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Herbs & Plants

Copal

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Botanical Name: Protium copal
Common Name: Copal, Pom

Habitat :Protium copal is native to Guatemalan in South America, also grows in several places in Africa

Description:
Copal is a name given to tree resin that is particularly identified with the aromatic resins used by the cultures of pre-Columbian Mesoamerica as ceremonially burned incense and other purposes. More generally, the term copal describes resinous substances in an intermediate stage of polymerization and hardening between “gummier” resins and amber. The word copal is derived from the Nahuatl language word copalli, meaning “incense
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To the pre-Columbian Maya and contemporary Maya peoples it is known in the various Mayan languages as pom (or a close variation thereof), although the word itself has been demonstrated to be a loanword to Mayan from Mixe–Zoquean languages.

Copal is still used by a number of indigenous peoples of Mexico and Central America as an incense and during sweat lodge ceremonies.  It is available in different forms. The hard, amber-like yellow copal is a less expensive version. The white copal, a hard, milky, sticky substance, is a more expensive version of the same resin.

Copal was also grown in East Africa, (the common species there being Hymenaea verrucosa) initially feeding an Indian Ocean demand for incense. By the 18th Century, Europeans found it to be a valuable ingredient in making a good wood varnish. It became widely used in the manufacture of furniture and carriages. By the late 19th and early 20th century varnish manufacturers in England and America were using it on train carriages, greatly swelling its demand.

In 1859 Americans consumed 68 percent of the East African trade, which was controlled through the Sultan of Zanzibar, with Germany receiving 24 percent. The American Civil War and the creation of the Suez Canal led to Germany, India and Hong Kong taking the majority by the end of that century.

East Africa apparently had a higher amount of subfossil copal, which is found one or two meters below living copal trees from roots of trees that may have lived thousands of years earlier. This subfossil copal produces a harder varnish. Subfossil copal is also well-known from New Zealand (Kauri gum), Japan, the Dominican Republic, Colombia and Madagascar. It often has inclusions and is sometimes sold as “young amber”. Copal can be easily distinguished from genuine amber by its lighter citrine colour and its surface getting tacky with a drop of acetone or chloroform

Medicinal Uses:
Chickleros who stayed in the bush for months relied on fresh copal resin to treat painful cavities, a piece of resin was stuffed into the cavity and, in a few days, the tooth broke apart and was easily expelled. The bark is scraped, powdered, and applied to wounds, sores, and infections.  Cut a piece of bark 2.5 cm x 15 cm; boil in 3 cups of water for 10 minutes and drink 1 cup before meals for stomach complaints and intestinal parasites.  It is also used as a remedy for fright and dizziness.

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

Resources:
http://belize.com/copal.html
http://www.marc.ucsb.edu/elpilar/features/trail/documents/plants/copal.htm
http://waynesword.palomar.edu/ecoph22.htm
http://en.wikipedia.org/wiki/File:Copal_with_insects_close-up.jpg

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Ailmemts & Remedies

Leigh’s disease

Alternative Name :Subacute Necrotizing Encephalomyelopathy (SNEM)

Definition:
Leigh’s disease is a rare neurometabolic disorder that affects the central nervous system.  This progressive disorder begins in infants between the ages of three months and two years. Rarely, it occurs in teenagers and adults. Leigh’s disease can be caused by mutations in mitochondrial DNA or by deficiencies of an enzyme called pyruvate dehydrogenase. Symptoms of Leigh’s disease usually progress rapidly. The earliest signs may be poor sucking ability,and the loss of head control and motor skills.These symptoms may be accompanied by loss of appetite, vomiting, irritability, continuous crying, and seizures. As the disorder progresses, symptoms may also include generalized weakness, lack of muscle tone, and episodes of lactic acidosis, which can lead to impairment of respiratory and kidney function.
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In Leigh’s disease, genetic mutations in mitochondrial DNA interfere with the energy sources that run cells in an area of the brain that plays a role in motor movements. The primary function of mitochondria is to convert the energy in glucose and fatty acids into a substance called adenosine triphosphate ( ATP). The energy in ATP drives virtually all of a cell’s metabolic functions. Genetic mutations in mitochondrial DNA, therefore, result in a chronic lack of energy in these cells, which in turn affects the central nervous system and causes progressive degeneration of motor functions.
There is also a form of Leigh’s disease (called X-linked Leigh’s disease) which is the result of mutations in a gene that produces another group of substances that are important for cell metabolism. This gene is only found on the X chromosome.

