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Panax ginseng

Botanical Name : Panax ginseng
Family: Araliaceae
Subfamily: Aralioideae
Tribe: Aralieae
Genus: Panax
Species: Panax ginseng
Kingdom: Plantae
Subkingdom: Tracheobionta
Division: Magnoliophyta
Class: Magnoliopsida
Subclass: Rosidae
Order: Apiales

Synonyms : Aralia ginseng. Panax chin-seng. Panax verus.

Common Name : Ginseng, Chinese ginseng

Habitat : Panax ginseng is native to E. Asia – China, Korea.(Manchuria, Chinese Tartary and other parts of eastern Asia, and is largely cultivated there as well as in Korea and Japan.) It grows on mountain forests.
Description:
Panax ginseng is a smooth perennial herb, with a large, fleshy, very slow-growing root, 2 to 3 inches in length (occasionally twice this size) and from 1/2 to 1 inch in thickness. Its main portion is spindle-shaped and heavily annulated (ringed growth), with a roundish summit, often with a slight terminal, projecting point. At the lower end of this straight portion, there is a narrower continuation, turned obliquely outward in the opposite direction and a very small branch is occasionally borne in the fork between the two. Some small rootlets exist upon the lower portion. The color ranges from a pale yellow to a brownish color. It has a mucilaginous sweetness, approaching that of liquorice, accompanied with some degree of bitterness and a slight aromatic warmth, with little or no smell. The stem is simple and erect, about a foot high, bearing three leaves, each divided into five finely-toothed leaflets, and a single, terminal umbel, with a few small, yellowish flowers. It is hardy to zone (UK) 6. The flowers are hermaphrodite (have both male and female organs) The fruit is a cluster of bright red berries.

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Cultivation:
Requires a moist humus rich soil in a shady position in a woodland. Ginseng is widely cultivated and also collected from the wild in the Orient for its root which is commonly used as a medicine. The root is prepared in a number of different ways, including by steaming it for 4 hours in wicker baskets over boiling water.

Propagation :
Seed – sow in a shady position in a cold frame preferably as soon as it is ripe, otherwise as soon as the seed is obtained. It can be very slow and erratic to germinate. Prick out the seedlings into individual pots when they are large enough to handle and grow them on in a shady positi
Edible Uses: ...Root – chewed. This probably refers to its medicinal uses. A tea is made from the root.

Medicinal Uses:
Ginseng was considered for generations to be a panacea by the Chinese and Koreans, although there are some disorders, such as acute inflammatory diseases, for which it is not recommended. It usually is not taken alone, but combined in formulas with other herbs. One of ginseng’s key investigators, Russian I.I. Brekhman, coined the term “adaptogen” to describe ginseng’s ability to regulate many different functions. It can have different responses, depending on what an individual needs. Studies show that ginseng increases mental and physical efficiency and resistance to stress and disease. Psychological improvements were also observed according to Rorschach. Studies done at the Chinese Academy of Medical Science in Beijing, China, showed that the ginsenosides increase protein synthesis and activity of neurotransmitters in the brain. They are also probably responsible for ginseng’s dual role of sedating or stimulating the central nervous system, depending on the condition it is being taken to treat. Studies also show that ginseng improves carbohydrate tolerance in diabetics. When volunteers were given 3 grams of ginseng along with alcohol, their blood alcohol level was 32% to 51% lower than that of the control group.

Ginseng appears to stimulate the immune system of both animals and humans. It revs up the white blood cells (macrophages and natural killer cells) that devour disease-causing microorganisms. Ginseng also spurs production of interferon, the body’s own virus-fighting chemical, and antibodies, which fight bacterial and viral infections. It reduces cholesterol, according to several American studies. It also increases good cholesterol. Ginseng has an anticlotting effect, which reduces the risk of blood clots. It reduces blood sugar levels. Ginseng protects the liver from the harmful effects of drugs, alcohol, and other toxic substances. In a pilot human study, ginseng improved liver function in 24 elderly people suffering from cirrhosis. Ginseng can minimize cell damage from radiation. In two studies, experimental animals were injected with various protective agents, then subjected to doses of radiation similar to those used in cancer radiation therapy. Ginseng provided the best protection against damage to healthy cells, suggesting value during cancer radiation therapy.

