Scientists from the University of Southampton (UK) have reengineered the fundamental process of photosynthesis to power useful chemical reactions that could be used to produce biofuels, pharmaceuticals, and fine chemicals. Photosynthesis is the pivotal biological reaction on the planet, providing the food we eat, the oxygen we breathe, and removing CO2 from the atmosphere. Photosynthesis in plants and algae consists of two reactions, the light-reactions absorb light energy from the sun and use this to split water (H2O) into electrons, protons, and oxygen, and the dark-reactions which use the electrons and protons from the light reactions to “fix” CO2 from the atmosphere into simple sugars that are the basis of the food chain. Importantly, the light reactions have a much higher capacity than the dark reactions resulting in much of the absorbed light energy being wasted as heat rather than being used to “fix” CO2. Co-author Dr. Adokiye Berepiki, a Postdoctoral Research Fellow from Ocean and Earth Sciences at the University of Southampton, said: "In our study, we used synthetic biology methods to engineer an additional enzyme in-between the light-reactions and before the dark-reactions. We have therefore 'rewired' photosynthesis such that more absorbed light is used to power useful chemical reactions. This study therefore represents an innovation whereby a range of additional valuable chemical reactions can be powered by the sun in plants and algae." In the study, published online on July 20, 2016 in ACS Synthetic Biology, the “wasted” electrons were rewired to degrade the widespread environmental pollutant atrazine (a herbicide used in agriculture). Atrazine was banned from the EU over 20 years ago, but is still one of the most prevalent pesticides in groundwater.
A receptor for the dopamine neurotransmitter (DRD2—dopamine receptor D2) promotes growth and spread of pancreatic cancer -- and schizophrenia drugs, which block the function of this receptor, slowed tumor growth and metastatic spread in mice, according to researchers at McGill University and the German Cancer Research Center. Cancer of the pancreas is an extremely aggressive disease with a dismal prognosis. “While the overall five-year survival rate of all cancer patients stands at 63%, it is only about 5% for pancreatic cancer – a number that has remained largely unchanged for the last three decades,” notes Yasser Riazalhosseini, Ph.D., Professor of Human Genetics at McGill and corresponding author of the new study, published online on August 28, 2016 in the journal Gastroenterology. “The tumors do not cause any signs or symptoms for a long time and are therefore diagnosed late,” says Jörg Hoheisel from the German Cancer Research Center (Deutsches Krebsforschungszentrum, or DKFZ) in Heidelberg, who co-led the study with Dr. Riazalhosseini. “In addition, the tumor biology is very aggressive, i.e., the cancer starts spreading metastases early on. And to make things even worse, pancreatic cancer rapidly develops resistance against available chemotherapy drugs.” The new Gastroenterology article is titled “Expression of DRD2 is Increased in Human Pancreatic Ductal Adenocarcinoma and Inhibitors Slow Tumor Growth in Mice.” Along with colleagues from Heidelberg, Tübingen, Liverpool, and Verona, the McGill and DKFZ researchers undertook a large-scale analysis of gene activities in 195 pancreatic cancer cases. “We leveraged quantitative and computational biology approaches that we have established in order to identify genes that may play a central role in several pancreatic cancer-relevant signaling pathways.
The glycemic index of a given food, a value that aims to quantify how fast blood sugar rises after eating that food, can vary by an average of 20 percent within an individual and 25 percent among individuals, report scientists from the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HRNCA) at Tufts University. In randomized, controlled, repeated tests involving 63 healthy adults, researchers found that individual blood sugar responses after consuming a fixed amount of white bread could range across all three glycemic index categories (low, medium, or high). Part of this variability could be attributed to insulin index and baseline HbA1c levels, which reflect long-term glucose control--evidence that glycemic index values are influenced by an individual's metabolic responses to food. The new study, published online in the American Journal of Clinical Nutrition on September 7, 2016 suggests that glycemic index has limited utility as a tool to predict how a food affects blood sugar levels. The article is titled “Estimating the Reliability of Glycemic Index Values and Potential Sources of Methodological and Biological Variability.” "Glycemic index values appear to be an unreliable indicator even under highly standardized conditions, and are unlikely to be useful in guiding food choices," said lead study author Nirupa Matthan, Ph.D., a scientist in the Cardiovascular Nutrition Laboratory at the USDA HNRCA. "If someone eats the same amount of the same food three times, their blood glucose response should be similar each time, but that was not observed in our study. A food that is low glycemic index for you one time you eat it could be high the next time, and it may have no impact on blood sugar for me.
