Miracles of God are never limited and can be discovered in the most eccentric of ways. Such is the case of the mystery healing of asthmatics in Hyderabad, a city in India. The weirdness is to an extent of absurdity whereby the patient is made to swallow a live sardine wrapped in a yellow herbal paste.

As funny as it sounds, it is a practice that has been followed for nearly a century now, by a single family named Goud. They are the only trustees of this medicine, and have not commercialized it nor given out the recipe of this secret elixir.

As legend goes, the medicine was gifted to the Gouds by a Hindu Saint about 170 years ago, and he had warned them that the treatment would lose its effectiveness if commercialized. Not just it, he also blessed a well around their area Doodhbowli, which is in a mile’s distance from historic monument, Charminar in Hyderabad. The Goud family use the water from that well to mix the medicine. Currently there are three Goud brothers performing the treatment, and they strictly to adhere to the practice of their ancestors. And still to date, the medicine and treatment is free of charge. There is an alternative to the fish, for thick-headed vegetarians, they can swallow a banana instead of the fish. However the Goud’s emphasize on the importance of fish. Since the therapy is based to a large extent on the effectiveness of the fish. As the live fish moves down, it opens up the pores in the windpipe blocked by phlegm or mucus, making way for the herbal paste.

The treatment is said to be very simple. After swallowing the live fish, the patient is given another three doses of a different medicine on three successive auspicious days called ‘Arudra Karthi,’ ‘Punarvasu Karthi’ and ‘Pushyami Karthi’, which fall every 15 days in a regulated span of 45 days. Along with this, the patient is also put on a strict diet for a period of 45 days which is said to be harder than swallowing the fish itself by some patients, abstaining from most edibles. Harinath Goud, one of the three Goud brothers says, “unless you strictly adhere to the diet, the effect of the medicine will not be optimum.”

Simultaneously every fortnight, morning and evening, two pills made out of the paste are to be taken without fail with warm water. The reason for the fortnightly gap is as much of a enigma as the medicine, and is religiously marked on every patient’s calendar. The patient’s life resumes to normal on the 46^th day, but this is not the end of the treatment. The miracle also takes some time to show its success, and the Goud’s suggest that the fish medicine has to be taken for three consecutive years.

But does this treatment really work? Sheela Chakravorty, a patient who is satisfied with the results said: “The first time I took the fish, it was hard to follow the diet. I was tempted to eat, not delicacies, but simple things such as eggs and coffee, and maybe use a few spices that weren’t allowed. The next year, I was more relaxed and took it upon myself to follow it through. And I did. Today, I am 75 percent cured.”

Most patients notice an improvement in their state in the first year itself. However there isn’t any fixed pattern to recovery by this treatment. And then again there are a few people, who have shown no change, and the reason for this could be not strictly following the diet.

There is almost no scientific explanation for the cure. Yet thousands of asthmatics come to Hyderabad for this treatment both from India and other foreign countries to date to experiment this ‘wonder-therapy’ or like some say ‘God’s blessing,’ and many return eased off from this suffering of wheezing and severe breathing disorder.

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Bronx, N.Y. – Researchers at Albert Einstein College of Medicine of Yeshiva University in collaboration with Nurses’ Health Study investigators have shown that levels of certain related proteins found in blood are associated with a greatly reduced risk for developing type 2 diabetes up to a decade or more later. The findings, published Thursday, May 3, in the online edition of Diabetes, could open a new front in the war against diabetes.

These proteins are part of what is called the IGF axis. This axis was named for insulin-like growth factor-1, (IGF-1), so called because it has biological effects similar to those of insulin (the hormone that regulates blood glucose levels) but has a greater effect on cell growth than insulin. The researchers also looked at levels of several proteins known as IGF binding proteins, or IGFBPs, that may have strong effects independent of IGF-1.

Researchers have hypothesized that the IGF axis may influence risk for developing diabetes – an idea supported by laboratory and mouse studies, and a few initial studies in humans. However, the current study  is the first large, prospective investigation of several components of the IGF-axis and the risk for developing diabetes, according to co-senior author Howard Strickler, M.D., M.P.H., professor of epidemiology & population health at Einstein.

In the current study, the researchers analyzed levels of IGF-1, IGFBP-1, IGFBP-2, and IGFBP-3 in blood taken from 742 women in the Nurses’ Health Study who years later developed type 2 diabetes as well as a similar number of women in the study who did not develop diabetes. None of the women had any signs or symptoms of the disease at the time their blood samples were taken. The median time between the taking of blood samples and diabetes onset was nine years.

