Effects of Barometric Pressure and Temperature on Acute Ischemic Stroke Hospitalization in Augusta, GA.

Several studies worldwide have demonstrated significant relationships between meteorological parameters and stroke events. However, authors often reported discordant effects of both barometric pressure and air temperature on stroke occurrence. The present study investigated whether there was an association between weather parameters (barometric pressure and temperature) and ischemic stroke hospitalization. The aim of the study was to find out whether daily barometric pressure may be used as a prognostic variable to evaluate the workload change of a neurological intensive care unit. We conducted a retrospective review study in which we collected the independent (barometric pressure and temperature) and dependent variables (stroke hospitalization) every 24 h for the periods 10/1/2016-4/30/2017 at Augusta University Medical Center of Augusta, GA. We analyzed the data with zero-inflated Poisson model to assess the relationship between the barometric pressure, temperature, and daily stroke hospitalization. The results showed that there was a significantly correlation between daily barometric pressure variation and daily stroke hospitalization, especially on elder male patients (≥ 65). Stroke events were more likely to occur in the patients with risk factors than in those without risk factors when exposed to barometric pressure and temperature changes. Decreased barometric pressure and increased temperature were associated with increased daily stroke hospitalization. Furthermore, there was a potential delayed effect of increased stroke events after cold temperature exposure. Barometric pressure and temperature changes over the preceding 24 h are associated with daily stroke hospitalization. These findings may enhance our understanding of relationship between stroke and weather and maybe used in the development of public health strategies to minimize the weather-related stroke risk.

Femoral artery diameter and arteriogenic cytokines in healthy women.

Animal studies have identified monocyte chemoattractive protein-1 (MCP-1) and vascular endothelial growth factor (VEGF) as critical mediators of arterial diameter enlargement in response to chronic increases in blood flow (arteriogenesis). Furthermore, cellular studies have shown that the shear stresses resulting from increased blood flow stimulate synthesis of MCP-1, which in turn stimulates synthesis of VEGF. The purpose of this study was to determine if these mechanisms are evident in healthy women. Resting femoral artery diameter and blood flow, lean leg mass, MCP-1 and VEGF concentrations, and aerobic capacity were measured in 34 healthy women along with plasma concentrations of lipids associated with cardiovascular disease risk. Femoral artery diameter was independently related to metabolically active (lean) leg mass (b=0.41, P=0.008) and aerobic capacity (b=0.45, P=0.004). Plasma MCP-1 correlated negatively with the ratio of femoral artery diameter to lean leg mass (b=-0.42, P=0.009) and positively with serum triglycerides (b=0.46, P=0.005). Plasma VEGF exhibited similar correlations and strongly correlated with MCP-1 (R=0.92, P<0.0001). The results indicate that circulating MCP-1 and VEGF concentrations are associated with both arteriogenic and atherogenic stimuli in healthy women.

Leptin, blood pressure, and aerobic capacity in women.

BACKGROUND: In animals, the adipocyte-derived hormone leptin induces increased blood pressure centrally via the hypothalamus, and one study has reported that exercise training decreases hypothalamic leptin receptor expression. In humans, high circulating leptin concentrations are associated with high blood pressure, but the possible influence of physical activity or aerobic capacity on this association is unknown. METHODS: Forty-two healthy women, 25-40 years of age, with diverse ranges of body fatness and aerobic capacities, were studied under basal resting conditions. Blood pressure (sphygmomanometry), arterial stiffness (pulse wave velocity (PWV)), percent body fat (dual energy X-ray absorptiometry), circulating concentrations of leptin, soluble leptin receptor (sLR) (enzyme-linked immunoassay), and nitric oxide (Griess reaction) were measured. RESULTS: Serum leptin correlated with percent body fat (R(2) = 0.74, P < 0.0001) but was not significantly associated with aerobic capacity. Blood pressure correlated positively with serum leptin concentrations and had a negative interaction with aerobic capacity for both systolic (overall model: R(2) = 0.33, P = 0.002) and diastolic (R(2) = 0.48, P < 0.0001) pressure. The relation between leptin and blood pressure was attributable solely to women with below-median aerobic capacity even though their body fat percentages and leptin concentrations were similar to those of women above the median. The results could not be attributed to differences in peripheral factors such as sLR or nitric oxide concentrations or to differences in arterial stiffness determined by aortic PWV. CONCLUSIONS: Circulating leptin concentrations are related to body fatness, but the hypertensive influence of leptin is modified by physical fitness.

Anti-inflammatory influence of P-selectin on human mononuclear cells.

The purpose of this study was to determine if P-selectin, an adhesion molecule involved in the transendothelial movement of leukocytes, might also have a direct influence on the function of cells that come into contact with it. Human peripheral blood mononuclear cells were incubated on immobilized P-selectin or a control substrate (bovine serum albumin, BSA) and stimulated with bacterial lipopolysaccharide (LPS). After 24 h, the concentrations of proinflammatory cytokines in the supernatants of LPS-stimulated cells incubated on P-selectin were <50% of those produced by cells incubated on BSA (interleukin-1beta: P=0.001, tumor necrosis factor-alpha: P=0.004, and interferon-gamma : P=0.026). In contrast, cells incubated on P-selectin produced 74% more of the anti-inflammatory cytokine interleukin-10 than cells incubated on BSA (P=0.013). Neither P-selectin nor BSA stimulated cytokine production in the absence of LPS. Thus, P-selectin modulated the cytokine secretion of peripheral blood mononuclear cells in a coordinated manner that reduced the inflammatory potential of the cells.