Research in Medicine

cancer fighting nanorobot may be able to target tumors

Could nanorobots be the next big cancer-fighting tool? Researchers from Chonnam National University in Gwangju, South Korea have created so-called “Bacteriobot,” a genetically-modified non-toxic salmonella bacteria that delivers cancer treatments that target tumors.

The bacteria is attracted to chemicals released by cancer cells. The Bacteriobot then goes directly to the tumors and releases the medication stored inside, attacking the problem areas. Traditional cancer treatments often wreak havoc on healthy tissues and other internal organs, so any treatment that can target just the tumors while sparing other tissue is highly sought after.

“First of all, the main feature of Bacteriobot is that the robot has a sensing function to diagnose the cancer, and it’s attacking the cancer itself as it uses the bacteria’s brain while moving toward the tumor region with its flagella,” Park Jong-Oh, director of robot research initiative at Chonnam National University, told Reuters.

Nanorobots in medicine isn’t an entirely new approach. CNET reported that Duke researchers were able to create a nanorobot called a “DNA nanocage” that could hold and release a biomolecule as well.

Source: inagist

Indo-American leads possible treatment for diabetes

In a significant discovery, a team of researchers led by an Indian-American has found that a single gene dysfunction in mice results in developing fasting hypoglycemia, one of the major symptoms of Type 2 diabetes.

The discovery by researchers, led by Prof. Bellur S Prabhakar, focused on a gene MADD for the study and may enable a new potential treatment for diabetes patients.
If MADD is not functioning properly, insulin is not released into the bloodstream to regulate blood sugar levels, said Prabhakar, professor and head of microbiology and immunology at University of Illinois at Chicago.

In previous work, Prabhakar isolated several genes from human beta cells, including MADD, which is also involved in certain cancers. Small genetic variations found among thousands of human subjects revealed that a mutation in MADD was strongly associated with Type 2 diabetes in Europeans and Han Chinese.

People with this mutation had high blood glucose and problems of insulin secretion – the “hallmarks of type 2 diabetes”, Prabhakar said.

But it was unclear how the mutation was causing the symptoms, or whether it caused them on its own or in concert with other genes associated with Type 2 diabetes.

To study the role of MADD in diabetes, Prabhakar and his colleagues developed a mouse model in which the MADD gene was deleted from the insulin-producing beta cells. All such mice had elevated blood glucose levels, which the researchers found was due to insufficient release of insulin.

“We didn’t see any insulin resistance in their cells, but it was clear that the beta cells were not functioning properly,” Prabhakar said.

Examination of the beta cells revealed that they were packed with insulin. “The cells were producing plenty of insulin, they just weren’t secreting it,” he said.

Prabhakar said that the work shows that Type 2 diabetes can be directly caused by the loss of a properly functioning MADD gene alone.

“Without the gene, insulin can’t leave the beta cells, and Blood sugar levels are chronically high,” he said.

In the future, the researchers plan to look into effects of a drug that allows for the secretion of insulin in MADD-deficient beta cells.

“If this drug works to reverse the deficits associated with a defective MADD gene in the beta cells of our model mice, it may have potential for treating people with this mutation who have an insulin-secretion defect and/or type 2 diabetes,” he said.

Type 2 diabetes affects roughly 8 per cent of Americans and over 366 million people worldwide. It can cause serious complications, including cardiovascular disease, kidney failure, loss of limbs and blindness.

Source: The Sen Times

New breakthrough brings Muscular Dystrophy Defect drug closer to reality

Researchers have revealed an atomic-level view of a genetic defect that causes a form of muscular dystrophy, myotonic dystrophy type 2.

The scientists from The Scripps Research Institute have used this information to design drug candidates with potential to counter those defects and reverse the disease.

“This the first time the structure of the RNA defect that causes this disease has been determined,” lead author Matthew Disney said. “Based on these results, we designed compounds that, even in small amounts, significantly improve disease-associated defects in treated cells.”

Myotonic dystrophy type 2 is a relatively rare form of muscular dystrophy that is somewhat milder than myotonic dystrophy type 1, the most common adult-onset form of the disease.

