Cyagen Biosciences

During the past several years, there has been an increasing public awareness of mental illness and their societal and health consequences. Eating disorders represent one of the most damaging groups of mental illnesses. Current estimates are that anorexia nervosa claims the life of an astonishing 10-20% of patients, and increases mortality rate by 6-fold. Based on these figures, anorexia is the single most deadly mental illness (1). Another surprising fact about eating disorders is that risk of anorexia and bulimia appears to be about 50% attributable to genetics (2). Despite this, there has been little progress toward identifying specific biological factors which are causal for eating disorders. There is good news, however, as some recent studies using animal models are beginning to provide much-needed insight into these complex and tragic illnesses. Researchers from Columbia University have reported a mouse model that recapitulates many aspects of human anorexia nervosa, includi

Invariably, everyone gets old. However, as a true testament to human stubbornness, research toward a “cure” for aging has never stopped. Over the past few decades, various approaches have allowed scientists to generate animal models with extended lifespans. In recent years, this trend has moved from lower organisms to mammalian model systems. There are now several rodent models with enhanced longevity. Many of these models are directly relevant to human aging. A new study has identified a deletion in exon 3 of human growth hormone receptor (GHR) to be prevalent in naturally long-lived men (1). The presence of two copies of this mutation may allow men to live about ten years longer than they otherwise would. This agrees with many findings from rodent models. Transgenic mice that overexpress GH age rapidly, while knockout mice lacking GHR are long-lived (2,3). In humans and mice, IGF1 signaling is also closely linked to longevity via a signaling pathway overlapping that of GH (4,5).

Introduction: Reduced heart function due to aging and disease is a major health problem. Heart attacks can have devastating impacts, often leading to the death of the patient or chronic morbidity for those that survive. A major reason for the sensitivity of the circulatory system to heart malfunction is that heart muscle cells (cardiomyocytes) of adult mammals generally do not divide. This means that when a cardiomyocyte dies, due to localized loss of blood supply, for example, that dead cell will never be replaced. Normally, heart tissue has a robust, healthy blood supply, but when a heart attack strikes, portions of heart tissue are deprived of blood flow, resulting in rapid cell death in those sections of the heart. Recovering the ability to heal Interestingly, newborn hearts can heal. In 2011, scientists discovered that newborn mice are able to regenerate cardiomyocytes to repair heart damage, but this ability is lost soon after birth (1). More recently, researchers disc

Introduction: Optogenenetics refers to a family of techniques which allow modulation of biological processes using light. Over the past 12 years, optogenetics has revolutionized neuroscience and is now expanding to impact many fields of biology. There are now genetic tools which can be used for photo-control of signal transduction, gene expression, apoptosis, histone modification, cytoskeletal dynamics, and many more processes. The incredible power of optogenetics comes from the very high spatial and temporal resolution possible using light, as opposed to chemical or genetic effects. Optogenetics can also be combined with other genetic or chemical approaches to further increase the level of experimental control. For example, optogenetic constructs can be targeted to specific cell types or subcellular locations, or can be engineered to require specific chemical cofactors, further limiting when and where light-induced effects will occur. The key component of an optogenetics ex

In many ways, regeneration is the ‘holy grail’ of medical research. To be able to completely heal from injuries and to regrow lost organs or tissues is a feat that most mammals are generally not capable of. However, many types of animals can regenerate to varying degrees, and some mammalian tissues do normally display regenerative capabilities. Studying model organisms has provided some insight into the biochemical pathways that allow regeneration in certain systems, as well as mechanisms that prevent regeneration in others. Here are a couple of recent studies which could represent major breakthroughs in regeneration research. Epigenetic barriers prevent regeneration in the eye   In adult mammals, the retina is almost completely incapable of regeneration. In contrast, bony fish can regenerate retinal tissue lost due to injury. The process of retinal regeneration in fish requires the generation of new neurons from Müller glial cells within the eye, driven by the activity of the pron

Last month, the Nobel Foundation recognized Jeffrey Hall, Michael Rosbash, and Michael Young "for their discoveries of molecular mechanisms controlling the circadian rhythm" 1 . This 24-hour "clock" influences many physiological processes, and has a well-understood biochemical basis elucidated by the work of many researchers over the past few decades. Interestingly, in addition daily circadian cycles, many organisms also display physiological cycles repeating twice a day. Most obviously, coastal animals possess a powerful “circatidal clock”, which oscillated with the 12.4-hour ebb and flow of the tides, influencing locomotion, metabolism, and many other physiological processes 2 . Even in humans, body temperature, hormone levels, blood pressure, and other functions fluctuate with a predictable 12-hour period, and some human diseases have even been associated with perturbed 12-hour cycles 3-9 . In a fascinating recent study, researchers used mathematical gene expr