Prospective comparison of plain abdominal radiography with conventional and digital renal tomography in assessing renal extracorporeal shock wave lithotripsy patients

Most publications citing the effectiveness of renal extracorporeal shock wave lithotripsy have used plain abdominal radiography to assess residual calculi after treatment. We compared radiologist sensitivity and specificity in the detection of calculi on plain abdominal radiographs versus conventional film-screen and digital renal tomograms in extracorporeal shock wave lithotripsy patients. Of the patients 50 were imaged before and within 24 hours after lithotripsy. Six radiologists evaluated the resultant 300 studies for the presence and location of calculi. The mean sensitivity for digital tomograms was 83% for pre-lithotripsy and post-lithotripsy studies, which was significantly higher than for plain abdominal radiography and conventional tomography after lithotripsy. However, there were significantly more false positive stone diagnoses associated with digital tomogram interpretation. Signal detection analysis verified the over-all superiority of digital tomography for post-extracorporeal shock wave lithotripsy imaging. Calculus detection by conventional and digital tomography is superior to detection by plain abdominal radiography. However, because we did not perform delayed imaging, it is not possible to say what impact digital tomography might have on the management of extracorporeal shock wave lithotripsy patients.     

Tissue-specific overexpression of lipoprotein lipase causes tissue-specific insulin resistance

Insulin resistance in skeletal muscle and liver may play a primary role in the development of type 2 diabetes mellitus, and the mechanism by which insulin resistance occurs may be related to alterations in fat metabolism. Transgenic mice with muscle- and liver-specific overexpression of lipoprotein lipase were studied during a 2-h hyperinsulinemic-euglycemic clamp to determine the effect of tissue-specific increase in fat on insulin action and signaling. Muscle-lipoprotein lipase mice had a 3-fold increase in muscle triglyceride content and were insulin resistant because of decreases in insulin-stimulated glucose uptake in skeletal muscle and insulin activation of insulin receptor substrate-1-associated phosphatidylinositol 3-kinase activity. In contrast, liver-lipoprotein lipase mice had a 2-fold increase in liver triglyceride content and were insulin resistant because of impaired ability of insulin to suppress endogenous glucose production associated with defects in insulin activation of insulin receptor substrate-2-associated phosphatidylinositol 3-kinase activity. These defects in insulin action and signaling were associated with increases in intracellular fatty acid-derived metabolites (i.e., diacylglycerol, fatty acyl CoA, ceramides). Our findings suggest a direct and causative relationship between the accumulation of intracellular fatty acid-derived metabolites and insulin resistance mediated via alterations in the insulin signaling pathway, independent of circulating adipocyte-derived hormones.     

Behavioral Impairment Under Alcohol: Cognitive and Pharmacokinetic Factors

This study tested the hypothesis that the intensity of behavioral impairment under alcohol is related to social drinkers' expectancies about impairment and their rates of rise in blood alcohol concentration (BAC). After subjects ( n = 30) were trained on a psychomotor task, they rated the impairment they expected from alcohol and then performed the task under alcohol (0.56 g/kg) or a placebo. Alcohol impaired performance, compared with placebo. Drinkers' expectations about impairment and their rates of rise in BAC were independent, and each factor predicted a significant portion of the variance in alcohol impairment among drinkers. More intense impairment under alcohol was associated with expectations of greater impairment and with swifter rates of rise in BAC. BACs obtained by drinkers during task performance were not related to the intensity of impairment they displayed. The study shows that a pharmacological and nonpharmacological variable can each affect a drinker's behavioral impairment under alcohol, and this finding contributes to our understanding of conditions where BAC per se may be an unreliable indicator of impairment.     