Both types of myotonic dystrophy are inherited disorders that involve progressive muscle wasting and weakness, and both are caused by a type of genetic defect known as a “RNA repeat expansion,” a series of nucleotides repeated more times than normal in an individual’s genetic code.

The repeat binds to the protein MBNL1, rendering it inactive and resulting in RNA splicing abnormalities-which lead to the disease.
Using information about the RNA’s structure and movement, the scientists were able to design molecules to improve RNA function.

The new findings were confirmed using sophisticated computational models that show precisely how the small molecules interact with and alter the RNA structure over time.
Those predictive models matched what the scientists found in the study-that these new compounds bind to the repeat structure in a predictable and easily reproducible way, attacking the cause of the disease.

The study is published in journal ACS Chemical Biology. (ANI)

Source: Yahoo news

Scientists discover new way of overcoming human stem cell rejection

Human embryonic stem cells have the capacity to differentiate into a variety of cell types, making them a valuable source of transplantable tissue for the treatment of numerous diseases, such as Parkinson’s disease and diabetes.

But there’s one major issue: Embryonic stem cells are often rejected by the human immune system.

Now, researchers from the University of California San Diego may have found an effective way to prevent this rejection in humans. Utilizing a novel humanized mouse model, the scientists have revealed a unique combination of immune suppressing molecules that stop the immune system from attacking the injected stem cells – without shutting the system down completely.

This discovery could ultimately help resolve some of the major problems currently limiting the use of embryonic stem cells for certain conditions, paving the way for the development of more effective human stem cell therapies.

“This is a generic way of immune suppression, so it could potentially be applied not just for stem cells therapies, but for organ transplants as well,” Yang Xu, a professor of biology at UC San Diego and lead author of the study, told FoxNews.com. “It can be very broad.”

Embryonic stem cells are different from the other cells in a patient’s body, making them “allogenic.” This means the immune system will recognize them as foreign agents and attack them.

One way of overcoming this rejection problem is to give patients immunosuppressant drugs, which suppress the entire immune system. While short term use of immunosuppressants has been successful for many organ transplants, embryonic stem cell therapies for chronic diseases require long term use of these drugs – which can often be very toxic and increase the risk of cancer.

“In order for the patient to really use this therapy, they have to decide: Do they want a lifelong use of immunosuppressant drugs, or are they willing to live with the symptoms of their disease,” Xu said.

Source: news.nom

Relapse of ‘cured’ HIV patients spurs AIDS science on

Scientists seeking a cure for AIDS say they have been inspired, not crushed, by a major setback in which two HIV positive patients believed to have been cured found the virus re-invading their bodies once more.

True, the news hit hard last month that the so-called “Boston patients” – two men who received bone marrow transplants that appeared to rid them completely of the AIDS-causing virus – had relapsed and gone back onto antiretroviral treatment.

But experts say the disappointment could lay the basis for important leaps forward in the search for a cure.

“It’s a setback for the patients, of course, but an advance for the field because the field has now gained a lot more knowledge,” said Steven Deeks, a professor and HIV expert at the University of California, San Francisco.

He and other experts say the primary practical message is that current tests designed to detect even very low levels of HIV present in the body are simply not sensitive enough.

As well as having the human immunodeficiency virus (HIV), the Boston patients both also had a type of blood cancer called lymphoma, for which they were treated using bone marrow transplants – one man in 2008 and the other in 2010.

They continued taking the antiretroviral AIDS drugs, but eight months after each patient’s transplant, doctors found they could not detect any sign of HIV in their blood.

In the early part of 2013, both patients decided to stop taking their AIDS drugs and both appeared to remain HIV-free – prompting their doctors, Timothy Henrich and Daniel Kuritzkes from Boston’s Brigham and Women’s Hospital, to announce at a conference in July that they may have been cured.

Yet in December came news that one of the men had begun to show signs of an HIV rebound by August, while the second patient had a relapse in November.

Henrich said the virus’ comeback underlined how ingenious HIV can be in finding hiding places in the body to evade attack efforts by the immune system and by drug treatment.

“Through this research we have discovered the HIV reservoir is deeper and more persistent than previously known and that our current standards of probing for HIV may not be sufficient,” he said, adding that both patients were “currently in good health” and back on antiretroviral therapy.