It is named after Denis Archibald Leigh, a British psychiatrist who first described the condition in 1951

Symptoms:
The symptoms of Leigh’s disease usually begin between the ages of 3 months and 2 years. Since the disease affects the central nervous system, symptoms may include:

•poor sucking ability
•difficulty holding up the head
•losing motor skills the infant had such as grasping a rattle and shaking it
•loss of appetite
•vomiting
•irritability
•continuous crying
•seizures
As Leigh’s disease becomes worse over time, the symptoms may include:
•generalized weakness
•lack of muscle tone (hypotonia)
•episodes of lactic acidosis (accumulation of lactic acid in the body and brain) that may impair breathing and kidney function
•heart problems

Causes:
It is an inherited disorder that usually affects infants between the age of three months and two years, but, in rare cases, teenagers and adults as well. In the case of the disease, mutations in mitochondrial DNA (mtDNA) or in nuclear DNA (gene SURF1  and some COX assembly factors) cause degradation of motor skills and eventually death.

Mitochondria are an essential organelle in eukaryotic cells. Their function is to convert the potential energy of glucose, amino acids, and fatty acids into adenosine triphosphate (ATP). Mitochondria carry their own DNA, called mitochondrial DNA [mtDNA]. The information stored in the mtDNA is used to produce several of the enzymes essential to the production of ATP.

Mutations in the mtDNA that cause the mitochondria to fail, to function improperly, a person is at risk for a number of disorders, including Leigh’s disease. In the case of Leigh’s disease, crucial cells in the brain stem have mutated mtDNA, creating poorly functioning mitochondria. This causes a chronic lack of energy in the cells, which, in turn, affects the central nervous system and inhibits motor functions.

Diagnosis:
Diagnosis of Leigh’s disease is based on the symptoms the infant or child has. Tests may show a deficiency of pyruvate dehydrogenase or the presence of lactic acidosis. Individuals with Leigh’s disease may have symmetrical patches of damage in the brain that may be discovered by brain scan. In some individuals, genetic testing may be able to identify the presence of a genetic mutation.

Treatment:
Leigh’s disease is a extremely rare disorder, and there is currently no cure, nor effective treatment. It usually affects infants under two years of age, but, in rarer cases, teenagers and adults as well. A high-fat, low-carbohydrate diet may be recommended. Adults may have puffiness and/or swelling of the eye area and the hands. It is currently treated with thiamin (vitamin B1), but even with treatment, infants rarely live longer than two or three years after the onset of the disease. In cases of older people, the disease takes longer, but is still almost always fatal.

Drug treatments may be needed for epilepsy, movement problems, and cardiac or renal complications.

Prognosis:
The prognosis for individuals with Leigh’s disease is poor. Individuals who lack mitochondrial complex IV activity and those with pyruvate dehydrogenase deficiency tend to have the worst prognosis and die within a few years. Those with partial deficiencies have a better prognosis, and may live to be 6 or 7 years of age. Some have survived to their mid-teenage years.

Resrarch:
The NINDS supports and encourages a broad range of basic and clinical research on neurogenetic disorders such as Leigh’s disease. The goal of this research is to understand what causes these disorders and then to apply these findings to new ways to diagnose, treat, and prevent them.

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.bbc.co.uk/health/physical_health/conditions/leigh1.shtml
http://rarediseases.about.com/od/mitochondrialdiseases/a/leighsdisease.htm
http://www.ninds.nih.gov/disorders/leighsdisease/leighsdisease.htm
http://en.wikipedia.org/wiki/Leigh’s_disease
http://baby-braden.blogspot.com/2008/10/diagnosis-leighs-disease.html

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Ailmemts & Remedies

Hereditary Non-polyposis Colorectal Cancer (HNPCC)

Definition:
HNPCC is an inherited genetic mutation that causes to develop colon, rectal  or bowel cancer.

In people with HNPCC, bowel cancer typically develops at a younger age than non-hereditary bowel cancer – around the ages of 40 to 50 rather than 60 to 70.

Some of the genes (basic units of heredity) that cause HNPCC are known. Nonpolyposis means that colorectal cancer can occur when only a small number of polyps is present (or polyps are not present at all). In HNPCC, colorectal cancer occurs primarily on the right side of the colon (you may see the  diagram). Sometimes other cancers can occur in families with HNPCC. They include cancer of the uterus, ovary, stomach, urinary tract, small bowel, and bile ducts. Other names for HNPCC are Lynch syndrome and cancer family syndrome.
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The gastrointestinal digestive tract is a hollow tube which begins at the mouth and ends at the anus. It has several parts including the esophagus, stomach, small intestine and colon (large intestine). Its total length is about 28 feet. The last 5-6 feet of the intestine is called the colon (large intestine, large bowel). The last 5 or 6 inches of the colon is the rectum. After food is digested, solid wastes move through the colon and rectum to the anus, where they are passed out of the body.

