3 Beta-hydroxysteroid dehydrogenase expression in rat spinal cord

In adult male rats, 3beta-hydroxysteroid dehydrogenase/delta5-delta4-isomerase (3beta-HSD) expressing cells were identified in the spinal cord from the cervical to the sacral segments. An in situ hybridization study, using an oligonucleotide common to the four known isoforms of rat 3beta-HSD, revealed its mRNA in gray matter. Measurements of optical densities in autoradiograms showed the following regional distribution: dorsal horn (layers I-III) > central canal (layer X) > or = ventral horn (layers VIII-IX) > ventral funiculus = lateral funiculus. At the cellular level, the number of grains was higher on the large motoneurons than on small neurons of the dorsal horn, but the grain density per cell was similar. Further evidence for the expression of 3beta-HSD in the spinal cord was obtained by western blot analysis, which revealed an immunoreactive protein of approximately 45 kDa in the dorsal and ventral parts of the spinal cord. Castration and adrenalectomy did not influence the expression of 3beta-HSD mRNA and protein. Gas chromatography/mass spectrometry measurements showed higher levels of pregnenolone and progesterone in the spinal cord than in the plasma. After castration and adrenalectomy, their levels remained elevated in the spinal cord, suggesting that these neurosteroids may be synthesized locally. The wide distribution of 3beta-HSD, and the high levels of pregnenolone and progesterone in the spinal cord even after castration and adrenalectomy, strongly suggest a potential endogenous production of progesterone and an important signalling function of this steroid in the spinal cord.     

Brainstem ischemia and preeclampsia.

Diffuse neurological manifestations of preeclampsia are due to endothelial involvement that lead to ischemia, hemorrhage, or edema. We analyzed clinical and radiological features and the course of brainstem ischemic strokes in a preeclampsia patient. We report a case of severe preeclampsia in a 30-year-old woman who was admitted 10 hr after a vaginal delivery at home. The pregnancy was at 39 wk, with no prenatal care. At her admission, she was conscious, and she had tetraparesia, swinging deep tendon reflex testing, drowsiness, and dysarthria; the BP was at 160/100 mmHg and 4 + proteinuria; magnetic resonance imaging revealed brainstem ischemic stroke. The evolution was favorable with symptomatic treatment. The patient was discharged on the 16th day; 2 months later she had a normal recovery. Brainstem strokes are rare. They are frequently due to hemorrhage; sometimes, they can also be ischemic. Their course is favorable.     

Lack of benefit of an active pectoral pulse generator on atrial defibrillation thresholds

INTRODUCTION: Atrial defibrillation can be achieved with standard implantable cardioverter defibrillator leads, which has led to the development of combined atrial and ventricular devices. For ventricular defibrillation, use of an active pectoral electrode (active can) in the shocking pathway markedly reduces defibrillation thresholds (DFTs). However, the effect of an active pectoral can on atrial defibrillation is unknown. METHODS AND RESULTS: This study was a prospective, randomized, paired comparison of two shock configurations on atrial DFTs in 33 patients. The lead system evaluated was a dual-coil transvenous defibrillation lead with a left pectoral pulse generator emulator. Shocks were delivered either between the right ventricular coil and proximal atrial coil (lead) or between the right ventricular coil and an active can in common with the atrial coil (active can). Delivered energy at DFT was 4.2 +/- 4.1 J in the lead configuration and 5.0 +/- 3.7 J in the active can configuration (P = NS). Peak current was 32% higher with an active can (P < 0.01), whereas shock impedance was 18% lower (P < 0.001). Moreover, a low threshold (< or = 3 J) was observed in 61% of subjects in the lead configuration but in only 36% in the active can configuration (P < 0.05). There were no clinical predictors of the atrial DFT. CONCLUSION: These results indicate that low atrial DFTs can be achieved using a transvenous ventricular defibrillation lead. Because no benefit was observed with the use of an active pectoral electrode for atrial defibrillation, programmable shock vectors may be useful for dual-chamber implantable cardioverter defibrillators.     

