Randolphsteele5338

Ambient BC concentration, ambient temperature, relative humidity, education level and air purifier use were significant determinants of personal BC exposure. Our findings highlight the need for detailed assessment of personal exposure on health risk assessment of BC and also help develop strategies for targeted risk reduction. BACKGROUND A new Air Quality Health Index (AQHI) was developed in Canada or several single cities as a promising health risk communication tool. OBJECTIVES To construct a national AQHI in China and compare its validity in predicting daily mortality risk with the existing Air Quality Index (AQI). METHODS We established the AQHI as the sum of excess total mortality risks associated with multiple air pollutants in 272 representative Chinese cities from 2013 to 2015 (termed as "total AQHI"). The mortality risks per unit change of air pollutant concentrations were determined according to a time-series analysis in each city. find more Separate AQHIs were established for subgroups classified by age and sex and for main cardiopulmonary diseases (termed as "specific AQHIs"). For validation, AQHIs and AQI were established using the data of 2015 (N = 272) and compared their associations with daily mortality using the data of 2013-2014 (N = 144). RESULTS The concentration-response coefficients of fine particulate matter, nitrogen dioxide and ozone were adopted in constructing AQHI. There were almost linear exposure-response relationships between AQHIs and daily mortality. The total AQHI and specific AQHIs had very similar associations with daily mortality. AQHI and AQI showed similar associations with daily cause-specific mortality in terms of average magnitude, numbers of cities of positive associations and model fit statistics. CONCLUSIONS AQHI may have comparable performance with AQI in communicating acute health risks of air pollution in China. There seems no need to establish specific AQHIs for different age groups, gender and causes of deaths. Substantial perfluoroalkyl acids (PFAAs) production still occurs in China, and the consumption of aquatic products is a critical exposure pathway of PFAAs in humans. In this study, specimens of 16 freshwater and 40 marine species were collected in the river-estuary-sea environment affected by a mega fluorochemical industry park in China in 2015, and the edible tissues of these organisms were analyzed for PFAA levels. Perfluorooctanoic acid (PFOA) was the dominating contaminant with an overall contribution of more than 90%, and concentrations as high as 2161 ng/g wet weight (measured in the freshwater winkle). All species with the greatest PFOA levels were benthic. The trophic magnification factor (TMF) of PFOA was 1.10 for freshwater species and 1.28 for marine species, indicating that PFOA was slightly magnifying. Analysis of carbon source indicated that freshwater species were more benthic feeding, while marine species were more pelagic feeding. Aquatic food consumption screening values of PFOA were modified according to estimated daily intake (EDI) values, which generated recommendations for limited meal categories and the do-not-eat category. Thus, this study provides recommendations for mitigating the health risks of PFAA-contaminated aquatic food, ranging from food selection to consumption frequency and proper food processing. Glucocorticoid (GC) treatments induce osteoporosis and chronic GC treatments have been suggested to induce delayed bone repair; however, the mechanisms by which GC induces delayed bone repair remain unclear. We herein investigated the roles of plasminogen activator inhibitor-1 (PAI-1) in GC-induced effects on bone repair after femoral bone injury using female mice with a PAI-1 deficiency and their wild-type counterparts. Dexamethasone (Dex) increased plasma PAI-1 levels as well as PAI-1 mRNA levels in the adipose tissues and muscles of wild-type mice. PAI-1 deficiency significantly blunted Dex-induced delayed bone repair in mice. Moreover, PAI-1 deficiency significantly blunted Runx2 mRNA levels suppressed by Dex as well as Dex-induced osteoblast apoptosis at the damaged site 7 days after bone injury in mice. On the other hand, PAI-1 deficiency did not affect adipogenic gene expression enhanced by Dex at the damaged site 7 days after bone injury in mice. In conclusion, we herein showed for the first time that PAI-1 is involved in delayed bone repair after bone injury induced by GC in mice. PAI-1 may influence early stage osteoblast differentiation and apoptosis during the osteoblastic restoration phase of the bone repair process. There is limited information about denosumab-related osteonecrosis of the jaw (DRONJ), unlike bisphosphonate-related ONJ (BRONJ). The mode of action is clearly different between denosumab and bisphosphonates. DRONJ occurs mainly following tooth extraction in cancer patients treated with the combination of denosumab and other drugs including chemotherapy. However, DRONJ animal models similar to these clinical situations have not been developed. The aims of this study were to 1) create a new model of high-prevalence chemotherapy/anti-RANKL antibody-related ONJ-like lesions to mimic patients receiving a denosumab/chemotherapy combination; and 2) compare the histopathological and immunopathological findings in the early stages of BRONJ-like and anti-RANKL antibody-related ONJ-like lesions. Cyclophosphamide (CY) and anti-mouse RANKL monoclonal antibody (mAb) or zoledronate combination therapy (CY/mAb and CY/ZA, respectively) was performed to create ONJ-like lesions in female C57BL/6J mice. Both maxillary first molerent antiresorptive-induced ONJ-like lesions in conjunction with lymphangiogenesis, although the histopathological findings were similar. These findings suggest that the pathogenesis of BRONJ and DRONJ may differ due to the distributions of F4/80+LYVE-1+ tube-like-structured cells. BACKGROUND Avoidant Restrictive Food Intake Disorder (ARFID) and Anorexia Nervosa (AN) cause significant underweight in children and young people (CYP). The association of low bone mineral density (BMD) and underweight CYP in AN is well established, but less is known about BMD in ARFID. METHODS Retrospective case-note review and analysis of BMD measures by DXA on underweight patients referred to a paediatric clinic for eating disorders between 2014 and 2019. Indications for BMD measurement were age > 5 years and underweight for at least 6 months. RESULTS Of 134 cases where BMD was measured, 118 (88%) had AN and 16 (12%) ARFID. Age range was 6-19 years. 19% were males. ARFID cases were more likely to be male, have lower Body Mass Index (BMI), BMI z-score (BMIz), and longer underweight duration. For all cases, BMI and BMIz were positively associated with BMD z-score (BMI coefficient 0.13,95%CI 0.04 to 0.22, p = 0.01; BMIz coefficient 0.34, 95%CI 0.17 to 0.51, p  less then  0.001) and bone mineral areal density z-score (BMI coefficient 0.