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To determine the utility of emergency physician-performed point-of-care biliary ultrasound in the evaluation of emergency department (ED) patients with isolated acute non-traumatic epigastric pain. This was a multi-center prospective observational study of adult patients presenting to the ED with isolated acute non-traumatic epigastric pain. Patients with abdominal tenderness at any site other than the epigastric region, or with a history of gall stones, cholecystectomy, gastrointestinal bleeding, chronic abdominal pain, trauma, or altered mental status were excluded. Emergency physician investigators performed point-of-care biliary ultrasound after clinical assessment. Demographic information, history, physical examination findings, laboratory results, additional diagnostic tests, and disposition data were collected. A total of 51 patients (39 women, 12 men) were enrolled. The mean age of the patients was 36.4 years ± 13.6 (SD). All subjects had isolated epigastric tenderness. Gallstones were found in 20/51 (39 %, 95 % CI 26–52 %) on point-of-care biliary ultrasound. Of the 20 patients who had gallstones, eight had sonographic signs of chloecystitis. The treating emergency physicians’ initial evaluation did not plan to include an ultrasound in 17/20 patients with gallstones. 19/20 patients were initially given a GI cocktail by the treating emergency physicians. Point-of-care biliary ultrasound detected gall stones in more than one-third of ED patients with isolated acute non-traumatic epigastric pain. All patients presenting to the ED with non-traumatic epigastric pain should be evaluated for biliary disease with an ultrasound imaging study. Bedside ultrasound can avoid misdiagnosis and expedite management in these patients.  相似文献   
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Endocannabinoid signaling critically regulates emotional and motivational states via activation of cannabinoid receptor 1 (CB1) in the brain. The nucleus accumbens (NAc) functions to gate emotional and motivational responses. Although expression of CB1 in the NAc is low, manipulation of CB1 signaling within the NAc triggers robust emotional/motivational alterations related to drug addiction and other psychiatric disorders, and these effects cannot be exclusively attributed to CB1 located at afferents to the NAc. Rather, CB1-expressing neurons in the NAc, although sparse, appear to be critical for emotional and motivational responses. However, the cellular properties of these neurons remain largely unknown. Here, we generated a knock-in mouse line in which CB1-expressing neurons expressed the fluorescent protein td-Tomato (tdT). Using these mice, we demonstrated that tdT-positive neurons within the NAc were exclusively fast-spiking interneurons (FSIs). These FSIs were electrically coupled with each other, and thus may help synchronize populations/ensembles of NAc neurons. CB1-expressing FSIs also form GABAergic synapses on adjacent medium spiny neurons (MSNs), providing feed-forward inhibition of NAc output. Furthermore, the membrane excitability of tdT-positive FSIs in the NAc was up-regulated after withdrawal from cocaine exposure, an effect that might increase FSI-to-MSN inhibition. Taken together with our previous findings that the membrane excitability of NAc MSNs is decreased during cocaine withdrawal, the present findings suggest that the basal functional output of the NAc is inhibited during cocaine withdrawal by multiple mechanisms. As such, CB1-expressing FSIs are targeted by cocaine exposure to influence the overall functional output of the NAc.Cannabinoid receptor type 1 (CB1) has been extensively implicated in a variety of psychological and psychiatric disorders, including drug addiction (1, 2). Recent studies suggest that CB1 within the nucleus accumbens (NAc), a key component of the brain reward circuit, plays a particularly important role in the development and maintenance of cocaine-induced behavioral alterations (3). Compared with the extensive expression of CB1 in the striatum, the mRNA and protein levels of CB1 within the NAc are sparse, leading to the notion that CB1 at afferent terminals projecting to the NAc are largely responsible for intra-NAc, CB1-dependent, cocaine-induced behaviors (46). However, a recent study primarily targeting CB1-expressing neurons demonstrates that inhibiting the expression of CB1 within the NAc antagonizes cocaine-induced reward responses (7). This and other results (8) suggest that CB1-expressing neurons in the NAc, although sparse, are critical for cellular and behavioral alterations induced by cocaine and other drugs of abuse.To examine these putative CB1-expressing neurons within the NAc, we generated a knock-in mouse line in which CB1-expressing neurons expressed the fluorescent protein td-Tomato (tdT). Our results show that tdT-positive neurons within the NAc were exclusively fast-spiking interneurons (FSIs). These FSIs were not only electrically connected with each other but exerted extensive inhibitory control on nearby medium spiny neurons (MSNs), the principal neurons in the NAc, via monosynaptic connections. Furthermore, the membrane excitability of these neurons became significantly up-regulated throughout short- and long-term withdrawal from repeated exposure to cocaine. These results suggest that CB1-expressing FSIs within the NAc are neural substrates targeted by cocaine exposure and influence the overall functional output of the NAc.  相似文献   
74.
Background: Alcohol dependence is more prevalent among those with any one of several anxiety or depressive (“internalizing”) disorders than among those in the general population. However, because internalizing disorders are highly intercorrelated, it is ambiguous whether alcohol dependence is related to internalizing psychopathology components that are: (i) unique to a particular internalizing disorder (“specific”); versus (ii) shared across a number of internalizing disorders (“general”). To clarify this ambiguity, we employed structural equation and logistic models to decompose the specific versus general components of internalizing psychopathology and then related these components separately to alcohol dependence. Methods: The data were based on face‐to‐face interviews of U.S. community residents collected in the 2001 to 2002 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC; N = 43,093). Results: Both analytic approaches demonstrated that increases in the general internalizing psychopathology load are accompanied by increases in the prevalence of alcohol dependence. Once the general internalizing psychopathology load is accounted for, knowing whether a particular internalizing disorder is present or absent provides little additional information regarding the prevalence of alcohol dependence. Conclusions: The components of internalizing psychopathology that are associated with alcohol dependence are shared and cumulative among common anxiety and depressive disorders. These findings have the potential to influence clinical and scientific conceptualizations of the association between alcohol dependence and internalizing psychopathology.  相似文献   
75.
Systemic inflammation is one of the pivotal pathogenetic principles in atherogenesis and progression of atherosclerosis. Patients with rheumatoid arthritis (RA) exhibit an increased cardiovascular risk that is not explained by traditional cardiovascular risk factors but rather by a chronic systemic inflammatory reaction. Reduction of inflammatory activity in RA patients was shown to reduce cardiovascular morbidity and mortality. Besides this specific approach traditional cardiovascular risk factors need to be carefully controlled in order to improve mortality in RA patients; however, this task is difficult to implement in everyday practice as RA patients usually have decisively different medical needs that need to be addressed irrespective of the well-acknowledged limitations of medical resources, such as time and costs.  相似文献   
76.
International Journal of Legal Medicine - Fluoride is a common stabilizing agent in forensic toxicology to avoid the frequent problem of degradation of drugs in blood samples especially described...  相似文献   
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It is plausible that infections post‐hematopoietic SCT play a role in the pathogenesis of BOS. A prospective study for children with history, questionnaire, examination, PFTs, and blood counts at one, three, six, nine, 12, 18, and 24 months post‐SCT was conducted. Between September 2009 and September 2011 (n = 39), six developed BOS at 200 days (range 94–282), three patients had probable clinical respiratory infection, and all six had higher neutrophil count compared to non‐BOS patients (4.7 vs. 2.4 at three months and 6.3 vs. 2.9 at six months ×109/L, p = 0.03). Contribution of clinical and subclinical infection needs to be considered in the pathogenesis of BOS.  相似文献   
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