INSPIRATION

Barely a decade ago, few HIV scientists would have dared put the words HIV and cure in the same sentence. Yet some intriguing and inspiring cases in recent years mean many now believe it is just a question of time before a cure is found.

First was the now famous case of Timothy Ray Brown, the so-called “Berlin patient,” whose HIV was eradicated by a complex treatment for leukemia in 2007 involving the destruction of his immune system and a stem cell transplant from a donor with a rare genetic mutation that resists HIV infection.

Such an elaborate, expensive and life-threatening procedure could never be used as a broad-spectrum approach for the world’s 34 million HIV patients. But the results in Brown focused scientific attention on a genetic mutation known as ‘CCR5 delta 32’ as a target for possible gene therapy treatment.

Then last March, French scientists who followed 14 HIV-positive people known as the “Visconti patients”, who were treated very swiftly with HIV drugs but then stopped treatment, said that even after seven years off therapy, they were still showing no signs of the virus rebounding.

That announcement came only weeks after news of the “functional cure” of an HIV-positive baby in Mississippi who received antiretroviral treatment for 18 months from the day she was born. By the time she was two this appeared to have stopped the virus replicating and spreading.

A “functional cure” is when HIV is reduced to such low levels that it is kept at bay even without treatment, though the virus can still be detected in the body.

Sharon Lewin, an HIV expert at Monash University in Australia, said all these developments, as well as the setback suffered by the Boston patients, inspired scientists to investigate many different approaches in the search for a cure.

“We’ve learnt many things here – and one of the most important is that a tiny, tiny amount of virus can get the whole thing going again,” she told Reuters. “It’s a clear message that we need better ways to pick up the virus.”

Scientists are now more convinced than ever that a two-pronged approach which aims to firmly suppress the virus while bolstering the immune system provides the best way forward.

“We need to attack in two ways – reduce the virus to very low levels and also to boost the immune response. We can’t do one without the other,” said Lewin.

“So we still have to think of other creative ways to control HIV. And it’s still early days… before we can say which approach is likely to be the winner.”

Source: orlando sentinel

Vitamin E may slow spread of mild-to-moderate Alzheimer’s disease

Researchers say vitamin E might slow the progression of mild-to-moderate Alzheimer’s disease — the first time any treatment has been shown to alter the course of dementia at that stage.

In a study of more than 600 older veterans, high doses of the vitamin delayed the decline in daily living skills, such as making meals, getting dressed and holding a conversation, by about six months over a two-year period.

The benefit was equivalent to keeping one major skill that otherwise would have been lost, such as being able to bathe without help. For some people, that could mean living independently rather than needing a nursing home.

Vitamin E did not preserve thinking abilities, though, and it did no good for patients who took it with another Alzheimer’s medication. But those taking vitamin E alone required less help from caregivers — about two fewer hours each day than some others in the study.

“It’s not a miracle or, obviously, a cure,” said study leader Dr. Maurice Dysken of the Minneapolis VA Health Care System. “The best we can do at this point is slow down the rate of progression.”

The U.S. Department of Veterans Affairs sponsored the study, published Tuesday by the Journal of the American Medical Association.

No one should rush out and buy vitamin E, several doctors warned. It failed to prevent healthy people from developing dementia or to help those with mild impairment (“pre-Alzheimer’s”) in other studies, and one suggested it might even be harmful.

Still, many experts cheered the new results after so many recent flops of once-promising drugs.

“This is truly a breakthrough paper and constitutes what we have been working toward for nearly three decades: the first truly disease-modifying intervention for Alzheimer’s,” said Dr. Sam Gandy of Mount Sinai School of Medicine in New York. “I am very enthusiastic about the results.”

About 35 million people worldwide have dementia, and Alzheimer’s is the most common type. In the U.S., about 5 million have Alzheimer’s. There is no cure and current medicines just temporarily ease symptoms.

Researchers don’t know how vitamin E might help, but it is an antioxidant, like those found in red wine, grapes and some teas. Antioxidants help protect cells from damage that can contribute to other diseases, says the federal Office on Dietary Supplements. Many foods contain vitamin E, such as nuts, seeds, grains, leafy greens and vegetable oils. There are many forms, and the study tested a synthetic version of one — alpha-tocopherol — at a pharmaceutical grade and strength, 2,000 international units a day.