Asians have always considered ginseng particularly beneficial for the elderly. As people age, the senses of taste and smell deteriorate, which reduces appetite. In addition, the intestine’s ability to absorb nutrients declines. Ginseng enjoys a reputation as an appetite stimulant and one study showed it increases the ability of the intestine to absorb nutrients, thus helping prevent undernourishment. This is a yin tonic, taken in China for fevers and for exhaustion due to a chronic, wasting disease such as tuberculosis. It can help coughs related to lung weaknessIn the 1960s, a Japanese scientist, Shoji Shibata, at the Meiji College of Pharmacy in Tokyo, identified a unique set of chemicals that are largely responsible for ginseng’s actions. They are saponins, biologically active compounds that foam in water. Ginseng’s unique saponins were dubbed “ginsenosides.”

Research reveals that ginseng can have beneficial effects on metabolic function, immunity, mood, and physiological function at the most basic cellular level. It does not benefit everyone; recent studies of elite athletes reveal that it has no demonstrable effects on athletic performance. Yet in older people, studies show that it reduces fatigue, improves performance, and boosts mood. This makes sense in classic terms because why would world-class athletes, with superior yang energy, want to take a root for people with “devastated ” yang? But if you are recovering from a drawn-out illness, feeling fatigued, or feeling the effects of age’ if you are experiencing a “collapse” of your “chi”, ginseng may be right for you.

As an adaptogenic, ginseng’s action varies. In China, ginseng is best known as a stimulant, tonic herb for athletes and those subject to physical stress, and as a male aphrodisiac. It is also a tonic for old age, and is traditionally taken by people in northern and central China fro late middle age onward, helping them to endure the long hard winters.

Ginseng has been researched in detail over the past 20-30 years in China, Japan, Korea, Russian, and many other countries. Its remarkable “adaptogenic” quality has been confirmed. Trials show that ginseng significantly improves the body’s capacity to cope with hunger, extremes of temperature, and mental and emotional stress. Furthermore, ginseng produces a sedative effect when the body requires sleep. The ginsenosides that are responsible for this action are similar in structure to the body’s own stress hormones. Ginseng also increases immune function and resistance to infection, and supports liver function.

In Asian countries, ginseng has long been recognized as effective n reducing alcohol intoxication and also as a remedy for hangovers. A clinical experiment demonstrated that ginseng significantly enhanced blood alcohol clearance in humans. In regards to cancer, a number of experiments have shown that ginseng can help restore physiological balance within the system and significantly reduce the side effects when used along with anticancer drugs. For diabetes, when patients are treated with ginseng at the early stages, conditions can return to normal. In advanced stages, the blood glucose level is significantly lowered. When combined with insulin, insulin requirements are reduced while still effectively lowering blood glucose level. Other symptoms such as fatigue and decreased sexual desire are also alleviated.

There is some evidence that ginseng, taken in small amounts over a long period of time, improves regulation of the adrenals so that stress hormones are produced rapidly when needed and broken down rapidly when not needed. Whole root is best. Extracts, even those that contain specific guaranteed-potency ginsenosides, don’t have some of the other compounds in ginseng that may be beneficial. Its not recommended to take even good quality extracts for more than 2-3 weeks at a time, but the whole ginseng root, in small amounts can be taken every day for a year or more.

At the Institute of Immunological Science at Hokkaido University in Sapporo, Japan, researchers have been studying a ginsenoside, Rb2. In mice given lung tumors,’ oral administration of ginsenoside Rb2 caused a marked inhibition of both neovascularization and tumor growth,’ they write. Neovascularization, also called angiogenesis, is the tendency of tumors to create tiny blood vessels that feed their malignant growth.

