The magnitude of protection matched IPC. IPC requited less S1365 phosphorylation, as TSC2SE hearts gained no benefit and failed to activate mTORC1 with IPC. IR metabolism was altered in TSC2SA, with increased mitochondrial oxygen consumption rate and glycolytic capacity (stressed/maximal extracellular acidification) after myocyte hypoxia-reperfusion. In whole heart, lactate increased and long-chain acyl-carnitine levels declined during ischemia. The relative IR protection in TSC2SA was lost by lowering glucose in the perfusate by 36%. Adding fatty acid (palmitate) compensated for reduced glucose in WT and TSC2SE but not TSC2SA which had the worst post-IR function under these conditions. Conclusions TSC2-S1365 phosphorylation status regulates myocardial substrate utilization, and its decline activates mTORC1 biasing metabolism away from fatty acid oxidation to glycolysis to confer protection against IR. This pathway is also engaged and reduced TSC2 S1365 phosphorylation required for effective IPC.
  The multifaceted nature of learning in diagnostic radiology residency requires a variety of assessment methods. However, the scope and quality of assessment tools has not been formally examined. A scoping review was performed to identify assessment tools available for radiology resident training and to evaluate the validity of these tools.
 
  A literature search was conducted through multiple databases and on-line resources. Inclusion criteria were defined as any tool used in assessment of radiology resident competence. Data regarding residents, evaluators and specifics of each tool was extracted. Each tool was subjected through a validation process with a customized rating scale using the 5 categories of validity content, response process, internal structure, relations to other variables, and consequences.
 
  The initial search returned 447 articles; 35 were included. The most evaluated competency being overall knowledge (31%), most common published journal was 
  (24%)
  evaluations were most commonly set in the United States (57%). In terms of validation, we found low adherence to modern integrated validity, with 34% of studies including a definition of validity. When specifically examining the 5 domains of validation evidence presented, most were either absent or of low rigor (70%). Only one study presented a modern definition of validation (3%, 1/35).
 
  We identified 35 evaluation tools covering a variety of competency areas. However, few of these tools have been validated. Development of new validated assessment tools or validation of existing tools is essential for the ongoing transition to a competency-based curriculum.
 We identified 35 evaluation tools covering a variety of competency areas. However, few of these tools have been validated. Development of new validated assessment tools or validation of existing tools is essential for the ongoing transition to a competency-based curriculum.We investigated the association between plasma microRNA (miR)-204 and coronary artery calcification (CAC) in patients with type 2 diabetes mellitus (T2DM). We consecutively enrolled 179 individuals with T2DM who underwent coronary computed tomography at Anzhen Hospital from January 2015 to September 2016. The CAC score (CACS) was expressed in Agatston units and >10 Hounsfield units were defined as CAC-positive status. Significant CAC was observed in 98 (54.7%) patients. Plasma miR-204 levels (relative expression) were significantly lower in patients with significant CAC than controls (1.001 ± 0.100 vs 0.634 ± 0.211, P less then .001).  https://www.selleckchem.com/products/suzetrigine.html  Plasma miR-204 levels were also negatively correlated with the glycosylated hemoglobin A1c (HbA1c) level (r = -0.702, P less then .001), CACS (r = -0.710, P less then .001), and the United Kingdom Prospective Diabetes Study (UKPDS) score (r = -0.355, P less then .001). After multivariate logistic analyses, plasma miR-204 levels were still significantly and independently associated with the presence of CAC (odds ratio = 0.103, CI = 0.018-0.583, P less then .001) after adjustment for conventional risk factors. Receiver operating characteristic curve analysis showed that plasma miR-204 levels can predict the severity and extent of CAC, and the specificity was higher than that of the traditional risk factors UKPDS score and HbA1c. In conclusion, the downregulation of miR-204 was independently associated with CAC in patients with T2DM.Background Despite compelling epidemiological evidence that circadian disruption inherent to long-term shift work enhances atherosclerosis progression and vascular events, the underlying mechanisms remain poorly understood. A challenge to the use of mouse models for mechanistic and interventional studies involving light-dark patterns is that the spectral and absolute sensitivities of the murine and human circadian systems are very different, and light stimuli in nocturnal mice should be scaled to represent the sensitivities of the human circadian system. Methods and Results We used calibrated devices to deliver to low-density lipoprotein receptor knockout mice light-dark patterns representative of that experienced by humans working day shifts or rotating shift schedules. Mice under day shifts were maintained under regular 12 hours of light and 12 hours of dark cycles. Mice under rotating shift schedules were subjected for 11 weeks to reversed light-dark patterns 4 days in a row per week, followed by 3 days of regular light-dark patterns. In both protocols the light phases consisted of monochromatic green light at an irradiance of 4 µW/cm2. We found that the shift work paradigm disrupts the foam cell's molecular clock and increases endoplasmic reticulum stress and apoptosis. Lesions of mice under rotating shift schedules were larger and contained less prostabilizing fibrillar collagen and significantly increased areas of necrosis. Conclusions Low-density lipoprotein receptor knockout mice under light-dark patterns analogous to that experienced by rotating shift workers develop larger and more vulnerable plaques and may represent a valuable model for further mechanistic and/or interventional studies against the deleterious vascular effects of rotating shift work.