Exercise echocardiography after stabilization of unstable angina: correlation with exercise thallium-201 single photon emission computed tomography.

The diagnostic usefulness of predischarge exercise echocardiography in 35 patients with unstable angina who responded to medical therapy was correlated with exercise thallium-201 single photon emission computed tomography (TI-SPECT) performed, on the average, three days after the exercise echocardiography. None of the patients had myocardial infarction prior to hospitalization or before TI-SPECT and none had left bundle-branch block on their rest electrocardiogram (ECG). Exercise echocardiography was positive in 21 patients and TI-SPECT in 24. The results of the two techniques were concordant in 28 of 35 patients (agreement = 80%, k = 0.57 +/- 0.14, p less than 0.001). Wall-by-wall comparison of the distribution of exercise-induced wall motion abnormalities with reversible thallium defects showed complete or partial correlation in all of 19 patients in whom both the tests were positive. A positive exercise ECG and positive exercise echocardiography identified 11 of 11 patients with angiographically verified significant coronary artery disease (CAD) and 11 of 12 patients (92%) with positive TI-SPECT. Thus, exercise echocardiography is a valuable addition to routine predischarge exercise test in the noninvasive diagnosis of myocardial ischemia and shows a good correlation with TI-SPECT in detecting and localizing ischemia in patients with unstable angina stabilized on medical therapy.     

The nociceptin/orphanin FQ receptor agonist Ro 64-6198 reduces alcohol self-administration and prevents relapse-like alcohol drinking.

Effects of the opioid receptor like-1 (ORL-1) receptor agonist Ro 64-6198 (0.1, 0.3, and 1.0 mg/kg intraperitoneally (i.p.)) on operant ethanol self-administration and activation of self-administration by ethanol deprivation were studied in male Wistar rats. Acute administration of Ro 64-6198 caused a dose-dependent reduction of ethanol self-administration. In comparison, the opioid antagonist naltrexone (0.1, 0.3, and 1.0 mg/kg i.p.) inhibited ethanol self-administration at all doses tested. Ethanol deprivation for 10 days significantly increased ethanol self-administration during the first 2 days after deprivation. Daily pretreatment with Ro 64-6198 (0.3 mg/kg) or naltrexone (0.3 mg/kg) during the last 3 days of ethanol deprivation abolished the deprivation-induced increase in ethanol intake. Thus, stimulation of the ORL-1 receptors by Ro 64-6198 reduced the acute reinforcing effects of ethanol and prevented relapse-like behavior in the ethanol-deprivation model in a similar manner as a blockade of opioid receptors by naltrexone. Ro 64-6198 at 0.1 and 0.3 mg/kg doses did not alter self-administration of 0.2% saccharin solution, indicating an apparent selectivity of this compound in modification of ethanol reward. These findings add further support to the idea that Ro 64-6198 and potentially other synthetic ORL-1 receptor agonists are as effective as naltrexone in blocking the actions of ethanol important for its addictive potential in animal experiments, and therefore may have therapeutic value in the treatment of alcoholism.     

Post-Traumatic Bone Mineral Loss in Tibial Shaft Fractures Treated with a Weight-Bearing Brace

The bone mineral content in the upper ends of the tibia and the fibula was measured in 27 patients with tibial shaft fracture. The loss of bone mineral associated with the fracture did not differ between patients who were allowed weight-bearing in a functional below-knee brace and patients treated with a long leg plaster cast without weight-bearing.     

The effect of plaque control and surgical pocket elimination on the establishment and maintenance of periodontal health. A longitudinal study of periodontal therapy in cases of advanced disease

Abstract The present clinical study was initiated in 1969 to test the hypothesis that microbial plaque is the cause of periodontal disease and that hence even advanced cases of periodontitis can be cured in patients willing to exercise optimal plaque control. The material consisted of 75 patients with severe destruction of the periodontal tissues. The patients were selected for the study because of their ability to maintain plaque-free dentition. Following an initial examination, a preliminary treatment plan was presented to the patients. This plan included detailed instructions in plaque control measures, scaling, root planing and emergency dental care, including endodontic therapy and extractions. Three to six months after the termination of the so-called presurgical treatment, surgical elimination of pathologically deepened pockets was performed. The patients were recalled every 3 to 6 months after the end of the treatment. At these reexaminations the following parameters were assessed: Plaque Index, Gingival Index, Pocket Depths, Marginal alveolar bone topography and height. The results demonstrate that it is possible to treat periodontal disease successfully, even in advanced stages, in patients willing to maintain plaque-free dentition.     

