Blighted ovum

A blighted ovum, also called an anembryonic pregnancy or anembryonic gestation, occurs when a gestational sac develops without an embryo — often due to chromosomal abnormalities in the fertilized egg. This may be from a poor-quality sperm or egg. Or, it may occur due to abnormal cell division.

Signs of a Blighted Ovum

• Abdominal cramps

• Vaginal spotting or bleeding

• A period that is heavier than usual.

A blighted ovum usually occurs in the first few weeks of pregnancy, often before a woman even knows she's pregnant. However, a woman might miss a period and have a positive pregnancy test. This is because the placenta secretes human chronic gonadotropic (HCG), a pregnancy hormone. Symptoms of early pregnancy — such as breast tenderness — are possible as well. But when the placenta stops growing and hormone levels decrease, the pregnancy symptoms subside. At this point, minor abdominal cramping and light spotting or bleeding are possible. An ultrasound will show an empty gestational sac.

A blighted ovum eventually results in miscarriage. Some women choose to wait for the miscarriage to happen naturally, while others take medication to trigger the miscarriage. In some cases, a procedure called dilation and curettage (D&C) is used to remove the placental tissues.

Most women who've had a blighted ovum go on to have successful pregnancies. If you experience multiple consecutive miscarriages, you might consider testing to identify any underlying causes.

Smoking Causes Genetic Damage Within Minutes After Inhaling

In research described as "a stark warning" to those tempted to start smoking, scientists are reporting that cigarette smoke begins to cause genetic damage within minutes -- not years -- after inhalation into the lungs.

Their report, the first human study to detail the way certain substances in tobacco cause DNA damage linked to cancer, appears in Chemical Research in Toxicology, one of 38 peer-reviewed scientific journals published by the American Chemical Society.

Stephen S. Hecht, Ph.D., and colleagues point out in the report that lung cancer claims a global toll of 3,000 lives each day, largely as a result of cigarette smoking. Smoking also is linked to at least 18 other types of cancer. Evidence indicates that harmful substances in tobacco smoke termed polycyclic aromatic hydrocarbons, or PAHs, are one of the culprits in causing lung cancer. Until now, however, scientists had not detailed the specific way in which the PAHs in cigarette smoke cause DNA damage in humans.

The scientists added a labeled PAH, phenanthrene, to cigarettes and tracked its fate in 12 volunteers who smoked the cigarettes. They found that phenanthrene quickly forms a toxic substance in the blood known to trash DNA, causing mutations that can cause cancer. The smokers developed maximum levels of the substance in a time frame that surprised even the researchers: Just 15-30 minutes after the volunteers finished smoking. Researchers said the effect is so fast that it's equivalent to injecting the substance directly into the bloodstream.

"This study is unique," writes Hecht, an internationally recognized expert on cancer-causing substances found in cigarette smoke and smokeless tobacco. "It is the first to investigate human metabolism of a PAH specifically delivered by inhalation in cigarette smoke, without interference by other sources of exposure such as air pollution or the diet. The results reported here should serve as a stark warning to those who are considering starting to smoke cigarettes," the article notes.

When good cholesterol is even better

HDL's efficiency, not just quantity, appears important for heart health

By Tina Hesman Saey

How much good cholesterol a person has is not as important as how well that good cholesterol works to stop heart disease, a new study suggests.
High-density lipoprotein — also known as HDL, or “good” cholesterol — is healthy for the heart, previous studies have indicated. People with high blood levels of the molecule tend to have lower risk of developing heart disease than people with low levels. But a new study suggests that the amount of good cholesterol in the blood may not be the most important factor in protecting against clogged arteries and cardiovascular disease. The study, published January 13 in the New England Journal of Medicine, shows that HDL’s efficiency at removing fats from arteries is a better predictor of who will develop heart disease than is the level of good cholesterol in the blood.
The results “suggest that just measuring HDL levels isn’t enough to figure out what’s going on,” says Jay Heinecke, an endocrinologist at the University of Washington in Seattle, who wrote an editorial comment on the research in the same issue of the journal. “It opens up the idea that there’s a lot we don’t know about HDL.”

