Mapping rat brain structures activated during ethanol withdrawal: role of glutamate and NMDA receptors.

Brain structures activated during ethanol withdrawal have been mapped by visualizing c-fos mRNA expression. The regional distribution of c-fos mRNA in brain during ethanol withdrawal can be mimicked by acute injection of N-methyl-D-aspartic acid (NMDA) and is stereospecifically blocked by the NMDA receptor antagonist, MK-801. The findings reveal that the dentate gyrus and piriform cortex are selectively activated during ethanol withdrawal and suggest that this may be mediated by glutamate activation of NMDA receptors.     

Comparison of fMRI statistical software packages and strategies for analysis of images containing random and stimulus-correlated motion.

The objectives of this study were to use computer-generated phantoms containing real subject motion to: (1) compare the sensitivity of four commonly used fMRI software packages and (2) compare the sensitivity of three statistical analysis strategies with respect to motion correction. The results suggest that all four packages perform similarly in fMRI statistical analysis with SPM2 having slightly higher sensitivity. The most sensitive analysis technique was to perform motion correction and include the realignment parameters as regressors in the general linear model. This approach applies to all four packages examined and can be most beneficial when stimulus-correlated motion is present.     

Adenosine as a vasodilator in primary pulmonary hypertension

BACKGROUND. The acute administration of vasodilator drugs to patients with primary pulmonary hypertension has been advocated to identify those with reversible pulmonary vasoconstriction. Unfortunately, the usefulness of the drugs currently available is limited by accompanying systemic hypotension. A vasodilator with effects confined to the pulmonary circulation would therefore be advantageous in such patients. METHODS AND RESULTS. The purine nucleoside adenosine was infused into the pulmonary artery in seven patients with primary pulmonary hypertension (baseline pulmonary vascular resistance [PVR], 442-1,295 dyne/cm/sec-5) to determine its effect on PVR. In all patients, there was a dose-dependent and significant reduction (mean maximal percent decrease from baseline, 38.9%; p less than 0.001) in PVR mediated through a decrease in pulmonary artery pressure and an increase in cardiac output. Systemic vascular resistance (SVR) also decreased, but the ratio of PVR to SVR decreased (maximal mean percent decrease from baseline) by 10.5% (p less than 0.025), indicating that adenosine has a preferential vasodilator effect on the pulmonary circulation when administered in this manner. CONCLUSIONS. Because of its pharmacokinetic and vasodilator properties, adenosine may have a specific role in the investigation of primary pulmonary hypertension.     

Salivary disease in childhood

Salivary disease in childhood is uncommon. Clinical features are much the same as in adult disease, however, congenital, inflammation, and functional disease is more common. Management is governed by the same general principles in all age groups. Congenital abnormalities are rare. Inflammation, either bacterial or viral, is the most common disease. Chronic sialadenitis usually resolves at puberty. Neoplasia is rare, and the majority of tumors are benign and occur in the parotid gland. Malignancy is suggested by rapid growth, pain, skin fixation, and lymphadenopathy. Surgical treatment of sialorrhea should only be considered after careful assessment. Relocation of the submandibular ducts is the treatment of choice.     

Peripheral arteriovenous fistula as a cause of neonatal cardiac failure

A newborn infant presented with cardiac failure secondary to a peripheral cavernous haemangioma. She was successfully treated surgically but was later diagnosed as having GM1 gangliosidosis.     

Alcohol and sleep apnea

Acute ingestion of ethanol induces vasodilation and swelling of respiratory mucosa; it depresses respiratory centers resulting in hypotonia of oropharyngeal dilator muscles and inducing or aggravating sleep apnea. However, no association between the sleep apnea syndrome (SAS) and Alcohol Use Disorders (AUD) has been demonstrated.