Effect of 2 ppm ozone exposure on rat lung lipid fatty acids

Based on in vitro studies, the initial damage to lung cells by ozone exposure is believed to result in part from the breakdown of lipid polyunsaturated fatty acids to aldehydes, ozonides, and peroxides. The present study measured lipid breakdown products in lungs isolated from rats pretreated with [1-14C]acetate 12 h before exposure for 4 h to either air or 2 ppm ozone. Lipid fatty acid breakdown was indicated by a 112% increase in thiobarbituric acid-reactive substances on ozone exposure and by changes in chemical and radioactive measurements of mono- and dicarboxylic acids formed by treatment of lipid fractions with hydrogen peroxide. Ozone exposure resulted in a 63% increase in recovery of short-chain fatty acids accounted for by increased recoveries of malonic acid by 37%, hexanoic acid by 47%, nonanoic acid by 118%, and azelaic acid by 107%. Recovery of glutaric acid was enhanced 15-fold by ozone exposure. Although decreases in tissue arachidonic acid could not be detected, oleic acid was significantly decreased by 36%. Recovery of radiolabel as short-chain fatty acids was increased by 65% on ozone exposure and was mainly accounted for by enhanced labeling of nonanoic and glutaric acid fractions. The failure to observe significant increases in 14C recovery in the other fractions suggested ozone-induced breakdown of unlabeled fatty acids. These results demonstrate the cleavage of unsaturated fatty acid double bonds following in vivo exposure of lungs to ozone. Breakdown of arachidonic and oleic acids was specifically identified by increased recoveries of glutaric and nonanoic acids, respectively.     

Iotrol versus metrizamide in lumbar myelography: a double-blind study

In a prospective, randomized, double-blind study, 49 patients underwent lumbar myelography using iotrol (24 patients) or metrizamide (25 patients). The diagnostic imaging adequacy of iotrol was comparable with that of metrizamide. After iotrol myelography, adverse reactions were fewer, less severe, and of shorter duration than were those following metrizamide myelography. Thirteen of 24 patients (54%) receiving iotrol reported some adverse reactions compared with 24 of 25 patients (96%) receiving metrizamide. Five moderate and one severe adverse reaction occurred in the group receiving iotrol. Fourteen moderate and eight severe adverse reactions occurred in the group receiving metrizamide. Thirty-eight patients underwent electroencephalography both before and after myelography (19 iotrol and 19 metrizamide). None of the EEGs obtained after iotrol myelography changed from baseline, while seven of the EEGs obtained after metrizamide myelography showed changes from baseline. Iotrol was judged superior to metrizamide as a contrast medium in this patient population.     

Adaptation of a perfused rat hemidiaphragm preparation to the study of intermediary metabolism

Glucose catabolism of a vascular perfused rat hemidiaphragm was determined at rest and during stimulation of the phrenic nerve with trains of either 5 (T5) or 15 (T15) pulses (20 msec intervals) per second. Tissues were perfused and bathed in HEPES-buffered medium containing 11 mM D-[U-14C, 5-3H]glucose, equilibrated with 100% O2. Resting glucose catabolism via the Emden-Meyerhof pathway was indicated by a 3H2O production rate per hemidiaphragm of 1.45 +/- 0.07 mumol/h, of which 47% was recovered as [14C]lactate with the remainder assumed to be metabolised by mitochondria. During the first 30 min of T5 and T15 stimulation, peak isometric tension declined from an initial value of 105 +/- 8 g by 54% and 79%, respectively. The resulting peak tensions of 48 and 22 g remained constant for the next 60 min. These tensions were associated with linear rates of 3H2O production of 2.93 +/- 0.41 and 2.84 +/- 0.25 mumol/h. Stimulation by T5 and T15 increased mitochondrial metabolism of glucose by 64% and 95%, respectively, with no significant alterations in lactate formation from either exogenous or endogenous sources. The results suggest that the initial decline in tension is due to fatigue of the fast anaerobic myofibers; whereas, the sustained force beyond 30 min is attributable to the mitochondrial-rich slow myofibers.     

Interferon-induced depressive illness in hep C patients responds to SSRI antidepressant treatments

This paper examines the role of selective serotonin reuptake inhibitors (SSRIs) in the treatment of hepatitis-C virus (HCV) patients who have developed interferon-α induced depression. A 2-year data analysis of HCV psychiatric liaison clinic has been undertaken. The diagnosis, treatment, and progress of those patients who were treated with interferon-α (INF-α) are reported. 53 of the 78 patients enrolled at the HCV Clinic and treated with INF-α were referred for psychiatric consultation. Six patients developed major depressive illness following INF therapy. They were all treated with SSRIs and they made full recovery. This is a significant observation and is concordant with other studies. Its biochemical ramifications are presented. It is concluded that INF-induced depression is fully reversible. A hypothesis is proposed that SSRIs modulate the neuro-protective neurotoxic ratio by possibly inhibiting the indole-2,3-dioxygenase induction of the kynurenine pathway.     

Luxatio erecta: the inferior glenohumeral dislocation

Luxatio erecta, or inferior glenohumeral dislocation, is a rare shoulder dislocation usually caused by a hyperabduction injury to the arm. We have reviewed the literature consisting of 80 cases of luxatio erecta and also discuss six additional cases that we have treated. The literature shows that either a fracture of the greater tuberosity or a rotator cuff tear was associated with this injury in 80% of patients; 60% of the patients reviewed sustained some degree of neurologic compromise, most commonly to the axillary nerve. These injuries usually resolved; the time for recovery varied from 2 weeks to 1 year. Only 3.3% of the cases demonstrated significant vascular compromise, but this is the highest incidence for any shoulder dislocation. Doppler studies of the affected arm or observation of the patient overnight are recommended because of the potentially disastrous complications of vascular insufficiency. If there is any indication of a vascular problem, immediate arteriogram is indicated. Although usually fairly easily reduced by overhead traction, the lesion is so rare that few physicians are familiar with the technique of reduction. Fluoroscopy was used in our most recent cases and was helpful in obtaining a complete and safe reduction.     

Follistatin and activin A production by the male reproductive tract

Follistatin is a binding protein for the activin and inhibin family of hormones, regulating their biological activity. In the male reproductive tract, the interaction of these factors is likely to be involved in the regulation of the proliferation of several cell types. We have investigated the presence of follistatin and activin A in seminal plasma using specific immunoassays and have localized follistatin and activin/inhibin subunits in the adult human testis, prostate and seminal vesicle to establish their likely sources. High concentrations of immunoreactive follistatin were present in seminal plasma in normal men (mean 97.9 ng/ml; 1.43 ng/ml in peripheral plasma) and were similar in men with oligo/azoospermia and following vasectomy. Follistatin immunoreactivity was localized to both Leydig and Sertoli cells of the testis, and to epithelial cells of the prostate gland and seminal vesicle, which are likely to be the predominant sources of the hormone in seminal plasma. Activin A was also present in seminal plasma in normal men but was undetectable following vasectomy, thus deriving from the testis. Consistent with this finding, the betaA-subunit was immunolocalized in Sertoli and Leydig cells but was not present in seminal vesicle or prostate gland. The functional significance of the high concentrations of follistatin secreted into seminal plasma by the prostate gland and/or seminal vesicle is uncertain, but they may regulate the biological activity of testis-derived activin A and inhibin B.