Contributory negligence

The doctrine of contributory negligence evolved from 19th century economic legal policy seeking to protect America's fledgling industries from liability for injuries resulting from their activities. These policies resulted in an anti-claimant environment that made it difficult for any plaintiff, including malpractice plaintiffs, to recover for their injuries. Since the onset of the 20th century, courts, spurred by state and federal legislative acts, have become more even-handed, and contributory negligence has become a limited defense in malpractice cases. This article defines some of the situations where courts have found that patient's actions have barred plaintiff recovery because of contributory negligence and offers the limited prediction that contributory negligence may be on the verge of once again becoming a major malpractice defense.     

The Emergency Medical Treatment and Labor Act (EMTALA)

The Emergency Medical Treatment and Labor Act (EMTALA) was enacted to prevent patient dumping. It provides patients a considerable amount of protection and leverage in obtaining care under emergency situations. The reimbursement strictures imposed by managed care organizations have compounded the problems. This article summarizes the Act's definition of role and duties of hospitals and physicians and the regulations to which these parties must adhere or face significant penalties.     

Synthesis and characterization of novel ceramide analogs for induction of apoptosis in human cancer cells

A variety of anti-cancer drugs elevate endogenous ceramide, thereby inducing apoptosis in tumor cells. Recently, we have introduced novel ceramide analogs of the beta-hydroxy alkyl amide type, which trigger pro-apoptotic signaling pathways without prior elevation of endogenous ceramide. They induce apoptosis specifically in rapidly dividing neuroblastoma cells, but not in resting or differentiated cells. We characterize new ceramide mimics that have been derived from N-acylation of serinol (S), diethanolamine (B), propanolamine (P), and tris(hydroxy-methyl)methylamine (T) with myristic (14), palmitic (16), or oleic (18) acid. The water solubility of these compounds exceeds that of ceramide by more than 100-fold (up to 5 mM). Apoptosis of human neuroblastoma, glioma, medulloblastoma, and adenocarcinoma cells is induced by N-(2-hydroxy-1-(hydroxymethyl)ethyl)-palmitoylamide, C16-serinol (S16), N-(2-hydroxy-1-(hydroxymethyl)ethyl)-oleoylamide, C18-serinol (S18), N-bis(2-hydroxyethyl)-myristoyl-amide (B16), and N-tris(hydroxymethyl)methyl-oleoylamide (T18) within 60 min of incubation, and is completed even after removal of the compound from the medium. This is most likely due to a rapid uptake of the analogs followed by their slow release from the cells. Alteration of the acyl chain length to less than 14 methylene units, removal of the amino group, or reducing the number of hydroxyalkyl residues to less than two significantly lowers or eliminates the pro-apoptotic potential of these compounds. The target specificity of novel ceramide analogs for tumor cells, their water solubility, and fast pro-apoptotic mechanism indicates a high therapeutic potential for cancer treatment.     

Alcohol increases reliance on cues that signal acts of control

This study examined the effects of alcohol on the ability to execute and inhibit behavior in a context in which preliminary information signaled the likelihood that a response should be executed or suppressed. Adults (N = 24) performed a cued go/no-go task that required quick responses to go targets and suppression of responses to no-go targets. Cue dependency was manipulated by varying the predictive validity of the cues, and performance was tested under 3 doses of alcohol: 0.00 g/kg, 0.45 g/kg, and 0.65 g/kg. Dose-dependent increases in cue dependence were only observed with highly predictive cues. Results suggest that alcohol-induced increases in stimulus control over behavior might be most likely in situations when stimulus control over behavior has already been established.     

Cocaine improves inhibitory control in a human model of response conflict

The present study was designed to test the acute effects of cocaine on behavioral control in the presence and absence of motivational conflict. Adults (N = 14) with a history of stimulant use received oral cocaine hydrogen chloride (0, 100, 200, and 300 mg) and performed a cue-dependent go/no-go task to measure inhibitory and activational mechanisms of behavioral control either with or without motivated conflict between the inhibition and the activation of responses. Cocaine improved response inhibition in both conflict conditions, as evident by a decrease in inhibitory failures following active doses. The current study provides a useful model to investigate the effects of other drugs reported to have performance-enhancing effects.