Dr. Gerald Zon’s latest “Zone in with Zon” blog post, dated December 8, 2014, and published by TriLink BioTechnologies of San Diego, is entitled, “Broccoli May Reduce the Symptoms of Autism.” Although initially skeptical, Dr. Zon was persuaded to investigate the assertion because autism is such a common and difficult disorder and because the ABC News report (“Broccoli Sprout Extract May Help Curb Autism Symptoms”) referred to a supportive article in PNAS, a highly reputable scientific journal. In his blog, Dr. Zon first describes what autism is, saying that “autism is more accurately referred to as “autism spectrum disorder” (ASD) because it covers a wide range of complex neurodevelopment disorders, characterized by social impairments, communication difficulties, and restricted, repetitive, and stereotyped patterns of behavior. Classical ASD is the most severe form of ASD, while other conditions along the spectrum include a milder form known as Asperger syndrome, as well as childhood disintegrative disorder and pervasive developmental disorder not otherwise specified (PDD-NOS). Although ASD varies significantly in character and severity, it occurs in all ethnic and socioeconomic groups and affects every age group. Experts estimate that 1 out of 68 persons have an ASD. Interestingly, males are four times more likely to have an ASD than females.” With regard to the causes of autism, Dr. Zon notes that scientists are still not sure what causes ASD, although there seems to be agreement that both genetics and environment play roles. He notes that “thankfully for many children, symptoms improve with treatment and with age; however, children whose language skills regress early in life—before the age of 3—appear to have a higher than normal risk of developing epilepsy or seizure-like brain activity.”
Take a look in your pantry: the miracle ingredient for fighting obesity may already be there. A simple potato extract may limit weight gain from a diet that is high in fat and refined carbohydrates, according to scientists at McGill University. The results of their recent study were so surprising that the investigators repeated the experiment just to be sure. Investigators fed mice an obesity-inducing diet for 10 weeks. The results soon appeared on the scale: mice that started out weighing on average 25 grams put on about 16 grams. But mice that consumed the same diet but with a potato extract gained much less weight: only 7 more grams. The benefits of the extract are due to its high concentration of polyphenols, a beneficial chemical component from the fruits and vegetables we eat. “We were astonished by the results,” said Professor Luis Agellon, one of the study’s authors. “We thought this can’t be right – in fact, we ran the experiment again using a different batch of extract prepared from potatoes grown in another season, just to be certain.” The rate of obesity due to over-eating continues to rise in Canada, affecting 1 in every 4 adults. Obesity increases the risk of cardiovascular disease and cancer. According to this study, potato extracts could be a solution for preventing both obesity and type 2 diabetes. The study was published in the November 2014 issue of Molecular Nutrition & Food Research. “The daily dose of extract comes from 30 potatoes, but of course we don’t advise anyone to eat 30 potatoes a day,” says Dr. Stan Kubow, principal author of the study, “as that would be an enormous number of calories.” What the investigators envisage instead is making the extract available as a dietary supplement or simply as a cooking ingredient to be added in the kitchen.
Scientists can now explore nerves in mice in much greater detail than ever before, thanks to a new approach developed by scientists at the European Molecular Biology Laboratory (EMBL) in Monterotondo, Italy, applied for the first time to neurons in living mice. The work, published online on December 8, 2014 in Nature Methods, enables researchers to easily use artificial tags, broadening the range of what they can study and vastly increasing image resolution. “Already we’ve been able to see things that we couldn’t see before,” says Dr. Paul Heppenstall from EMBL, who led the research. “Structures such as nerves arranged around a hair on the skin; we can now seethem under the microscope, just as they were presumed to be. The technique, called SNAP-tagging, had been used for about a decade in studies using cell cultures – cells grown in a lab dish – but Dr. Heppenstall’s group is the first to apply it to neurons in living mice. It allows researchers to use virtually any labels they want, making it easier to overcome the challenges that often come with studying complex tissues and animals. To study nerves in the skin, for instance, Dr. Heppenstall’s lab can employ artificial dyes that are small enough to cross the barrier posed by the skin itself, and stand out better from the skin’s natural fluorescence. And because these are artificial, custom-made tags, they can be designed to do more than just highlight particular structures. Scientists can produce tags that destroy certain structures or cells, for instance.