In the study, some people’s good cholesterol was more efficient at relieving the white blood cells of a cholesterol burden than other people’s, found researchers led by Daniel Rader at the University of Pennsylvania School of Medicine in Philadelphia. Healthy people with this trait, known technically as a higher cholesterol efflux capacity, had less thickening of their carotid arteries than did people with less efficient cholesterol-clearing HDL. And, in a separate group of people, HDL functioning was a better indicator than HDL levels of whether the person had heart disease, the team found.

Doctors won’t be able to test their patients’ HDL efficiency any time soon. “We don’t yet have an assay or a test that can be used in a clinical setting,” says Rader. But the work does shed light on some important questions about how good cholesterol works.

“It says that the good cholesterol is more complicated than the bad cholesterol story,” says Christopher Cannon, a cardiologist at Brigham and Women’s Hospital in Boston. Bad cholesterol can build up in arteries, thickening the vessels and narrowing the space blood can squeeze through, so reducing artery damage is as straightforward as lowering the amount of bad cholesterol in the blood. “But good cholesterol actually has to do something to pull bad cholesterol out of the arteries” and send it to the liver for disposal, Cannon says. Exactly how the molecule accomplishes that task efficiently remains to be seen, and is next on the list for Rader and his colleagues to study.

“Now they have to put themselves to work,” says Valentin Fuster, director of the Mount Sinai Heart center in New York City, ticking off a list of research questions raised by the finding. Measurements of thickening of the carotid artery, which feeds oxygen-rich blood to the head and neck, aren’t good indicators of what is happening to arteries feeding the heart, he notes. While the study has value, Fuster would like to see more work showing how HDL efficiency affects arterial disease and how cholesterol-clearing capacity relates to other heart disease risk factors, such as age.

Gene breakthrough in diabetes study

Scientists have identified a gene which plays a role in how a commonly used diabetes drug works - creating a new area for drug development in the future.

Metformin is a drug taken by millions of people with diabetes across the globe and has been in use for more than 50 years.

It has been shown to protect against heart disease and eye and kidney disease in people with Type 2 diabetes and has also been shown to have benefits against cancer. But scientists have not known exactly how metformin works.

New research carried out at the University of Dundee, Oxford University and the Wellcome Trust Sanger Institute as part of the Wellcome Trust Case Control Consortium shed light on how the body works with and makes use of metformin.

Dr Ewan Pearson, Professor Colin Palmer and colleagues based in the Biomedical Research Institute at the University of Dundee used data from a clinical information system of patients with diabetes linked to donated blood samples from 20,000 people in the Tayside area of Scotland in the research.

They were able to determine how well metformin worked in 2,800 people and identified an area of chromosome 11, which includes a gene called ATM (Ataxia Telangiectasia Mutated), that altered how well people responded to metformin.

ATM is a gene that is known to be involved in the DNA damage response system of cells, a mechanism that if faulty can lead to the development of cancer, Dr Pearson said.

"We were expecting to find genes involved in blood sugar regulation so the finding that ATM is involved in metformin response was totally unexpected. Although ATM has been widely studied by cancer scientists, no one previously thought it had a role in how this commonly used diabetes drug worked."

Prof Palmer said: "This is an important development in defining how individuals may respond differently to diabetes drugs, but further work is required before we have enough information to be able to reliably use genetic testing in the clinic to guide treatment of common forms of Type 2 diabetes."

The research was funded by the Wellcome Trust and Diabetes UK and is published in the journal Nature Genetics. Diabetes UK has now awarded Dr Pearson further funding to continue his research using new genetic techniques on 8,000 people with Type 2 diabetes.

Study finds evidence of increased lung cancer risk among tuberculosis patients

Although a clear association of tuberculosis with lung cancer remains to be established, a new study published in the January issue of theJournal of Thoracic Oncology provides compelling evidence of increased lung cancer risk among people with tuberculosis.

Researchers at China Medical University and Hospital in Taiwan randomly selected 1 million patients covered under the country’s National Health Insurance (NHI) program. All patients aged 20 years and older with a new diagnosis of tuberculosis between 1998 and 2000 were identified as the exposed cohort and all people without tuberculosis history were the non-exposed cohort. Patients with any cancer diagnosis were excluded to ensure that all participants were cancer-free at the start of both cohorts. Overall, 716,872 adults were eligible for the analysis – 4,480 in the tuberculosis cohort and 712,392 in the non-tuberculosis cohort.