What are Polyps: Polyps are abnormal, mushroom-like growths. When found in the gastrointestinal tract, they occur most commonly inside the colon (large intestine, large bowel). Polyps vary in size from less than one-tenth of an inch to 1-2 inches. They may be so large as to block part of the intestine. In some people polyps may be inherited, while in others they are not inherited. Certain types of polyps can turn into colon cancer or rectal cancer.

HNPCC is also called Lynch syndrome. Henry T. Lynch (professor of medicine at Creighton University Medical Center), characterized the syndrome in 1966. In his earlier work, he described the disease entity as “cancer family syndrome.” The term “Lynch syndrome” was coined in 1984 by other authors, and Lynch himself coined the term HNPCC in 1985. Since then, the two terms have being used interchangeably, until more recent advances in the understanding of the genetics of the disease led to the term HNPCC falling out of favor.

How HNPCC is inherited: People with HNPCC have a 50% chance of passing the HNPCC gene to each of their children (see diagram p. 5). The gene can be passed on even if the parent has had surgery to remove his or her own colon. Individuals who do not inherit the gene cannot pass it to their own children. The vast majority of individuals with HNPCC develop cancer.
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Some individuals with HNPCC do not have an affected parent. These individuals, who are the first to have the condition, are referred to as having a new mutation (newly altered gene). They can, however, pass this HNPCC gene to their children.
In the United States, about 160,000 new cases of colorectal cancer are diagnosed each year. Hereditary nonpolyposis colorectal cancer is responsible for approximately 2 percent to 7 percent of all diagnosed cases of colorectal cancer. The average age of diagnosis of cancer in patients with this syndrome is 44 years old, as compared to 64 years old in people without the syndrome.

Symptoms:–
Symptoms include a change in bowel habit (needing to visit the toilet more frequently, with diarrhoea or constipation), the passage of blood with faeces, weight loss(Unusual and continuing lack of energy), change in appetite, abdominal pain and even an abdominal mass.

It should be emphasized that there is no safety in simply waiting for symptoms to develop. It is vital that persons at risk make every effort to have examinations starting by age 25 or 5 to 10 years before the age of the earliest colorectal cancer diagnosed in the family, even if they do not have symptoms.
Causes and risk factors:-
The genes affected are known as repair genes, which means they normally detect and repair damage in DNA that occurs when DNA is copied during cell division. However, when the genetic mutations are present, mistakes in DNA persist. The faulty DNA accumulates leading to uncontrolled cell growth and hence a risk of cancer.

The genes associated with HNPCC can sometimes cause other cancers, such as stomach, small intestine, liver, gall-bladder, ovary, endometrium (the lining of the womb), kidney, brain, skin and prostate gland.

Diagnosis: –
Persons at risk for HNPCC usually have a family history of two successive generations of colon cancer or at least one generation with colon cancer and one generation with polyps. Men and women at risk for HNPCC need examinations of the entire colon. Women at risk should also have yearly endometrial screening. Two tests, colonoscopy and barium enema, are available to tell whether polyps or cancer is present in the colon. For patients at risk for HNPCC, colonoscopy is the preferred method of screening.

1.Colonoscopy is an examination by means of a flexible, lighted tube, slightly larger in diameter than an enema tube, that is inserted into the colon. Tiny amounts of tissue may be removed from any part of the colon for microscopic study during this procedure. Before a person undergoes a colonoscopy a sedative is given; many persons sleep through the whole procedure and feel little or no discomfort. During this procedure it is sometimes necessary for the doctor to insert some air into the colon. Occasionally, air will cause the same kind of discomfort as a gas pain.

2.Barium enema is a test in which a white liquid called barium is inserted as an enema into the colon. This test allows the colon to be outlined when an x-ray picture is taken. If polyps are present they can be seen on the x-ray. The barium enema feels much like an ordinary enema, causing a feeling of fullness. This test should not be performed on pregnant women because of the risk of x-rays to the fetus.

For both of these tests of the colon, the patient must undergo a preparation before examination. The preparation, which includes a liquid diet and laxatives, clears stool from the colon so that all areas of the colon can be inspected. Exact instructions will be provided by the doctor before the examination.

A blood test for the HNPCC gene will tell at-risk family members if they have inherited the gene mutation identified in the family. However, gene tests do not reveal the presence of polyps or cancer.