Years ago, another study found that the same form and dose helped people with more advanced Alzheimer’s, and many were prescribed it. But vitamin E fell out of favor after a 2005 analysis of many studies found that those taking more than 400 units a day were more likely to die of any cause.

The new study involved 613 veterans, nearly all male, 79 years old on average, with mild to moderate Alzheimer’s, at 14 VA centers. All were already taking Aricept, Razadyne or Exelon — widely used, similar dementia medicines.

Participants were placed in four groups and given either vitamin E, another dementia medicine called memantine (its brand name is Namenda), both pills or dummy pills.

After a little more than two years of follow-up, those on vitamin E alone had a 19 percent lower annual rate of decline in daily living skills compared to the placebo group. Memantine made no difference, and vitamin E did not affect several tests of thinking skills.

“It’s a subtle effect but it’s probably real,” Dr. Ron Petersen, the Mayo Clinic’s Alzheimer’s research chief, said of the benefit on daily living from vitamin E. “That has to be weighed against the potential risks” seen in earlier studies, he said.

Heather Snyder, director of medical and scientific operations for the Alzheimer’s Association, said the group’s position is that “no one should take vitamin E for Alzheimer’s disease or other memory issues except under the supervision of a physician,” because it can interfere with blood thinners, cholesterol drugs and other medicines.

The new results also need to be verified in a fresh study that includes more women and minorities, she said.

Source: fox news

Scientists use drug to repair a rare birth defect

University of British Columbia and Vancouver Coastal Health scientists have developed a potential cure for a rare eye disease, showing for the first time that a drug can repair a birth defect.

They formulated the drug Ataluren into eye drops, and found that it consistently restored normal vision in mice who had aniridia, a condition that severely limits the vision of about 5,000 people in North America. A small clinical trial with children and teens is expected to begin next year in Vancouver, the US and the UK.

Aniridia is caused by the presence of a “nonsense mutation” – an extra “stop sign” on the gene that interrupts production of a protein crucial for eye development. Aniridia patients don’t have an iris (the coloured ring around the pupil), and suffer many other eye abnormalities.

Ataluren is believed to have the power to override the extra stop sign, thus allowing the protein to be made. The UBC-VCH scientists initially thought the drug would work only in utero – giving it to a pregnant mother to prevent aniridia from ever arising in her foetus. But then they gave their specially formulated Ataluren eye drops, which they call START, to two-week-old mice with aniridia, and found that it actually reversed the damage they had been born with.

“We were amazed to see how malleable the eye is after birth,” said Cheryl Gregory-Evans, associate professor of ophthalmology and visual sciences and a neurobiologist at the Vancouver Coastal Health Research Institute. “This holds promise for treating other eye conditions caused by nonsense mutations, including some types of macular degeneration. And if it reverses damage in the eye, it raises the possibility of a cure for other congenital disorders. The challenge is getting it to the right place at the right time.”

Bad vision at birth, worse vision later: Aniridia is apparent at birth because of the missing iris. Toddlers with aniridia need eyeglasses to see, sunglasses or darkened contact lenses to protect their eyes from overexposure to light, and cannot read small text. Their eyes are continually moving, making it difficult for them to focus, and have higher internal pressure (glaucoma), which damages the optic nerve as they get older. They are also prone to corneal damage in their teens and early adulthood. Eventually, most people with aniridia are considered legally blind, and must resort to Braille or expensive electronic aids to read.

An eye affected with aniridia on the bottom compared to an unaffected eye.

The plasticity of the eye: The reversal of tissue damage in young mice, published by the Journal of Clinical Investigation, fits with the fact that mammals’ eyes aren’t fully formed at birth. Human babies don’t discern colours until they are six months old, and their depth perception isn’t fully developed until the age of five.

Nonsense suppressor: Ataluren, made by the New Jersey-based PTC Therapeutics, is thought to be a “nonsense suppressor” – it silences the extra “stop codon” on the gene and allows a complete protein to be assembled. The drug is currently being tested as a treatment for cystic fibrosis and Duchenne muscular dystrophy, which are also caused by nonsense mutations.

