BACKGROUND: We investigated whether limited abdominal magnetic resonance imaging (MRI) is as effective as transabdominal ultrasound (US) in evaluating patients presenting with acute right upper quadrant pain. METHODS: Twenty-four patients underwent evaluation with a limited abdominal MRI using single-shot fast spin-echo sequences and a right upper quadrant US within 24 h. Two MRI and two US readers independently evaluated the images for gallstones, gallbladder wall thickness, pericholecystic fluid, acute cholecystitis, visualization of the common bile duct, and requests for further imaging. US and MRI findings were compared. Surgical pathology was the gold standard. RESULTS: MRI and US demonstrated no statistically significant difference in the diagnosis of gallbladder wall thickening, the presence of gallstones or pericholecystic fluid, or the diagnosis of acute cholecystitis (p > 0.05). The sensitivity of both for acute cholecystitis was 50%, with specificities of 89% and 86% for US and MRI, respectively. US readers more frequently requested additional tests and displayed more variability in whether they could adequately see the common bile duct. CONCLUSION: Limited MRI is equivalent to US in diagnosing gallstones, gallbladder wall thickening, pericholecystic fluid, and acute cholecystitis in patients presenting with symptoms of acute right upper quadrant pain. Especially in sonographically challenging patients, limited MRI may provide a faster, easier method of diagnosis.

Abdomen, Acute↗

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Putative atherogenic factors in patients with chronic renal failure.

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Arteriosclerosis↗

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Parotid salivary secretion in diabetic autonomic neuropathy.

Parotid salivary flow rates and amylase concentrations were measured in three groups of eight subjects each (normal control, non-neuropathic diabetic, and neuropathic diabetic). Flow rates were significantly reduced in neuropathic diabetic patients as compared with normal controls (p less than 0.001) and non-neuropathic diabetic patients (p less than 0.02). Amylase concentrations were similar. These data are consistent with parasympathetic denervation of the parotid gland in diabetic neuropathy and provide evidence for a widespread distribution of autonomic denervation in diabetes.

Adult↗

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Interactions between dihydropyridine receptors and ryanodine receptors in striated muscle.

Excitation-contraction coupling in both skeletal and cardiac muscle depends on structural and functional interactions between the voltage-sensing dihydropyridine receptor L-type Ca(2+) channels in the surface/transverse tubular membrane and ryanodine receptor Ca(2+) release channels in the sarcoplasmic reticulum membrane. The channels are targeted to either side of a narrow junctional gap that separates the external and internal membrane systems and are arranged so that bi-directional structural and functional coupling can occur between the proteins. There is strong evidence for a physical interaction between the two types of channel protein in skeletal muscle. This evidence is derived from studies of excitation-contraction coupling in intact myocytes and from experiments in isolated systems where fragments of the dihydropyridine receptor can bind to the ryanodine receptors in sarcoplasmic reticulum vesicles or in lipid bilayers and alter channel activity. Although micro-regions that participate in the functional interactions have been identified in each protein, the role of these regions and the molecular nature of the protein-protein interaction remain unknown. The trigger for Ca(2+) release through ryanodine receptors in cardiac muscle is a Ca(2+) influx through the L-type Ca(2+) channel. The Ca(2+) entering through the surface membrane Ca(2+) channels flows directly onto underlying ryanodine receptors and activates the channels. This was thought to be a relatively simple system compared with that in skeletal muscle. However, complexities are emerging and evidence has now been obtained for a bi-directional physical coupling between the proteins in cardiac as well as skeletal muscle. The molecular nature of this coupling remains to be elucidated.

Amino Acid Sequence↗

PubMedDate not supplied

Verrucoside, a new cytotoxic pregnane glycoside from a gorgonian Eunicella verrucosa.

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Animals↗

PubMedDate not supplied

Limited brain access for leptin in obesity.

Obesity is a major health problem that contributes to the development of type 2 diabetes, hypertension, dyslipidemia, and cardiovascular disease. The current pharmacological therapies for obesity are limited and may have significant side effects. Leptin therapy was shown to effectively cause weight loss in obese rats, however its effectiveness in humans is still under investigation. Obese humans have significantly elevated plasma leptin concentrations compared with lean individuals. Plasma leptin concentrations strongly correlated with percentage of body fat. Leptin concentration in the cerebrospinal fluid (CSF) is correlated, in a nonlinear manner, with plasma leptin levels and body mass index (BMI). The ratio of CSF leptin levels to serum leptin levels was 4 times greater in lean individuals than in obese individuals. One interpretation of this finding is that human obesity could be secondary to a central resistance to leptin action, causing a relative leptin deficiency in the CNS. Six years after the discovery of leptin we still do not have a clear understanding of how leptin accesses its targets in the brain, or whether there is defect in this process in the brain of obese individuals. In this manuscript we will review the different leptin gateways to the brain and the potential sites where a defect in leptin action may be present, as well as some potential clinical implications of leptin. A better understanding of how leptin reaches the brain and how it modulates the release of hypothalamic neuropeptides will be important in understanding the role that leptin plays in the pathophysiology of obesity.

Animals↗

PubMedDate not supplied

Neural control of the forms of acetylcholinesterase in slow mammalian muscles.

The 'heavy', collagen-tailed form of acetylcholinesterase (AChE), having a s(0)20,w of 16S in mammals, occurs at vertebrate muscle endplates and has been widely regarded as a marker of neuronal influence on muscle in vivo. However, an interesting exception has been described by Bacou et al., in a previous report in Nature. They found, in a slow-twitch muscle of the rabbit, that after denervation the 16S form of AChE increases markedly, rather than disappearing. Such a phenomenon would modify current concepts of neuromuscular regulation. We report here, however, that this exception is apparent rather than real in terms of endplate AChE regulation.

Acetylcholinesterase↗