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A: Yes this is an expected behavior in that function. By the way, to mimic the open your web browser from your terminal, youcan use curl commands such as: curl HIV-1 infection induces impairment of endothelial nitric oxide synthase in humanumbilical vein endothelial cells. HIV-1 may cause endothelial dysfunction, although the underlying mechanisms remain elusive.
Here we evaluate the relationship between HIV-1 infection and nitric oxide synthase (NOS) in human umbilical vein endothelialcells (HUVEC). Infection of HUVEC with HIV-1 strains BaL, NL4-3, and NL4-3-NL-C34 increased concentrations of HIV-1
p24 core antigen and HIV-1 RNA in the culture supernatant, respectively, without altering cell viability. HUVEC-derived
macrophages infected with BaL or NL4-3 viruses augmented production of TNF-alpha, IL-1beta, and IL-6. In contrast,
supernatants from cultures of HIV-1-infected HUVEC induced monocyte chemoattractant protein-1 production by HUVEC,
whereas that from the NL4-3-NL-C34 virus-infected cultures inhibited. Infection of HUVEC with HIV-1, BaL, NL4-3, orNL4-3-NL-C34 cells significantly decreased the production of nitrite, a stable metabolite of nitric oxide, and increased
inducible nitric oxide synthase (iNOS) protein. HIV-1-infected HUVEC decreased both endothelial constitutive nitric oxidesynthase (ecNOS) and iNOS protein expression, whereas treatment of the cells with 10-11 M cocaine caused a greater reductionof iNOS protein expression compared with that of ecNOS. Cocaine-induced iNOS mRNA expression was increased by HIV-1infection. In contrast, treatment with 10-11 M cocaine reduced ecNOS mRNA expression, which was further enhanced byHIV-1 infection. The study indicates that HIV-1 infection impairs both ecNOS and iNOS, and decreases the nitric oxide activityof HUVEC in part by the up-regulation of cocaine-induced iNOS mRNA expression.package
com.github.zhangkaitao.onechart.chart; ba244e880a
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