Sodium transport in airway epithelium correlates with lung compliance in healthy newborn infants

To study the relation between sodium transport in airway epithelium and postnatal pulmonary adaptation, we measured nasal potential difference at 1 to 4 hours and lung compliance at 21 to 48 hours after birth in 20 healthy infants. Sodium transport correlated with lung compliance ( r 2 = 0.40, P < .003). Airway sodium transport plays a role in postnatal pulmonary adaptation.     

Matrilysins-1 and -2 (MMP-7 and -26) and metalloelastase (MMP-12), unlike MMP-19, are up-regulated in necrotizing enterocolitis

OBJECTIVES: Necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of premature infants characterized histologically by extensive tissue injury and inflammation. Matrix metalloproteinases (MMP) are involved in tissue remodeling and cell migration, both being important aspects of inflammatory disease. The aim of this study was to investigate whether MMPs play a role in the pathogenesis of NEC. METHODS: Expression of MMP-1, -7, -9, -10, -12, -19 and -26 was studied using in situ hybridization/immunohistochemistry in samples intestinal tissue removed from 15 patients with NEC; in 7 of them control samples were obtained at closure of stomas. Six intestinal samples from patients with intestinal atresia and four samples of necrosis were also included in the material examined. Laminin-5 was immunostained to find migrating enterocytes and cytokeratin to delineate mucosal epithelium. RESULTS: MMP-7 protein was upregulated in the epithelium of 12/18 NEC samples. MMP-26 was induced in stromal cells of 12/17 NEC specimens. Stromal expression was found for MMP-1 and -12 mRNAs in 7/18 samples. MMP-1 was also detected in the epithelium of regenerating areas. Both NEC and stoma samples expressed MMP-9 in inflammatory cells. Epithelial MMP-19 was downregulated in NEC. CONCLUSIONS: Our results suggest that several MMPs may be major factors in tissue destruction and remodeling in NEC. Targeted inhibition of matrilysins, using synthetic MMP inhibitors or blockers of their signal transduction pathways, may represent a novel therapeutic option for the treatment of intestinal inflammation associated with NEC.     

The NMDA NR2B subunit-selective receptor antagonist, CP-101,606, enhances the functional recovery the NMDA NR2B subunit-selective receptor and reduces brain damage after cortical compression-induced brain ischemia

Using a novel in vivo model for cerebral ischemia produced by short-lasting compression of a well-defined brain area of sensorimotor cortex we studied neuroprotective effects of the NMDA NR2B subunit selective antagonist, CP-101,606, in Sprague-Dawley rats. Cortical compression for 30 min produced a consistent and highly reproducible functional impairment, that is paresis of contralateral hind and fore limbs. The neurological deficit was accompanied by marked brain damage in cerebral cortex, hippocampus and thalamus as identified by Fluoro-Jade, a marker of general neuronal cell death. Using a daily performed beam walking test it was shown that untreated animals recovered from their functional impairment within 5-7 days following surgery. Intravenous administration of increasing doses (1, 5, 10, 20 mg/kg) of the NMDA NR2B subunit receptor specific antagonist, CP-101,606, dose-dependently improved the rate of functional recovery and protected against the ischemic brain damage in cerebral cortex, hippocampus, and thalamus as identified 2 days after the ischemic insult. Based upon these results, we conclude that NMDA NR2B receptor subunits represent potential targets to reduce not only the functional deficits, but also neuronal death in cortex and several midbrain regions produced by moderate, transient, cerebral ischemia.