Treatment:
If a polyp is found, removal through the colonoscope may be sufficient, although surgery may be recommended for some patients. If cancer is found at examination, the doctor will recommend colon surgery. Removing the entire colon is the only way to completely prevent the development of colon cancer or to treat existing cancer.

Several different operations are currently available for treatment of HNPCC. The three most commonly performed operations are total colectomy with: 1) ileorectal anastomosis, 2) ileoanal pull-through (pouch procedure), or 3) ileostomy. All three operations involve removal of all or most of the colon. After a complete discussion of these operations, the patient and surgeon together can decide which one is best. Women with HNPCC may also consider surgical removal of the uterus, ovaries, and Fallopian tubes.

In some cases, after colon removal, a person may have an ileostomy. An ileostomy is an opening on the abdomen through which stool leaves the body An ileostomy can be temporary or permanent. In most cases it is necessary to wear an appliance called an ileostomy bag to collect body wastes.

An ileostomy should not be considered a handicap, although it is an inconvenience. With proper care, there should be no odor or uncleanliness. Thousands of people of every age and of both sexes have had ileostomy surgery. After surgery, people can be just as busy, successful, and involved in daily routines as before surgery; in fact, they may be more active because of improved health.

However, someone with the abnormal genes can be screened for tumours.

However, someone known to have an abnormal HNPCC gene (or others in the family) can be screened for tumours with regular colonoscopy, gastroscopy and hysteroscopy, so problems may be caught much earlier when treatment is more likely to be effective.

Seven genes have been identified as causing the majority of cases of HNPCC: MSH2, MLH1, PMS1, PMS2, MSH6, TGFBR2 and MLH3. Blood tests may be used to detect them. These genes for HNPCC are inherited in an autosomal dominant pattern, which means that a person has a 50% chance of passing the abnormal gene on to each of their children. However this doesn’t mean a 50% chance of cancer in the child as not all those who inherit the genetic mutation will go on to develop cancer.

Antenatal screening is not usually offered.

Follow up  care after surgery:-
Early diagnosis of HNPCC in many patients has led to early surgery, resulting in prevention or cure of colon cancer and increased life span. However, other complications of this hereditary condition may still occur. For example, individuals with HNPCC appear to be at an increased risk for cancer of the endometrium (uterus), ovary, stomach, urinary tract, small bowel, and bile ducts. If you have had surgery for HNPCC, follow the guidelines below.

Exam guidlines for people with HNPCC aand who have had surgery:–
1.Sigmoidoscopy every year (depending on type of surgery).

2.Annual hemoccult test.

3.Annual physical exam.

4.For women: annual gynecological exam, including endometrial screening with biopsy (consider vacuum curettage or Pipel biopsy).

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

Resource:
http://www.bbc.co.uk/health/physical_health/conditions/hnpcc1.shtml
http://en.wikipedia.org/wiki/Hereditary_nonpolyposis_colorectal_cancer
http://www.macgn.org/cc_hnpcc1.html

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Ailmemts & Remedies Pediatric

Cytomegalovirus

Definition
Cytomegalovirus (say: si-toe-meg-ah-low-vi-russ), or CMV, is a very common virus. It  is a viral genus of the viral group known as Herpesviridae or herpesviruses. It is typically abbreviated as CMV: The species that infects humans it is commonly known as human CMV (HCMV) or human herpesvirus-5 (HHV-5), and is the best studied of all cytomegoloviruses. Within Herpesviridae, CMV belongs to the Betaherpesvirinae subfamily, which also includes the genera Muromegalovirus and Roseolovirus. It is related to other herpesviruses within the subfamilies of Alphaherpesvirinae that includes herpes simplex viruses (HSV)-1 and -2 and varicella-zoster virus (VZV), and the Gammaherpesvirinae subfamily that includes Epstein-Barr virus. All herpesviruses share a characteristic ability to remain latent within the body over long periods. Although they may be found throughout the body, CMV infections are frequently associated with the salivary glands in humans and other mammals. Other CMV viruses are found in several mammal species, but species isolated from animals differ from HCMV in terms of genomic structure, and have not been reported to cause human disease.

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People are usually infected by the time they are 2 years old or during their teenage years and carry the virus for life (usually in a dormant or inactive state). The majority of adults carry the virus by the time they are 40 years of age.

Many people are infected with CMV and don’t even know it because the virus rarely causes symptoms and usually does not cause long-term problems.

However, CMV can cause problems in people who have weak immune systems and in a newborn if the mother gets the infection during pregnancy.

