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Archive - May 20, 2018

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Giraffes Surprise Biologists Yet Again; Increased Understanding Much Needed to Aid Conservation Efforts for This “Vulnerable” Species

New research from the University of Bristol in the UK has highlighted how little we know about giraffe behavior and ecology. It is commonly accepted that group sizes of animals increase when there is a risk of predation, because larger group sizes reduce the risk of individuals being killed, and there are “many eyes” to spot any potential predation risk. Now, however, in the first study of its kind, Bristol PhD student Zoe Muller from the School of Biological Sciences has found that this is not true for giraffes, and that the size of giraffe groups is not influenced by the presence of predators. Muller said, "This is surprising, and highlights how little we know about even the most basic aspects of giraffe behavior." This study investigates how the grouping behavior of giraffes differed in response to numerous factors, such as predation risk, habitat type, and the characteristics of individuals. Habitat type had some effect on group size, but the main effect on group size was in the behavior of adult females, who were found to be in smaller groups when they had calves. This is contrary to another popular belief that female giraffes form large groups to communally care for their young - this study, published recently in the Journal of Zoology presents the first evidence to show that, actually, the opposite is true. Giraffe populations have declined by 40 percent in the last 30 years, and there are now thought to be fewer than 98,000 individuals remaining in the wild. In recognition of their drastic decline in the wild, giraffes have recently been listed as "Vulnerable" on the International Union for Conservation in Nature's Red List of Threatened Species.

New Molecular Insights into How Neurons Communicate During Learning; Synaptic Nanomodules Underlie Organization & Plasticity of Spine Synapses

(BY RACHEL DERITA, PhD Candidate,Thomas Jefferson University, Department of Cancer Biology) The laboratory of Matthew Dalva, PhD, and Director of the Synaptic Biology Center at Thomas Jefferson University in Philadelphia, has gained new insight into how synapses change upon learning in the brain. These findings come from a study published in Nature Neuroscience on April 23, 2018. The article is titled : Synaptic Nanomodules Underlie the Organization and Plasticity of Spine Synapses.” It was already known that upon learning, connections between neurons strengthen and become bigger. But this new study showed specifically that molecules involved in transmitting signals between neurons organize in clumps called “nanomodules” that dance and multiply when neurons are stimulated by signals that mimic learning. Super-resolution live-cell microscopy was used to show this dynamic behavior of molecules during neuronal communication on a cellular and molecular level by zooming into synapses in real-time. When further analyzing the behavior of these nanomodules, it was discovered that key molecules on the pre-synaptic side (such as vesicular glutamate transporter; VGLUT) not only clustered, but lined up and tracked with the post-synaptic proteins (such as post-synaptic density protein 95; PSD-95). When stimulated with signals to strengthen the synaptic connection between two neurons, a stationary nanomodule would begin to move around the synaptic spine, and the pre- and post-synaptic components would still track with each other. The nanomodules also had a uniform size and multiplied when the neurons were stimulated to grow and nearly touch each other across the synapse. The number of nanomodules was positively correlated with the size of the spines.

Research Offers Deeper Understanding of Role of Retinoblastoma Gene in Aggressive Prostate Cancer

(BY RACHEL DERITA, PhD Candidate,Thomas Jefferson University, Department of Cancer Biology) In prostate cancer, there is a continual effort to better stratify patients. Current standards of care for all patients are identical, but each case is not. A recent study (published on December 4, 2017 in the Journal of Cl inical Investigation) from Thomas Jefferson University’s Sidney Kimmel Cancer Center (SKCC) identified loss of the retinoblastoma (RB) susceptibility gene as a cause of what senior author Karen Knudsen, PhD, Director of the SKCC, describes as “major reprogramming of gene expression, allowing induction of pathways that promote features that induce characteristics of lethal disease.” That article is titled “Differential Impact of RB Status on E2F1 Reprogramming in Human Cancer.” RB was the first “gatekeeper” gene (genes that are responsible for controlling cell growth and keeping it in check) discovered for cancer. Loss or damage to RB allowed cancer to thrive and be more aggressive, but the exact mechanism of how this happened remained unclear. The JCI -piublshed study involved tumor and cell-free DNA analysis of samples from patients with” advanced, lethal-stage” prostate cancer from multiple institutions across the US and international institutions in the UK, Italy, Belgium, Finland, and Sweden. RB function may be disrupted in several different ways, but it was found that complete loss of the RB gene, compared to inactivation, was associated with the transcriptional reprogramming linked to aggressive disease. This reprogramming, interestingly, was unique and different from the typical cell-cycle genes that RB controls as a gatekeeper.