without adequate magnesium, the excess calcium can actually become toxic and contribute to health conditions like kidney stones.

Magnesium helps prevent calcium from combining with oxalate, which, as mentioned, is the most common type of kidney stone. Green leafy vegetables like spinach and Swiss chard are excellent sources of magnesium, and one of the simplest ways to make sure you’re consuming enough of these is by juicing your vegetables. Vegetable juice is an excellent source of magnesium, as are some beans, nuts like almonds, and seeds, pumpkin seeds, sunflower seeds, and sesame seeds. Avocadoes are also a good source.

2. Eat Calcium-Rich Foods (But Be Careful with Supplements)

In the past, kidney stone sufferers have been warned to avoid foods high in calcium, as calcium is a major component of the majority of kidney stones. However, there is now evidence that avoiding calcium may do more harm than good. The Harvard School of Public Health conducted a study of more than 45,000 men,14 and the men who had diets rich in calcium had a one-third lower risk of kidney stones than those with lower calcium diets. It turns out that a diet rich in calcium actually blocks a chemical action that causes the formation of the stones.

It binds with oxalates (from foods) in your intestine, which then prevents both from being absorbed into your blood and later transferred to your kidneys. So, urinary oxalates may be more important to formation of calcium-oxalate kidney stone crystals than is urinary calcium. It is important to note that it is the calcium from foods that is beneficial — not calcium supplements, which have actually been found to increase your risk of kidney stones by 20 percent.
3. Avoid Non-Fermented Soy:

Soybeans and soy-based foods may promote kidney stones in those prone to them, as they may contain high levels of oxalates, which can bind with calcium in your kidney to form kidney stones. This is just one reason why unfermented soy — the type found in soy milk, soy burgers, soy ice cream, and even tofu — is not a health food. If you were to carefully review the thousands of studies published on soy, I strongly believe you would reach the same conclusion as I have — which is, the risks of consuming unfermented soy products FAR outweigh any possible benefits.

If you’re interested in enjoying the health benefits of soy, choose fermented soy, as after a long fermentation process, the phytate (which blocks your body’s uptake of essential minerals) and anti-nutrient levels of soybeans (including oxalates) are reduced, and their beneficial properties become available to your digestive system.

In the conclution it can be said that the good news is  there’s plenty you can do to reduce your risk of kidney stones.

Sources:Mercola.com

Jute

Botanical Name:Corchorus capsularis
Family: Malvaceae
Subfamily: Grewioideae
Genus:     Corchorus
Kingdom: Plantae
Order:     Malvales

Common Name : Jute
Habitat :Jute is native to tropical and subtropical regions throughout the world.A tropical plant in essence, Jute thrives in hot, humid conditions and in soils that have high levels of sand and clay. It is little wonder then, that the Ganges River Delta is at the centre of global Jute production. This area also encounters heavy rainfall during the monsoon season that further benefits Jute growth and the reliability of a good crop.

Description:
Jute plants are tall, usually annual herbs, reaching a height of 2–4 m, unbranched or with only a few side branches. The leaves are alternate, simple, lanceolate, 5–15 cm long, with an acuminate tip and a finely serrated or lobed margin. The flowers are small (2–3 cm diameter) and yellow, with five petals; the fruit is a many-seeded capsule. It thrives almost anywhere, and can be grown year-round.

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Jute plant has about 40–100 species, including:
Corchorus aestuans
Corchorus capsularis
Corchorus carnarvonensis
Corchorus cunninghamii
Corchorus erodiodes
Corchorus junodi
Corchorus olitorius
Corchorus sidoides
Corchorus tridens
Corchorus walcottii

Cultivation:
Jute needs a plain alluvial soil and standing water. The suitable climate for growing jute (warm and wet) is offered by the monsoon climate, during the monsoon season. Temperatures from 20 degree cent. to 40degree cent. and relative humidity of 70%–80% are favourable for successful cultivation. Jute requires 5–8 cm of rainfall weekly, and more during the sowing time.

Edible Uses:
In Nigeria, leaves of Corchorus olitorius are prepared in sticky soup called ewedu together with ingredients such as sweet potato, dried small fish or shrimp. The leaves are rubbed until foamy or sticky before adding to the soup. The leaves of the Jute plant are widely used in Nigeria to prepare a sticky soup. Amongst the Yoruba of Nigeria, the leaves are called Ewedu, and in the Hausa-speaking northern Nigeria, the leaves are called turgunuwa or lallo. The jute leaves are cut into shreds and added to the soup which would normally contain other ingredients such as meat and/or fish, pepper, onions, and other spices. Likewise, the Lugbara of Northwestern Uganda eat the leaves as soup, locally called pala bi. Jute is also a totem for Ayivu, one of the Lugbara clans.

In the Philippines, especially in Ilocano-dominated areas, this vegetable, locally known as saluyot, can be mixed with either bitter gourd, bamboo shoots, loofah, or sometimes all of them. These have a slimy and slippery texture.

In Bengal the leaf is used and cooked as  jute vegetable called as pat shak.