Causes:
CMV gets into body fluids, such as saliva, blood, urine, semen and breast milk. A person is able to transmit (or “shed”) the virus to others only when it is active in his or her system (not dormant). It can be spread from one person to another through sexual contact and contact with blood and other body fluids. CMV can rarely be transmitted by blood transfusion or organ transplantation. In developed countries, blood supplies are screened for CMV when they’re to be used for those at greatest risk from the infection.

 Symptoms:

Usually, CMV does not cause symptoms or only causes mild symptoms. A few people will have symptoms that are similar to mononucleosis. Symptoms of CMV can include:

•Sore throat
•Swollen lymph nodes (lymph glands)
•Fever
•Headache
•Fatigue
•Weakness
•Muscle aches
•Loss of appetite


People who have weakened immune systems due to conditions like human immunodeficiency virus (HIV) or because they received an organ transplant and are taking immunosuppressant medicines may have severe symptoms. (Immunosuppressant medicines are medicines that lower or suppress the immune system.) Symptoms of severe CMV include:
•Blindness
•Pneumonia
•Diarrhea
•Bleeding ulcers in the esophagus (windpipe) or intestines
•Inflammation of the brain (encephalitis)
•Seizures

If a pregnant woman transmits CMV to her unborn baby, miscarriage, stillbirth or death of the newborn may occur. Newborns who survive are at an increased risk for hearing loss and mental retardation. However, only 1% of newborns who are infected with CMV during pregnancy experience problems from the virus. Most are born healthy, or with only mild CMV symptoms.

Who’s affected?
In most cases, CMV is harmless, but for some people infection can have disastrous consequences.

People with weakened immune systems (because of HIV, for example) can suffer serious illness. They may experience high fever for two or three weeks, accompanied by hepatitis and jaundice.

Other serious complications include pneumonia, inflammation of the brain (encephalitis) and blindness as a result of inflammation of the retina at the back of the eye.

CMV remains in the body for life. For those with strong immune systems, it remains inactive. If the immune system is weakened through illness or medical treatments, CMV may be reactivated, causing further medical problems and distress.

If a pregnant woman becomes infected with CMV for the first time, the virus may pass through the placenta and infect her unborn baby. If this happens early in pregnancy, the risk of miscarriage increases, as does the chance of the baby being born with malformations. For example, CMV infection in the womb is the leading cause of congenital deafness.

If the infection is contracted later in pregnancy, stillbirth and premature labour are more likely. A newborn baby may suffer severe illness shortly after birth – jaundice, enlargement of the liver and blood disorders.

Diagnosis:
CMV is diagnosed with a blood test.

CMV is more likey to cause vision problems in people who have weakened immune systems, so if you have conditions such as HIV or AIDS, your doctor may recommend that you visit an eye doctor to find out whether the virus has infected your eyes. Be sure to let your doctor know if you are having any painless blurring of your vision, “floaters” only in one eye, light flashes or areas of blindness. You should also let your doctor(s) know if you are experiencing frequent shortness of breath with flu-like symptoms, or if you are having problems hearing.

Treatment:
For otherwise healthy people, CMV usually doesn’t require treatment. If your immune system is weakened, your doctor may use one of several different medicines to treat CMV infection. However, because CMV is a virus, regular antibiotics won’t work against it. Antiviral drugs are usually prescribed, which slows the virus down (but cannot cure CMV).

If you are pregnant, your doctor may want to test you for CMV to determine if there is a risk for your unborn baby. If you do carry the virus, your doctor may suggest a test called amniocentesis, which collects a sample of the amniotic fluid for testing. It can help determine whether your unborn baby has CMV.

If you are pregnant and your baby has CMV, you doctor will likely check your baby once he or she is born for any problems or birth defects so they can be treated early. Treatable symptoms in newborns include pneumonia, hearing loss and inflammation of the eye.

Prevention:
In child care centers, as many as 70% of children ages 1 to 3 can shed the virus. Careful, frequent hand washing with soap and water may help prevent the spread of CMV.

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.bbc.co.uk/health/physical_health/conditions/cmv1.shtml
http://familydoctor.org/online/famdocen/home/common/infections/common/viral/743.html
http://en.wikipedia.org/wiki/Cytomegalovirus
http://medippt.files.wordpress.com/2010/10/cytomegalovirus.jpg

http://health.allrefer.com/health/cmv-immunocompromised-host-cmv-cytomegalovirus.html

http://archive.microbelibrary.org/ASMOnly/Details.asp?ID=658

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Suppliments our body needs

Zinc

Introduction:

Zinc is a kind of metallic chemical element. It is considered to be a transition metal, similar to nickel and mercury. It has the chemical symbol of ZN with an atomic number of 30. In its pure form it has a kind of light blue color. It tends to be quite brittle at room temperature but, once it is heated, it transforms into something very soft and easy to shape. In fact, it is often added to other metals in order to make them more malleable....CLICK & SEE

People have been using zinc for centuries. The ancient Hindi civilization were the first to find many applications for it. By the 1500s, though, it made its way to Europe via trade. There, it was considered rare and was quite expensive to obtain. Today, however, people have found many zinc sources and it is considered a relatively abundant chemical.

