Lumbosacral glioblastoma and leptomeningeal gliomatosis complicating the course of a cervicothoracic astrocytoma WHO grade II

CASE REPORT: The reported female patient underwent sub-total resection of an intra-medullary cervicothoracic astrocytoma classified as WHO grade II in 1984 at the age of 18 months and received local irradiation. In 1989, a local recurrence was diagnosed and a partial resection was performed. Sixteen years later, a small recurrent cervicothoracic tumour was found and spinal seeding to the equine nerve roots and the left cerebellar cortex was apparent on MRI. The patient was implanted with a ventriculoperitoneal shunt for a pseudo-tumour cerebri producing papilloedema, which eventually lead to amaurosis. After an extended biopsy, the invasive lumbosacral tumour was classified as glioblastoma multiforme. Two months later, the patient died after rapid progression of the caudal cranial nerve dysfunction. DISCUSSION AND CONCLUSION: Anaplastic progression and dissemination of spinal astrocytomas even two decades after initial diagnosis and treatment are rare. Therapies and diagnostic follow-up strategies are discussed.     

Pyridoxine Deficiency and Ethanol-induced Liver Injury

It has been suggested that pyridoxine deficiency may potentiate ethanol-induced liver injury. Our purpose was to clarify the effect of pyridoxine deficiency on ethanol-associated liver injury by comparing liver histology, serum liver enzymes, and the viability of cultured hepatocytes from pyridoxine-deficient and pyridoxine-sufficient rats that had been chronically fed ethanol-enriched diets. Our data fail to substantiate that pyridoxine-deficient animals are more susceptible to the hepatotoxic effects of ethanol than pair-fed pyridoxine-sufficient controls. Furthermore, the addition of pyridoxine to hepatocyte cultures fails to prevent in vitro cytotoxicity of added ethanol. Pyridoxine deficiency may augment ethanol-induced enhancement of hepatic urea synthesis. These data suggest that pyridoxine deficiency may contribute to the abnormal plasma amino acid profiles and nitrogen balance of chronic alcoholics, but that it does not potentiate ethanol-induced liver injury.     

Effects of different perfusates on functional parameters of isolated perfused dog kidneys.

BACKGROUND: The isolated perfused canine kidney has been established as a valid model for conducting both renal physiology and transplantation research. This model is of particular importance for developing new strategies to improve graft function after renal transplantation. In the present study, a newly developed method using isolated haemoperfused porcine kidneys was adapted for use in canine kidneys. In contrast to haemoperfusion, synthetic perfusion media can be standardized and can prevent the initiation of blood-mediated reperfusion reactions. Thus, an additional aim was to determine whether blood could be replaced by synthetic cell-free perfusion solutions. METHODS: Canine kidneys (n = 30) were harvested from donors euthanized in veterinary practices for causes unrelated to the present study. The kidneys were isolated and perfused with autologous blood or cell-free synthetic electrolyte buffer (Tyrode solution). During perfusion, we monitored renal perfusate flow (RPF), glomerular filtration rate (GFR), electrolyte and glucose reabsorption, oxygen consumption and urine concentration. RESULTS: Changes in perfusion medium did not affect the RPF. In contrast, GFR, urine concentration and oxygen consumption were significantly higher, whereas fractional excretion of sodium and glucose were significantly lower in blood- than in Tyrode-perfused kidneys. CONCLUSIONS: This system offers a simple model for studying whole-organ functional alterations after acute renal ischaemia. Renal function indicators were below values reported during in vivo physiological conditions. These functions were better conserved when kidneys were perfused with autologous blood than with Tyrode.     

Progressive increase in the angle of deviation in acquired nonaccommodative esotropia of childhood.

