State University of New York System

About: State University of New York System is a education organization based out in Albany, New York, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 54077 authors who have published 78070 publications receiving 2985160 citations.

Neurocan is upregulated in injured brain and in cytokine-treated astrocytes.

Abstract: Injury to the CNS results in the formation of the glial scar, a primarily astrocytic structure that represents an obstacle to regrowing axons. Chondroitin sulfate proteoglycans (CSPG) are greatly upregulated in the glial scar, and a large body of evidence suggests that these molecules are inhibitory to axon regeneration. We show that the CSPG neurocan, which is expressed in the CNS, exerts a repulsive effect on growing cerebellar axons. Expression of neurocan was examined in the normal and damaged CNS. Frozen sections labeled with anti-neurocan monoclonal antibodies 7 d after a unilateral knife lesion to the cerebral cortex revealed an upregulation of neurocan around the lesion. Western blot analysis of extracts prepared from injured and uninjured tissue also revealed substantially more neurocan in the injured CNS. Western blot analysis revealed neurocan and the processed forms neurocan-C and neurocan-130 to be present in the conditioned medium of highly purified rat astrocytes. The amount detected was increased by transforming growth factor beta and to a greater extent by epidermal growth factor and was decreased by platelet-derived growth factor and, to a lesser extent, by interferon gamma. O-2A lineage cells were also capable of synthesizing and processing neurocan. Immunocytochemistry revealed neurocan to be deposited on the substrate around and under astrocytes but not on the cells. Astrocytes therefore lack the means to retain neurocan at the cell surface. These findings raise the possibility that neurocan interferes with axonal regeneration after CNS injury.

Platelets and thrombolytic therapy.

Abstract: FIBRINOLYTIC therapy is a major advance in the treatment of occlusive vascular disease. Problems remain, however, including resistance to fibrinolytic therapy, delays in reperfusion, reocclusion after successful thrombolysis, and serious hemorrhage.1 2 3 Increasing evidence indicates that platelets have an important role in both delaying reperfusion and mediating reocclusion. In addition, preliminary data suggest that some thrombi resist lysis because they are rich in platelets and that platelet dysfunction contributes to the hemorrhagic diathesis associated with thrombolytic therapy. It is worthwhile, therefore, to review the complex interrelations between platelets and fibrinolysis, with emphasis on the therapeutic potential (and risks) of combining thrombolytic . . .

Physiologic Evidence for a Dual A-V Transmission System

Abstract: A study of the transmission of early premature contractions between atria and ventricles and in the retrograde direction in the dog heart suggests the existence of two parallel A-V conduction pathways communicating with each other over one or more branches. The evidence is based on the excessive delay of very early premature responses in traversing the node, suggesting that a slowly conducting pathway recovers earlier than the normal "fast" pathway; on the echoing back to the chamber of origin of early premature responses; and on ventricular electrograms of "abnormal" configuration obtained during early premature responses. These observations and the hypothesis to which they lead provide a natural explanation for reciprocal rhythm and nodal paroxysmal tachycardia.

Interpretation of Cloud-Climate Feedback as Produced by 14 Atmospheric General Circulation Models

Abstract: Understanding the cause of differences among general circulation model projections of carbon dioxide-induced climatic change is a necessary step toward improving the models An intercomparison of 14 atmospheric general circulation models, for which sea surface temperature perturbations were used as a surrogate climate change, showed that there was a roughly threefold variation in global climate sensitivity Most of this variation is attributable to differences in the models' depictions of cloud-climate feedback, a result that emphasizes the need for improvements in the treatment of clouds in these models if they are ultimately to be used as climatic predictors

Paxillin LD4 Motif Binds PAK and PIX through a Novel 95-kD Ankyrin Repeat, ARF–GAP Protein: A Role in Cytoskeletal Remodeling

Abstract: Paxillin is a focal adhesion adaptor protein involved in the integration of growth factor- and adhesion-mediated signal transduction pathways. Repeats of a leucine-rich sequence named paxillin LD motifs (Brown M.C., M.S. Curtis, and C.E. Turner. 1998. Nature Struct. Biol. 5:677–678) have been implicated in paxillin binding to focal adhesion kinase (FAK) and vinculin. Here we demonstrate that the individual paxillin LD motifs function as discrete and selective protein binding interfaces. A novel scaffolding function is described for paxillin LD4 in the binding of a complex of proteins containing active p21 GTPase–activated kinase (PAK), Nck, and the guanine nucleotide exchange factor, PIX. The association of this complex with paxillin is mediated by a new 95-kD protein, p95PKL (paxillin-kinase linker), which binds directly to paxillin LD4 and PIX. This protein complex also binds to Hic-5, suggesting a conservation of LD function across the paxillin superfamily. Cloning of p95PKL revealed a multidomain protein containing an NH2-terminal ARF–GAP domain, three ankyrin-like repeats, a potential calcium-binding EF hand, calmodulin-binding IQ motifs, a myosin homology domain, and two paxillin-binding subdomains (PBS). Green fluorescent protein- (GFP-) tagged p95PKL localized to focal adhesions/complexes in CHO.K1 cells. Overexpression in neuroblastoma cells of a paxillin LD4 deletion mutant inhibited lamellipodia formation in response to insulin-like growth fac- tor-1. Microinjection of GST–LD4 into NIH3T3 cells significantly decreased cell migration into a wound. These data implicate paxillin as a mediator of p21 GTPase–regulated actin cytoskeletal reorganization through the recruitment to nascent focal adhesion structures of an active PAK/PIX complex potentially via interactions with p95PKL.