Both groups were followed from 2001 through 2007. Results showed that patients with tuberculosis were 10.9 times more likely than non-tuberculosis patients to develop lung cancer (26.3 versus 2.41 per 10,000 person-years). Mortality was also much higher in the patients with tuberculosis than in the non-tuberculosis patients (51.1 versus 8.2 per 10,000 person-years).

“Tuberculosis is a very common chronic disease worldwide; people in the developing and undeveloped areas suffer with it mostly,” said Dr. Chih-Yi Chen, one of the researchers. “It is well known that lung cancer is causally associated with smoking. Less attention has been focused on whether people with tuberculosis are also at higher risk of developing lung cancer. With the universal health insurance claims data of Taiwan, we identified 4,480 patients with tuberculosis from a group of 716,872 people and followed them for eight years or longer. The incidence of lung cancer in these tuberculosis patients was 11 times greater than people without tuberculosis. The risk of lung cancer may increase further to almost 16 times greater if patients with tuberculosis also suffer from chronic obstructive pulmonary disease. This study suggests that it is also important to watch out for lung cancer prevention in the campaign against tuberculosis.”

The research was supported by the National Science Council, Executive Yuan, Taiwan; the Department of Health Clinical Trial and Research Center of Excellence; China Medical University Hospital; and Taiwan Department of Health, China Medical University Hospital Cancer Research of Excellence.

About the Journal of Thoracic Oncology:

The Journal of Thoracic Oncology (JTO) is the official monthly journal of the International Association for the Study of Lung Cancer (IASLC). It is a prized resource for medical specialists and scientists who focus on the detection, prevention, diagnosis and treatment of lung cancer. It emphasizes a multidisciplinary approach, including original research (clinical trials and translational or basic research), reviews and opinion pieces.

To find out more about the JTO please visit journals.lww.com. To learn more about the IASLC please visit iaslc.org.

PhD Position in Biology, Computer Science, Neuroscience, and Interdisciplinary Areas

Study Subject: 
Biology,
Computer Science,
Neuroscience

Employer: 
Institute of Science and Technology

Level: 
PhD

Scholarship Description:

The Graduate School at IST Austria invites applicants from all countries to its PhD program. IST Austria is a new institution located on the outskirts of Vienna dedicated to cutting-edge basic research in the natural sciences and related disciplines. The language at the Institute and the Graduate School is English.

The PhD program combines advanced coursework and research, with a focus on Biology, Computer Science, Neuroscience, and interdisciplinary areas.

IST Austria offers internationally competitive PhD salaries supporting 4-5 years of study.

Applicants must hold either a Bachelor or Master degree or equivalent.

Scholarship Application Deadline: 15 January 2011

Further Scholarship Information and Application click Here

CSIR-Nehru Science Postdoctoral Research Fellowship Scheme

Job Description: Council of Scientific and Industrial Research (CSIR), an ensemble of 37 state-of-the art institutes, is amongst the foremost scientific and industrial research organizations. Over the years, this unique organization has helped India usher in a scientific milieu, creating and nurturing talent in a wide variety of S&T domains, spawned many organizations, many disciplines and most importantly has served as a nursery and training ground for most of India?s talented scientists and technologists. CSIR annually publishes over 3800 papers in science journals and holds over 3000 patents.

“CSIR-Nehru Science Postdoctoral Research Fellowship Scheme” has been instituted to identify promising young researchers with innovative ideas and provide them with training and research opportunities in niche areas of basic science, engineering, medicine and agriculture. The scheme aims at facilitating their transition from mentored to independent research career. CSIR intends to offer one hundred (100) such fellowships every year to promising fresh PhD holders for working in CSIR laboratories with state-of-art R&D facilities.

Eligibility: PhD degree holders within three years of award of PhD degree, or those who have submitted PhD theses. Applicants who are about to submit thesis are also eligible to apply, but their selection will be subject to the condition that they would have submitted thesis before the expiry of the validity of the award offer. Applicants should have research publications in high impact SCI journals.