PURPOSE: Although the angle of deviation in patients with congenital esotropia has been shown to increase during the early preoperative period, few data exist regarding this change in other forms of childhood esotropia. The primary objective of this study was to investigate whether the angle of deviation increases with time in patients with acquired nonaccommodative esotropia (ANAET). METHODS: The medical records of all children whose ANAET was diagnosed at East Tennessee State University College of Medicine from August 1, 1995, through October 1, 2001, were retrospectively reviewed. All patients were assessed for any change in the amount of their strabismic angle and associated risk factors. RESULTS: Eighty-two patients with ANAET were identified, and all except 3 underwent more than one examination. Of the 79 children who underwent more than one examination, 26 (32.9%) displayed an angle increase of > or =10 prism diopters (PD) during a median follow-up period of 2.9 months. The ANAET of those patients whose angle increased by > or =10 PD was diagnosed (28.4 months of age vs 45.5 months of age, P =.003), and they underwent surgery (35.9 months of age vs 53.3 months of age, P =.003) at a significantly younger median age than those whose angle increased <10 PD. CONCLUSIONS: The angle of deviation of approximately one third of patients with ANAET in this study increased at least 10 PD in the early preoperative period. This increase occurs more often in younger patients and underscores the importance of performing serial measurements of the deviating angle before surgical intervention is undertaken.     

Incidence and Clinical Significance of Ventricular Late Potentials in Idiopathic Dilated Cardiomyopathy Compared to Coronary Artery Disease

Objective: This prospective study was designed to compare incidence and clinical significance of ventricular late potentials between patients with idiopathic dilated cardiomyopathy (IDC) and postinfarct patients (CAD) using exactly the same method of signal-averaged electrocardiography (SAECG) in both patient groups. Methods: Time-domain analysis of SAECG was performed in 120 consecutive patients with IDC, 120 patients with CAD, and 60 healthy controls. Ventricular late potentials were detected in 27 of 120 patients with IDC (23%) compared to 41 of 120 patients with CAD (34%; P < 0.05). Results: Ventricular late potentials were found in 2 of 60 controls (3%). During 15 ± 7 months follow-up, serious arrhythmic events occurred in 17 of 120 patients with IDC (14%) and in 13 of 120 patients with CAD (11%). The sensitivity of ventricular late potentials for future arrhythmic events was 35% for IDC compared to 77% for CAD (P < 0.05). The positive predictive value of late potentials detected by time-domain analysis was 22% for IDC versus 24% for CAD (P = ns). Conclusion: In this selected patient population with IDC and CAD, time-domain analysis of SAECG revealed a lower incidence of ventricular ate potentials in patients with IDC as compared to postinfarct patients. Whereas ventricular late potentials had a high sensitivity but a low positive predictive value for identification of postinfarct patients with serious arrhythmic events during follow-up, both sensitivity and positive predictive value of ventricular late potentials for future serious arrhythmic events were low in the setting of IDC.     

Akromioklavikulargelenkverletzungen

There is some controversy over the treatment of acromioclavicular injuries. The use of the Rockwood classification as the basis for decisions on whether operative or nonoperative treatment is indicated is discussed critically, and the authors' preferred operative technique is described and illustrated by examples. We treat injuries classified according to the Rockwood classification as types I and II with conservative methods. In type III injuries the patient's age, job and free time activities determine whether or not surgery is indicated. In the case of type IV or type VI injuries we always perform temporary internal fixation of the acromioclavicular joint, using transarticular K-wire fixation or hookplate osteosynthesis. Satisfactory results of both operative and nonoperative treatment are reported in the literature. The authors' own results are presented.     

The feasibility of sensitization studies using fewer test animals

The possibility of reducing the number of animals in sensitization studies (maximization method) is discussed on the basis of results from 20 sensitization tests. It appears that the number of test animals in sensitization studies may be reduced to ten treated animals and five control animals without prejudice to the quality of the test.     

Cerebrospinal fluidCHOLINESTERASES—MARKERS for loss ofcholinergic basal forebrain neurons?

The present study was conducted to test the hypothesis that cholinergic basalforebrain neurons are a major source of cerebrospinal fluid (CSF) cholinesterases. To address thisquestion enzyme activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) inboth CSF and parietal cortex were assayed following selective lesion of basal forebrain cholinergicneurons by a single intracerebroventricular application of the cholinergic immunotoxin192IgG-saporin. Cholinergic immunolesions led to a dramatic decrease in total AChE activity inparietal cortex, which was due to the specific loss of the G4 molecular form while the activity ofthe G1 form was increased as compared to nonlesioned animals. In contrast, the total enzymeactivity of BChE and its molecular forms were not affected by cholinergic lesion in both parietalcortex and CSF. The data suggest, that cholinergic basal forebrain neurons are seemingly not amajor source of cholinesterases in the CSF, and do not provide any evidence for using CSFcholinesterases as a diagnostic marker of basal forebrain cholinergic cell loss in humans.