Scientists at the University of Southampton have discovered variations in an enzyme belonging to the immune system that leaves individuals susceptible to ankylosing spondylitis. The variation in ERAP1 can be detected by genetic testing which, if available, could lead to people becoming aware of the risk of the condition earlier. Ankylosing spondylitis is a chronic inflammatory disease which mainly affects joints in the spine. In severe cases, it can eventually cause complete fusion and rigidity of the spine, called "Bamboo spine." It tends to first develop in teenagers and young adults with most cases first starting in people aged 20-30. Ankylosing spondylitis is around three times more common in men than in women and there are around 200,000 people in the UK who have been diagnosed with the condition. Although there is currently no cure, treatments and medications can reduce symptoms and pain, and very early diagnosis may even help to slow progression of the disease. It can take up to 10 years to make a diagnosis so a genetic test could revolutionise management of ankylosing apondylitis, the researchers say. Professor Tim Elliott, who led the study with Dr. Edd James at the University of Southampton, comments: "These natural variations in ERAP1, which are normally involved in T cell immunity, predispose individuals to ankylosing spondylitis. We have also discovered how variations in ERAP1 change its enzyme function - and this means that it might actually be a target for developing new drugs to treat ankylosing spondylitis.
Dinosaurs did it. Human beings and monkey do it. And even birds do it. They walk on two legs. And although humans occupy a special position amongst mammals as they have two legs, the upright gait is not reserved only for man. In the course of evolution many animals have developed the bipedal gait - the ability to walk on two legs. "Birds are moving forward on two legs as well, although they use a completely different technique from us humans," Dr. Emanuel Andrada from the Friedrich Schiller University in Jena, Germany, says. Human beings keep their upper bodies generally in an upright position and the body's center of gravity is directly above the legs. The bodies of birds on the other hand are horizontally forward-facing, which appears to be awkward at first glance. Hence the motion scientist analyzed - together with colleagues - which effect this posture has on the movement of their legs and on their stability when they walk. The first detailed analysis of its kind has now been published online on November 5, 2014 by the scientists in the Proceedings of the Royal Society B. To this end, the team had quails walking through a high-speed X-ray installation at varying speeds. While the installation monitored the movements of the animals meticulously, the scientists were able to measure the power at work in the birds’ legs. From this data, the Jena research team could develop a computer model of the whole motion sequence, which served to simulate and analyze the stability and the energy balance in connection to different gaits.
Triple-negative breast cancer is as bad as it sounds. The cells that form these tumors lack three proteins that would make the cancer respond to powerful, customized treatments. Instead, doctors are left with treating these patients with traditional chemotherapy drugs that only show long-term effectiveness in 20 percent of women with triple-negative breast cancer. Now, researchers at The Johns Hopkins University have discovered a way that breast cancer cells are able to resist the effects of chemotherapy -- and they have found a way to reverse that process. A report of their findings was published online in PNAS on December 1, 2014. Triple-negative breast cancers account for about 20 percent of all breast cancers in the United States, and 30 percent of all breast cancers in African-American women. In addition to being resistant to chemotherapy, these cancers are known to include a high number of breast cancer stem cells, which are responsible for relapses and for producing the metastatic tumors that lead to the death of patients with cancer. Previous research revealed that triple-negative breast cancer cells show a marked increase in the activity of many genes known to be controlled by the protein hypoxia-inducible factor (HIF). Given these past results, a research team directed by Gregg Semenza, M.D., Ph.D., of Johns Hopkins, decided to test whether HIF inhibitors could improve the effectiveness of chemotherapy. "Our study showed that chemotherapy turns on HIF and that HIF enhances the survival of breast cancer stem cells, which are the cancer cells that must be killed to prevent relapse and metastasis," says Dr. Semenza, the C. Michael Armstrong Professor of Medicine at Johns Hopkins and a Johns Hopkins Kimmel Cancer Center expert. "The good news is that we have drugs that block HIF from acting."
Scientists at the Institute for Biologically Inspired Engineering at Harvard University and Harvard's School of Engineering and Applied Sciences (SEAS) have shown that a non–surgical injection of programmable biomaterial that spontaneously assembles in vivo into a 3D structure could fight and even help prevent cancer and also infectious diseases such as HIV. Their findings were reported online on December 8, 2014 in Nature Biotechnology. "We can create 3D structures using minimally–invasive delivery to enrich and activate a host's immune cells to target and attack harmful cells in vivo," said the study's senior author David Mooney, Ph.D., who is a Wyss Institute Core Faculty member and the Robert P. Pinkas Professor of Bioengineering at Harvard’s SEAS. Tiny biodegradable rod–like structures made from silica, known as mesoporous silica rods (MSRs) (see image), can be loaded with biological and chemical drug components and then delivered by needle just underneath the skin. The rods spontaneously assemble at the vaccination site to form a three–dimensional scaffold, like pouring a box of matchsticks into a pile on a table. The porous spaces in the stack of MSRs are large enough to recruit and fill up with dendritic cells, which are "surveillance" cells that monitor the body and trigger an immune response when a harmful presence is detected. "Nano–sized mesoporous silica particles have already been established as useful for manipulating individual cells from the inside, but this is the first time that larger particles, in the micron–sized range, have been used to create a 3D in vivo scaffold that can recruit and attract tens of millions of immune cells," said co-lead author Jaeyun Kim, Ph.D., an Assistant Professor of Chemical Engineering at Sungkyunkwan University and a former Wyss Institute Postdoctoral Fellow.
