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.

Context: Intermittent hypoxia (IH)-induced activation of pro-inflammatory pathways is a major contributing factor to the cardiovascular pathophysiology associated with obstructive sleep apnea (OSA). Obesity is commonly associated with OSA although it remains unknown whether adipose tissue is a major source of inflammatory mediators in response to IH. The aim of this study was to test the hypothesis that IH leads to augmented inflammatory responses in human adipocytes when compared to cells of non-adipocyte lineages.', 'Human primary subcutaneous and visceral adipocytes, human primary microvascular pulmonary endothelial cells (HUMEC-L) and human primary small airway epithelial cells (SAEC) were exposed to 0, 6 or 12 cycles of IH or stimulated with tumor necrosis factor (TNF)-. IH led to a robust increase in NF-B DNA-binding activity in adipocytes compared with normoxic controls regardless of whether the source of adipocytes was visceral or subcutaneous. Notably, the NF-B response of adipocytes to both IH and TNF- was significantly greater than that in HUMEC-L and SAEC. Western blotting confirmed enhanced nuclear translocation of p65 in adipocytes in response to IH, accompanied by phosphorylation of I-B. Parallel to p65 activation, we observed a significant increase in secretion of the adipokines interleukin (IL)-8, IL-6 and TNF- with IH in adipocytes accompanied by significant upregulation of mRNA expression. PCR-array suggested profound influence of IH on pro-inflammatory gene expression in adipocytes.\Question: Are human adipocytes highly sensitive to intermittent hypoxia induced NF-kappaB activity and subsequent inflammatory gene expression?
Human adipocytes demonstrate strong sensitivity to inflammatory gene expression in response to acute IH and hence, adipose tissue may be a key source of inflammatory mediators in OSA.

Context: The aim of this study was to evaluate the effect of local injection of vasopressin on blood loss and secondary impact on complications during cesarean section in patients with placenta previa.', 'We retrospectively reviewed the medical records of all patients diagnosed with placenta previa admitted to our hospital. Two consecutive periods were compared. During period B, 59 patients underwent the local injection of a vasopressin solution (4 U in 20 mL of saline) into the placental implantation site after placental delivery. During period A, 50 patients underwent cesarean section without vasopressin injection, and were analyzed as a control group. The estimated blood loss was recorded, as were the complications during surgery. In addition, the expression of the vasopressin V1 receptor in uterine smooth muscle was evaluated by immunohistochemistry.', 'The mean estimated blood loss was significantly lower in the vasopressin group than in the control group. There were no statistically significant differences with surgical complications. The vasopressin V1 receptor was highly expressed in smooth muscle cells in the lower segment of the uterine body, whereas the immunoreactivity for the oxytocin receptor was faint in the lower segment.\Question: Does local injection of vasopressin reduce the blood loss during cesarean section in placenta previa?
The local injection of vasopressin into the placental implantation site significantly reduced the blood loss without increasing the morbidity.

Context: Although excessive sympathetic activation in viral myocarditis and the protective effects of sympathetic inhibition with -blockers are clear, the effects of enhancing vagal tone on viral myocarditis remain unclear. In several models, vagus nerve activation with the 7 nicotinic acetylcholine receptor (7-nAChR) agonists has been demonstrated to ameliorate inflammation. This study was therefore designed to examine the effects of cholinergic stimulation with 7-nAChR agonist nicotine in a murine model of acute viral myocarditis.', 'BALB/C mice were infected by an intraperitoneally injection with coxsackievirus B3. Nicotine and methyllycaconitine (an 7-nAChR antagonist) were administered at doses of 0.4mg/kg and 0.8mg/kg three times per day for 7 or 14 consecutive days, respectively. The effects of nicotine and methyllycaconitine on survival rate, myocardial histopathological changes, cardiac function, cytokine levels, viral RNA, malondialdehyde, and superoxide dismutase contents were investigated.', 'Nicotine significantly increased survival rate of the infected mice, decreased myocardial inflammation, and improved the impairment of left ventricular function in murine coxsackievirus B3-induced myocarditis compared with methyllycaconitine. The proinflammatory cytokines TNF-, IL-1, IL-6 and IL-17A were significantly decreased in the infected mice treated with nicotine compared with methyllycaconitine. Nicotine had no significant anti-oxidative and antiviral effects in coxsackievirus B3-infected mice.\Question: Does nicotine inhibit the production of proinflammatory cytokines of mice infected with coxsackievirus B3?
The results indicate that cholinergic stimulation with nicotine significantly reduced the severity of viral myocarditis in mice. The findings suggest that alpha7 nAChR agonists may be a promising new strategy for patients with myocarditis.