Coronary bypass surgery early after thrombolytic therapy for acute myocardial infarction

The safety of coronary bypass operations after coronary reperfusion with streptokinase for acute myocardial infarction is not well documented. Therefore we studied 23 consecutive patients (mean age, 59.5 years; 22 men) undergoing bypass operations a median of 5 days (range, 1 to 23 days) after thrombolysis (streptokinase). The control group consisted of 169 concurrent patients of similar mean age (58.8 years) having bypass operations for standard indications. The preoperative angiographic ejection fraction was 68 +/- 14% in the control patients and 61 +/- 14% in the streptokinase group (p less than 0.05). The number of diseased vessels (70% stenosis or greater) averaged 2.6 in control and 2.3 in streptokinase patients. A previous myocardial infarction had occurred in 42% of the controls and all of the streptokinase patients. Aortic cross-clamp times did not differ between the two groups (80 +/- 35 minutes for the controls and 68 +/- 25 minutes for the streptokinase group). Cardiopulmonary bypass times were similar: 108 +/- 45 minutes in the controls versus 109 +/- 28 minutes in the streptokinase group. Grafts per patient averaged 3.7 +/- 1.5 for the controls versus 2.8 +/- 1.1 for the streptokinase patients (p less than 0.01). Difficult operative hemostasis was noted in 4% of both groups. Inotropic support was given postoperatively to 11% of the control and 13% of the streptokinase patients (p = not significant). Measured blood loss during the first 48 hours postoperatively was similar, averaging 809 ml in controls and 776 ml in the streptokinase group. Blood product replacement was also comparable: mean, 713 ml in the control group versus 759 ml in the streptokinase group.(ABSTRACT TRUNCATED AT 250 WORDS)     

No linkage or association between multiple sclerosis and the myelin basic protein gene in affected sibling pairs.

Myelin basic protein was examined as a candidate gene for susceptibility to multiple sclerosis using two adjacent amplification fragment length polymorphisms (AmpFLPs), containing seven and six highly informative alleles respectively. No allelic association was found with multiple sclerosis, comparing 77 cases and 88 controls, and there was no evidence for linkage in 73 affected sibling pairs, using the methods of identity by descent and identity by state.     

'Acute on chronic' effect of depot leuprolide in patients with stage D2 cancer of prostate

During a phase III open study of depot leuprolide for stage D2 cancer of the prostate, we studied the effect of depot leuprolide on chronic leuprolide users. To determine whether there was a transient elevation of testosterone or luteinizing hormone (LH) 4-24 h and 3-5 days following the monthly injections, we monitored the changes of testosterone and LH before injection and 24 h post-injection in 10 patients who have been under depot leuprolide Rx for 24-36 weeks, and in 35 patients before injection and 3-5 days post-injection who have received depot leuprolide for 8-24 weeks prior to monitoring. Comparison of the data between pre-injection within 24 h and 3-5 days post-injection showed no significant changes of testosterone and LH values between these levels for either testosterone (P = 0.31) or LH (P = 0.45). We therefore conclude that there was no 'acute on chronic' effect of depot formulation in chronic users of depot leuprolide.     

Uroscopy in the 21st century: high-field NMR spectroscopy

From the experiments described, it can be seen that there are different research approaches that can be taken and these are summarized in Table 1. Whereas much scientific research is principally hypothesis led, there remains, nevertheless, an important place for exploratory research. High resolution NMR can measure, directly and simultaneously, a wide range of endogenous metabolites in biological fluids and has the unique capability of providing structural information on the metabolites detected. It has proved to be a powerful research tool with which to study inherited metabolic diseases, renal disease, drug metabolism, and toxicity, and can be used to monitor the effects of drug therapy. For instance, by using a library of experimental toxins one can map the metabolic profile of site-specific nephron injury. With this approach in man one could eventually take an unknown disease such as Balkan nephropathy and predict the initial site of tubular injury, the mode of injury and therefore the kind of toxin capable of producing that injury. NMR spectroscopic techniques are still advancing rapidly, with ever increasing sensitivity and sophistication of NMR pulse sequences to enhance structural elucidation in complex mixtures. Given the advances in directly coupled HPLC-NMR and even HPLC-NMR-mass spectroscopy it is likely that these technologies in conjunction with pattern recognition will make major contribution to our understanding of renal processes and provide new diagnostic insights in the 21st century.      

Activation of guinea pig eosinophil respiratory burst by leukotriene B4: role of protein kinase C

Leukotriene B4 (LTB4) and the protein kinase C activator, 4-beta-phorbol dibutyrate (PDBu), both induced a pronounced and concentration-dependent stimulation of hydrogen peroxide (H2O2) generation by purified guinea pig peritoneal eosinophils in the concentration range 1 nM-1 microM. The LTB4 response was inhibited competitively by the specific LTB4 receptor antagonist, U-75302, with a KB of 25 nM, while the concentration-response curves for both stimuli were shifted rightwards (3.8-fold and 2.8-fold for LTB4 and PDBu, respectively) by the competitive protein kinase C inhibitor, 1-O-hexadecyl-2-O-methylglycerol at a concentration of 300 microM. LTB4 appears, therefore, to induce respiratory burst in eosinophils via a receptor-mediated mechanism involving protein kinase C.     

Localization of a gene for otosclerosis to chromosome 15q25-q26

Among white adults otosclerosis is the single most common cause of hearing impairment. Although the genetics of this disease are controversial, the majority of studies indicate autosomal dominant inheritance with reduced penetrance. We studied a large multi- generational family in which otosclerosis has been inherited in an autosomal dominant pattern. Five of16 affected persons have surgically confirmed otosclerosis; the remaining nine have a conductive hearing loss but have not undergone corrective surgery. To locate the disease- causing gene we completed genetic linkage analysis using short tandem repeat polymorphisms (STRPs) distributed over the entire genome. Multipoint linkage analysis showed that only one genomic region, on chromosome 15q, generated a lod score >2.0. Additional STRPs were typed in this area, resulting in a lod score of 3.4. STRPs FES (centromeric) and D15S657 (telomeric) flank the 14. 5 cM region that contains an otosclerosis gene.