Shyama Kuruvilla and colleagues present findings across 12 country case studies of multisectoral collaboration, showing how diverse sectors intentionally shape new ways of collaborating and learning, using “business not as usual” strategies to transform situations and achieve shared goals
Therapeutic hypothermia initiated during cardiopulmonary resuscitation (CPR) in pre-clinical studies appears to be highly protective against sudden cardiac arrest injury. Given the challenges to implementing CPR cooling clinically, insights into its critical mechanisms of protection could guide development of new CPR drugs that mimic hypothermia effects without the need for physical cooling. Here, we used Akt1-deficient mice that lose CPR hypothermia protection to identify hypothermia targets. Adult female C57BL/6 mice (Akt1 +/+ and Akt1 +/- ) underwent 8 min of KCl-induced asystolic arrest and were randomized to receive hypothermia (30 ± 0.5°C) or normothermia. Hypothermia was initiated during CPR and extended for 1 h after resuscitation. Neurologically scored survival was measured at 72 h. Other outcomes included mean arterial pressure and target measures in heart and brain related to contractile function, glucose utilization and inflammation. Compared to northothermia, hypothermia improved both 2h mean arterial pressure and 72h neurologically intact survival in Akt1 +/+ mice but not in Akt1 +/- mice. In Akt1 +/+ mice, hypothermia increased Akt and GSK3β phosphorylation, pyruvate dehydrogenase activation, and NAD + and ATP production while decreasing IκBα degradation and NF-κB activity in both heart and brain at 30 min after CPR. It also increased phospholamban phosphorylation in heart tissue. Further, hypothermia reduced metabolic and inflammatory blood markers lactate and Pre-B cell Colony Enhancing Factor. Despite hypothermia treatment, all these effects were reversed in Akt1 +/- mice. Taken together, drugs that target Akt1 and its effectors may have the potential to mimic hypothermia-like protection to improve sudden cardiac arrest survival when administered during CPR.
in 1%8, represented the proceedings of the sixth annual meeting of the ACNP. The second edition, Psychopharmacology: A Generation of Progress, published in 1976, became a widely cited reference in basic neuroscience, psychiatry, and neurology, and this volume promises to be the same. It contains 184 chapters written by 271 contributors in 1,840 pages. It is divided into three major sections: Basic Neurobiology (J. T. Coyle and I. J. Kopin, associate editors), Biological Psychiatry (W. E. Bunney, Jr. and K. L. Davis), and Clinical Psychopharmacology (C. R. Schuster, R. I. Shader, and G. M. Simpson).The scope and depth of the volume in the clinical aspects and the scientific foundations of psychiatry leave no question that this will be a highly useful reference work for practising psychiatrists, research psychiatrists, and psychopharmacologists. As a neurologist, I reviewed the work with regard to its potential usefulness for members of the neuroscience community outside of psychiatry and psychopharmacology. For all neuroscientists, this volume is a valuable resource, owing particularly to the strength of the basic neurobiology section. There are 48 chapters in this section, covering the neuroanatomy and neurochemistry of the classic neurotransmitter systems; neurotransmitter receptors and their heterogeneity; neurotoxins in animal models and human disease; and the molecular biology, chemistry, and anatomy of the neuropeptides. To have this range of neuroscience updated succinctly and definitively by established authorities in each area and collected in a single volume provides a valuable resource indeed.The neurologist with an interest in movement disorders has much to find in this book. Within the basic neurobiology section, chapters of potential interest include those devoted to muscarinic cholinergic and dopaminergic receptor heterogeneity, neural transplantation, and MPTP-induced parkinsonism. Also of potential interest are the chapters devoted to the design of clinical trials of drugs, the design and validation of clinical rating scales, and the pharmacokinetics of centrally acting agents. Two movement disorders related to psychotropics, tardive dyskinesia and neuroleptic malignant syndrome, are reviewed thoroughly but concisely. My one disappointment here was in the lack of coverage of other psychotropic drug-induced movement disorders including acute dystonia, akathisia, and parkinsonism. Perhaps the editorial decision to limit the contents to a single volume led to the exclusion of subjects in which there is less news to report. Nevertheless, there is enough information here to make this a highly valued source for the next generation, at least. As all neurologists know, Jean-Martin Charcot, professor of neurology at SalpCtrikre in Paris from 1862 until his death in 1893 at age 67, was one of the leading clinical neurologists of his day and is considered by many the greatest of all time. Charcot meticulously examined thousands of patients at the huge hospital. By combining his clinical evaluations with post...
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