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BACKGROUND This study's purpose was to determine if age, fall height, fall mechanism, landing surface, and landing position are associated with injury severity and hospital outcomes among pediatric fall patients. METHODS A retrospective review was conducted of patients aged ≤18 years who sustained fall-related injuries admitted to an American College of Surgeons verified Level 1 trauma center from January 1, 2006 through December 31, 2015. RESULTS Patient age, fall mechanism, landing position, and landing surface were associated with the need for surgery. Patient age, fall mechanism, and landing position were also associated with intensive care unit admissions. Fall mechanism was the only variable associated with injury severity. No variables were associated with the need for mechanical ventilation or mortality. CONCLUSIONS Patient age, fall mechanism, landing surface, and landing position need to be considered with regard to injury severity and patient outcomes among pediatric fall patients. BACKGROUND The aim of this study was to evaluate quetiapine-associated pulmonary complications (PC) in critically injured trauma patients. METHODS Injured adults admitted during 2016 to the ICU at a Level I trauma center were analyzed. Outcomes were evaluated by competing risks survival analysis. RESULTS Of 254 admissions, 40 (15.7%) had PC and 214 (84.3%) were non-events. PC patients were more severely injured, had longer hospital stays and were more likely to die. Patients administered quetiapine were more likely to develop PC and acquire PC earlier than those without quetiapine. Quetiapine was a positive risk factor for PC (sHR 2.24, p = 0.013). Stratification by ventilator use revealed non-ventilated patients administered quetiapine had the highest risk for PC (sHR 4.66, p = 0.099). CONCLUSIONS Quetiapine exposure in critically injured trauma patients was associated with increased risk of PC. Guidelines for treatment of delirium with quetiapine in critically injured trauma patients should account for this risk. The Comprehensive Primary Care (CPC) initiative was an alternative payment model implemented from 2012 to 2016 to strengthen primary care by enhancing core functions, including access to care. The association between interventions to enhance access and patients' perception of access is unknown. We performed a cross-sectional analysis of CPC practice surveys and CAHPS patient survey responses pertaining to access and timeliness in 2016. There were regional differences in both patients' perceptions of access and interventions to enhance access, but no association between interventions and patients' perceptions. Practices with fewer clinicians and whose patients had fewer chronic conditions had better perceived access. Published by Elsevier Inc.Bone marrow adipose tissue (BMAT) has recently been found to induce osteoclastogenesis by secreting RANKL. Although Type 1 diabetes mellitus (T1DM) has been reported to be associated with increased BMAT and bone loss, little is known about the relationship between BMAT and osteoclasts in T1DM. We studied the role of BMAT in the alterations of osteoclast activities in early-stage T1DM, by using a streptozotocin-induced T1DM mouse model. Our results showed that osteoclast activity was enhanced in the long bones of T1DM mice, accompanied by increased protein expression of RANKL. However, RANKL mRNA levels in bone tissues of T1DM mice remained unchanged. Meanwhile, we found that BMAT was significantly increased in the long bones of T1DM mice, and both mRNA and protein levels of RANKL were elevated in the diabetic BMAT. More importantly, RANKL protein was mainly expressed on the cell membranes of the increased adipocytes, most of which were located next to the metaphyseal region. These results suggest that the enhanced bone resorption in early-stage diabetic mice is induced by RANKL derived from BMAT rather than the bone tissue itself. Collagen Triple Helix Repeat Containing 1 (CTHRC1) has been picked out as a cancer-related, secreted glycoprotein that possesses multifaceted functions such as wound repair, the formation of adipose tissue, hepatocytes fibrosis, and bone remodeling. selleck kinase inhibitor This study aims to explore the biological function and the profound regulative mechanism of CTHRC1 in human prostate cancer (PCa). We found that CTHRC1 was upregulated in patients with PCa. The knockdown of CTHRC1 suppressed PCa cell proliferation, invasion, migration, and colony formation significantly. The expression of CTHRC1 was down-regulated and up-regulated by miR-30e-5p mimics and inhibitors, respectively, in PCa cells. The dual-luciferase reporter assay validated the binding of miR-30e-5p with CTHRC1 mRNA, indicating the regulation of CTHC1 by miR-30e-5p. In consequence, this study demonstrated that CTHRC1 acts as an oncogenic gene and targeting the miR-30e-5p-CTHRC1 axis may provide novel therapeutic treatment for PCa. Caspase recruitment domain 6 (CARD6) was initially implicated in the immune system and oncogenesis, which has also been emerged to play an important role in cardio-metabolic diseases. Nevertheless, the potential role of CARD6 on macrophage activation remains unknown. In the present study, we observed a decreased CARD6 expression in bone marrow derived macrophages (BMDMs) and mouse peritoneal macrophages (MPMs) isolated from ApoE deficiency mice and administrated with OX-LDL, which were tested by RT-PCR and western bolt analysis. Moreover, the immunofluorescence co-staining revealed that a weaker immunoreactivity of CARD6 was found and primary located in cytoplasm of macrophages induced by OX-LDL. Phenotypically, loss-of-function of CARD6 dramatically increased pro-inflammatory M1 macrophage but decreased resolving M2 macrophage markers expression. Additionally, CARD6 knockdown significantly promoted cholesterol uptake but attenuated cholesterol efflux, which lead to increased foam cell formation. Mechanistically, a downregulated AMP-activated protein kinase (AMPK) expression was required for the promoted effect of CARD6 knockdown on macrophage activation. Taken together, these results suggest that CARD6 protects against macrophage activation partially through activation of AMPK-dependent mechanism.
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