Zinc is used to make metal alloys and is usually an ingredient in making batteries and coins. Zinc oxide, on the other hand, is an ingredient in sun screen. Zinc is also needed by the body. An average person needs 11 mg of zinc ever day; lack of zinc can lead to hair loss and diarrhea. Too much zinc, on the other hand, can cause anemia. Luckily it is possible to get the recommended daily allowance of zinc through food. Some foods that are rich in zinc are seeds and whole grains. However, it is also possible to get zinc supplements, or on the other hand, multi-vitamins that are enriched with zinc.

Dietary supplement:
Zinc is included in most single tablet over-the-counter daily vitamin and mineral supplements. It is believed to possess antioxidant properties, which protect against accelerated aging of the skin and muscles of the body, although studies differ as to its effectiveness. Zinc also helps speed up the healing process after an injury.

The efficacy of zinc compounds when used to reduce the duration or severity of cold symptoms is controversial. Zinc gluconate glycine and zinc acetate are used in throat lozenges or tablets to reduce the duration and the severity of cold symptoms. Preparations include zinc oxide, zinc acetate, and zinc gluconate.

You may click to see : Alternative treatments used for the common cold#Zinc preparations

Zinc preparations can protect against sunburn in the summer and windburn in the winter.[51] Applied thinly to a baby’s diaper area (perineum) with each diaper change, it can protect against diaper rash.

The Age-Related Eye Disease Study determined that zinc can be part of an effective treatment for age-related macular degeneration. Zinc supplementation is an effective treatment for acrodermatitis enteropathica, a genetic disorder affecting zinc absorption that was previously fatal to babies born with it.

Zinc lactate is used in toothpaste to prevent halitosis. Zinc pyrithione is widely applied in shampoos because of its anti-dandruff function Zinc ions are effective antimicrobial agents even at low concentrations. Gastroenteritis is strongly attenuated by ingestion of zinc, and this effect could be due to direct antimicrobial action of the zinc ions in the gastrointestinal tract, or to the absorption of the zinc and re-release from immune cells (all granulocytes secrete zinc), or both

Biological role:
Zinc is an essential trace element, necessary for plants, animals, and microorganisms. Zinc is found in nearly 100 specific enzymes (other sources say 300), serves as structural ions in transcription factors and is stored and transferred in metallothioneins. It is “typically the second most abundant transition metal [ sic ] in organisms” after iron and it is the only metal which appears in all enzyme classes.

In proteins, Zn ions are often coordinated to the amino acid side chains of aspartic acid, glutamic acid, cysteine and histidine. The theoretical and computational description of this zinc binding in proteins (as well as that of other transition metals) is difficult.

There are 2–4 grams of zinc distributed throughout the human body. Most zinc is in the brain, muscle, bones, kidney, and liver, with the highest concentrations in the prostate and parts of the eye. Semen is particularly rich in zinc, which is a key factor in prostate gland function and reproductive organ growth.

In humans, zinc plays “ubiquitous biological roles”. It interacts with “a wide range of organic ligands”, and has roles in the metabolism of RNA and DNA, signal transduction, and gene expression. It also regulates apoptosis. A 2006 study estimated that about 10% of human proteins (2800) potentially bind zinc, in addition to hundreds which transport and traffic zinc; a similar in silico study in the plant Arabidopsis thaliana found 2367 zinc-related proteins.

In the brain, zinc is stored in specific synaptic vesicles by glutamatergic neurons and can “modulate brain excitability”. It plays a key role in synaptic plasticity and so in learning. However it has been called “the brain’s dark horse” since it also can be a neurotoxin, suggesting zinc homeostasis plays a critical role in normal functioning of the brain and central nervous system

Enzymes:
Zinc is a good Lewis acid, making it a useful catalytic agent in hydroxylation and other enzymatic reactions. The metal also has a flexible coordination geometry, which allows proteins using it to rapidly shift conformations to perform biological reactions. Two examples of zinc-containing enzymes are carbonic anhydrase and carboxypeptidase, which are vital to the processes of carbon dioxide (CO2) regulation and digestion of proteins, respectively.
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In vertebrate blood, carbonic anhydrase converts CO2 into bicarbonate and the same enzyme transforms the bicarbonate back into CO2 for exhalation through the lungs. Without this enzyme, this conversion would occur about one million times slower at the normal blood pH of 7 or would require a pH of 10 or more. The non-related ?-carbonic anhydrase is required in plants for leaf formation, the synthesis of indole acetic acid (auxin) and anaerobic respiration (alcoholic fermentation).