A case-control study in Korea compared about 2,000 patients admitted tot eh Korea Cancer Center Hospital in Seoul to another 2,000 noncancer patients. Those with cancer were about half as likely to use ginseng as those without cancer. Cancer risk was lower with those who took ginseng for a year but much lower for those who took ginseng for up to 20 years. Fresh ginseng, white ginseng extract, white ginseng powder, and red ginseng were all associated with reduced cancer risk.

Known Hazards : Side effects include inability to fall asleep, increase in heart rate and blood pressure. Overuse or prolonged use may cause over stimulation (diarrhoea, nervousness, skin eruption). Caution with other stimulants needed. Avoid in patients with psychosis and manic disorders. Not recommended during pregnancy and breast feeding

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:
https://en.wikipedia.org/wiki/Panax_ginseng
http://www.hardingsginsengfarm.com/botgin.htm
http://www.herbnet.com/Herb%20Uses_FGH.htm
http://www.pfaf.org/user/Plant.aspx?LatinName=Panax+ginseng

Adrenoleukodystrophy

Alternative Names:  Adrenoleukodystrophy; Adrenomyeloneuropathy; Childhood cerebral adrenoleukodystrophy; ALD; Schilder-Addison Complex


Definition:

Adrenoleukodystrophy (ALD),  is a rare, inherited disorder that leads to progressive brain damage, failure of the adrenal glands and eventually death. ALD is a disease in a group of genetic disorders called leukodystrophies. Adrenoleukodystrophy progressively damages the myelin sheath, a complex fatty neural tissue that insulates many nerves of the central and peripheral nervous systems. Without functional myelin, nerves are unable to aid in the conduction of an impulse, which leads to increasing disability.

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Patients with X-linked ALD have defects in the ATP-binding cassette, sub-family D (ALD), member 1 transporter protein, which is encoded by the ABCD1 gene. The ABCD1 (aka ALDP) protein is indirectly involved in the break down of very long-chain fatty acids (VLCFAs) found in the normal diet. Lack of this protein can give rise to an over-accumulation of VLCFAs which can lead to damage to the brain, adrenal gland, and peripheral nervous system.

There are several different types of the disease which can be inherited, but the most common form is an X-linked condition. X-linked ALD primarily affects males, but about one in five women with the disease gene develop some symptoms. Adrenomyeloneuropathy is a less-severe form of ALD, with onset of symptoms occurring in adolescence or adulthood. This form does not include cerebral involvement, and should be included in the differential diagnosis of all males with adrenal insufficiency. Although they share a similar name, X-linked ALD and neonatal adrenoleukodystrophy (NALD), a peroxisome biogenesis disorder, are completely different diseases.

Although this disorder affects the growth and/or development of myelin, leukodystrophies are different from demyelinating disorders such as multiple sclerosis where myelin is formed normally but is lost by immunologic dysfunction or for other reasons.

Causes:

There are several types of ALD, which may be inherited in two different ways, and which can cause different patterns of disease even among people in the same families.

ALD is most commonly inherited as an X-linked condition. This means the abnormal gene is found on the X chromosome.

Because women have two X chromosomes, they have a spare normal gene as well as the abnormal one, so generally only carry the condition (although they may have a mild form of the disease). Men have only one X, so they are affected by the condition.

X-linked ALD may occur in three forms, with onset of symptoms in either childhood or adulthood.

Neonatal ALD is much less common. In this type of ALD the faulty gene isn’t X-linked but is found on one of the other chromosomes. This means both boys and girls can be affected.

