instruction:
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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Context: Various pathways involved in the pathogenesis of sJIA have been identified through gene expression profiling in peripheral blood mononuclear cells (PBMC), but not in neutrophils. Since neutrophils are important in tissue damage during inflammation, and are elevated as part of the acute phase response, we hypothesised that neutrophil pathways could also be important in the pathogenesis of sJIA. We therefore studied the gene profile in both PBMC and neutrophils of sJIA patients treated with tocilizumab.', 'We studied the transcriptomes of peripheral blood mononuclear cells (PBMC) and neutrophils from eight paired samples obtained from 4 sJIA patients taken before and after treatment, selected on the basis that they achieved ACR90 responses within 12 weeks of therapy initiation with tocilizumab. RNA was extracted and gene expression profiling was performed using Affymetrix GeneChip Human Genome U133 Plus 2.0 microarray platform. A longitudinal analysis using paired t-test (p<0.05 and FC1.5) was applied to identify differentially expressed genes (DEGs) between the two time points followed by ingenuity pathway analysis. Gene Set Enrichment Analysis (GSEA) and quantitative real-time PCR were then performed to verify the microarray results.', 'Gene ontology analysis in neutrophils revealed that response to tocilizumab significantly altered genes regulating mitochondrial dysfunction and oxidative stress (p=4.6E-05). This was independently verified with GSEA, by identifying a set of oxidative genes whose expression correlated with response to tocilizumab. In PBMC, treatment of sJIA with tocilizumab appeared to affect genes in Oncostatin M signalling and B cell pathways.\Question: Are mitochondrial and oxidative stress genes differentially expressed in neutrophils of sJIA patients treated with tocilizumab : a pilot microarray study?
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For the first time we demonstrate that neutrophils from sJIA patients responding to tocilizumab showed significantly different changes in gene expression. These data could highlight the importance of mitochondrial genes that modulate oxidative stress in the pathogenesis of sJIA.

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Context: Although few studies have examined cardiovascular disease in Asian-American subgroups separately, limited data in Asian Americans strongly suggest that some subgroups are at increased risk. The present study examined modifiable cardiovascular risk factor profiles as a function of Asian ethnicity.', 'This descriptive cross-sectional pilot study recruited Asian-American women (N=147) in northeast Florida including Cambodians (n=39), Chinese (n=36), Filipinos (n=49), and Vietnamese (n=23). Risk factors included blood pressure, body mass index, waist circumference and blood lipids.', 'Filipino participants (41%) had 4 risk factors compared to 21% Cambodian, 13% Vietnamese and 0% Chinese. The Chinese had significantly more participants (44%) with the absence of CVD risk factors compared to all other subgroups. Obesity rate (18%), mean BMI: 26 5 kg/m(2) and mean triglycerides (173 103 mg/dL) were highest in Filipinas (n=49). The Chinese (n=36) had a low rate (4%) of obesity with a mean BMI of 23 3 kg/m(2) and the least risk factors along with the lowest triglycerides (88 44 mg/dL). Cambodians (n=39; BMI of 24 3 kg/m(2)) and Vietnamese (n=23; BMI: 22 3 kg/m(2)) had low rates of obesity with comparable rates of unhealthy lipids and hypertension as the Filipinas.\Question: Does one size fit all : cardiovascular health disparities as a function of ethnicity in Asian-American women?
answer:
Modifiable CVD risk factor profiles significantly differed as a function of ethnicity supporting the premise that Asian-American women cannot be categorized as one group and the traditional "one size fits all" prevention or treatment of CVD risk factors should be re-considered.

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Context: Vitamin D and the vitamin D receptor (VDR) appear to be important immunological regulators of inflammatory bowel diseases (IBD). Defective autophagy has also been implicated in IBD, where interestingly, polymorphisms of genes such as ATG16L1 have been associated with increased risk. Although vitamin D, the microbiome and autophagy are all involved in pathogenesis of IBD, it remains unclear whether these processes are related or function independently.', 'We investigated the effects and mechanisms of intestinal epithelial VDR in healthy and inflamed states using cell culture models, a conditional VDR knockout mouse model (VDR(IEC)), colitis models and human samples.', 'Absence of intestinal epithelial VDR affects microbial assemblage and increases susceptibility to dextran sulfate sodium-induced colitis. Intestinal epithelial VDR downregulates expressions of ATG16L1 and lysozyme, and impairs antimicrobial function of Paneth cells. Gain and loss-of-function assays showed that VDR levels regulate ATG16L1 and lysozyme at the transcriptional and translational levels. Moreover, low levels of intestinal epithelial VDR correlated with reduced ATG16L1 and representation by intestinal Bacteroides in patients with IBD. Administration of the butyrate (a fermentation product of gut microbes) increases intestinal VDR expression and suppresses inflammation in a colitis model.\Question: Does intestinal epithelial vitamin D receptor deletion lead to defective autophagy in colitis?
answer:
Our study demonstrates fundamental relationship between VDR, autophagy and gut microbial assemblage that is essential for maintaining intestinal homeostasis, but also in contributing to the pathophysiology of IBD. These insights can be leveraged to define therapeutic targets for restoring VDR expression and function.