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.
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Question: Context: Hypercholesterolemia is a well-established risk factor for the development of kidney injury. Considering that female sex hormones may play a preventative role in both cardiovascular and renal diseases, the aim of the present study was to evaluate the effects of female sex hormones on hypercholesterolemia-induced renal dysfunction.', "Apolipoprotein E-deficient (ApoE) and C57 control female mice underwent an ovariectomy (OVX) or sham surgery and after 2 months, creatinine clearance, uremia and proteinuria were determined. Renal oxidative stress and lipid deposition were also quantified. Values are presented as meanSEM. Statistical analyses were performed using Two-way ANOVA followed by Tukey's post hoc test.", 'Creatinine clearance (L/min) was similar between C57 (17117) and ApoE (14026) mice underwent sham surgery. OVX resulted in a reduced glomerular filtration rate in both C57 (1128, ~-35%, p<0.05) and ApoE (6110, ~-56%, p<0.05) animals. Plasma levels of urea (mg/dL) were higher in both ApoE groups (Sham: 737; OVX: 738, p<0.05) when compared to C57 animals (Sham: 493; OVX: 604), with no changes among ovariectomized groups. Proteinuria levels (mg/24 h) were similar between C57 (Sham: 25.15.7; OVX: 33.74.7) and ApoE sham animals (26.43.5), however, 24-h urine protein excretion was augmented in ApoE OVX animals (49.65.8, p<0.05). Histological kidney analysis demonstrated that the absence of female sex hormones resulted in increased oxidative stress, which was more severe in ApoE mice (C57 Sham: 9.20.4; C57 OVX: 22.91.0; ApoE Sham: 13.90.7; ApoE OVX: 34.01.4 au x 103, p<0.05). As expected, ApoE mice presented higher lipid deposition, which was not affected by OVX (C57 Sham: 00; C57 OVX: 00; ApoE Sham: 6.81.6; ApoE OVX: 5.20.8% x 10-2, p<0.05). Ovariectomy resulted in a similar reduction in ER- protein expression in the renal cortex (C57: 0.780.04; ApoE: 0.810.04 au, p<0.05) when compared to sham animals (C57:1.000.04; ApoE: 1.030.03 au).\Question: Do endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice?

Answer: Taken together these data indicate that female sex hormones may delay hypercholesterolemia-induced renal dysfunction and emphasizes the importance of plasma cholesterol control in post-menopausal women.

Question: Context: To test whether extension of the C-terminus of human chorionic gonadotropin (hCG) alpha-subunit (halpha) alters the bioactivity of the recombined alphabeta heterodimer.', 'The stop codon of halpha was mutated to produce a 24 amino acid extension.', 'The extended halpha (alpha(+24)) was co-expressed with hCGbeta in COS-7 cells and the receptor binding and in vivo bioactivity of the secreted hormone was compared with its wild-type counterpart.', 'This extension did not impair the binding of hCG to rat LH/CG receptors and provoked a sixfold reduction in its stimulatory activity of testosterone secretion in rat Leydig cells.\Question: Does human chorionic gonadotropin with C-elongated alpha-subunit retain full receptor binding and partial agonist activity?

Answer: The extension of alpha by itself does not lead to inhibition of the alphabeta heterodimer to LH receptors but the structure of the extension appears to play an important role. It is thus possible that one-chain hCG chimeras with the beta N-terminus fused to the alpha C-terminus might be active.

Question: Context: Epigenetic modifications play an important role in the regulation of gene transcription and cellular function. Here, we examined if pro-inflammatory factors present in the inflamed joint of patients with rheumatoid arthritis (RA) could regulate histone deacetylase (HDAC) expression and function in fibroblast-like synoviocytes (FLS).', 'Protein acetylation in synovial tissue was assessed by immunohistochemistry. The mRNA levels of HDAC family members and inflammatory mediators in the synovial tissue and the changes in HDAC expression in RA FLS were measured by quantitative (q) PCR. FLS were either transfected with HDAC5 siRNA or transduced with adenoviral vector encoding wild-type HDAC5 and the effects of HDAC5 manipulation were examined by qPCR arrays, ELISA and ELISA-based assays.', 'Synovial class I HDAC expression was associated with local expression of tumour necrosis factor (TNF) and matrix metalloproteinase-1, while class IIa HDAC5 expression was inversely associated with parameters of disease activity (erythrocyte sedimentation rate, C-reactive protein, Disease Activity Score in 28 Joints). Interleukin (IL)-1 or TNF stimulation selectively suppressed HDAC5 expression in RA FLS, which was sufficient and required for optimal IFNB, CXCL9, CXCL10 and CXCL11 induction by IL-1, associated with increased nuclear accumulation of the transcription factor, interferon regulatory factor 1(IRF1).\Question: Do inflammatory cytokines epigenetically regulate rheumatoid arthritis fibroblast-like synoviocyte activation by suppressing HDAC5 expression?

Answer:
Inflammatory cytokines suppress RA FLS HDAC5 expression, promoting nuclear localisation of IRF1 and transcription of a subset of type I interferon response genes. Our results identify HDAC5 as a novel inflammatory mediator in RA, and suggest that strategies rescuing HDAC5 expression in vivo, or the development of HDAC inhibitors not affecting HDAC5 activity, may have therapeutic applications in RA treatment.