Carboxypeptidase cleaves peptide linkages during digestion of proteins. A coordinate covalent bond is formed between the terminal peptide and a C=O group attached to zinc, which gives the carbon a positive charge. This helps to create a hydrophobic pocket on the enzyme near the zinc, which attracts the non-polar part of the protein being digested.

Other proteins:
Zinc serves a purely structural role in zinc fingers, twists and clusters. Zinc fingers form parts of some transcription factors, which are proteins that recognize DNA base sequences during the replication and transcription of DNA. Each of the nine or ten Zn2+ ions in a zinc finger helps maintain the finger’s structure by coordinately binding to four amino acids in the transcription factor. The transcription factor wraps around the DNA helix and uses its fingers to accurately bind to the DNA sequence.

In blood plasma, zinc is bound to and transported by albumin (60%, low-affinity) and transferrin (10%). Since transferrin also transports iron, excessive iron reduces zinc absorption, and vice-versa. A similar reaction occurs with copper. The concentration of zinc in blood plasma stays relatively constant regardless of zinc intake. Cells in the salivary gland, prostate, immune system and intestine use zinc signaling as one way to communicate with other cells.

Zinc may be held in metallothionein reserves within microorganisms or in the intestines or liver of animals.[156] Metallothionein in intestinal cells is capable of adjusting absorption of zinc by 15–40%. However, inadequate or excessive zinc intake can be harmful; excess zinc particularly impairs copper absorption because metallothionein absorbs both metals

Dietary intake
Foods and spices containing zincIn the U.S., the Recommended Dietary Allowance (RDA) is 8 mg/day for women and 11 mg/day for men. Median intake in the U.S. around 2000 was 9 mg/day for women and 14 mg/day in men.[159] Red meats, especially beef, lamb and liver have some of the highest concentrations of zinc in food.

The concentration of zinc in plants varies based on levels of the element in soil. When there is adequate zinc in the soil, the food plants that contain the most zinc are wheat (germ and bran) and various seeds (sesame, poppy, alfalfa, celery, mustard). Zinc is also found in beans, nuts, almonds, whole grains, pumpkin seeds, sunflower seeds and blackcurrant.

Other sources include fortified food and dietary supplements, which come in various forms. A 1998 review concluded that zinc oxide, one of the most common supplements in the United States, and zinc carbonate are nearly insoluble and poorly absorbed in the body. This review cited studies which found low plasma zinc concentrations after zinc oxide and zinc carbonate were consumed compared with those seen after consumption of zinc acetate and sulfate salts. However, harmful excessive supplementation is a problem among the relatively affluent, and should probably not exceed 20 mg/day in healthy people, although the U.S. National Research Council set a Tolerable Upper Intake of 40 mg/day.

For fortification, however, a 2003 review recommended zinc oxide in cereals as cheap, stable, and as easily absorbed as more expensive forms. A 2005 study found that various compounds of zinc, including oxide and sulfate, did not show statistically significant differences in absorption when added as fortificants to maize tortillas. A 1987 study found that zinc picolinate was better absorbed than zinc gluconate or zinc citrate. However, a study published in 2008 determined that zinc glycinate is the best absorbed of the four dietary supplement types available.

Deficiency:
Zinc deficiency is usually due to insufficient dietary intake, but can be associated with malabsorption, acrodermatitis enteropathica, chronic liver disease, chronic renal disease, sickle cell disease, diabetes, malignancy, and other chronic illnesses. Symptoms of mild zinc deficiency are diverse. Clinical outcomes include depressed growth, diarrhea, impotence and delayed sexual maturation, alopecia, eye and skin lesions, impaired appetite, altered cognition, impaired host defense properties, defects in carbohydrate utilization, and reproductive teratogenesis. Mild zinc deficiency depresses immunity, although excessive zinc does also. Animals with a diet deficient in zinc require twice as much food in order to attain the same weight gain as animals given sufficient zinc.

