The purpose of this study was to quantify and integrate key emergency department (ED) and radiology department workflow time intervals within the ED length of stay (LOS) for patients presenting with acute abdomen who require CT.An 11-month retrospective review was performed of all patients presenting to the ED with an acute abdomen who required abdominal CT. Nine key time points associated with ED LOS and CT workflow were collected: triage, physician assessment, CT request, porter schedule, CT start, CT complete, provision of first CT report, ED disposition decision, and physical discharge. The median and 90th percentile times for each interval were reported.Ninety-six percent (2194/2292) of ED encounters during the study period met the inclusion criteria. The median ED LOS was 9.22 hours (90th percentile, 15.7 hours). Intervals associated with CT workflow accounted for 29% of the total LOS. Radiology turnaround time accounted for 32% of the entire CT workflow interval. Timeline analysis found three unique patterns of ED disposition: disposition after initial imaging report, disposition before report, and disposition before CT.To our knowledge, this study is the first to quantify the contribution of CT-related workflow time intervals within the context of ED LOS. We have shown that patients do not have identical ED transit pathways, and this may under- or overestimate time interval calculations. These results show the importance of site-specific ED LOS timeline analysis to identify potential targets for quality improvement and serve as baseline targets for measuring future quality improvement initiatives.
A healthy skeletal muscle mass is essential in attenuating the complications of obesity. Importantly, healthy muscle function is maintained through adequate repair following overuse and injury. The purpose of this study was to investigate the impact of diet-induced obesity (DIO) on skeletal muscle repair and the functionality of the muscle satellite cell (SC) population. Male C57BL/6J mice were fed a standard chow or high-fat diet (60% kcal fat; DIO) for 8 weeks. Muscles from DIO mice subjected to cardiotoxin injury displayed attenuated muscle regeneration, as indicated by prolonged necrosis, delayed expression of MyoD and Myogenin, elevated collagen content, and persistent embryonic myosin heavy chain expression. While no significant differences in SC content were observed, SCs from DIO muscles did not activate normally nor did they respond to exogenous hepatocyte growth factor (HGF) despite similar receptor (cMet) density. Furthermore, HGF release from crushed muscle was significantly less than that from muscles of chow fed mice. This study demonstrates that deficits in muscle repair are present in DIO, and the impairments in the functionality of the muscle SC population as a result of altered HGF/c-met signaling are contributors to the delayed regeneration.
OBJECTIVE. CT or MRI is most commonly used for characterizing focal hepatic lesions. However, findings on CT and MRI are occasionally indeterminate. Contrast-enhanced ultrasound (CEUS), with its unique characteristics as a purely intravascular contrast agent and real-time evaluation of enhancement, is a useful next step. The purpose of this article is to review the evidence for performing CEUS in the assessment of indeterminate hepatic lesions seen on CT and MRI. CONCLUSION. CEUS is a useful problem-solving tool in the evaluation of liver lesions that are indeterminate on CT and MRI. Uses include detection of arterial phase hyperenhancement; differentiation between hepatocellular carcinoma and intrahepatic cholangiocarcinoma; determination of benign versus malignant tumor thrombus, benign versus neoplastic cystic hepatic lesions, and hepatocellular adenoma versus focal nodular hyperplasia; and monitoring for recurrence in postablative therapies. CEUS can help establish a confident diagnosis and determine the need for further invasive diagnosis or treatment.
Background Diet-induced obesity is a rising health concern which can lead to the development of glucose intolerance and muscle insulin resistance and, ultimately, type II diabetes mellitus. This research investigates the associations between glucose intolerance or muscle insulin resistance and tissue specific changes during the progression of diet-induced obesity. Methodology C57BL/6J mice were fed a normal or high-fat diet (HFD; 60% kcal fat) for 3 or 8 weeks. Disease progression was monitored by measurements of body/tissue mass changes, glucose and insulin tolerance tests, and ex vivo glucose uptake in intact muscles. Lipid metabolism was analyzed using metabolic chambers and ex vivo palmitate assays in intact muscles. Skeletal muscle, liver and adipose tissues were analyzed for changes in inflammatory gene expression. Plasma was analyzed for insulin levels and inflammatory proteins. Histological techniques were used on muscle and liver cryosections to assess metabolic and morphological changes. Principal Findings/Conclusions A rapid shift in whole body metabolism towards lipids was observed with HFD. Following 3 weeks of HFD, elevated total lipid oxidation and an oxidative fiber type shift had occurred in the skeletal muscle, which we propose was responsible for delaying intramyocellular lipid accumulation and maintaining muscle’s insulin sensitivity. Glucose intolerance was present after three weeks of HFD and was associated with an enlarged adipose tissue depot, adipose tissue inflammation and excess hepatic lipids, but not hepatic inflammation. Furthermore, HFD did not significantly increase systemic or muscle inflammation after 3 or 8 weeks of HFD suggesting that early diet-induced obesity does not cause inflammation throughout the whole body. Overall these findings indicate skeletal muscle did not contribute to the development of HFD-induced impairments in whole-body glucose tolerance following 3 weeks of HFD.
