Black and Hispanic Men Perceived to Be Large Are at Increased Risk for Police Frisk,Search, and Force

Social justice issues remain some of the most pressing problems in the United States. One aspect of social justice involves the differential treatment of demographic groups in the criminal justice system. While data consistently show that Blacks and Hispanics are often treated differently than Whites, one understudied aspect of these disparities is how police officers'' assessments of suspects'' size affects their decisions. Using over 3 million cases from the New York Police Department (NYPD) Stop, Question, and Frisk (SQF) Database, 2006–2013, this study is the first to explore suspects'' race, perceived size, and police treatment. Results indicate that tall and heavy black and Hispanic men are at the greatest risk for frisk or search. Tall and heavy suspects are at increased risk for experiencing police force, with black and Hispanic men being more likely to experience force than white men across size categories.     

Differential expression of guinea pig class II major histocompatibility complex antigens on vascular endothelial cells in vitro and in experimental allergic encephalomyelitis

Previous studies have shown that vascular endothelial cells do not normally express major histocompatibility complex (MHC) Class II antigens either in vivo or in vitro. In this investigation it was found that endothelial in the central nervous system (CNS) of normal guinea pigs constitutively express MHC Class II antigens recognized by the monoclonal antibodies HLA-DR, 27E7, and MSgp8. This phenotype is retained when these CNS-derived endothelial cells are propagated in tissue culture. Furthermore, examination of CNS tissue taken from animals in the acute phase of chronic relapsing experimental allergic encephalomyelitis shows that additional epitopes of the MHC Class II antigen, detected by the monoclonal antibodies CI.13.1 and 22C4, are present during the diseased state. This study not only demonstrates constitutive expression of certain MHC Class II determinants by guinea pig endothelial cells, but also shows that other Class II determinants can be differentially expressed in certain disease states.     

Lactation-associated redistribution of the glial fibrillary acidic protein within the supraoptic nucleus

Summary Three clones of myeloproliferative virus (MPV)-transformed rat fibroblasts (NRK) with different growth properties and morphology were transplanted to athymic nude mice. Presence of carbohydrate-binding proteins was inferred by fluorescence microscopy using fluorescent, glycosylated markers. Salt and detergent extracts of tumors from this model system were fractionated under identical conditions on different sets of Sepharose columns, to which lactose, asialofetuin, melibiose, mannan and fucose had been covalently linked. Successive elution by chelating reagent and specific sugar resulted in isolation of the different Ca²⁺-dependent and Ca²⁺-independent endogenous carbohydrate-binding proteins that were assayable as agglutinins. In comparison, the different tumors displayed a pattern with qualitative and quantitative alterations. Since protein-carbohydrate interaction mediated by carbohydrate-binding proteins (lectins) is of importance for cognitive processes, it is remarkable that the pattern of membrane glycoproteins, isolated by affinity chromatography on resins with immobilized plant lectins, had also been found to reveal certain individual properties for receptors specific for peanut agglutinin (PNA) and Ulex europaeus agglutinin (UEA). These demonstrated differences within the system of protein-carbohydrate interaction suggest that endogenous lectins and their ligands have potential significance as markers defining a certain phenotype within this tumor model system.Dedicated to Prof. Dr. W. Lamprecht on the occasion of his 60th birthday     

The Vancouver Lymphadenopathy-AIDS Study: 4. Effects of exposure factors,cofactors and HTLV-III seropositivity on number of helper T cells.

Results of testing for antibody to human T-lymphotropic virus (HTLV-III) and absolute numbers of helper T cells in 219 participants in the Vancouver Lymphadenopathy-AIDS (acquired immune deficiency syndrome) Study were analysed. The mean absolute helper T-cell counts in the 141 HTLV-III seronegative and the 78 seropositive men were 897/mL and 659/mL respectively (p less than 0.001). Established AIDS risk factors such as elevated lifetime number of male sexual partners and frequent receptive anal intercourse did not appear to have any significant effect on number of helper T cells that was independent of HTLV-III antibody status. Seropositive men with less than 100, 100 to 500 or more than 500 male sexual partners in their lifetime had mean absolute helper T-cell counts of 667/mL, 651/mL and 662/mL respectively. Most other risk factors, as well, did not appear to exert any effect on absolute number of helper T cells that was independent of the effect of HTLV-III antibody status. However, independent effects of a history of mononucleosis or hepatitis and of cigarette smoking were noted. The data support the hypothesis that no immune dysfunction beyond that due to the initial infection alone arises from repeated exposure to HTLV-III. Most risk factors appear to act as exposure factors, exerting their effect on the immune system merely by increasing the probability of contact with the agent. The independent effects of a history of mononucleosis or hepatitis suggest that viral agents may be cofactors in the production of immune dysfunction.     

Ethanol and the γ-Aminobutyric Acid-Benzodiazepine Receptor Complex

Abstract: Ethanol appears to enhance γ-aminobutyric acid (GABA)-mediated synaptic transmission. Using radioligand binding techniques, we investigated the possibility that the GABA-benzodiazepine receptor complex is the site responsible for this effect. Ethanol at concentrations up to 100 m M failed to alter binding of [³H]flunitrazepam (FNZ), [³H]Ro 15-1788, or [³H]methyl-γ-carboline-3-carboxylate (MBCC) to benzodiazepine receptors, or of [³H]muscimol to GABA receptors in rat brain membranes. Scatchard analyses of the binding of these radioligands at 4°C and 37°C revealed no significant effects of 100 m M ethanol on receptor affinity or number. A variety of drugs as well as chloride ion increased binding of [³H]FNZ and/or [³H]muscimol, but these influences were not modified by ethanol. These findings indicate that ethanol probably potentiates GABAergic neurotransmission at a signal transduction site beyond the GABA-benzodiazepine receptor complex.     

Compartmentation and regulation of acetylcholine synthesis at the synapse.

Acetylcholine and choline release was measured by using an automated and modified version of the chemiluminescence technique of Israel & Lesbats [(1981) Neurochem. Int. 3, 81-90]. A comparison of acetylcholine and choline release from synaptosomes demonstrated that acetylcholine release was K+-stimulated and inhibited by the Ca2+ ionophore A23187 and cyanide. Choline release, however, did not vary markedly under different conditions, suggesting that it is not associated with acetylcholine release at the nerve ending. Total acetylcholine synthesis in synaptosomal preparations was measured concurrently with the incorporation of [14C]acetyl and [3H]choline moieties by using the chemiluminescence method. Under sub-optimal glucose concentrations or in the absence of treatment of the synaptosomes with the acetylcholinesterase inhibitor phospholine, the incorporation of radioactivity exceeded total synthesis, indicating that cycling between acetylcholine and its precursors may occur. After treatment with phospholine, acetyl-group incorporation from D-[U-14C]glucose occurred without dilution of the precursor at optimal (1.0 mM) and low (0.1 mM) glucose concentrations; however, at very low (0.01 mM) glucose concentrations, dilution by a small endogenous pool occurred. [14C]Acetyl incorporation into acetylcholine was compared with various metabolic parameters. A closer correlation was observed between [14C]acetyl-group incorporation into acetylcholine and the calculated acetyl-carrier efflux from the mitochondria than with the calculated pyruvate-dehydrogenase-complex flux. The results are discussed with respect to the regulation of acetylcholine concentrations at the synapse and the mechanism whereby turnover occurs.