A retrospective analysis of hypertension screening at a mass gathering in India: implications for non-communicable disease control strategies.

Cardiovascular disease is the leading case of mortality from non-communicable diseases (NCD) in India. The government's National Programme for Prevention and Control of Cancer, Diabetes, Cardiovascular Diseases and Stroke seeks to increase capacity building, screening, referral and management of NCDs across India, and includes community-based outreach and screening programmes. The government in India routinely provides basic care at religious mass gatherings. However, in 2015, at the Kumbh Mela in Nashik and Trimbakeshwar, the state government extended its services to include a hypertension screening programme. We examine here the value and implications of such opportunistic screening at mass gatherings. At the Kumbh, 5760 persons voluntarily opted for hypertension screening, and received a single blood pressure measurement. In all, 1783 (33.6%) screened positive, of whom, 1580 were previously unaware of their diagnosis. Of the 303 that had previously known hypertension, 240 (79%) were prescribed medications, and 160 were compliant (that is, 52.8% under treatment). Fifty-five (18%) had normal blood pressure readings (BP under control). The data also demonstrated higher prevalence (39%) of hypertension among tobacco users compared to non-users (28%) (P<0.001). Poor recording of phone numbers (0.01%) precluded any phone-based follow-up. The low rates of hypertension awareness, treatment and control underscore the ongoing challenge of both hypertension screening and management in India.

Nicotine induces endothelial TNF-alpha expression, which mediates growth retardation in vitro.

PURPOSE: Atherosclerosis is understood as the common pathologic manifestation of arterial injury caused by a variety of etiologies. One well-established etiologic agent is nicotine. We hypothesized that cytokines of endothelial origin are involved with the pathologic changes found in atherosclerosis associated with smoking. We chose to assay for TNF-alpha due to its many biologic actions that are similar to those found in peripheral vascular disease. METHODS: Human umbilical vein endothelial cells (HUVEC) were plated in endothelial growth medium (EGM-2) on plastic coverslips until 75% confluent. Free base nicotine (FBN) was diluted in EGM-2 to a concentration of 10(-8) M and added to experimental cells. At 1, 3, and 24 h, coverslips were removed and fixed. Immunohistochemical staining was performed using anti-TNF-alpha. Digital image analysis (DIA) was performed to quantify expression of TNF-alpha. An intensity stain index measuring area and intensity of stain/total cellular area was determined for each time point (n = 5). Additional HUVEC were plated in 12-well plates in EGM-2 at 2 x 10(3) cells/cm(2) on T(-2) day. FBN was diluted in medium to 10(-9) M and added to wells with and without 0.9 microg/ml anti-TNF-alpha on T(0) day. Cell counts were performed in triplicate on days T(2-5) utilizing hemocytometry. Data was analyzed using Student's t test and ANOVA, with a 95% confidence interval. RESULTS: Dose response determinations showed that the minimal concentration required to show statistically significant cell retardation is 10 (-9) M. Accordingly, this concentration was used for subsequent proliferation studies. DIA showed a threefold increase in TNF-alpha activity at 1 h and a twofold increase at 3 h. Activity returned to baseline by 24 h. Cell growth was significantly decreased in cells exposed to nicotine when compared to controls on days T(2)-T(5) (P < 0.05). In cells exposed to anti-TNF-alpha and nicotine there was inhibition of the growth retardation seen in the cells containing nicotine alone. Differences between the control group and the anti-TNF-alpha group were not statistically significant. CONCLUSION: These data demonstrate the ability of endothelial cells to secrete TNF-alpha in response to nicotine at levels found in serum after smoking and also shows that endothelial cell growth retardation as a consequence of nicotine exposure may be TNF-alpha mediated.

Age-adjusted outcomes in traumatic flail chest injuries in the elderly.

Severe chest trauma does not independently predict poor outcome in elderly patients. We chose a specific injury, flail chest, to determine whether age factored into outcome of these patients. A retrospective chart review of all trauma admissions to our Level I trauma center between January 1994 and January 1998 sustaining flail chest was undertaken. Sixty-eight patients were identified, but ten patients were excluded because of death on arrival. Fifty-eight patients were included in the study and separated into groups. The first group comprised those under the age of 55 (n = 32) and the second comprised those over age 55 (n = 26). Parameters evaluated were age, Injury Severity Score (ISS), neurologic injury, the need for mechanical ventilation, need for tracheostomy, length of stay, and death. Statistical analysis was performed with Wilcoxon t test, chi2, and logistic regression where appropriate. A 95 per cent confidence interval was sought as determinant of significance. Of the 58 surviving patients analyzed there was no significant difference between the groups regarding ISS, length of stay, days on the ventilator, head injury, tracheostomy, or development of pneumonia or adult respiratory distress syndrome. The likelihood of death was shown to increase by 132 per cent for every 10 years starting at the second decade and continuing to the eighth decade of life. The likelihood of death also increased by 30 per cent for each unit increase in ISS. The likelihood of death decreased by 23 per cent for every day survived in the hospital. Blunt chest trauma directly impacts respiratory mechanics. Elderly patients are more likely to have comorbid conditions and less likely to tolerate traumatic respiratory compromise. Age (and its effects on the body) is the strongest predictor of outcome with flail chest and is associated with an increased mortality (P < or = 0.05).

Insulin stimulates lipoprotein lipase activity and synthesis in adipocytes from septic rats.

Gram-negative sepsis suppresses lipoprotein lipase (LPL) activity in adipose tissue which contributes, in part, to the altered clearance of triglycerides. The suppression in LPL activity occurs when plasma insulin concentrations are elevated and insulin-stimulated glucose utilization is impaired. This study was planned to evaluate whether the presence of insulin resistance was responsible for the decrease in adipose LPL activity. Adipocytes were isolated from epididymal fat pads 24 h after inducing sepsis in male Lewis rats by intravenous injection of 4 x 10(8) colonies of live Escherichia coli/100 g body wt. The decrease in heparin-releasable (HR) LPL activity in adipocytes from the septic rats was evident at the time of isolation and maintained in a 20-h culture. After overnight incubation with insulin (10(-8) M), HR LPL activity was stimulated to a greater extent in adipocytes from septic rats (298%) than in adipocytes from control rats (88%). The insulin stimulation of LPL activity during sepsis could not be attributed to insulin-like growth factor-I (IGF-I) as adipocytes from septic rats appeared to be IGF-I resistant. Insulin-treatment (10(-8) M) increased LPL synthesis 99% in adipocytes from control rats and 136% in adipocytes from septic rats. Insulin treatment also led to a 65 and 62% increase in LPL mass in adipocytes from control and septic rats, respectively. These findings indicate that the sepsis-induced decrease in adipose LPL is not due to insulin resistance with respect to LPL. The insulin stimulation of LPL activity in adipocytes from septic rats appears to be mediated by an increase in LPL synthesis.