See also page [598][1] and [www.cmaj.ca/lookup/doi/10.1503/cmaj.150663][2] Patients presenting with suspected cognitive decline should undergo a detailed history, physical examination and cognitive screening to establish functional impairment.[1][3] Laboratory investigations to rule out medical
AMP-activated protein kinase (AMPK) is a master regulator of metabolism. While Muscle-specific AMPK β1β2 double-knockout (β1β2M-KO) mice display alterations in metabolic and mitochondrial capacity, their severe exercise intolerance suggested a secondary contributor to the observed phenotype. We find that tibialis anterior (TA), but not soleus, muscles of sedentary β1β2M-KO mice display a significant myopathy (decreased myofiber areas, increased split and necrotic myofibers, and increased centrally nucleated myofibers. A mitochondrial- and fiber-type-specific etiology to the myopathy was ruled out. However, β1β2M-KO TA muscles displayed significant (P<0.05) increases in platelet aggregation and apoptosis within myofibers and surrounding interstitium (P<0.05). These changes correlated with a 45% decrease in capillary density (P<0.05). We hypothesized that the β1β2M-KO myopathy in resting muscle resulted from impaired AMPK-nNOSμ signaling, causing increased platelet aggregation, impaired vasodilation, and, ultimately, ischemic injury. Consistent with this hypothesis, AMPK-specific phosphorylation (Ser1446) of nNOSμ was decreased in β1β2M-KO compared to wild-type (WT) mice. The AMPK-nNOSμ relationship was further demonstrated by administration of 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR) to β1β2-MKO muscles and C2C12 myotubes. AICAR significantly increased nNOSμ phosphorylation and nitric oxide production (P<0.05) within minutes of administration in WT muscles and C2C12 myotubes but not in β1β2M-KO muscles. These findings highlight the importance of the AMPK-nNOSμ pathway in resting skeletal muscle.—Thomas, M. M., Wang, D. C., D'Souza, D. M., Krause, M. P., Layne, A. S., Criswell, D. S., O'Neill, H. M., Connor, M. K., Anderson, J. E., Kemp, B. E., Steinberg, G. R., and Hawke, T. J. Musclespecific AMPK β1β2-null mice display a myopathy due to loss of capillary density in nonpostural muscles. FASEB J. 28, 2098–2107 (2014). www.fasebj.org
To determine the incidence of temporal lobe dysplasia (TLD) detected on prenatal ultrasound in thanatophoric dysplasia (TD) over an 11-year period in a tertiary referral center.An 11-year retrospective review of perinatal autopsies from 2002 to 2013 was performed to identify cases of TD. The ultrasound images and corresponding reports of all TD cases were examined for the presence of TLD. The same set of images subsequently underwent a retrospective review by a perinatal radiologist with knowledge of the features of TLD to determine whether they could be identified.Thirty-one cases of TD underwent perinatal autopsy, and prenatal ultrasound imaging was available for review in 24 (77%). Mean gestational age at diagnosis of TD was 21.3 (range, 18-36) weeks. TLD was identified and reported in 6/24 (25%) cases; all six cases occurred after 2007. Retrospective interpretation of the ultrasound images identified features of TLD in 10 additional cases. In total, 16/24 (67%) cases displayed sonographic evidence of TLD. Temporal trends showed that TLD features were present in 50% (5/10) of all TD cases between 2002 and 2006 and in 79% (11/14) of those detected between 2007 and 2013.At present, the detection rate of TLD by ultrasound is low but may be increased by modified brain images that enhance visualization of the temporal lobes. Prenatal identification of TLD may help in the prenatal diagnosis of TD and thus provide more accurate prenatal counseling and guide molecular investigations to confirm the specific diagnosis of TD.