A team of researchers, including several from the University of California, Riverside, has found that flowers are a hot spot of transmission of bacteria that end up in the microbiome of wild bees. The research, which was pubished onine on September 3, 2016 in the journal Microbial Ecology, shows, for the first time, that multiple flower and wild bee species share several of the same types of bacteria. Bees therefore obtain both food and bacteria from flowers. These bacteria may play important roles in bee health. The new article is titled "Flowers and Wild Megachilid Bees Share Microbes." The research on the wild bee microbiome, or the community of microorganisms that live in the bee, follows similar work on the human microbiome that has surged in popularity in the past decade. There has been research on the microbiome of honeybees and bumblebees, but very little on wild bees. While wild bees don't get the same amount of attention as honey bees or bumblebees, they are a critical piece of the pollination puzzle. Wild bees could become more important because of the decline in numbers of honey bees due to colony collapse disorder, which has resulted in the loss of more than 10 million hives in the past decade. Currently, honey bees are relied on for almost all commercial pollination needs. “We are putting all our pollination needs in one basket," said Quinn McFrederick, Ph.D., an Assistant Professor of Entomology at UC Riverside, who is the lead author of the paper. "What if this collapses?” Like honey bees, wild bees pollinate crops, but there is no way to effectively manage them so they can be shipped to a site, as honeybees are, to pollinate a specific crop, such as almond trees in central California.
There may be a way to switch off the urge for compulsive drinking, according to a new study in animal models, which was led by scientists at The Scripps Research Institute (TSRI) in California. “We can completely reverse alcohol dependence by targeting a network of neurons,” said TSRI Assistant Professor Olivier George, Ph.D., who led the study. The new findings, published in the September 7, 2016 issue of The Journal of Neuroscience, build on the results of previous studies showing that frequent alcohol use can activate specific groups of neurons. The new article is titled “Recruitment of a Neuronal Ensemble in the Central Nucleus of the Amygdala Is Required for Alcohol Dependence.” The more a person drinks, the more that person reinforces activation in the neuronal “circuit,” which then drives further alcohol use and addiction. It’s as if the brain carves a special path between alcohol and reward. For the new study, the researchers investigated whether there was a way to influence only the select neurons that form these circuits. In both humans and rats, these neurons make up only about five percent of the neurons in the brain’s central amygdala. TSRI Research Associate Giordano de Guglielmo, Ph.D., who was the study’s first author, spearheaded the experiment in rat models of alcohol dependence, which were designed to express a special protein to distinguish only the neurons activated by alcohol. The rats gave the researchers a potential new window into how these circuits form in human brains, where alcohol-linked neurons are harder to identify without the use of protein labels. The rats were then injected with a compound that could specifically inactivate only alcohol-linked neurons. Dr.
An internationally significant study of healthy twins, 65 years of age or older, has unlocked important clues about how genes influence the development of key grey matter structures, paving the way for a genetic blueprint of the human brain. A team led by researchers from University of New South Wales (UNSW) Medicine analyzed the MRI scans of 322 individuals from the Older Australian Twins Study. The objective was to map the genetic relatedness (or heritability) of cortical and subcortical structures in their brains. These structures are responsible for functions ranging from memory and visual processing, to motor control. The new work was reported online on September 6, 2016 in Scientific Reports. The open-access article is titled “Distinct Genetic Influences on Cortical and Subcortical Brain Structures.” "We know that genes strongly underpin brain development," says lead researcher Associate Professor Wei Wen from the Centre for Healthy Brain Ageing (CHeBA) at UNSW. "But we still don't understand which specific genes are implicated, or how they contribute to different brain structures. In order to identify these genes, we need to first know whether they are shared by different parts of the brain, or unique to a single structure," he says. "This is the first attempt to examine genetic correlations between all of the brain's structures, using the twin design." The UNSW-led team analyzed MRI scans of 93 sets of identical twins and 68 sets of fraternal twins. These participants were all Caucasian men and women without dementia, with an average age of 70, living in the Eastern states of Australia. The scientists measured the volume of their brain structures (12 structures in total) and, using statistical and genetic modeling, determined the heritability for each.
Whooping cranes are changing migration patterns in response to climate and land use change, and these new patterns are being determined by the older, more experienced, members of the population. Researchers from Senckenberg Biodiversity and Climate Research Centre, the Goethe University Frankfurt, the U.S. Geological Survey, the University of Maryland, and the International Crane Foundation investigated a behavior known as "shortstopping," which is the shortening of a migration route by shifting wintering grounds toward the breeding grounds. Shortstopping can benefit migrating birds by decreasing the amount of energy that they use on long-distance flights. They also can arrive at the breeding grounds earlier, which can be beneficial. This requires that the birds find suitable overwintering sites closer to breeding grounds, and due to climate and land use change, suitable sites can now be found at higher latitudes. "Our results show that when migratory groups winter closer to the breeding grounds, the first groups to use these new sites include older birds. For each additional year of age of the oldest bird in the group, the distance between breeding and wintering grounds was reduced by 40 km, or almost 25 miles," said Claire Teitelbaum, Ph.D., a Senckenberg & Goethe University Frankfurt researcher, and lead author of the study. "We also found that site familiarity may be an important factor in where migratory groups short-stop. Older birds often chose overwintering sites which they were familiar with from previous migrations." The population studied is a reintroduced population, established by the Whooping Crane Eastern Partnership. In 2001, the Partnership began releasing captive-reared birds and teaching them to migrate using ultralight aircraft.