Clinical trial: The forthcoming clinical trial, involving about 30 patients, will be led by Gregory-Evans in Vancouver, and is being supported by the Vision for Tomorrow Foundation, a US-based charity focused on aniridia and albinism (an absence of pigmentation in skin, hair and eyes that results in poor vision). If START is proven to be safe and effective, children with aniridia would use the drops twice a day for the rest of their lives. The drug would probably not reverse the condition in adults because their eyes would already be damaged beyond repair.

A gritty solution: Gregory-Evans’ first attempt at creating Ataluren eye drops proved unsuccessful. The drug didn’t dissolve, and thus irritated the mice’s eyes. So she turned to Kishor Wasan, a professor and associate dean in the Faculty of Pharmaceutical Sciences, who ground the drug into a very fine powder and combined it with a solution that adhered better to the eye.

A multidisciplinary team: Gregory-Evans also collaborated with her husband, Kevin Gregory-Evans, the Julia Levy BC Leadership Chair in Macular Research and an ophthalmologist at the VCH Eye Care Centre, who treats BC patients with aniridia. He administered the vision tests for the mice used in the study.

Funding from a UBC alumna: Cheryl Gregory-Evans’ position and this research were funded by the Sharon Stewart Testamentary Trust. Stewart, of Victoria, was born with aniridia, and at the time of her graduation from UBC in 1968, she only had five per cent of her vision. She died in 2008 and donated over $6 million to UBC for aniridia research.

Source; India Medical Times

 

Science Confirms Turmeric As Effective As 14 Drugs

 

Turmeric is one the most thoroughly researched plants in existence today. Its medicinal properties and components (primarily curcumin) have been the subject of over 5600 peer-reviewed and published biomedical studies. In fact, our five-year long research project on this sacred plant has revealed over 600 potential preventive and therapeutic applications, as well as 175 distinct beneficial physiological effects.

This entire database of 1,585 ncbi-hyperlinked turmeric abstracts can be downloaded as a PDF at our Downloadable Turmeric Document page, and acquired either as a retail item or with 200 GMI-tokens, for those of you who are already are members and receive them automatically each month.

Given the sheer density of research performed on this remarkable spice, it is no wonder that a growing number of studies have concluded that it compares favorably to a variety of conventional medications, including:

Lipitor/Atorvastatin(cholesterol medication): A 2008 study published in the journal Drugs in R & D found that a standardized preparation of curcuminoids from Turmeric compared favorably to the drug atorvastatin (trade name Lipitor) on endothelial dysfunction, the underlying pathology of the blood vessels that drives atherosclerosis, in association with reductions in inflammation and oxidative stress in type 2 diabetic patients.

Corticosteroids (steroid medications): A 1999 study published in the journal Phytotherapy Research found that the primary polyphenol in turmeric, the saffron colored pigment known as curcumin, compared favorably to steroids in the management of chronic anterior uveitis, an inflammatory eye disease.

A 2008 study published in Critical Care Medicine found that curcumin compared favorably to the corticosteroid drug dexamethasone in the animal model as an alternative therapy for protecting lung transplantation-associated injury by down-regulating inflammatory genes.

An earlier 2003 study published in Cancer Letters found the same drug also compared favorably to dexamethasone in a lung ischaemia-repurfusion injury model.
Prozac/Fluoxetine & Imipramine (antidepressants): A 2011 study published in the journal Acta Poloniae Pharmaceutica found that curcumin compared favorably to both drugs in reducing depressive behavior in an animal model.
Aspirin (blood thinner): A 1986 in vitro and ex vivo study published in the journal Arzneimittelforschung found that curcumin has anti-platelet and prostacyclin modulating effects compared to aspirin, indicating it may have value in patients prone to vascular thrombosis and requiring anti-arthritis therapy.
Anti-inflammatory Drugs: A 2004 study published in the journal Oncogene found that curcumin (as well as resveratrol) were effective alternatives to the drugs aspirin, ibuprofen, sulindac, phenylbutazone, naproxen, indomethacin, diclofenac, dexamethasone, celecoxib, and tamoxifen in exerting anti-inflammatory and anti-proliferative activity against tumor cells.
Oxaliplatin (chemotherapy drug): A 2007 study published in the International Journal of Cancer found that curcumin compares favorably with oxaliplatin as an antiproliferative agenet in colorectal cell lines.
Metformin (diabetes drug): A 2009 study published in the journal Biochemitry and Biophysical Research Community explored how curcumin might be valuable in treating diabetes, finding that it activates AMPK (which increases glucose uptake) and suppresses gluconeogenic gene expression (which suppresses glucose production in the liver) in hepatoma cells. Interestingly, they found curcumin to be 500 times to 100,000 times (in the form known as tetrahydrocurcuminoids(THC)) more potent than metformin in activating AMPK and its downstream target acetyl-CoA carboxylase (ACC).