Though CSIR Nehru Science Postdoctoral Research Fellowship is open to Indian nationals, Persons of Indian Origin (PIO) and Overseas Citizen of India (OCI), a certain number (up to 20%) of fellowships may be offered to foreign nationals.

Maximum Age Limit: 32 years, relaxable upto 5 years in case of SC/ST/OBC/Physically handicapped and women candidates.

Tenure: Two years and extendable for maximum one more year based on outstanding performance and recommendation from the Director of the CSIR lab where working.

Remuneration: CSIR Nehru Science Postdoctoral Fellows will be paid a consolidated fellowship of Indian Rs. 35,000/- per month plus House Rent Allowance (HRA) as admissible and a contingency grant of Rs. 3.0 lakh per annum. 25% of the contingency grant can be used for domestic and international travel including per diem expenses.

Mode of selection: Eligible candidates can apply in the prescribed format, available on the website www.csirhrdg.res.in, any time of the year. However, the selections will be made twice a year, in the months of June and December. Applications received two months before the scheduled interview date will be considered for short listing and calling for interview. Eligible candidates must route their applications through the sponsoring CSIR laboratory.

Selections to the “CSIR-Nehru Science Postdoctoral Research Fellowships” will be made based on the presentation of the proposed research project followed by interview of short listed candidates by specially constituted Committees. Applicants from abroad may also be considered in absentia, if eligible. Selection of foreign nationals will be subjected to clearance by ISTADS, CSIR.

Accommodation and other benefits: Accommodation may be provided by CSIR laboratories if available. CSIR rules on leased accommodation are being reviewed in the light of „Sixth Pay Commission? recommendations and will be made applicable as and when approved. CSIR Nehru Science Postdoctoral Fellows will be entitled for Medical benefits as per the CSIR rules for Research Associates.

Other relevant information:

(i) Candidates who have worked for their PhD from a particular CSIR laboratory will not be eligible for becoming a PDF in the same CSIR laboratory under this scheme.

(ii) 20% of the fellowship amount will be paid as lump sum at the end of completion of 1st and 2nd year, respectively.

(iii) Selected candidates are expected to join within four months of effective date of award.

All other rules and regulations will be as applicable to CSIR Research Associates (can be seen at www.csirhrdg.res.in). Further, in all matters, the decision of CSIR shall be final.

List of CSIR laboratories and their R&D activities can be seen at www.csir.res.in. For more information about CSIR labs, please visit the website of the individual Laboratory.

How to Apply

Please read the instructions, given at Annexure-I, carefully before filling the Application Form. The Application Proforma is given as Annexure-II. Application received without the Attestation of the Director of the Sponsoring CSIR laboratory will be rejected.

Where to Apply

Applications duly filled in the prescribed format and complete in all respect should be sent to:

Ms Sushila Khilnani,

Scientist-G

Human Resource Development Group,

CSIR Complex, Library Avenue,

Pusa, New Delhi-110012

Email : skhilnani@csirhrdg.res.in

Tel : 011-25846077

“Application for CSIR-Nehru Science Postdoctoral Research Fellowship” should clearly be written on top of the envelope containing application form.

More detail for CSIR-Nehru Science Postdoctoral Research Fellowship Scheme

Black Raspberries May Prevent Colon Cancer, Study Finds

Black raspberries are highly effective in preventing colorectal tumors in two mouse models of the disease, according to a University of Illinois at Chicago study.

The findings are published in the November issue of Cancer Prevention Research.

Colorectal cancer is the third most common cancer and the second leading cause of cancer-related death in both men and women in the U.S., according to the National Cancer Institute.

Building on previous research that found black raspberries have antioxidant, anti-cancer, anti-neurodegenerative and anti-inflammatory properties, the researchers looked at the fruit's ability to prevent colon cancer.

"We saw the black raspberry as a natural product, very powerful, and easy to access," said Dr. Wancai Yang, assistant professor of pathology at the UIC College of Medicine and senior author of the study, whose research focuses on the interactions of genetic and nutritional factors in the development of intestinal cancer and tumor prevention.

