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.
question:
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.

question:
Context: Treatment of difficult asthma with oral corticosteroids (OCS) may suppress the hypothalamic-pituitary-adrenal axis.', 'In this study we have checked if the substitution of OCS with very high doses of ciclesonide may restore the adrenal function without losing the control of the disease.', 'In 5 patients with difficult, uncontrolled asthma despite treatment with OCS, inhaled and systemic glucocorticosteroids were replaced with very high doses of ciclesonide (1600-2400 g/day). The symptoms of asthma and the lung function were assessed at baseline and on the 28(th), 56(th) and 70(th) day of treatment, whereas the levels of cortisol and adrenocorticotropic hormone (ACTH) in the morning were measured at baseline and on the 28(th) and the 56(th) day of treatment.', 'In all patients, the control of asthma symptoms, measured with Asthma Control Test questionnaire, improved from the mean score of 9.4 to 19.8 in 70 days. In 4 subjects force expiratory volume in 1 s improved gradually through the entire study reaching a mean improvement of 585 ml in 70 days. The ACTH levels were normalized in 3 patients after 28 days of observation and in all patients after 56 days. The cortisol level was normalized in 4 patients after 28 days and in another subject after 56 days of treatment with ciclesonide.\Question: Does switching from systemic steroids to ciclesonide restore the hypothalamic pituitary-adrenal axis?
answer:
Switching from prednisone to very high doses of ciclesonide normalized the hypothalamic-pituitary adrenal axis function and also improved the disease control and the lung function in these 5 patients with difficult asthma.

question:
Context: Accelerated thrombus formation induced by exposure to combustion-derived air pollution has been linked to alterations in endogenous fibrinolysis and platelet activation in response to pulmonary and systemic inflammation. We hypothesised that mechanisms independent of inflammation contribute to accelerated thrombus formation following exposure to diesel exhaust particles (DEP).', 'Thrombosis in rats was assessed 2, 6 and 24 h after administration of DEP, carbon black (CB; control carbon nanoparticle), DQ12 quartz microparticles (to induce pulmonary inflammation) or saline (vehicle) by either intra-tracheal instillation (0.5 mg, except Quartz; 0.125 mg) or intravenous injection (0.5 mg/kg). Thrombogenicity was assessed by carotid artery occlusion, fibrinolytic variables and platelet-monocyte aggregates. Measures of inflammation were determined in plasma and bronchoalveolar lavage fluid. Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI)-1 were measured following direct in vitro exposure of human umbilical vein endothelial cells (HUVECs) to DEP (10-150 g/mL).', 'Instillation of DEP reduced the time to thrombotic occlusion in vivo, coinciding with the peak of DEP-induced pulmonary inflammation (6 h). CB and DQ12 produced greater inflammation than DEP but did not alter time to thrombotic occlusion. Intravenous DEP produced an earlier (2 h) acceleration of thrombosis (as did CB) without pulmonary or systemic inflammation. DEP inhibited t-PA and PAI-1 release from HUVECs, and reduced the t-PA/PAI-1 ratio in vivo; similar effects in vivo were seen with CB and DQ12. DEP, but not CB or DQ12, increased platelet-monocyte aggregates.\Question: Does platelet activation independent of pulmonary inflammation contribute to diesel exhaust particulate-induced promotion of arterial thrombosis?
answer:
DEP accelerates arterial thrombus formation through increased platelet activation. This effect is dissociated from pulmonary and systemic inflammation and from impaired fibrinolytic function.