Cellular basis for progesterone neuroprotection in the injured spinal cord

Progesterone (PROG) exerts beneficial and neuroprotective effects in the injured central and peripheral nervous system. In the present work, we examine PROG effects on three measures of neuronal function under negative regulation (choline acetyltransferase [ChAT] and Na,K-ATPase) or stimulated (growth-associated protein [GAP-43]) after acute spinal cord transection injury in rats. As expected, spinal cord injury reduced ChAT immunostaining intensity of ventral horn neurons. A 3-day course of intensive PROG treatment of transected rats restored ChAT immunoreactivity, as assessed by frequency histograms that recorded shifts from predominantly light neuronal staining to medium, dark or intense staining typical of control rats. Transection also reduced the expression of the mRNA for the alpha3 catalytic and beta1 regulatory subunits of neuronal Na,K-ATPase, whereas PROG treatment restored both subunit mRNA to normal levels. Additionally, the upregulation observed for GAP-43 mRNA in ventral horn neurons in spinal cord-transected rats, was further enhanced by PROG administration. In no case did PROG modify ChAT immunoreactivity, Na,K-ATPase subunit mRNA or GAP-43 mRNA in control, sham-operated rats. Further, the PROG-mediated effects on these three markers were observed in large, presumably Lamina IX motoneurons, as well as in smaller neurons measuring approximately <500 micro2. Overall, the stimulatory effects of PROG on ChAT appears to replenish acetylcholine, with its stimulatory effects on Na,K-ATPase seems capable of restoring membrane potential, ion transport and nutrient uptake. PROG effects on GAP-43 also appear to accelerate reparative responses to injury. As the cellular basis for PROG neuroprotection becomes better understood it may prove of therapeutic benefit to spinal cord injury patients.     

Somatostatin receptor scintigraphy in forty-eight patients with the Zollinger-Ellison syndrome

In patients with the Zollinger-Ellison syndrome, which is either sporadic or integrated into multiple endocrine neoplasia type 1, accurate localization of all the tumours is difficult and may have therapeutic implications. In an attempt to improve this localization, somatostatin receptor scintigraphy using [¹¹¹In-DTPA-D-Phe¹]-octreotide was performed prospectively in 48 consecutive patients with the Zollinger-Ellison syndrome. Thirty of them had the sporadic type of this disease. Scintigraphic data were compared with data obtained by conventional imaging methods, and also, in 32 selected patients, with those obtained by endoscopic ultrasonography. Somatostatin receptor scintigraphy showed abnormal tracer uptake in 39 patients (81%), in whom it correctly identified 50 of the 60 tumoral sites (83%) previously localized by the other imaging methods. In 17 patients (35%) somatostatin receptor scintigraphy disclosed abnormal tracer uptake at 18 different tumoral sites: 14 were located in the abdomen, including four in the liver and eight in the duodenopancreatic area, and four outside the abdomen, including two in the mediastinum. Six of the ten tumoral sites which were not correctly identified by somatostatin receptor scintigraphy were located in the duodeno-pancreatic area. However, in the 20 patients for whom conventional techniques failed to visualize any tumour in the duodenopancreatic area, somatostatin receptor scintigraphy was positive in ten (50%) whereas endoscopic ultrasonography was only positive in five (25%). In our patients with the Zollinger-Ellison syndrome, somatostatin receptor scintigraphy appeared to be a useful new addition to the battery of tests used for tumour detection.     

Diagnostic contribution of HBME-1 and anti-cytokeratin-19 antibodies in thyroid pathology: a retrospective study of 163 cases

The objective of our study was to estimate the expression of 2 antibodies HBME-1 and anti-cytokeratin-19 and their diagnostic importance in thyroid pathology. MATERIAL AND METHODS: 163 thyroid lesions were retrospectively examined by immnohistochemistry. RESULTS: 92% (46/50 cases) of papillary carcinomas expressed HBME-1 as well as 50% (8/16 cases) of follicular carcinomas and 15% (6/40 cases) of follicular adenomas. 8 insular carcinomas, 5 anaplastic carcinomas, 20 cases of Basedow disease and lymphocytic thyroiditis, and the 24 cases of nodular goiters did not express it or very focally. Anti-cytokératine-19 marked 92% of papillary carcinomas, 56.2% of follicular carcinomas, 100% of the medullar carcinomas and 45% of follicular adenomas. Whereas the cases of anaplastic carcinomas, Basedow disease, thyroiditis and the cases of nodular goiters were negative or focally marked. CONCLUSION: HBME-1 is an excellent marker for papillary carcinoma which can be helpful in the diagnosis of its follicular variant; the association with anti-cytokératine-19 increases its specificity.