The researchers used two strains of mice, Apc1638 and Muc2, which each have a specific gene knocked out, causing the mice to develop either intestinal tumors (in the case of Apc1638) or colitis in the case of Muc2. Colitis is an inflammation of the large intestine that can contribute to the development of colorectal cancer.

Both mouse strains were randomized to be fed either a Western-style, high-risk diet (high in fat and low in calcium and vitamin D) or the same diet supplemented with 10 percent freeze-dried black raspberry powder for 12 weeks.

The researchers found that in both mouse strains the black raspberry-supplemented diet produced a broad range of protective effects in the intestine, colon and rectum and inhibited tumor formation.

In the Apc1638 mice, tumor incidence was reduced by 45 percent and the number of tumors by 60 percent. The researchers found that black raspberries inhibited tumor development by suppressing a protein, known as beta-catenin, which binds to the APC gene.

In the Muc2 mice, tumor incidence and the number of tumors were both reduced by 50 percent, and black raspberries inhibited tumor development by reducing chronic inflammation associated with colitis.

The researchers now hope to obtain funding to begin clinical trials in humans, said Yang. Because black raspberries not only prevent cancer but also inflammation, they may also protect against other diseases, such as heart disease.

Yang is a member of the UIC Cancer Center. Co-authors are Xiuli Bi of UIC, Wenfeng Fang of UIC and Wuhan University in China, and Li-Shu Wang and Gary Stoner of the Ohio State University.

The research was funded by UIC's department of pathology and the National Cancer Institute.

ELISA

Enzyme-linked Immunosorbent Assays (ELISAs) combine the specificity of antibodies with the sensitivity of simple enzyme assays, by using antibodies or antigens coupled to an easily-assayed enzyme. ELISAs can provide a useful measurement of antigen or antibody concentration. There are two main variations on this method: The ELISA can be used to detect the presence of antigens that are recognized by an antibody or it can be used to test for antibodies that recognize an antigen. An ELISA is a five-step procedure: 

1) coat the microtiter plate wells with antigen

2) block all unbound sites to prevent false positive results

3) add antibody to the wells

4) add anti-mouse IgG conjugated to an enzyme 

5) reaction of a substrate with the enzyme to produce a colored product, thus indicating a positive reaction. 

There are many different types of ELISAs. One of the most common types of ELISA is "sandwich ELISA."

Southern Blot

Southern Blotting The first blotting technique to be devised is known as Southern blotting after its originator E. M. Southern.

This technique is capable of detecting a single specific restriction fragment in the highly complex mixture of fragments produced by cleavage of the entire human genome with a restriction enzyme. In such a complex mixture, many fragments will have the same or nearly the same length and thus migrate together during electrophoresis. Even though all the fragments are not separated completely by gel electrophoresis, an individual fragment within one of the bands can be identified by hybridization to a specific DNA probe. To accomplish this, the restriction fragments present in the gel are denatured with alkali and transferred onto a nitrocellulose filter or nylon membrane by blotting.

This procedure preserves the distribution of the fragments in the gel, creating a replica of the gel on the filter, much like the replica filter produced from clones in a library. (The blot is used because probes do not readily diffuse into the original gel.) The filter then is incubated under hybridization conditions with a specific radiolabeled DNA probe, which usually is generated from a cloned restriction fragment. The DNA restriction fragment that is complementary to the probe hybridizes, and its location on the filter can be revealed by autoradiography.