Symptoms:
Childhood cerebral type:

•Changes in muscle tone, especially muscle spasms and spasticity
•Crossed eyes (strabismus)
•Decreased understanding of verbal communication (aphasia)
•Deterioration of handwriting
•Difficulty at school
•Difficulty understanding spoken material
•Hearing loss
•Hyperactivity
•Worsening nervous system deterioration
*Coma
*Decreased fine motor control
*Paralysis
•Seizures
•Swallowing difficulties
•Visual impairment or blindness

Adrenomyelopathy:
•Difficulty controlling urination
•Possible worsening muscle weakness or leg stiffness
•Problems with thinking speed and visual memory

.
Adrenal gland failure (Addison type):

•Coma
•Decreased appetite
•Increased skin color (pigmentation)
•Loss of weight, muscle mass (wasting)
•Muscle weakness
•Vomiting

Diagnosis:

The diagnosis is established by clinical findings and the detection of serum very long-chain free fatty acid levels. MRI examination reveals white matter abnormalities, and neuro-imaging findings of this disease are somewhat reminiscent of the findings of multiple sclerosis. Genetic testing for the analysis of the defective gene is available in some centers.

Neonatal screening may become available in the future, which may permit early diagnosis and treatment.

Genetics:

X-linkedX-linked ALD (X-ALD) is the most common form of ALD. In X-ALD, the defective ABCD1 gene resides on the X chromosome (Xq28). The incidence of X-ALD is at least 1 in 20,000 male births.[6] The ABCD1 (“ATP-binding cassette, subfamily D, member 1”) gene was discovered in 1993 and codes for a peroxisome membrane protein necessary for the ?-oxidation of VLCFAs.

X-ALD is characterized by excessive accumulation of very long-chain fatty acids (VLCFA), which are fatty acids with chains of 25–30 carbon atoms. The most common is hexacosanoate, with a 26 carbon skeleton. The elevation in (VLCFA) was originally described by Moser et al. in 1981.[8] The precise mechanisms through which high VLCFA concentrations in affected organs cause the disease is still unknown.

Autosomal
Neonatal adrenoleukodystrophy (NALD) is one of three autosomal dominant disorders which belong to the Zellweger spectrum of peroxisome biogenesis disorders (PBD-ZSD).The other two disorders are Zellweger syndrome (ZS), and infantile Refsum disease (IRD). NALD is most frequently caused by mutations in the PEX1, PEX5, PEX10, PEX13, and PEX26 genes.

Treatment:

There’s no cure for ALD, and the nervous system progressively deteriorates, with death usually occurring between one and ten years after the start of symptoms.

Research suggests that a mixture of oleic acid and euric acid, known as Lorenzo’s oil, may delay or reduce symptoms in boys with X-linked ALD by lowering levels of VLCFAs. The most benefit is seen when the treatment is used before symptoms develop, before irreversible damage has occurred.

Bone marrow transplants have also been used with some success in boys in the early stages of X-linked ALD but are not without considerable risk. Newer treatments that may lower brain levels of VLCFA are being tested. Treatment with docosahexanoic acid (DHA) may help young children with neonatal ALD.

Genetic research has identified the transporter proteins and their faulty genes, starting the path towards gene therapy.

Research directions:
Active clinical trials are currently in progress to determine if the proposed treatments are effective:

*Glyceryl Trioleate (Lorenzo’s oil) for Adrenomyelneuropathy.
*Beta Interferon and Thalidomide  This study is closed.
*Combination of Glyceryl Trierucate and Glyceryl Trioleate (Lorenzo’s Oil) in assymptomatic patients.
*Hematopoietic stem cell transplantation.

Prognosis:
Treatment is symptomatic. Progressive neurological degeneration makes the prognosis generally poor. Death occurs within one to ten years of presentation of symptoms. The use of Lorenzo’s Oil, bone marrow transplant, and gene therapy is currently under investigation.

Possible Complications:
•Adrenal crisis
•Vegetative state (long-term coma)

Prevention:
Genetic counseling is recommended for prospective parents with a family history of X-linked adrenoleukodystrophy. Female carriers can be diagnosed 85% of the time using a very-long-chain fatty acid test and a DNA probe study done by specialized laboratories.