Each component of the IGF axis (IGF-1 and IGFBP-1, -2, and -3) had a significant independent association with diabetes risk – most notably IGFBP-1 and -2. Compared with women in the bottom 20 percent with respect to their levels of IGFBP-1, having high levels of IGFBP-1 (top 20 percent) was associated with a three-fold reduction in risk for diabetes, while high levels of IGFBP-2 were associated with a more than five-fold reduction in diabetes risk.

“Our data provide important new evidence that circulating IGF-axis proteins may have a role in the development of type 2 diabetes,” said Dr. Strickler.

The findings have potential clinical implications. First of all, IGF-axis proteins could help in stratifying people at risk for diabetes. “For example,” said Dr. Strickler, “we know that obesity is a major risk factor for diabetes. But some overweight individuals don’t develop diabetes, while some thin people do. If our findings are confirmed, they could help doctors more precisely determine who is actually at risk for the disease.”

The proteins may also prove useful as targets for novel therapies to prevent or treat diabetes. But Dr. Strickler cautions that it’s too early to apply these findings to clinical practice. “IGF-axis proteins have other effects, some beneficial and some not,” he notes. “We need to learn more about the connection between the IGF-axis and diabetes before we recommend that people get tested for these substances, and before deciding how we can exploit the IGF-1 axis to help address diabetes.”

The Diabetes paper is titled, “The Insulin-Like Growth Factor Axis and Risk of Type 2 Diabetes in Women.” The first author was Swapnil Rajpathak (who was at Einstein at the time this work was conducted). The other senior author is Frank B. Hu, M.D., Ph.D, of Harvard School of Public Health,Boston, MA.

Additional contributors include Meian He, M.D., Ph.D., (Harvard and Huazhong University of Science and Technology, Wuhan, Hubei, China); Qi Sun M.D., Sc.D., (Harvard); Jeannette Beasley, Ph.D., R.D., M.P.H., (Fred Hutchinson Cancer Research Center, Seattle, WA);  Michael Pollak, M.D., (McGill University, Montreal, Quebec, Canada); and Robert Kaplan, Ph.D., Radhika Muzumdar M.D., M.B.B.S., Thomas Rohan, M.D., Ph.D., Mimi Kim, Sci.D.,  Jeffrey Pessin, Ph.D., and Judith Wylie-Rosett, Ed.D., all of Einstein. Co-author Marc Gunter, Ph.D., contributed to the paper while at Einstein.

The study was supported by grants from the National Institutes of Health. Laboratory testing and data analysis were supported in part by NIDDK 5-R01-DK-080792.

The NHS is supported by grants CA-87969, DK-58845, and DK-58785 from the National Institute of Diabetes and Digestive and Kidney Diseases and the National Institute of Child Health and Human Development. Q.S. was supported by a career development award (K99HL098459) from the National Heart, Lung, and Blood Institute. The authors report no conflicts of interest.

For more information, please visit www.einstein.yu.edu  and follow on Twitter @EinsteinMed.

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Cincinnati, OH, U.S.A.- Researchers have rejuvenated aged hematopoietic stem cells to be functionally younger, offering intriguing clues into how medicine might one day fend off some of the ailments of old age.

Scientists at Cincinnati Children‘s Hospital Medical Center and the Ulm University Medicine in Germany report their findings online May 3 in the journal Cell Stem Cell. The paper brings new perspective to what has been a life science controversy – countering what used to be broad consensus that the aging of hematopoietic stem cells (HSCs) was locked in by nature and not reversible by therapeutic intervention.

HSCs are stem cells that originate in the bone marrow and generate all of the body’s red and white blood cells and platelets. They are an essential support mechanism of blood cells and the immune system. As humans and other species age, HSCs become more numerous but less effective at regenerating blood cells and immune cells. This makes older people more susceptible to infections and disease, including leukemia.

Researchers in the current study determined a protein that regulates cell signaling – Cdc42 – also controls a molecular process that causes HSCs from mice to age. Pharmacologic inhibition of Cdc42 reversed HSC aging and restored function similar to that of younger stem cells, explained Hartmut Geiger, PhD, the study’s principal investigator and a researcher in the Division of Experimental Hematology/Cancer Biology at Cincinnati Children’s, and the Department of Dermatology and Allergic Diseases, Ulm University Medicine.

“Aging is interesting, in part because we still don’t understand how we age,” Geiger said. “Our findings suggest a novel and important role for Cdc42 and identify its activity as a target for ameliorating natural HSC aging. We know the aging of HSCs reduces in part the response of the immune system response in older people, which contributes to diseases such as anemia, and may be the cause of tissue attrition in certain systems of the body.”

