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: 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?

Answer: 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.

Question: Context: This study examines the prevalence and correlates of self-reported premenstrual symptoms among a large, population-based sample of reproductive age, active-duty women.', 'Data were obtained from a combined dataset of two large-scale mail surveys designed to represent the total force. Subjects included in the present study were 6026 active-duty women of all branches of military service stratified by service, paygrade group, race/ethnicity, and location. A multivariate approach is used to evaluate the interrelationships among psychosocial and lifestyle correlates of premenstrual symptoms or pain after controlling for demographic differences in women who reported premenstrual symptoms or pain during the past 3 months (cases) and those who did not (controls).', 'Premenstrual symptoms were reported by nearly 2 of every 3 reproductive age women. Women reporting premenstrual symptoms were more likely to report other symptoms of menstrual dysfunction, two or more current medical conditions, migraines, and healthcare provider visits in the past year. After controlling for the protective effects of taking Depo-Provera (Upjohn, Kalamazoo, MI) and ever being pregnant, younger age, trying to lose weight, heavier drinking, poorer self-perceived health, and overall job stress were the most significant predictors of premenstrual symptoms. The greatest risk factor was a high level of job stress, with an almost 3-fold increase in risk relative to those without symptoms.\Question: Does psychosocial and lifestyle correlate of premenstrual symptoms among military women?

Answer: Work stress may mediate the relationship among depression and premenstrual symptoms. Further research is needed to elucidate the biological interrelationships among work stress, hormonal function, and premenstrual symptomatology.

Question: Context: Seasonal allergic rhinitic (SAR) subjects are more physiologically reactive to airborne irritants than non-rhinitic (NR) subjects; however the mechanism underlying this difference is unclear.', 'We sought to determine whether irritant-induced nasal airflow limitation involves neuropeptide release into nasal lining fluid, and if so, whether such release occurs differentially by rhinitic status.', "Eight SAR and 8 NR subjects were exposed to 1.0 ppm chlorine and filtered air in random order during separate visits; exposures were via nasal mask and lasted 15 min. Rhinomanometry was performed before, immediately post-, and 15 min post-exposure. Following a minimum of 2 weeks' time, exposures and symptom reporting were repeated with nasal lavage pre- and post-exposure. Neuropeptides (substance P, cacitonin gene-related protein, vasoactive intestinal peptide, and neuropeptide Y) as well as markers of plasma leakage (albumin and urea) and glandular secretion (lysozyme and 7F10-mucin) were measured using standard methods.", 'Cl(2) provocation significantly increased nasal airway resistance in SAR but not NR subjects (p<0.05). Neuropeptide levels in nasal lavage fluid, on the other hand, were unaffected, with the exception of a paradoxical increase in vasoactive intestinal peptide in non-rhinitic controls post-Cl(2) provocation.\Question: Does chlorine inhalation produce nasal airflow limitation in allergic rhinitic subjects without evidence of neuropeptide release?

Answer:
Irritant-induced nasal airflow limitation is more pronounced among SAR than NR subjects. We could not, however, demonstrate a role for neuropeptide release in the nasal congestive response of SAR subjects.