Prenatal diagnosis of X-linked adrenoleukodystrophy is also available. It is done by evaluating cells from chorionic villus sampling or amniocentesis.

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/adrenoleukodystrophy1.shtml
http://en.wikipedia.org/wiki/Adrenoleukodystrophy
http://www.nlm.nih.gov/medlineplus/ency/article/001182.htm

http://health.bwmc.umms.org/imagepages/17277.htm

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Bubble Boy Disease

Other Names: Severe combined immunodeficiency (SCID), or Boy in the Bubble Syndrome, (also known as “Alymphocytosis,” “Glanzmann–Riniker syndrome,” “Severe mixed immunodeficiency syndrome,” and “Thymic alymphoplasia”


Definition:

It is a genetic disorder in which both “arms” (B cells and T cells) of the adaptive immune system are crippled, due to a defect in one of several possible genes. SCID is a severe form of heritable immunodeficiency. It is also known as the “bubble boy” disease because its victims are extremely vulnerable to infectious diseases and some of them, such as David Vetter, become famous for living in a sterile environment.

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David Vetter poses inside of his bubble in his Houston home in this Dec. 17, 1976

The body’s immune system fights against diseases and infections. The SCID syndromes are inherited disorders that result in severe defects in the immune system. White blood cells (which fight infection) are produced in the bone marrow by stem cells. In people with SCID, the bone marrow stem cells are absent or defective. This leaves the affected person open to any and all germs around him because he has no way to fight them off.

Prevalence:-
The most commonly quoted figure for the prevalence of SCID is around 1 in 100,000 births, although this is regarded by some to be an underestimate of the true prevalence; and a figure of about 1 in 65,000 live births has been reported for Australia.

Recent studies indicate that one in every 2,500 children in the Navajo population inherit severe combined immunodeficiency. This condition is a significant cause of illness and death among Navajo children. Ongoing research reveals a similar genetic pattern among the related Apache people.

Types
:-
1. X-linked severe combined immunodeficiency:

Most cases of SCID are due to mutations in the gene encoding the common gamma chain (?c), a protein that is shared by the receptors for interleukins IL-2, IL-4, IL-7, IL-9, IL-15 and IL-21. These interleukins and their receptors are involved in the development and differentiation of T and B cells. Because the common gamma chain is shared by many interleukin receptors, mutations that result in a non-functional common gamma chain cause widespread defects in interleukin signalling. The result is a near complete failure of the immune system to develop and function, with low or absent T cells and NK cells and non-functional B cells.
The common gamma chain is encoded by the gene IL-2 receptor gamma, or IL-2R?, which is located on the X-chromosome. Therefore, immunodeficiency caused by mutations in IL-2R? is known as X-linked severe combined immunodeficiency. The condition is inherited in an X-linked recessive pattern.


2.Adenosine deaminase deficiency:-

The second most common form of SCID after X-SCID is caused by a defective enzyme, adenosine deaminase (ADA), necessary for the breakdown of purines. Lack of ADA causes accumulation of dATP. This metabolite will inhibit the activity of ribonucleotide reductase, the enzyme that reduces ribonucleotides to generate deoxyribonucleotides. The effectiveness of the immune system depends upon lymphocyte proliferation and hence dNTP synthesis. Without functional ribonucleotide reductase, lymphocyte proliferation is inhibited and the immune system is compromised.

3. Omenn syndrome:

The manufacture of immunoglobulins requires recombinase enzymes derived from the recombination activating genes RAG-1 and RAG-2. These enzymes are involved in the first stage of V(D)J recombination, the process by which segments of a B cell or T cell’s DNA are rearranged to create a new T cell receptor or B cell receptor (and, in the B cell’s case, the template for antibodies).Certain mutations of the RAG-1 or RAG-2 genes prevent V(D)J recombination, causing SCID.