Technology that can map out the genes at work in a snake or lizard’s mouth has, in many cases, changed the way scientists define an animal as venomous. If oral glands show expression of some of the 20 gene families associated with “venom toxins,” that species gets the venomous label. But, a new study from The University of Texas at Arlington (UT-Arlington) challenges that practice, while also developing a new model for how snake venoms came to be. The work, which was published online on October 21, 2014 in the journal Molecular Biology and Evolution, is based on a painstaking analysis comparing groups of related genes or “gene families” in tissue from different parts of the Burmese python, or Python molurus bivittatus. A team led by assistant professor of biology Dr. Todd Castoe, and including researchers from Colorado and the United Kingdom, found similar levels of these so-called toxic gene families in python oral glands and in tissue from the python brain, liver, stomach, and several other organs. Scientists say those findings demonstrate much about the functions of venom genes before they evolved into venoms. It also shows that just the expression of genes related to venom toxins in oral glands of snakes and lizards isn’t enough information to close the book on whether something is venomous. “Research on venom is widespread because of its obvious importance to treating and understanding snakebite, as well as the potential of venoms to be used as drugs, but, up until now, everything was focused in the venom gland, where venom is produced before it is injected,” Dr. Castoe said. “There was no examination of what’s happening in other parts of the snake’s body.
A new treatment for adult-onset diabetes and obesity developed by researchers at Indiana University (IU) and the German Research Center for Environmental Health has essentially cured lab animals of obesity, diabetes, and associated lipid abnormalities through improved glucose sensitivity, reduced appetite, and enhanced calorie burning. In preclinical trials, the new peptide (image)-- a molecular integration of three gastrointestinal hormones -- lowered blood sugar levels and reduced body fat beyond all existing drugs, according to the work co-led by IU Distinguished Professor of Chemistry Dr. Richard DiMarchi and Dr. Matthias Tschöp, Director of the Institute for Diabetes and Obesity at the German Research Center for Environmental Health. The new findings were published online on December 8, 2014 in in Nature Medicine. These preclinical results advance the clinical work the team announced last year that a peptide combining the properties of two endocrine hormones, GLP-1 and GIP, was an effective treatment for adult-onset diabetes. This new molecule includes a third hormone activity, glucagon. "This triple hormone effect in a single molecule shows results never achieved before,” said co-first author Dr. Brian Finan, a scientist at the Helmholtz Diabetes Center who earned his Ph.D. in biochemistry at IU in Dr. DiMarchi’s lab. “A number of metabolic control centers are influenced simultaneously, namely in the pancreas, liver, fat depots, and brain.” In constructing the new single-cell molecules with triple-hormone action, the researchers found they could reduce body weight in rodents by about 30 percent, almost twice as much as the GLP-1/GIP double hormone. The molecules are called triple agonists -- three hormones combined molecularly that can bind to and activate receptors to produce certain biological responses.
As one of the most diverse plant families, the orchid now has had its first whole genome sequenced and the result will ultimately appear as a cover story in Nature Genetics and was published, in advance, online, on November 24, 2014, in an open-access article in Nature Genetics. This study was an international collaboration, including the National Orchid Conservation Center of China (NOCCC), BGI-Shenzhen, Tsinghua University, Ghent University, Chengkong University, and Institute of Botany Chinese Academy of Sciences. The research team carried out the whole genome sequencing of Phalaenopsis equestris (image), which is an important parental species for breeding of commercial phalaenopsis strains. P. equestris is also the first plant sequenced that has crassulacean acid metabolism (CAM). The assembled genome contains 29,431 predicted protein-coding genes. The average intron length is 2,922 base pairs, which is much longer than seen in any sequenced plant genomes. Further analysis indicated that transposable elements in introns are the major reason for the large size of introns in the orchid genome. The orchid genome contains a high degree of heterozygosity, thus posing a great challenge for the whole genome sequencing and assembly. In this study, researchers found that due to heterozygosity, the derived contigs were likely to be under-assembled and may be enriched for genes involved in self-incompatibility pathways. Those genes could be candidates for further research on the mechanism of self-incompatibility in the orchid. It was also reported that the evidence was found for an orchid-specific paleopolyploidy event that preceded the radiation of most orchid clades, which explained why orchid developed into one of the largest plant families on earth.