Innate immune responses reverse HIV cognitive disease in mice: Profile by RNAseq in the brain.

Antiretroviral therapy controls immunodeficiency in people with HIV but many develop mild neurocognitive disorder. Here we investigated HIV brain disease by infecting mice with the chimeric HIV, EcoHIV, and probing changes in brain gene expression during infection and reversal with polyinosinic-polycytidylic acid (poly I:C). EcoHIV-infected C57BL/6 mice were treated with poly I:C and monitored by assay of learning in radial arm water maze, RNAseq of striatum, and QPCR of virus burden and brain transcripts.

Prevention and treatment of HIV infection and cognitive disease in mice by innate immune responses.

HIV associated neurocognitive impairment afflicts roughly half of infected individuals on antiretroviral therapy. This disease currently has no treatment. We have previously shown that type I interferon is induced by and partially controls infection and neuropathogenesis in mice infected by chimeric HIV, EcoHIV.

[Diagnostic Significance of BIOMED-2 Standardized Gene Rearran-gement System in Patients with Non-Hodgkin's Lymphoma].

Objective: To detect the immunoglobulin(Ig) and T cell receptor(TCR) gene rearrangement in bone marrow of non-Hodgkin's lymphoma(NHL) patients by using BIOMED-2 standardized system, and to explore the potential clinical significance of Ig/TCR gene rearrangement.

Methods: DNA was extracted in bone marrow and Formalin-fixed and Paraffin-embedded(FFPE) samples of NHL patients, the Ig/TCR gene rearrangements were analyzed by using BIOMED-2 multiple primers system and multiplex PCR assay.

Results: Among 235 T-NHL cases, 71.

TLR4 regulates cardiac lipid accumulation and diabetic heart disease in the nonobese diabetic mouse model of type 1 diabetes.

Toll-like receptor (TLR)4 regulates inflammation and metabolism and has been linked to the pathogenesis of heart disease. TLR4 is upregulated in diabetic cardiomyocytes, and we examined the role of TLR4 in modulating cardiac fatty acid (FA) metabolism and the pathogenesis of diabetic heart disease in nonobese diabetic (NOD) mice. Both wild-type (WT) NOD and TLR4-deficient NOD animals had increased plasma triglyceride levels after the onset of diabetes.

Flt3L controls the development of radiosensitive dendritic cells in the meninges and choroid plexus of the steady-state mouse brain.

Antigen-presenting cells in the disease-free brain have been identified primarily by expression of antigens such as CD11b, CD11c, and MHC II, which can be shared by dendritic cells (DCs), microglia, and monocytes. In this study, starting with the criterion of Flt3 (FMS-like receptor tyrosine kinase 3)-dependent development, we characterize the features of authentic DCs within the meninges and choroid plexus in healthy mouse brains. Analyses of morphology, gene expression, and antigen-presenting function established a close relationship between meningeal and choroid plexus DCs (m/chDCs) and spleen DCs.

Effect of chromium picolinate supplementation on growth performance and meat characteristics of swine.

The purpose of this study was to evaluate the effect of supplemental chromium (Cr) in the form of chromium picolinate (CrPic) on swine growth performance, meat quality, and protein deposition in skeletal muscle. Forty-eight piglets were divided into three groups randomly, fed with three different dietary levels of Cr (common basal feedstuff supplemented with a dose of 1.61 μg/g or 3.

Cellular and humoral immune responses in the early stages of diabetic nephropathy in NOD mice.

This study was designed to examine immunopathology of diabetic nephropathy in non-obese diabetic (NOD) mice and to investigate the involvement of cellular and humoral immunity at various time points after diabetes onset. We found that the glomeruli of diabetic NOD mice were infiltrated with T and B cells, as well as CD11c+ dendritic cells, which had close contact with CD4+ and CD8+ T cells in the infiltrates. We also found that IgG deposits in the glomeruli of diabetic NOD mice were accompanied by the presence of complement C3.

Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction.

In addition to its role in cell adhesion, beta-catenin is an important signaling molecule in the Wnt/Wingless signaling pathway. Recent studies have indicated that beta-catenin is stabilized by hypertrophic stimuli and may regulate cardiac hypertrophic responses. To explore the role and requirement of beta-catenin in cardiac development and hypertrophy, we deleted the beta-catenin gene specifically in cardiac myocytes by crossing loxP-floxed beta-catenin mice with transgenic mice expressing a Cre recombinase under the control of the alpha-myosin heavy chain promoter.