Zebrafish Provide New Hope for Cancer Treatment

ScienceDaily (Dec. 20, 2010) — The imaging of tumour growth in zebrafish has revealed for the first time how newly formed cancer cells have the capacity to co-opt the immune system into spreading the disease, leading the way for investigations into potential therapies for eliminating early-stage cancer in humans. Using different coloured fluorescent tags, scientists at the University of Bristol labelled immune cells and tumour-forming cells in the translucent zebrafish in order to track their behaviour and interactions by live cell imaging.
These dramatic findings, which are the result of a collaboration between academic colleagues in the UK (University of Bristol and University of Manchester) and Italy (Institute of Molecular Oncology, Milan) are published in the online, open access journal PLoS Biology.
Tests showed that cancer cells are less likely to proliferate if white blood cells can be prevented from contacting the precursor cancer cells, suggesting that white blood cells -- the immune cells -- have the ability to promote disease by providing some kind of growth signal. Interestingly, the chemical compound that acts as a draw between the two sets of cells was shown here to be hydrogen peroxide -- commonly used as a disinfectant or antiseptic, but also a natural by-product produced by the body's metabolic process.
Describing the work, Paul Martin, Professor of Cell Biology at the University of Bristol's Schools of Biochemistry and Physiology & Pharmacology, who supervised post-doctoral fellow Yi Feng in the research project, said: "By visualizing the earliest interactions between cancer cells and their host environment, we have shown that even from their earliest stages tumours don't just avoid being destroyed by the immune system. Rather, they appear to court an immune response, co-opting the body's innate immune system to aid and abet their growth."
The team used a method to switch on the human oncogene, HRAS, in specific pigment cells (melanocytes) in the skin of early stage zebrafish embryos. Studies were carried out using zebrafish because they conserve many of the molecular and cellular components of tumour formation seen in mammals and are almost translucent, making it easy to see the cells as they move around and grow. Researchers monitored the first hours and days of development and as the embryo grew, some of the cells were transformed, ie, made cancerous by HRAS. Those transformed cells were found to actively attract the innate immune cells. The researchers got the same results, after inserting HRAS into different, mucous-secreting cells, and again when experimenting with a different oncogene, SRC. They discovered that the tumour cells produced hydrogen peroxide and that immune cells were drawn up the hydrogen peroxide gradient towards the cancer.
The researchers' movies show that the immune cells appear to engulf cancerous cells in a bid to destroy them. However, other cells formed cytoplasmic tethers linking them to cancerous cells and in some cases the cancerous cells appeared to drag the immune cells back when they started to leave the region. In order to see whether the tumour was avoiding destruction or actually co-opting the immune cells, the researchers blocked the immune response in three different ways: they prevented the development of immune cells for the first three days of the zebrafish embryos' life, and separately, they used two different strategies to limit hydrogen peroxide production. In each case, immune cells failed to migrate to the cancer site. And each time, when the immune response was blocked, fewer cancer cells formed.
Professor Martin added: "Yi's movies in Zebrafish larvae give us the first insight into how immune cells sense and then attempt to deal with the earliest stages of cancer. Now we can look closer to discover why it is that immune cells seem to aid growth of these young cancer cells and figure out ways for guiding immune cells how better to search and destroy."

UCSB researchers discover new biotechnology to identify and engineer substrates for proteases

This technology should help solve the puzzles of cancer, Alzheimer’s, atherosclerosis and infectious diseases.

Santa Barbara, California – May 1 , 2006 – Researchers at UC Santa Barbara have developed a new biotechnology that enables scientists to identify and engineer protease substrates, giving them the means of crafting pharmaceuticals to outsmart disease. Their work, authored by Patrick Daugherty, an assistant professor of Chemical Engineering, and Kevin Boulware, a PhD candidate, are published online today in the Proceedings of the National Academy of Sciences.
Proteases (or peptidases) are encoded by about two percent of genes in the human genome and play key roles in nearly all diseases. They act as "molecular scissors" by attaching to specific sequences contained within other proteins, called substrates, and cutting them in specific locations. For example, proteases are responsible for digesting food, for determining the proper time for cells to die, and for removing damaged proteins from the body.

But the substrates for most proteases are unknown, and this has limited researchers' ability to facilitate or thwart protease action. By identifying substrates, scientists gain the ability to regulate protein function, creating the capacity to speed up, slow down or eliminate particular protease actions. Daugherty's approach also makes it easier to measure protease action and thus develop pharmaceuticals that control protease activity.

Daugherty and Boulware developed a general combinatorial approach to identify optimal substrates of proteases, using quantitative kinetic screening of cellular libraries of peptide substrates (CLiPS). The results suggest that CLiPS will be broadly useful for characterizing proteases and developing optimal substrates for therapeutic applications.