Groups at risk for zinc deficiency include the elderly, vegetarians, and those with renal insufficiency. The zinc chelator phytate, found in seeds and cereal bran, can contribute to zinc malabsorption in those with heavily vegetarian diets. There is a paucity of adequate zinc biomarkers, and the most widely used indicator, plasma zinc, has poor sensitivity and specificity. Diagnosing zinc deficiency is a persistent challenge.

Nearly two billion people in the developing world are deficient in zinc. In children it causes an increase in infection and diarrhea, contributing to the death of about 800,000 children worldwide per year. The World Health Organization advocates zinc supplementation for severe malnutrition and diarrhea. Zinc supplements help prevent disease and reduce mortality, especially among children with low birth weight or stunted growth. However, zinc supplements should not be administered alone, since many in the developing world have several deficiencies, and zinc interacts with other micronutrients.

Zinc deficiency is crop plants’ most common micronutrient deficiency; it is particularly common in high-pH soils. Zinc-deficient soil is cultivated in the cropland of about half of Turkey and India, a third of China, and most of Western Australia, and substantial responses to zinc fertilization have been reported in these areas. Plants that grow in soils that are zinc-deficient are more susceptible to disease. Zinc is primarily added to the soil through the weathering of rocks, but humans have added zinc through fossil fuel combustion, mine waste, phosphate fertilizers, limestone, manure, sewage sludge, and particles from galvanized surfaces. Excess zinc is toxic to plants, although zinc toxicity is far less widespread.

KNOWN HAZARDS:

Toxicity:
Although zinc is an essential requirement for good health, excess zinc can be harmful. Excessive absorption of zinc suppresses copper and iron absorption. The free zinc ion in solution is highly toxic to plants, invertebrates, and even vertebrate fish.[173] The Free Ion Activity Model is well-established in the literature, and shows that just micromolar amounts of the free ion kills some organisms. A recent example showed 6 micromolar killing 93% of all Daphnia in water.

The free zinc ion is a powerful Lewis acid up to the point of being corrosive. Stomach acid contains hydrochloric acid, in which metallic zinc dissolves readily to give corrosive zinc chloride. Swallowing a post-1982 American one cent piece (97.5% zinc) can cause damage to the stomach lining due to the high solubility of the zinc ion in the acidic stomach.

There is evidence of induced copper deficiency at low intakes of 100–300 mg Zn/day; a recent trial had higher hospitalizations for urinary complications compared to placebo among elderly men taking 80 mg/day. The USDA RDA is 15 mg Zn/day. Even lower levels, closer to the RDA, may interfere with the utilization of copper and iron or adversely affect cholesterol. Levels of zinc in excess of 500 ppm in soil interfere with the ability of plants to absorb other essential metals, such as iron and manganese. There is also a condition called the zinc shakes or “zinc chills” that can be induced by the inhalation of freshly formed zinc oxide formed during the welding of galvanized materials.

The U.S. Food and Drug Administration (FDA) has stated that zinc damages nerve receptors in the nose, which can cause anosmia. Reports of anosmia were also observed in the 1930s when zinc preparations were used in a failed attempt to prevent polio infections. On June 16, 2009, the FDA said that consumers should stop using zinc-based intranasal cold products and ordered their removal from store shelves. The FDA said the loss of smell can be life-threatening because people with impaired smell cannot detect leaking gas or smoke and cannot tell if food has spoiled before they eat it. Recent research suggests that the topical antimicrobial zinc pyrithione is a potent heat shock response inducer that may impair genomic integrity with induction of PARP-dependent energy crisis in cultured human keratinocytes and melanocytes.

Poisoning:
In 1982, the United States Mint began minting pennies coated in copper but made primarily of zinc. With the new zinc pennies, there is the potential for zinc toxicosis, which can be fatal. One reported case of chronic ingestion of 425 pennies (over 1 kg of zinc) resulted in death due to gastrointestinal bacterial and fungal sepsis, while another patient, who ingested 12 grams of zinc, only showed lethargy and ataxia (gross lack of coordination of muscle movements). Several other cases have been reported of humans suffering zinc intoxication by the ingestion of zinc coins.

Pennies and other small coins are sometimes ingested by dogs, resulting in the need for medical treatment to remove the foreign body. The zinc content of some coins can cause zinc toxicity, which is commonly fatal in dogs, where it causes a severe hemolytic anemia, and also liver or kidney damage; vomiting and diarrhea are possible symptoms. Zinc is highly toxic in parrots and poisoning can often be fatal. The consumption of fruit juices stored in galvanized cans has resulted in mass parrot poisonings with zinc

You may click to see :Use  Zinc For Cold & Flue
Resources:
http://brainz.org/what-zinc/
http://en.wikipedia.org/wiki/Zinc

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