Cerebral metabolic effects of sequential periods of hypothermic circulatory arrest

During repair of congenital heart defects, extended periods of hypothermic circulatory arrest (CA) have been shown to cause short-term cerebral metabolic and flow abnormalities as well as long-term neuropsychologic dysfunction. Occasionally, a second period of CA is required during the same operative setting to revise a complicated repair. However, the metabolic effects of two consecutive periods of CA on the brain are unclear. In this study, we compared the recovery of cerebral metabolism after 60 minutes of CA with that after two sequential 30-minute periods of CA separated by a brief period of rewarming (30'SEQ). Fifteen neonatal piglets (2 to 3 kg) were placed on cardiopulmonary bypass at 100 mL.kg-1 x min-1 and cooled to 18 degrees C. Each animal then underwent either 60 minutes of uninterrupted cardiopulmonary bypass at 18 degrees C, 60 minutes of CA, or two 30-minute periods of CA separated by a brief period of rewarming. After these experimental periods, animals were rewarmed to 37 degrees C and weaned from cardiopulmonary bypass. Data were obtained before cardiopulmonary bypass and after cardiopulmonary bypass at 37 degrees C and included measurements of cerebral blood flow by xenon 133 clearance, arterial and sagittal sinus blood gases, and cerebral metabolism (mL O2.100 g-1 x min-1). Our results demonstrated that acute recovery of cerebral metabolism was significantly impaired after 60 minutes of CA and that recovery of cerebral metabolism after two sequential 30-minute periods of CA was significantly better than after 60 minutes of continuous CA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Fatal varicella-zoster encephalitis; a rare complication of herpes zoster

In a 82-year-old woman varicella zoster encephalitis was diagnosed, a rare complication of shingles. The case was remarkable for its rapid and fatal course in a patient without an underlying disease. At autopsy, the histological picture of an acute haemorrhagic encephalitis was seen, also a rare finding.     

Month of birth and schizophrenia in Taiwan: effect of gender, family history and age at onset

Schizophrenic patients have been shown to have a moderate excess of winter births in the areas where seasonal variations in weather are large. In this report, we examined the seasonality of schizophrenic births in Taiwan, which has a subtropical climate. Using nationwide hospitalization data (2429 male and 1320 female schizophrenic patients), we applied the life table method to compare the risk of schizophrenia among 12 cohorts of month-of-birth for males and females, respectively. Differences among the risks of the 12 cohorts were tested using the logrank test. The samples were further stratified by family history and age at onset. There was a significant association between the risk of being admitted as a schizophrenic and month of birth for both males and females. The cohorts born in November and January had the highest risks. After stratification, the association was significant only for non-familial, male, and early onset schizophrenic patients. The results indicate that seasonally varying factors might increase the risk of schizophrenia, especially in those without a family history of the disease. Men are more vulnerable to such factors than women, and the schizophrenics resulting from such insults tend to be early onset.     

Chemokine regulation of experimental autoimmune encephalomyelitis: temporal and spatial expression patterns govern disease pathogenesis

Experimental autoimmune encephalomyelitis (EAE) is a CD4+ Th1-mediated demyelinating disease of the central nervous system that serves as a model for multiple sclerosis (MS). There are several considerations that suggest a role for chemokines in the disease process. First, chemokines are highly expressed in the central nervous system with a tight temporal relationship to disease activity. Second, in vivo neutralization studies showed a distinct role for specific chemokines in the evolution of the process. Third, the selective and differential expression of chemokines in differing models of EAE bears a close relationship to the patterns of inflammatory pathology. Fourth, the spatial distribution of chemokine expression could plausibly contribute to lesion architecture. Finally, preliminary observations in MS material suggest that chemokine expression observed in EAE may provide useful information regarding the pathogenesis of inflammation in MS. We propose that temporal and spatial expression of chemokines are crucial factors, complementing adhesion molecule up-regulation, that regulate EAE disease activity.     

Enzymatic amplification of lactate dehydrogenase-elevating virus

To improve the detection of lactate dehydrogenase-elevating virus (LDV), we developed a PCR assay. Primers were selected from ORF7, encoding nucleocapsid protein VP1. No specific amplification was observed with any other common murine virus or with RNAs from the closely related Lelystad virus and equine arteritis virus. In experimentally infected mice, LDV could be detected in plasma in both the acute and the persistent phases. LDV was also detected by the PCR in contaminated pools of Plasmodium berghei parasites which were maintained in mice, both by a direct analysis of the samples and by testing of plasma from mice inoculated with these pools. There was a complete agreement between the results of the PCR assay and the lactate dehydrogenase (LDH) enzyme assay of plasma from the inoculated mice. In contrast to the results of the LDH enzyme assay, no false-positive reactions were obtained in the PCR assay with negative control samples showing visible hemolysis. Storage of plasma samples at room temperature and at 4, -20, and -80 degrees C for up to 8 days did not influence the results of the PCR. These results show that the PCR is a valuable technique which may replace the LDH test as a diagnostic tool.     

Suprascapular neuropathy after distal clavicle excision

Two cases of suprascapular neuropathy after excision of the distal clavicle are reported. Both patients were treated successfully with neurolysis of the suprascapular nerve starting at the upper trunk of the brachial plexus. Anatomic dissections revealed that the suprascapular nerve is quite close (<1.4 cm) to the posterior aspect of the distal clavicle, within 2 to 3 cm of the acromioclavicular joint. To avoid the complication of suprascapular neuropathy that could be associated with this close relationship, it is recommended that no more than 1 cm of the distal clavicle be removed posteriorly. It is also recommended that minimal periosteal elevation should be performed on the posteroinferior border of the distal clavicle.     

STZ transport and cytotoxicity. Specific enhancement in GLUT2-expressing cells

The glucose analog streptozotocin (STZ) has long been used as a tool for creating experimental diabetes because of its relatively specific beta-cell cytotoxic effect, but the mechanism by which systemic injection of STZ causes beta-cell destruction is not well understood. In the current study, we have used insulinoma (RIN) and AtT-20ins cell lines engineered for overexpression of GLUT2 or GLUT1 to investigate the role of glucose transporter isoforms in mediating STZ cytotoxicity. The in vivo effects of STZ were evaluated by implantation of RIN cells expressing or lacking GLUT2 into athymic nude rats. The drug had a potent cytotoxic effect on RIN cells expressing GLUT2, but had no effect on cells lacking GLUT2 expression, as indicated by histological analysis and measurement of the blood glucose levels of treated animals. The preferential cytotoxic effect of STZ on GLUT2-expressing cell lines was confirmed by in vitro analysis of GLUT2-expressing and untransfected RIN cells, as well as GLUT2- and GLUT1-overexpressing AtT-20ins cells. Consistent with these data, only GLUT2-expressing RIN or AtT-20ins cells transported STZ efficiently. We conclude that expression of GLUT2 is required for efficient killing of neuroendocrine cells by STZ, and this effect is related to specific recognition of the drug as a transported substrate by GLUT2 but not GLUT1.