Of the roughly 1,000 proteases in the human genome, only about ten percent of the targets have been identified, but Daugherty believes that scientists will identify nearly all of them in the next five to ten years. "This technology will give us a scalable tool that will allow us to effectively tackle this challenge," he says.

Mice missing protein burn more fat

PHILADELPHIA — Scientists are learning how they might stoke the body’s fat-burning furnace by turning up a molecular thermostat.

Mice lacking a protein that responds to the hunger-promoting hormone ghrelin burn more energy in their brown fat than other mice, Yuxiang Sun of Baylor College of Medicine in Houston reported December 13 at the American Society for Cell Biology’s annual meeting. This revved-up brown fat helps keep mice lean and energetic into middle age. The finding could eventually lead to a way to help people fight obesity.

Brown fat burns energy instead of just storing it the way white fat does. This metabolically active fat is important in helping rodents and other animals maintain their body temperature. Recently researchers learned that adult humans have brown fat, and that the amount of energy burned by brown fat decreases with age and weight. The discovery has spurred interest in learning how to turn brown fat on.

Sun and her colleagues didn’t start out trying to rev up brown fat. Because the hormone ghrelin has been shown to make animals eat more, the researchers reasoned that blocking the molecule’s activity might reduce appetite and help animals and people lose weight. Sun and her colleagues genetically engineered mice to completely lack either ghrelin or the ghrelin receptor, a protein that interacts with ghrelin and sets off a series of biological reactions in cells that leads to the hormone’s effect.

Disappointingly, mice lacking either molecule ate and exercised just as much as normal mice. But mice lacking the ghrelin receptor burned more energy and stayed lean even as they aged, while normal mice and mice lacking ghrelin tended to gain weight as they got older.

Mice missing ghrelin had a hard time maintaining their body temperature when placed in the cold. But mice without the ghrelin receptor stayed warm. Those pieces of evidence led Sun and her colleagues to examine brown fat in the mutant mice.

Sun’s team found that removing the ghrelin receptor causes brown fat cells to make more of a protein called UCP1. That protein makes the cell’s power plants less efficient and as a result, they release more heat. These inefficient brown fat cells may burn their own supply of fat and then gobble up fat that otherwise would be stored in white fat cells, leading to leaner rodents, Sun speculated.

If researchers can discover why removing the ghrelin receptor turns up brown fat’s furnace, it may be possible to design a drug that will do the same thing. “There may be more than just exercise and willpower that can keep us in shape,” Sun said.

There is no question that increasing the activity of brown fat can have a big effect on weight, said Lewis Landsberg, an endocrinologist at Northwestern University in Evanston, Ill. About 10 percent of a rodent’s total energy expenditure comes from brown fat. Extrapolating to humans, turning up brown fat to burn a similar amount of a person’s calories would be about equal to the energy burned while walking 2.5 miles each day, he said.

Landsberg said that it is not clear whether removing the ghrelin receptor directly affects the energy expenditure of brown fat or if the mutation somehow spurs the sympathetic nervous system to turn up the furnace.

Sun hopes to answer that question by removing the ghrelin receptor in just brown fat cells.

Cells reprogrammed to treat diabetes

PHILADELPHIA — Sperm-forming stem cells in the testes can be converted to insulin-producing cells that could replace diseased ones in the pancreas, researchers from Georgetown University Medical Center in Washington, D.C., reported December 12 at the annual meeting of the American Society for Cell Biology. The new technique is edging closer to producing the amount of insulin needed to cure diabetes in humans.

Ian Gallicano, a developmental biologist at Georgetown, and his colleagues isolated sperm-producing stem cells from the testes of organ donors. These cells could easily revert to an embryonic state, capable of making nearly any cell in the body. The Georgetown researchers treated the cells with chemicals to coax them into mimicking beta-islet cells from the pancreas, the same kind of cells that are compromised in diabetes.

Reprogrammed sperm-producing cells cured diabetes in mice for about a week before their insulin levels dropped again. “If you’re a mouse and you have diabetes, you’re in good shape these days,” Gallicano says.