4.Bare lymphocyte syndrome:-

MHC class II is not expressed on the cell surface of all antigen presenting cells. Autosomal recessive. The MHC-II gene regulatory proteins are what is altered, not the MHC-II protein itself.

5.JAK3 :-  Janus kinase-3 (JAK3) is an enzyme that mediates transduction downstream of the ?c signal. Mutation of its gene also causes SCID.

6.Artemis/DCLRE1C:-
Mortan Cowan, MD, director of the Pediatric Bone Marrow Transplant Program at the University of California-San Francisco, noted that although researchers have identified about a dozen genes that cause SCID, the Navajo and Apache population has the most severe form of the disorder. This is due to the lack of a gene designated Artemis. Without the gene, children’s bodies are unable to repair DNA or develop disease-fighting cells.


Symptoms:

Chronic diarrhea, ear infections, recurrent Pneumocystis jirovecii pneumonia, and profuse oral candidiasis commonly occur. These babies, if untreated, usually die within 1 year due to severe, recurrent infections. However, treatment options are much improved since David Vetter.


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The list of signs and symptoms mentioned in various sources for SCID includes the 35 symptoms listed below:

Causes
:
Click to see :New Genetic Cause Of Boy In The Bubble Syndrome :

New gene mutation found to cause ‘bubble boy disease’ :


How Gene Defects Cause Disease :


Diagnosis:

Several US states are performing pilot studies to diagnose SCID in newborns through the use of T-cell recombinant excision circles.[citation needed] Wisconsin and Massachusetts (as of February 1, 2009) screen newborns for SCID.

Despite these pilot programs, standard testing for SCID is not currently available in newborns due to the diversity of the genetic defect. Some SCID can be detected by sequencing fetal DNA if a known history of the disease exists. Otherwise, SCID is not diagnosed until about six months of age, usually indicated by recurrent infections. The delay in detection is because newborns carry their mother’s antibodies for the first few weeks of life and SCID babies look normal.

You may click to see :Diagnostic Tests for SCID :

Treatment
:-
The most common treatment for SCID is bone marrow transplantation, which has been successful using either a matched related or unrelated donor, or a half-matched donor, who would be either parent. The half-matched type of transplant is called haploidentical and was perfected by Memorial Sloan Kettering Cancer Center in New York and also Duke University Medical Center which currently does the highest number of these transplants of any center in the world. David Vetter, the original “bubble boy”, had one of the first transplantations but eventually died because of an unscreened virus, Epstein-Barr (tests were not available at the time), in his newly transplanted bone marrow from his sister. Today, transplants done in the first three months of life have a high success rate. Physicians have also had some success with in utero transplants done before the child is born and also by using cord blood which is rich in stem cells.

More recently gene therapy has been attempted as an alternative to the bone marrow transplant. Transduction of the missing gene to hematopoietic stem cells using viral vectors is being tested in ADA SCID and X-linked SCID. In 1990, 12-year-old Ashanthi DeSilva became the first patient to undergo successful gene therapy. Researchers collected samples of Ashanthi’s blood, isolated some of her white blood peripheral T cells, and incorporated into them a virus engineered to contain a healthy immune system enzyme: adenosine deaminase (ADA) gene. These cells were then injected back into her body. She is now given a weekly shot of ADA that without would have her destined for a life of isolation. In 2000, the first gene therapy “success” resulted in SCID patients with a functional immune system. These trials were stopped when it was discovered that two of ten patients in one trial had developed leukemia resulting from the insertion of the gene-carrying retrovirus near an oncogene. In 2007, four of the ten patients have developed leukemias [11]. Work is now focusing on correcting the gene without triggering an oncogene. No leukemia cases have yet been seen in trials of ADA-SCID, which does not involve the gamma c gene that may be oncogenic when expressed by a retrovirus.

