From 1999 to 2010, prevalence of hypertension remained stable. Hypertension awareness, management, and control were improved, but remained poor; nevertheless, there has been no improvement since 2007.

Background: SII and SIRI are two novel systemic inflammation indexes that were suggested in predicting poor outcomes in cancers. However, no studies have examined their effect on cardiovascular diseases (CVDs) and all-cause mortality. Thus, this study aims to investigate associations between SII, SIRI, and the risks for CVDs and all-cause mortality. Methods: A total of 85,154 participants from the Kailuan cohort were included and followed up for incidents of CVDs (including MI, stroke) and all-cause death for 10 years. Multiple Cox regression was used to calculate the adjusted hazard ratios (HRs). Results: During the follow-up period, 4262 stroke events, 1233 MI events, and 7225 allcause deaths were identified, respectively. Compared with the lowest quantile (Q1) of SII or SIRI, after adjusted for most cardiovascular risk factors, both indexes showed positive associations with the risk for stroke (adjusted HRs in Q4 were 1.264 (95% CI: 1.157,1.382) for SII, 1.194 (95% CI: 1.087,1.313) for SIRI), and all-cause death (adjusted HRs in Q4 were 1.246 (95% CI: 1.165,1.331) for SII, 1.393 (95% CI: 1.296,1.498) for SIRI). Additionally, higher SII and SIRI are also associated with increased risk of hemorrhagic stroke and ischemic stroke. Higher SIRI but not SII exhibited a higher MI risk, the adjusted HR in Q4 was 1.204 (1.013,1.431). The significant association remained after additional adjustment for CRP. Subgroup analysis and sensitivity analysis displayed consistent results except for SIRI with MI, where the association did not arrive at significance in subjects aged ≥60. Conclusion: Elevated SII and SIRI increased the risk of stroke, two stroke subtypes, and all-cause death. Higher SIRI, but not SII associated with increased MI incidence, and the association of SIRI was only significant in subjects aged <60.

No abstract

This study examines the use of ambient measurements of a number of "photochemical indicators" as a basis for determining ozone-NO-hydrocarbon sensitivity and for evaluating the performance of ozone models. The successful photochemical indicators are: 0/NO , 0/NO (where NO = NO-NO), 0/HN0, H0/HN0, and H0/NO. Results of Urban Airshed Model (UAM-IV) simulations for Atlanta, GA, New York, NY, and Los Angeles, CA, show that high values of these species ratios are correlated with NO-sensitive chemistry and low values are associated with reactive organic gases (ROG)-sen-sitive chemistry. Correlations between measured 0 and NO in Atlanta and between 0 and NO in Los Angeles are consistent with theory and reflect the difference between likely NO-sensitive chemistry in Atlanta and hydrocarbon-sensitive chemistry in Los Angeles. Measured 0, NO and NO are used to evaluate model performance during two air pollution events in Atlanta and Los Angeles. The performance evaluation includes model scenarios for each city with different anthropogenic and biogenic emission rates and different NO-ROG sensitivity predictions. Simulations with different NO-ROG chemistry are found to give similar predictions for peak ozone but different values for photochemical indicators. Comparison with measured values of photochemical indicators provides a more stringent test of model performance than evaluation versus observed ozone.

This study investigated the effects of short-term food restriction or supplementation on folliculogenesis and plasma and intrafollicular metabolite and hormone concentrations. Ewes were randomly assigned to three groups: the control group received a maintenance diet (M) while the supplemented group and restricted group received 1.5!M and 0.5!M respectively on days 6-12 of their estrous cycle. Estrus was synchronized by intravaginal progestogen sponges for 12 days. On days 7-12, blood samples were taken. After slaughter, the ovarian follicles were classified and the follicular fluid was collected. Compared with restriction, supplementation shortened the estrous cycle length, decreased the number of follicles 2.5-3.5 mm and follicular fluid estradiol (E 2 ) concentration, increased the number of follicles O3.5 mm and plasma glucose, insulin and glucagon concentrations, and augmented the volume of follicles O2.5 mm. Restricted ewes had higher intrafollicular insulin concentration, but it was similar to that of supplemented ewes. Compared with follicles %2.5 mm, the intrafollicular glucose and E 2 concentrations were increased and the testosterone, insulin, and glucagon concentrations and lactate dehydrogenase (LDH) activity were decreased in follicles O2.5 mm. Only in restricted ewes were intrafollicular LDH and testosterone concentrations in follicles %2.5 mm not different from those in follicles %2.5 mm. In conclusion, the mechanism by which short-term dietary restriction inhibits folliculogenesis may involve responses to intrafollicular increased E 2 , testosterone, and LDH levels in late-stage follicles. This may not be due to the variation of intrafollicular insulin level but rather due to decreased circulating levels of glucose, insulin, and glucagon.