Transplantation of human cortex with Alzheimer's disease into rat occipital cortex; a model for the study of Alzheimer disease

Summary Senile dementia of the Alzheimer type (SDAT) is a major problem in the human senescent population. As this pathology cannot be reproduced in animals, research into its development is greatly impeded. The technique of implantation of the nervous tissue has been utilized in order to establish an animal model and to test the possible existence of a transmissible agent. When human temporal cortex with Alzheimer's disease is implanted in the occipital cortex of 7-week-old rats, human cerebral tissue containing abundant tangles induces in the receiver cortex a reactive fibrous gliosis. In the processes of the astrocytes, twisted filaments are evident among bundles of normal filaments. These alterations could be induced by the metabolising of abnormal filament subunits or by some infectious agent introduced by the implant.This study is supported by grant No. 2.4517.82 of Fonds de la Recherche Fondamentale Collective of Belgium.     

Neurosecretion and hydroelectrolytic regulation in Artemia salina (author's transl)]

The activity of Artemia protocerebral median neurosecretory cells is stimulated when animals are grown in media whose tonicity is lower than that of sea weater. The substance liberated by these cells could regulate the tonicity of the internal medium.     

EphrinB2 is the entry receptor for Nipah virus, an emergent deadly paramyxovirus

Nipah virus (NiV) is an emergent paramyxovirus that causes fatal encephalitis in up to 70 percent of infected patients, and there is evidence of human-to-human transmission. Endothelial syncytia, comprised of multinucleated giant-endothelial cells, are frequently found in NiV infections, and are mediated by the fusion (F) and attachment (G) envelope glycoproteins. Identification of the receptor for this virus will shed light on the pathobiology of NiV infection, and spur the rational development of effective therapeutics. Here we report that ephrinB2, the membrane-bound ligand for the EphB class of receptor tyrosine kinases (RTKs), specifically binds to the attachment (G) glycoprotein of NiV. Soluble Fc-fusion proteins of ephrinB2, but not ephrinB1, effectively block NiV fusion and entry into permissive cell types. Moreover, transfection of ephrinB2 into non-permissive cells renders them permissive for NiV fusion and entry. EphrinB2 is expressed on endothelial cells and neurons, which is consistent with the known cellular tropism for NiV. Significantly, we find that NiV-envelope-mediated infection of microvascular endothelial cells and primary cortical rat neurons is inhibited by soluble ephrinB2, but not by the related ephrinB1 protein. Cumulatively, our data show that ephrinB2 is a functional receptor for NiV.     

Oxidative metabolism of the limbic system in prepuberal rats

Resumen El consumo de oxígeno por amigdala, en ratas prepúberes, es mayor en machos que en hembras, hembras tratadas en el día 5° con propionato de testosterona y machos castrados postnatalmente. En los machos prepúberes, la castración origina una disminución en el consumo de oxígeno por amígdala.     

Oxidative metabolism of the limbic system in androgenized rats

Resumen Se ha estudiado el metabolismo oxidativo de amígdala e hipocampo en ratas en fase de estro, diestro y androgenizadas postnatalmente con testosterona. En estos animales desaparecen las variaciones observadas en animales cíclicos, presentando unos valores semejantes a los de diestro.     

X-ray analyses of peptide-inhibitor complexes define the structural basis of specificity for human and mouse renins.

X-ray analyses have defined the three-dimensional structures of crystals of mouse and human renins complexed with peptide inhibitors at resolutions of 1.9 and 2.8 A, respectively. The exquisite specificity of renin arises partly from ordered loop regions at the periphery of the binding cleft. Although the pattern of main-chain hydrogen bonding in other aspartic proteinase inhibitor complexes is conserved in renins, differences in the positions of secondary structure elements (particularly helices) also lead to improved specificity in renins for angiotensinogen substrates.     

Permanent El Niño during the Pliocene warm period not supported by coral evidence

The El Ni?o/Southern Oscillation (ENSO) system during the Pliocene warm period (PWP; 3-5 million years ago) may have existed in a permanent El Ni?o state with a sharply reduced zonal sea surface temperature (SST) gradient in the equatorial Pacific Ocean. This suggests that during the PWP, when global mean temperatures and atmospheric carbon dioxide concentrations were similar to those projected for near-term climate change, ENSO variability--and related global climate teleconnections-could have been radically different from that today. Yet, owing to a lack of observational evidence on seasonal and interannual SST variability from crucial low-latitude sites, this fundamental climate characteristic of the PWP remains controversial. Here we show that permanent El Ni?o conditions did not exist during the PWP. Our spectral analysis of the δ(18)O SST and salinity proxy, extracted from two 35-year, monthly resolved PWP Porites corals in the Philippines, reveals variability that is similar to present ENSO variation. Although our fossil corals cannot be directly compared with modern ENSO records, two lines of evidence suggest that Philippine corals are appropriate ENSO proxies. First, δ(18)O anomalies from a nearby live Porites coral are correlated with modern records of ENSO variability. Second, negative-δ(18)O events in the fossil corals closely resemble the decreases in δ(18)O seen in the live coral during El Ni?o events. Prior research advocating a permanent El Ni?o state may have been limited by the coarse resolution of many SST proxies, whereas our coral-based analysis identifies climate variability at the temporal scale required to resolve ENSO structure firmly.     

Eisosomes mark static sites of endocytosis

Endocytosis functions to recycle plasma membrane components, to regulate cell-surface expression of signalling receptors and to internalize nutrients in all eukaryotic cells. Internalization of proteins, lipids and other cargo can occur by one of several pathways that have different, but often overlapping, molecular requirements. To mediate endocytosis, effectors assemble transiently underneath the plasma membrane, carry out the mechanics of membrane deformation, cargo selection and vesicle internalization, and then disassemble. The mechanism by which endocytosis initiates at particular locations on the plasma membrane has remained unknown. Sites of endocytosis might be formed randomly, induced by stochastic protein and/or lipid clustering. Alternatively, endocytosis might initiate at specific locations. Here we describe large immobile protein assemblies at the plasma membrane in the yeast Saccharomyces cerevisiae that mark endocytic sites. These structures, termed eisosomes (from the Greek 'eis', meaning into or portal, and 'soma', meaning body), are composed primarily of two cytoplasmic proteins, Pil1 and Lsp1. A plasma membrane protein, Sur7, localizes to eisosomes. These structures colocalize with sites of protein and lipid endocytosis, and their components genetically interact with known endocytic effectors. Loss of Pil1 leads to clustering of eisosome remnants and redirects endocytosis and endocytic effector proteins to these clusters.