But cells need to make much more insulin in order to cure diabetes in humans. In islet cells in the human pancreas, insulin accounts for about 10 percent of the proteins secreted by the cell. No stem cell from the testes or anywhere else has come close to making that amount of insulin, Gallicano says. He and his colleagues have developed a new way of programming insulin-producing cells and are getting closer to the goal of creating islet-like cells in which insulin accounts for 1 to 10 percent of the proteins in the cells.
Although testes-derived stem cells would be useful only for men, Gallicano thinks the tricks he’s developing could be adapted to other stem cells that could help women with diabetes too.

Apartments share tobacco smoke

Children in nonsmoking families have higher levels of secondhand exposure if they live in multifamily dwellings.
By Janet Raloff

Children who grow up in apartment buildings are more likely to inhale secondhand tobacco smoke than are kids living in detached homes, a new study finds — even if no one in their household ever lights a cigarette.

“This is the first study to show significant evidence of increased tobacco-smoke exposure among children who live in multi-unit housing,” reports pediatrician Jonathan Winickoff of the Massachusetts General Hospital for Children in Boston, who directed the study. Compared to children who grew up in detached houses, his team finds that those living in apartments excreted 45 percent more cotinine, which is a marker of nicotine exposure. The findings were released online December 13 in Pediatrics.

“Our new study is really the last link in the chain of evidence demonstrating the need for smoke-free buildings,” Winickoff says, “because it proves that children are absorbing that smoke.”

Overall, depending on the type of dwelling in which they lived, cotinine concentrations were quite low, averaging 0.053 to 0.075 nanograms per milliliter of urine among all 5,002 kids, aged 6 to 18. But a host of studies have linked even low-level exposures to behavioral changes and increased risk of allergy and asthma.

“The 2006 surgeon general’s report is clear: There’s really no safe level of secondhand smoke,” notes Gary Adamkiewicz of the Harvard School of Public Health, an environmental health scientist unaffiliated with the new research.

In the new study, Winickoff’s team examined data collected as part of the National Health and Nutrition Examination Survey conducted between 2001 and 2006 by the U.S. Centers for Disease Control and Prevention. Almost three-quarters of children excreted cotinine, including 84.5 percent living in apartments and 70 percent of those from detached homes. There was less than a 1 percent probability that the difference was due to chance. The prevalence of cotinine residues in children from attached homes fell in between.

The common occurrence of the smoke marker among children living in detached houses points to the importance of community exposures, Winickoff says. Kids may have been exposed by being near a parent's smoky clothing, by walking though doorways where smokers are clustered, riding in cars with a smoker or hanging out indoors where smokers previously have lit up.

While dramatic, the new findings hardly come as a surprise, since another recent study measured nicotine from tobacco smoke tainting the air in roughly 90 percent of 49 low-income apartments inhabited by nonsmokers.

“Our study confirmed on-the-ground evidence that folks who live in multi-family housing were reporting,” explains Adamkiewicz, an author of that study. People in nonsmoking residences often could smell smoke, which likely seeped in through ventilation systems, cracks around plumbing or under doors.

Concentrations that his team measured were low — “but not trivial,” he says. They were highest in those households where the residents had reported smelling smoke most frequently. By analyzing air movement in and out of an apartment, “we could calculate how many cigarettes someone would have had to have smoked to yield this level of nicotine in the air,” he says. “And in the apartments of nonsmokers, it started to approach a cigarette a day.” His team reported its findings in the December 2009 Tobacco Control.

The new study takes those results a step further, Winickoff says. “Although we now protect bartenders and people in restaurants in many places from secondhand smoke, we’ve forgotten to protect one critical segment: where children live.” But owing to the strong data that his team has just turned up, he says, “Landlords are soon going to be deciding not whether to go smokefree but how soon to go smokefree.”

And if they don’t, the Department of Housing and Urban Development may force the issue, says toxicologist Bruce Lanphear of Simon Fraser University in Vancouver, British Columbia. “You can’t ban smoking in private housing,” he acknowledges, “but HUD can ban smoking in public housing if there’s sufficient evidence to suggest that it’s in the best interest of kids’ health.”

Another reason the new study is important: It points to housing-related issues, Lanphear says, that at least on a population level may explain why kids in certain ethnic and low-income communities “have higher rates of wheezing or learning problems.”

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