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.

[EX Q]: Context: Both obesity and type 2 diabetes are among the risk factors for breast cancer development. Combined effect of these metabolic abnormalities on breast cancer risk however, has not been examined in premenopausal women. We tested this association in type 2 diabetic women, categorized as obese, overweight and normal body weight groups based on BMI.', 'A total of 101 subjects were included in this study. Serum levels of IL-6, TNF-alpha, C reactive protein, leptin, TGF-alpha, adiponectin and insulin were measured by ELISA. Data were logarithmically transformed for variables not normally distributed. Analysis of variance with post-hoc Bonferroni was applied to compare the data between the groups. Simple and partial correlation coefficients between the variables were determined and a stepwise multiple linear regression analysis was performed to determine the relationships between the variables of interest.', 'Significantly increased levels of IL-6, C reactive protein, leptin and significantly decreased levels of adiponectin were found in obese group, while the levels of TNF-alpha and TGF-alpha were unaltered. A positive correlation between waist circumference and IL-6 was found in obese group. Similarly, C reactive protein, waist and hip circumferences were linearly correlated with BMI in obese group. Stepwise multiple linear regression analysis revealed several significant predictors for breast cancer risk.\Question: Do combined effects of obesity and type 2 diabetes contribute to increased breast cancer risk in premenopausal women?
[EX A]: Obesity and type 2 diabetes, owing to their effects on adipocytokines and inflammatory mediators, contribute to increased breast cancer risk in premenopausal women. This study emphasizes healthy life style and better management of these metabolic disorders to avoid the pathogenesis of breast cancer and of other chronic diseases.

[EX Q]: Context: The incidence and predictors of spontaneous hepatitis B surface-antigen (HBsAg) seroclearance in patients with chronic hepatitis B virus (HBV) were evaluated.', 'A total of 1427 patients with chronic HBV infection, who were followed between 1994 and 2013, were investigated in this retrospective study. All data were extracted from patient files.', 'Spontaneous HBsAg seroclearance occurred in 84 patients during 8798 person-years of follow-up. The patients were categorized into 3 groups at follow-up based on HBV DNA features as continuously <100 copies/mL (Group A), 0-10,000 copies/mL (Group B), and 0 to >10,000 copies/mL (Group C). Alanine aminotransferase features in the 2 groups were categorized as continuously normal (<40 U/L) and 0 to >40 U/L. Spontaneous HBsAg seroclearance was seen primarily in patients with Group A HBV DNA features, and continuously low HBV DNA values were the main predictor of HBsAg seroclearance (P < 0.001).\Question: Is a persistently low HBV DNA level a predictor of spontaneous HBsAg clearance in patients with chronic hepatitis B?
[EX A]: These results suggest that a continuously low viral load is the most important factor affecting spontaneous HBsAg seroclearance.

[EX Q]: Context: The microcirculation supplies oxygen (O2) and nutrients to all cells with the red blood cell (RBC) acting as both a deliverer and sensor of O2. In sepsis, a proinflammatory disease with microvascular complications, small blood vessel alterations are associated with multi-organ dysfunction and poor septic patient outcome. We hypothesized that microvascular autoregulation-existing at three levels: over the entire capillary network, within a capillary and within the erythrocyte-was impaired during onset of sepsis. This study had three objectives: 1) measure capillary response time within hypoxic capillaries, 2) test the null hypothesis that RBC O2-dependent adenosine triphosphate (ATP) efflux was not altered by sepsis and 3) develop a framework of a pathophysiological model.', 'This was an animal study, comparing sepsis with control, set in a university laboratory. Acute hypotensive sepsis was studied using cecal ligation and perforation (CLP) with a 6-hour end-point. Rat hindlimb skeletal muscle microcirculation was imaged, and capillary RBC supply rate (SR=RBC/s), RBC hemoglobin O2 saturation (SO2) and O2 supply rate (qO2=pLO2/s) were quantified. Arterial NOx (nitrite+nitrate) and RBC O2-dependent ATP efflux were measured using a nitric oxide (NO) analyzer and gas exchanger, respectively.', "Sepsis increased capillary stopped-flow (p=0.001) and increased plasma lactate (p<0.001). Increased plasma NOx (p<0.001) was related to increased capillary RBC supply rate (p=0.027). Analysis of 30-second SR-SO2-qO2 profiles revealed a shift towards decreased (p<0.05) O2 supply rates in some capillaries. Moreover, we detected a three- to fourfold increase (p<0.05) in capillary response time within hypoxic capillaries (capillary flow states where RBC SO2<20%). Additionally, sepsis decreased the erythrocyte's ability to respond to hypoxic environments, as normalized RBC O2-dependent ATP efflux decreased by 62.5% (p<0.001).\Question: Does sepsis impair microvascular autoregulation and delays capillary response within hypoxic capillaries?
[EX A]:
Sepsis impaired microvascular autoregulation at both the individual capillary and erythrocyte level, seemingly uncoupling the RBC acting as an "O2 sensor" from microvascular autoregulation. Impaired microvascular autoregulation was manifested by increased capillary stopped-flow, increased capillary response time within hypoxic capillaries, decreased capillary O2 supply rate and decreased RBC O2-dependent ATP efflux. This loss of local microvascular control was partially off-set by increased capillary RBC supply rate, which correlated with increased plasma NOx.