Geography and ecology are key factors that have influenced the genetic makeup of human groups in southern Africa, according to new research published online on September 1, 2016 in the journal GENETICS, a publication of the Genetics Society of America. The open-access article is titled “Fine-Scale Human Population Structure in Southern Africa Reflects Ecogeographic Boundaries.” By investigating the ancestries of twenty-two KhoeSan groups, including new samples from the Nama and the ≠Khomani, researchers conclude that the genetic clustering of southern African populations is closely tied to the ecogeography of the Kalahari Desert region. The name KhoeSan refers to several indigenous populations in southern Africa; KhoeSan people speak "click" languages and include both hunter-gatherer groups and pastoralists. They are genetically distinct and strikingly isolated from all other African populations, suggesting they were among the first groups to diverge from the ancestors of all humans. Much scientific interest has focused on the KhoeSan as researchers try to reconstruct this early divergence; however, little genetic material was collected until the past decade. Brenna Henn, Ph.D., of Stony Brook University in New York, has been studying southern African population genetics for over a decade. She notes that there is a tendency to lump all indigenous southern Africans into a single group - often called "Bushmen" - but in fact, the KhoeSan includes many distinct populations. She and her team set out to explore genetic diversity in the area and to better understand the differences between these KhoeSan groups."For the last twenty years or so, there has b een a lot of interest in understanding how genetic patterns are determined by geography in addition to language," says Dr.Henn.
Researchers at the Bellvitge Biomedical Research Institute (IDIBELL) in Spain have published a new Oncotarget work which highlights the importance of the tumor environment as a source of resistance to treatment in colorectal cancer, the fourth most common cancer and the leading cause of cancer death worldwide. The article describes how the presence of certain molecules in the environment of the tumor triggers processes that protect the tumor cells from the action of conventional chemotherapy. Resistance to treatment is one of the main obstacles that patients face during the course of the disease; therefore, understand the mechanisms by which it develops is essential to improve the prognosis. The study led by Dr David G. Molleví, researcher of the Program against cancer therapeutic resistance (PROCURE) of IDIBELL, reports how certain cytokines, chemokines and other soluble factors secreted by carcinoma -associated fibroblasts (CAFs), a type of normal cell which is closely associated with primary tumor cells, induce processes that slow down cell cycle, affecting the proliferation of tumor cells. In the presence of conventional chemotherapy, such factors allow stabilization and activation of selected downstream proteins that minimize the effectiveness of the treatment. However, it has also been reported that inhibition of the JAK/STAT signaling pathway, addict to many of these cytokines, might revert the process. The importance of tumor microenvironment (TME) as a relevant contributor to cancer progression and its role in the development of resistance to therapies has become increasingly apparent to researchers.
Scientists have discovered that esophageal cancer can be classified into three different subtypes, paving the way for testing targeted treatments tailored to patients' disease for the first time. This discovery, published online on September 5, 2016 in Nature Genetics, could help find drugs that target specific weaknesses in each subtype of the disease, which could make treatment more effective and boost survival. The article is titled “Mutational Signatures in Esophageal Adenocarcinoma Reveal Etiologically Distinct Subgroups with Therapeutic Relevance.” The authors, funded by Cancer Research UK and the Medical Research Council (MRC), looked at the complete genetic make-up of 129 esophageal cancers and were able to subdivide the disease into three distinct types based on patterns detected in the DNA of the cancer cells. These patterns are called “signatures.” In the first subtype, patients had faults in their DNA repair pathways. Damage to this pathway is known to increase the risk of breast, ovarian, and prostate cancers. Patients with this subtype may benefit from a new family of drugs called PARP inhibitors that kill cancer cells by exploiting this weakness in their ability to repair DNA. Patients with the second subtype had a higher number of DNA mistakes and more immune cells in the tumors, which suggests these patients could benefit from immunotherapy drugs already showing great promise in a number of cancer types such as skin cancer. Patients with the final subtype had a DNA signature that is mainly associated with the cell aging process and means that this group might benefit from drugs targeting proteins on the surface of the cancer cells which make cells divide.