Trial treatments of SCID have been gene therapy’s only success; since 1999, gene therapy has restored the immune systems of at least 17 children with two forms (ADA-SCID and X-SCID) of the disorder.

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Drugs and Medications used to treat SCID:
A new hope for gene therapy

Breakthrough for “Bubble Boy” Disease

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/Severe_combined_immunodeficiency#cite_note-Bolognia-0
http://rarediseases.about.com/od/immunedisorders/a/scid.htm
http://www.wrongdiagnosis.com/s/scid/intro.htm

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Bone Marrow ‘Cures AIDS Patient’

A bone marrow transplant using stem cells from a donor with natural genetic resistance to the AIDS virus has left an HIV patient free of infection for nearly two years, German researchers.

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The patient, an American living in Berlin, was infected with the human immunodeficiency virus that causes AIDS and also had leukemia.

The best treatment for the leukemia was a bone marrow transplant, which takes the stem cells from a healthy donor’s immune system to replace the patient’s cancer-ridden cells.

Dr Gero Hutter and Thomas Schneider of the Clinic for Gastroenterology, Infections and Rheumatology of the Berlin Charite hospital said on Wednesday the team sought a bone marrow donor who had a genetic mutation known to help the body resist AIDS infection.

The mutation affects a receptor, a cellular doorway, called CCR5 that the AIDS virus uses to get into the cells it infects.

When they found a donor with the mutation, they used that bone marrow to treat the patient. Not only did the leukemia disappear, but so did the HIV.

“As of today, more than 20 months after the successful transplant, no HIV can be detected in the patient,” the clinic said in a statement. “We performed all tests, not only with blood but also with other reservoirs,” Schneider told a news conference. “But we cannot exclude the possibility that it’s still there.”

The researchers stressed that this would never become a standard treatment for HIV. Bone marrow stem cell transplants are rigorous and dangerous and require the patient to first have his or her own bone marrow completely destroyed.

Patients risk death from even the most minor infections because they have no immune system until the stem cells can grow and replace their own.

HIV has no cure and is always fatal. Cocktails of drugs can keep the virus suppressed, sometimes to undetectable levels. But research shows the virus never disappears — it lurks in so-called reservoirs throughout the body.

Hutter’s team said they have been unable to find any trace of the virus in their 42-year-old patient, who remains unnamed, but that does not mean it is not there. “The virus is tricky. It can always return,” Hutter said.

The CCR5 mutation is found in about 3% of Europeans, the researchers said. They said the study suggests that gene therapy, a highly experimental technology, might someday be used to help treat patients with HIV.

Sources: The Times Of India

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Bromelain

The cochlea and vestibule, viewed from above.Image via Wikipedia

Scientists have used gene therapy on mouse embryos to grow hair cells with the potential to reduce hearing loss in adult animals, according to a study.

The proof-of-concept experiments are a crucial step toward therapies that could one day treat deafness and inner-ear disease in humans, said the study, published in the British journal Nature on Wednesday.

Sensory hair cells inside the cochlea, the auditory portion of the inner ear, convert sound waves into electrical impulses that are delivered to the brain.

The loss of these cells and the neurons they contain is the most common cause of hearing impairment and so-called nerve deafness. At birth, humans have about about 30,000 hair cells, which can be damaged by factors like infections, aging, genetic diseases, loud noise or treatment with certain drugs.

In most cases, damaged hair cells do not regrow in mature humans. But recent research has kindled hope that nerve deafness may one day be curable.

A team of scientists led by John Brigande at the Oregon Health and Science University, in Portland showed that implanting a gene known as Atoh1 into the inner ear of a mouse embryo coaxed non-sensory cells to become hair cells.

Earlier research had pointed to similar results, but this is the first study to show that the cells generated by the gene therapy are functional.

The production of extra, working hair cells in a mouse embryo could be an important step toward using similar therapies in human patients, the study by the researchers in US said.

Sources:The Times Of India

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