Another way in which turmeric and its components reveal their remarkable therapeutic properties is in research on drug resistant- and multi-drug resistant cancers. We have two sections on our site dedicated to researching natural and integrative therapies on these topics, and while there are dozens of substances with demonstrable efficacy against these chemotherapy- and radiation-resistant cancers, curcumin tops both lists:

Source: True Activist

New genetic clues for rheumatoid arthritis ‘cure’

An international team of researchers has found more than 40 new areas in DNA that increase the risk of rheumatoid arthritis.

The work is the largest genetic study ever carried out, involving nearly 30,000 patients.

The investigators believe new drugs could be developed to target these areas that could one day provide a cure for the disease.

The findings are published in the Journal Nature.

The research team compared the DNA of arthritis patients with those without the disease and found 42 ‘faulty’ areas that were linked with the disease. The hope is that drugs can be developed to compensate for these faults.

The lead researcher Professor Robert Plenge of Harvard Medical School found that one of these areas produced a weakness that was treated by an existing drug that was developed by trial and error, rather than specifically made to correct the genetic problem.

This finding, he says, shows such discoveries could be used to design new drugs.

“What this offers in the future is an opportunity to use genetics to discover new medicines for complex diseases like rheumatoid arthritis to treat or even cure the disease,” he said.

Complex diseases
Some have argued identifying genetic weak areas for complex diseases – known as single nucleotide polymorphisms (SNPs) – is not useful. There is little or no evidence, they argue, that “silencing the SNPs” with drugs will relieve any symptoms.

But Dr Plenge says the fact that he has found an established drug that treats the symptoms that arise from a particular SNP for rheumatoid arthritis validates this genetic approach.

“It offers tremendous potential. This approach could be used to identify drug targets for complex diseases, nut just rheumatoid arthritis, but diabetes, Alzheimer’s and coronary heart disease”

Fast track
The study also found SNPs in the rheumatoid arthritis patients that also occur in patients with types of blood cancer.

According to Prof Jane Worthington, director of the centre for genetics in Manchester, this observation suggests that drugs that are being used to treat the cancer could be effective against rheumatoid arthritis and so should be fast tracked into clinical trials.

“There are already therapies that have been designed in the cancer field that might open up new opportunities for retargeting drugs,” she told BBC News.

“It might allow us a straightforward way to add therapies we have to treat patients with rheumatoid arthritis”.

Source: escience

New genetic marker to predict bird flu severity

Australian scientists Tuesday said they have discovered a genetic marker that can accurately predict the severity of the H7N9 avian influenza.

Researchers at the University of Melbourne claimed that by using genetic markers to blood and lung samples, they discovered certain indicators that signal increased susceptibility to this avian influenza, a statement said.

Katherine Kedzierska, associate professor at the department of microbiology and immunology at the university, said that being able to predict which patient will be more susceptible to the emerging avian influenza strain will allow experts to better manage the disease.

“Higher than normal levels of cytokines (a type of protein), driven by a genetic variant of a protein called IFITM3, tells us that the severe disease is likely,” Kedzierska said.

“We call this a Cytokine Storm and people with the defective genetic variant of the protein IFITM3 are more likely to succumb to severe influenza infection,” she added.

Peter Doherty, a lead author of the study, said predicting how avian influenza works in individuals has implications for the management of disease and the resources on our health system.

Source: Business Standard