The findings are early and involve laboratory manipulation of mouse cells, so it remains to be seen what direct application they may have for humans. Still, the study expands what is known about the basic molecular and cellular mechanisms of aging – a necessary step to one day designing rational approaches to aiding a healthy aging process.

One reason the research team focused on Cdc42 is that previous studies have reported elevated activity of the protein in various tissue types of older mice – which have a natural life span of around two years. Also, elevated expression of Cdc42 has been found in immune system white blood cells in older humans.

In the current study, researchers found elevated activity of Cdc42 in the HSCs of older mice. They also were able to induce premature aging of HSCs in mice by genetically increasing Cdc42 activity in the cells. The aged cells lost structural organization and polarity, resulting in improper placement and spacing of components inside the cells. This disorganization contributed to the cells’ decreased functional efficiency.

The researchers then analyzed HSCs from older mice to see if inhibition of Cdc42 would reverse the aging process. They used a specific dose (5uM) of a pharmacologic inhibitor of Cdc42, CASIN, to reduce the protein’s activity in the cells – processing them for 16 hours ex vivo in laboratory cultures. This improved structural organization, increased polarity and restored functionality in the older cells to levels found in young cells.

To test the rejuvenated cells, the researchers used a process known as serial competitive transplantation. This included extracting HSCs from young (2-4 months) and aged (20-26 months) mice and processing them in laboratory cultures. Young and rejuvenated cells were then engrafted into recipient mice. This allowed scientists to compare how well young and rejuvenated aged HSCs started to repopulate and transform into different types of blood cells. It also confirmed that HSCs rejuvenated by targeting Cdc42 do function similarly to young stem cells.

Researchers next plan to test the Cdc42 inhibitor, CASIN, in mice to see how HSCs and various tissues in the laboratory models respond. In particular, they are testing red blood cell production, endurance and immune response in the mice. The research team is also acquiring samples of human HSCs to see how those cells respond in laboratory tests to Cdc42 expression.

The first author on the study was Maria Carolina Florian, PhD, from the University of Ulm. Also collaborating were Karin Doerr, Anja Niebel, Deidre Daria, Hubert Schrezenmeier, MD, PhD, Markus Rojewski and Karin Sharffetter-Kochanek, all from the University of Ulm, and Yi Zheng, PhD, and Marie-Dominique Filippi, PhD, of Cincinnati Children’s.

Funding support for the research came from the Deutsche Forschungsgemeinschaft and the National Institutes of Health.

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Last week, at the International Solid-State Circuits Conference (ISSCC), electrical engineer Ada Poon reported that she has developed a wireless device that swims through the blood-stream and delivers medicine throughout the body.

“Such devices could revolutionize medical technology,” Poon states in the Stanford University news release. Poon works as an assistant professor at the Stanford School of Engineering. She states, “Applications include everything from diagnostics to minimally invasive surgeries.”

Prior, implanted medical devices (such as pacemakers and cochlear implants) were usually powered by battery, and were heavy and stationary. Poon’s device, on the other hand, is wireless and self-propelled; it does not require batteries or cables to keep itself energized, and is instead powered by electromagnetic radio waves that come from a radio transmitter outside the body. According to Stanford University,

“The transmitter and the antennae [from the device] are magnetically coupled such that any change in current flow in the transmitter produces a voltage in the other wire – or, more accurately, it induces a voltage.”

Wireless implantable devices are not a new concept. Scientists have been working on this sort of device for half a century, using Maxwell’s equations– which consist of a set of equations that explain the fundamentals and relationship between electricity and magnetism– to perform calculations. However, scientists have stopped due to the equations results, which expressed that radio waves would exponentially decrease as it traveled through the body.

Poon identified several mistakes in their calculations. The scientists had assumed the body acted as a good conductor of electricity. It turns out that it is not so. Poon, instead, viewed the body as dielectric – a good electric insulator. Collaborating with graduate students David Pivonka and Anatoly Yakovlev, she used a different set of equations, from which she realized radio waves can still move through tissue and not decrease in energy. She further discovered that they can travel much farther than she or anyone previously expected.

Poon then developed two types of the self-propelled device. One powers itself by driving an electric current directly in the blood, propelling itself five centimeters per second. The other produces a current goes that back and forth through a loop of wire. It produces whooshing motion as maneuvers as if it were a kayak.

“There is considerable room for improvement and much work remains before such devices are ready for medical applications,” says Poon. “But for the first time in decades the possibility seems closer than ever.”

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