The specificity of human immunodeficiency virus type 1 (HIV-1) for human cells precludes virus infection in most mammalian species and limits the utility of small animal models for studies of disease pathogenesis, therapy, and vaccine development. One way to overcome this limitation is by human cell xenotransplantation in immune-deficient mice. However, this has proved inadequate, as engraftment of human immune cells is limited (both functionally and quantitatively) following transplantation of mature human lymphocytes or fetal thymus/liver. To this end, a human immune system was generated from umbilical cord blood-derived CD34 A genetically modified immunodeficient mouse with truncation or knockout of the interleukin-2 (IL-2) receptor (common cytokine receptor) gamma chain (␥ c ) provides a unique platform for permanent engraftment of human hematopoietic stem cells (HSCs). The attenuation of cell signaling pathways via ␥ c for IL-2, -4, -7, -9, -15, and -21 cytokines, which are involved in survival, differentiation, and function of lymphocytes, impairs the development of mouse lymphatic compartments. This provides a niche for human lymphoid and myeloid cell reconstitution and results in the development of a functional human immune system (HIS

Linear, sequential formatting for the escape room game design is recommended for use with recruits into nursing. The use of escape rooms for recruitment is a positive activity. [J Nurs Educ. 2018;57(3):184-187.].

Cognitive, behavioral, and motor impairments, during progressive human immunodeficiency virus type 1 (HIV-1) infection, are linked to activation of brain mononuclear phagocytes (MP; perivascular macrophages and microglia). Activated MPs effect a giant cell encephalitis and neuroinflammatory responses that are mirrored in severe combined immunodeficient (SCID) mice injected with human monocyte-derived macrophages (MDM). Whether activated human MDMs positioned in the basal ganglia affect hippocampal neuronal plasticity, the brain subregion involved in learning and memory, is unknown. Thus, immunohistochemical techniques were used for detection of newborn neurons (polysialylated neuronal cell adhesion molecule [PSA-NCAM]) and cell proliferation (Ki-67) to assay MDM effects on neuronal development in mouse models of HIV-1 encephalitis. Immunodeficient (C.B.-17/SCID and nonobese diabetic/SCID, NOD/SCID) and immune competent (C.B.-17) mice were injected with uninfected or HIV-1-infected MDM. Sham-operated or unmanipulated mice served as controls. Neuronal plasticity was evaluated in the hippocampal dentate gyrus (DG) at days 7 and 28. By day 7, increased numbers of Ki-67+ cells, PSA-NCAM+ cells and dendrites in DG were observed in sham-operated animals. In contrast, significant reductions in neuronal precursors and altered neuronal morphology paralleled increased microglial activation in both HIV-1-infected and uninfected MDM-injected animals. DG cellular composition was restored at day 28. We posit that activated MDM induce inflammation and diminish DG neuronal plasticity. These data provide novel explanations for the cognitive impairments manifested during advanced HIV-1 infection.

Sixty-two black bears were captured at different seasons during the years 1983–1987. Bears were anesthetized in their dens during the winter and parts of the fall and spring, while bears captured during the summer were snared prior to anesthesia. Radioimmunoassays for both Cortisol and progesterone were validated on black bear serum. An improved, rapid progesterone radioimmunoassay for black bear serum is reported. Serum glucose demonstrated a tendency for reduction during spring. Serum progesterone levels did not demonstrate seasonal differences and were significantly higher in females only during the summer ovulatory/postestrus period. Serum Cortisol was significantly elevated during the winter denning period as compared with the summer period. We conclude that differences in serum progesterone, Cortisol, and glucose may not be indicators of stress exposure, but of seasonal reproductive states and metabolic utilization of fat reserves.

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