In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

[Q]: Context: Infection of human immunodeficiency virus (HIV) has been associated with several chronic diseases, including pulmonary artery hypertension and atherosclerosis. However, the underlying mechanisms of these vascular complications are largely unknown. The objective of this study was to test a novel hypothesis that HIV Nef, an accessory HIV protein, may directly affect endothelial functions and gene expression in pulmonary arteries.', 'Fresh porcine pulmonary artery rings and human pulmonary artery endothelial cells (HPAECs) were treated with HIV Nef for 24 h. With a myograph device, vasomotor function was determined with thromboxane A2 analog, U46619, for contraction, bradykinin, and sodium nitroprusside for relaxation. The expression of endothelial nitric oxide synthase (eNOS) was determined with real-time PCR and immunohistochemistry. Nitric oxide (NO) production was determined by Calorimetric Nitric Oxide Assay kit. Superoxide anion levels were detected with lucigenin-enhanced chemiluminescence assay and dihydroethidium (DHE) staining.', 'The endothelium-dependent vasorelaxation in response to bradykinin was significantly reduced in HIV Nef-treated porcine pulmonary artery rings in a concentration-dependent manner. In response to bradykinin (10(-8) mol/L), HIV Nef (10 ng/mL) significantly reduced vasorelaxation by 32% compared with untreated controls (P < 0.05). In addition, HIV Nef significantly decreased eNOS expression in the vessels and HPAECs. HIV Nef at 10 ng/mL significantly decreased NO production in HPAECs by 21% compared with controls (P < 0.05). Furthermore, HIV Nef significantly increased superoxide anion production in porcine pulmonary arteries and HPAECs compared with controls (P < 0.05). Consequently, Mn (III) tetrakis porphyrin, a superoxide dismutase mimic, effectively blocked HIV Nef-induced vasomotor dysfunction and superoxide anion production. The specificity of HIV Nef action was confirmed by anti-Nef antibody blocking and Nef heat inactivation.\Question: Does hIV Nef protein cause endothelial dysfunction in porcine pulmonary arteries and human pulmonary artery endothelial cells?
[A]: HIV Nef protein significantly decreases endothelium-dependent vasorelaxation in porcine pulmonary arteries. It also reduces eNOS expression and induces oxidative stress in both porcine pulmonary arteries and HPAECs. This study demonstrates a new mechanism of HIV Nef, which causes endothelial dysfunction and may contribute to the human pulmonary artery disease in HIV-infected patients.

[Q]: Context: To test whether oral L-81 treatment could improve the condition of mice with diabetes and to investigate how L-81 regulates microsomal triglyceride transfer protein (MTP) activity in the liver.', 'Genetically diabetic (db/db) mice were fed on chow supplemented with or without L-81 for 4 wk. The body weight, plasma glucose level, plasma lipid profile, and adipocyte volume of the db/db mice were assessed after treatment. Toxicity of L-81 was also evaluated. To understand the molecular mechanism, HepG2 cells were treated with L-81 and the effects on apolipoprotein B (apoB) secretion and mRNA level of the MTP gene were assessed.', 'Treatment of db/db mice with L-81 significantly reduced and nearly normalized their body weight, hyperphagia and polydipsia. L-81 also markedly decreased the fasting plasma glucose level, improved glucose tolerance, and attenuated the elevated levels of plasma cholesterol and triglyceride. At the effective dosage, little toxicity was observed. Treatment of HepG2 cells with L-81 not only inhibited apoB secretion, but also significantly decreased the mRNA level of the MTP gene. Similar to the action of insulin, L-81 exerted its effect on the MTP promoter.\Question: Does pluronic L-81 ameliorate diabetic symptoms in db/db mice through transcriptional regulation of microsomal triglyceride transfer protein?
[A]: L-81 represents a promising candidate in the development of a selective insulin-mimetic molecule and an anti-diabetic agent.

[Q]: Context: To investigate the associations of IL17A, IL17F, IL23A, and IL23R copy number variants (CNVs) with Vogt-Koyanagi-Harada (VKH) syndrome and Behcet's disease (BD) and the possible mechanisms involved.", 'Two-stage case-control and functional studies.', 'A total of 1159 VKH patients, 1036 BD patients, and 2050 controls were enrolled.', 'TaqMan real-time polymerase chain reaction assay was used for genotyping of copy number variant. Cell proliferation was measured by colorimetric assay.', 'Association of CNVs in IL17A, IL17F, IL23A, and IL23R with BD and VKH syndrome and the functional roles of IL17F CNVs.', 'Increased frequencies of more than 2 copies of IL17F and IL23A were found in BD patients as compared with controls (IL17F: P=4.1710(-8); odds ratio [OR], 2.2; IL23A: P=2.8610(-11); OR, 2.8, respectively). A similar result was found for VKH syndrome (IL17F: P=2.8410(-13); OR, 2.7; IL23A: P=4.4610(-17); OR, 3.4, respectively). Interestingly, the association of IL17F and IL23A with BD was found only in male patients (IL17F: P=1.0610(-6); OR, 2.3; IL23A, P=3.8110(-8); OR, 2.8, respectively), but not in female patients. No association of CNVs in IL17A and IL23R was found for BD and VKH syndrome. IL17F protein levels were correlated positively with gene copy numbers (P=3.4310(-7)). Individuals with high IL17F copies showed enhanced peripheral blood mononuclear cells (PBMC) proliferation (P=5.6710(-3)).\Question: Do genetic variations of IL17F and IL23A show associations with Behcet 's disease and Vogt-Koyanagi-Harada syndrome?
[A]:
High gene copy numbers of IL17F and IL23A were associated with BD and VKH syndrome. Enhanced IL17F protein production and PBMC proliferation were associated with high IL17F copy numbers.