Chemical Constituents:
Per 100 g, the leaves are reported to contain 43-58 calories, 80.4-84.1 g H2O, 4.5-5.6 g protein, 0.3 g fat, 7.6-12.4 g total carbohydrate, 1.7-2.0 g fiber, 2.4 g ash, 266-366 mg Ca, 97-122 mg P, 7.2-7.7 mg Fe, 12 mg Na, 444 mg K, 6,410-7,850 ug beta-carotene equivalent, 0.13-0.15 mg thiamine, 0.26- 0.53 mg riboflavin, 1.1-1.2 mg niacin, and 53-80 mg ascorbic acid. Leaves contain oxydase and chlorogenic acid. The folic acid content is substantially higher than that of other folacin-rich vegetables, ca 800 micrograins per 100 g (ca 75% moisture) or ca 3200 micrograms on a zero moisture basis (Chen and Saad, 1981).
The seeds contain 11.3-14.8% oil (Watt and Breyer-Brandwijk, 1962), reportedly estrogenic (Sharaf et al, 1979), which contains 16.9% palmitic-, 3.7% stearic-, 1.8% behenic-, 1.1% lignoceiic-, 9.1% oleic-, 62.5% linoleic-, and 0.9% linolenic- acids as well as large portions of B, Mn, Mo, and Zn.

Medicinal Uses:
While perhaps better known as a fiber crop, jute is also a medicinal “vegetable”, eaten from Tanganyika to Egypt. Dried leaves were given me by an Egyptian friend who had brought them with him to this country. They are used in soups under the Arabic name  “Molukhyia.” In India the leaves and tender shoots are eaten. The dried material is there  known as “nalita.” Injections of olitoriside markedly improve cardiac insufficiencies and  have no cumulative attributes; hence, it can serve as a substitute for strophanthin.

Reported to be demulcent, deobstruent, diuretic, lactagogue, purgative, and tonic, tussah  jute is a folk remedy for aches and pains, dysentery, enteritis, fever, dysentery, pectoral  pains, and tumors (Duke and Wain, 1981; List and Horhammer, 1969-1979). Ayurvedics.

The leaves are used for ascites, pain, piles, and tumors. Elsewhere the leaves are used for  cystitis, dysuria, fever, and gonorrhea. The cold infusion is said to restore the appetite and  strength (Source: James A. Duke. 1983. Handbook of Energy Crops.http://www.worldjute.com/jute_news/medijut.html).

Other Uses:
Jute is a long, soft, shiny vegetable fiber that can be spun into coarse, strong threads. It is produced from plants in the genus Corchorus, which was once classified with the family Tiliaceae, more recently with Malvaceae, and has now been reclassified as belonging to the family Sparrmanniaceae. “Jute” is the name of the plant or fiber that is used to make burlap, Hessian or gunny cloth…..click & see

Jute is one of the most affordable natural fibers and is second only to cotton in amount produced and variety of uses of vegetable fibers. Jute fibers are composed primarily of the plant materials cellulose and lignin. It falls into the bast fiber category (fiber collected from bast or skin of the plant) along with kenaf, industrial hemp, flax (linen), ramie, etc. The industrial term for jute fiber is raw jute. The fibers are off-white to brown, and 1–4 metres (3–13 feet) long. Jute is also called “the golden fiber” for its color and high cash value.

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Jute is used in the manufacture of a number of fabrics such as Hessian cloth, sacking, scrim, carpet backing cloth (CBC), and canvas. Hessian, lighter than sacking, is used for bags, wrappers, wall-coverings, upholstery, and home furnishings. Sacking, a fabric made of heavy jute fibers, has its use in the name. CBC made of jute comes in two types. Primary CBC provides a tufting surface, while secondary CBC is bonded onto the primary backing for an overlay. Jute packaging is used as an eco-friendly substitute.

Jute floor coverings consist of woven and tufted and piled carpets. Jute Mats and mattings with 5 / 6 mts width and of continuous length are easily being woven in Southern parts of India, in solid and fancy shades, and in different weaves like, Boucle, Panama, Herringbone, etc. Jute Mats & Rugs are made both through Powerloom & Handloom, in large volume from Kerala, India. The traditional Satranji mat is becoming very popular in home décor. Jute non-wovens and composites can be used for underlay, linoleum substrate, and more.

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Jute has many advantages as a home textile, either replacing cotton or blending with it. It is a strong, durable, color and light-fast fiber. Its UV protection, sound and heat insulation, low thermal conduction and anti-static properties make it a wise choice in home décor. Also, fabrics made of jute fibers are carbon-dioxide neutral and naturally decomposable. These properties are also why jute can be used in high performance technical textiles.

The dry  jute stem is used as fire wood.

As a diversified byproducts from jute can be used in cosmetics,  paints, and other products.

Toxicity:
Contains HCN and several cardiac glycosides. Negm et al (1980) report the LD50 of tissue extracts to mice. The “lethal dose” of Corchoroside A to cats is 0.053-0.0768 mg/kg and Corchoroside B 0.059-0.1413, but some authors say that Corchoroside A is twice as active as Corchoroside B.

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/Jute

http://www.jute-rugs.co.uk/aboutjute.php

http://indianjute.blogspot.in/p/medicinal-use-herbal-use-of-jute-jute.html

http://www.worldjute.com/jute_news/medijut.html