Hunger and food insecurity are important factors that may affect an individual's nutritional state and should therefore be assessed in nutrition surveillance activities. The objective of this study was to determine the level of food insecurity and hunger among HIV-positive persons accessing antiretroviral therapy in British Columbia. A cross-sectional study was performed in the BC HIV/AIDS drug treatment program, a province-wide source of free-of-charge antiretroviral medications. In 1998-1999, participants completed a questionnaire focusing on personal information, health, and clinical status. Food and hunger issues were evaluated with the Radimer/Cornell questionnaire. Overall, 1213 responding men and women were classified as food secure (52%), food insecure without hunger (27%), or food insecure with hunger (21%). In both categories of food insecurity, individuals were significantly more likely to be women, aboriginals, living with children, and to have less education, a history of recreational injection drug and/or alcohol abuse, and an unstable housing situation (P < 0.05). In logistic multivariate modeling, income < or = Can$10,000 [adjusted odds ratio (AOR) 3.78, 95% CI (2.53-5.65)], shared household with children [AOR 3.68, 95% CI (1.98-6.84)] and unemployment [AOR 3.15, 95% CI (1.94-5.13)] were the strongest predictors of hunger. In HIV-positive individuals, the occurrence of food insecurity was nearly 5 times higher than in the general Canadian population. The results should stimulate further research to identify to what extent hunger-associated factors are reversible with interventions built on nutritional and/or social strategies.

South Asians have a phenotype of high fat mass and low lean mass, which may account for greater levels of insulin and HOMA compared with other ethnic groups.

The tachykinin neuropeptides substance P and neurokinin (NK) A have been postulated to participate in the inflammatory reaction in airways of smokers and asthmatics. We have examined the hypothesis that the expression of one or more of the three cloned tachykinin receptors (NK1, NK2, and NK3) is increased in inflammatory airway disorders, which could result in augmentation of the effect of released tachykinin neuropeptides. NK1 receptor and NK2 receptor but not NK3-receptor mRNA were detected by ribonuclease protection assay in RNA from both cartilaginous and membranous bronchi and subpleural lung. In lung samples containing membranous airways, NK2-receptor mRNA expression was increased fourfold in asthmatics compared with nonsmoking controls, whereas NK1-receptor mRNA levels were similar in the two groups. NK1- and NK2-receptor mRNA expression was increased twofold in smokers without airflow obstruction compared with nonsmokers, whereas NK1-receptor mRNA expression was significantly lower in patients with chronic obstructive pulmonary disease compared with smoking controls. In situ hybridization indicated NK1-receptor mRNA was expressed in submucosal glands and airway epithelial cells, whereas NK2-receptor and NK3-receptor mRNA were not detected. These observations have implications for the pathophysiology and treatment of both asthma and tobacco smoke-induced airway inflammation.

Background-Glucocorticoid-induced granulocytosis has been attributed to enhanced release of polymorphonuclear leukocytes (PMNs) from bone marrow, delayed apoptosis, and reduced egress of PMNs into tissues. This study was designed to determine the relative contributions of PMNs released from the bone marrow and those entering the circulation from the marginated pool to the granulocytosis produced by a single dose of dexamethasone (2.0 mg/kg) in rabbits. Methods and Results-PMN transit through the mitotic and postmitotic pools of the bone marrow and rate of release of PMNs into the circulation were measured by use of the thymidine analogue 5Ј-bromo-2Ј-deoxyuridine (BrdU) to pulse-label PMNs in the bone marrow. The shift of PMNs from the marginated to the circulating pool was measured with BrdU-labeled PMNs transferred from donor rabbits to recipients before dexamethasone was delivered. The data show that dexamethasone increased bone marrow release of PMNs and shortened their transit time through the postmitotic pool (PϽ0.001) but not the mitotic pool of the bone marrow (PϾ0.05). Dexamethasone slowed the clearance of BrdU-labeled PMNs from the circulation (PϽ0.05) and lengthened their disappearance (half-life) from the circulation compared with control (half-life, 4.95 versus 9.45 hours). At 6 hours after dexamethasone, bone marrow release contributed Ϸ10%, mobilization from the marginated pool Ϸ61%, and a lengthened half-life in the circulation Ϸ29% to the glucocorticoid-induced granulocytosis. Conclusions-We conclude that a single dose of dexamethasone causes a granulocytosis primarily by a shift of PMNs from the marginated to the circulating pool, with a minor contribution from marrow release. (Circulation. 1998;98:2307-2313.)