Arthurbranch7910

Cases of CAP in the ICU were clustered in patients from areas of the city with high poverty. The mortality of patients with CAP in ICU was 27% at 30 days and 47% at 1 year. In the US, the estimated number of patients hospitalized with CAP requiring ICU was 356,326 per year, and the estimated number of deaths at 30 days and one year was 96,206 and 167,474, respectively. CONCLUSIONS Almost one in five patients hospitalized with CAP requires intensive care. Poverty is associated with CAP in the ICU. Nearly half of patients with CAP in the ICU will die within one year. Due to its significant burden, CAP in the ICU should be a high priority in research agenda and health policy. BACKGROUND Little is known about the different risk of silicosis in metal mines and pottery factories. We aimed to compare the silicosis risks among silica-exposed workers in different industrial circumstances. RESEARCH QUESTION Are the silicosis risks among silica-exposed workers in industrial circumstances different? STUDY DESIGN AND METHODS We studied 39,808 workers followed from January 1, 1960 to December 31, 2003 in China. Cumulative respirable silica dust exposure (CDE) was estimated by linking a job-exposure matrix to personal work history. Silicosis of stage I or higher was diagnosed by Chinese pneumoconiosis Roentgen diagnostic criteria. RESULTS A total of 9,377 silicosis patients were diagnosed during 1,153,580.9 person-years follow-up in the cohort. Hazard ratios of silicosis for each 1 mg/m3-year increase in CDE were 1.08 (1.07-1.08) for tungsten mines, 1.41 (1.33-1.48) for iron and copper mines, 1.14 (1.11-1.17) for tin mines, and 1.03 (1.02-1.04) for pottery factories, respectively. When exposed to 0.05 mg/m3 of respirable silica dust for 45 years, the cumulative risks in metal mines (2.3%, 9.9%, 1.5% for tungsten mines, iron and copper mines, tin mine respectively) were still higher than those in pottery factories (0.6%). The joint effect of silica and smoking on silicosis was more than multiplicative. INTERPRETATION The risk of silicosis in metal miners is higher than that in pottery workers when exposed to the same level of silica dust. The silica dust exposed years should be under 10 years for metal miners and 40 years for pottery workers at 0.05 mg/m3 to keep lifetime risk within 0.1%. Current exposure limits should take into account for differences in various industrial circumstances. Smoking cessation could help reduce silicosis risk for silica-exposed workers. BACKGROUND Prematurity is a risk factor for impaired lung function. We sought to assess the long-term effect of palivizumab immunization and extreme prematurity ( less then 29 weeks) on respiratory symptoms and pulmonary function at adolescence. METHODS We examined survivors of extreme prematurity ( less then 29 weeks) at 13-18 years of age (study group, SG). SG babies born immediately prior to palivizumab immunization (non-palivizumab group, NPG) were compared to those born just after implementation (PG), as well as to a control group (CG). For SG patients, lung function at adolescence was further compared longitudinally to that at primary school age. RESULTS Sixty-four adolescents aged 15.76 ±1.52 years, mean ±SD, were included 46 SG (17 PG and 29 NPG) and 18 CG. For the SG, wheezing episodes, inhaler use and hospitalizations were uncommon. For the SG compared to the CG, FEV1% predicted was 82.60% ±13.54 vs. 105.83% ±13.12, mean ±SD, p less then 0.001, and LCI was 7.67 ±1.02 vs. 7.46 ±0.70, p=0.48, respectively. SG adolescents with BPD had a higher LCI than non-BPD (7.94±1.11 vs 7.20±0.60, p=0.002). PG and NPG adolescents were not significantly different. Comparing SG in adolescence to primary school age, we found improvement in mean FEV1% predicted bronchodilator response (0.37%±9.98 vs 5.67%±9.87, p=0.036) and mean PC20 (12.16±4.71 mg/ml vs 4.14±4.51 mg/ml, respectively, p less then 0.001). CONCLUSION Palivizumab did not provide any discernable long-term protective effect. Nevertheless, adolescent survivors of extreme prematurity showed good clinical and physiological outcomes, except for mildly raised LCI in BPD subjects. Airway hyper reactivity detected at primary school age, decreased by adolescence. Nicotine transfer via breast milk induces obesity in the adult offspring. We hypothesize that sympathetic nervous system (SNS) activity, brown adipose tissue (BAT) thermogenesis and white adipose tissue (WAT) lipogenesis/adipogenesis are altered in adult rats that were exposed to nicotine exclusively during the breastfeeding period. Lactating Wistar rats were separated into two groups nicotine (NIC), dams implanted with osmotic minipumps containing 6 mg/kg of nicotine at postnatal day (PN) 2; control, dams were implanted with saline-containing minipumps. Euthanasia occurred at PN120 or PN180. ALK phosphorylation NIC offspring had lower BAT SNS activity and higher BAT lipid content. NIC males showed lower UCP1, β3-AR and CPT1a, while NIC females showed lower UCP1, TRα1, CPT1a, suggesting lower thermogenesis. NIC males showed higher WAT SNS activity, WAT β3-AR, adrenal catecholamine, FAS, PPARγ and adipocytes area, while NIC females showed higher ACC, FAS, CEBPβ and PPARγ. These findings indicate increased lipogenesis/adipogenesis in both sexes, with a possible compensatory sympathetic activated-lipolysis in males. NIC males had higher hypothalamic pAMPK/AMPK, explaining the lower BAT sympathetic activity. Neonatal nicotine exposure reduces BAT SNS activity and thermogenesis, and, only in males, increases WAT adipogenesis/lipogenesis, despite higher WAT SNS activity. These alterations can be associated with obesogenesis in this programming model. Reactive carbonyls, including methylglyoxal (MG), are considered toxic compounds in foodstuffs because they irreversibly modify proteins and produce advanced glycation end products (AGEs). Therefore, we studied the long-term effect of increased MG intake in mature adult mice. Six-month-old C57BL/6N mice received MG by drinking water (2.5 mg/ml; i.e., 200-300 mg/kg BW/d) until death. This treatment caused an immediate strong increase in urine MG and a delayed moderate increase in plasma MG. At 24 months of age, mice administered MG showed no changes in the blood and tissue activity of glyoxalase-1 (Glo1), an intracellular MG-detoxifying enzyme; no signs of renal insufficiency and diabetes, including unchanged AGE modifications of plasma and vessel proteins; reduced tumour incidence; and slightly increased survival. Mice simultaneously deficient in the receptor for AGEs (RAGE) and overexpressing Glo1 exhibited higher basal plasma MG levels and did generally not respond to long-term MG intake. In vitro experiments supported the minor relevance of Glo1 in the detoxification of circulating MG but the important role of plasma albumin as an MG scavenger.