Radioautographic evidence for slow astrocyte turnover and modest oligodendrocyte production in the corpus callosum of adult mice infused with 3H-thymidine

To find out whether glial cells proliferate in the corpus callosum of adult mice, two series of experiments were carried out. The first one made use of 9-month-old "aged" male mice. Some of them were given 3H-thymidine as a 2-hour pulse to examine which cells became labeled and, therefore, had the ability to divide. Others were sacrificed after a continuous infusion of 3H-thymidine for 30 days to examine whether the label would then appear in different cells. In other aged animals, the 30-day infusion was followed by 60 or 180 days without 3H-thymidine to determine whether cells retained or lost their label with time. A second series of experiments was carried out in 4-month old "young adult" male mice to seek confirmation of the main conclusions. Following the 3H-thymidine pulse given to aged mice, only immature glial cells were labeled. After a 30-day infusion, 12.1% astrocytes and 1.1% oligodendrocytes were labeled, so that the net daily addition rate of astrocytes averaged 0.4% and of oligodendrocytes, 0.04%. In young adult mice, the rate after a 7-day infusion averaged 0.9% for astrocytes and 0.08% for oligodendrocytes. However, when the 30-day infusion into aged mice was followed by 60 and 180 days without 3H-thymidine, the labeled astrocytes decreased to 5.3% and 0%, respectively, whereas the number of labeled oligodendrocytes did not change significantly. The interpretation of the results is that the immature cells present in the corpus callosum of mice continue dividing throughout life and their progeny give rise to astrocytes and oligodendrocytes. In the case of astrocytes, the production of new cells occurs in parallel with a loss, so that the astrocyte population turns over. In the case of oligodendrocytes, there is a small production of new, apparently stable cells.     

Radiographical documentation of direct injury of the intracanalicular segment of the optic nerve in the orbital apex syndrome

In the radiographical evaluation of the orbital apex syndrome, standard radiographs, tomograms, and computed tomographic scans have proved useful in the demonstration of the bony pathology, especially for optic canal fractures. The limitation of these methods, however, remains in their inability to provide accurate delineation of the associated soft tissue pathology, including the presence of optic nerve sheath hematoma. Recent developments in computer technology and graphic imaging are now available to provide an accurate three-dimensional radiographical analysis of the extent of skeletal and soft tissue injury in the orbital apex syndrome. The physician, in essence, can perform a radiographical "living autopsy". The technique was used to evaluate a patient with bilateral apex syndrome. It clearly showed that a severe direct injury to the intracanalicular portion of the optic nerve was responsible for the development of blindness in this patient. The progression of optic nerve injury, from perineural sheath hematoma to the ultimate development of optic nerve atrophy and fibrosis, was radiographically documented.     

The random blood glucose level, a risk factor for mortality after acute myocardial infarction, in non-diabetic patients

The Correlation between blood glucose level and cardio-vascular events is well established in diabetic patients. In this study, fifty three non diabetic (M:30F:23), patients after acute myocardial infarction were studied for mortality in the following two years, retrospectively. Every patient had random venous glucose estimated on admission. This glucose level was correlated with all cause mortality. At the end of 2 years, 13 patients died and 40 remained alive. There was a significant difference of blood glucose between those who died and remained alive. The difference between the mean blood glucose level is between 0.6 mmol/L and 3.8 mmol/L higher for patients who died (mean = 8.62); compared with those that were still alive (mean = 6.69). This difference was particularly observed in the group of anterior wall infarction. The subgroup analysis also revealed that the difference between the mean blood glucose levels is 9 mmol/L for female patients with heart failure compared with those who did not suffer from heart failure (mean 6.8). The study concludes that, the higher glucose level is associated with increased all cause mortality in the following 2 years of first acute myocardial infarction.     

Capnocytophaga ochracea Septicemia

A case report describing Capnocytophaga ochracea (Bacteroides ochraceus) septicemia in a 21-year-old male patient receiving chemotherapy for acute lymphocytic leukemia is presented. The unusual features of this organism are discussed together with a review of the literature.     

New methods for the assessment of in vitro and in vivo stress cracking in biomedical polyurethanes

This article describes a new test method for the assessment of the severity of environmental stress cracking of biomedical polyurethanes in a manner that minimizes the degree of subjectivity involved. The effect of applied strain and acetone pre-treatment on degradation of Pellethane 2363 80A and Pellethane 2363 55D polyurethanes under in vitro and in vivo conditions is studied. The results are presented using a magnification-weighted image rating system that allows the semi-quantitative rating of degradation based on distribution and severity of surface damage. Devices for applying controlled strain to both flat sheet and tubing samples are described. The new rating system consistently discriminated between the effects of acetone pre-treatments, strain and exposure times in both in vitro and in vivo experiments. As expected, P80A underwent considerable stress cracking compared with P55D. P80A produced similar stress crack ratings in both in vivo and in vitro experiments, however P55D performed worse under in vitro conditions compared with in vivo. This result indicated that care must be taken when interpreting in vitro results in the absence of in vivo data.     

A virus disease of captive vervet monkeys (Cercopithecus aethiops) caused by a new herpesvirus

Summary A probable new member of the herpes virus group caused an outbreak of fatal infections in captive vervet monkeys. The pathological findings and some of the properties of the virus are described.Dedicated to ProfessorJohn V. Enders on the occasion of his 70th birthday.     

Isolation and characterization of entomopox virions from virus-containing inclusions of Amsacta moorei (Lepidoptera: Arctiidae)

Preparations of Amsacta moorei entomopox virions were obtained from virus-containing inclusions (VCI) by using a carbonate-thioglycolate solution (pH 10.7–11.5). The virions possessed a uniform coat (“halo”) surrounding the viral envelope and exhibited an RNA polymerase activity. The “halo” could be removed by prolonged exposure to the carbonate-thioglycolate solution. Virions obtained by this treatment, however, possessed low infectivity and no detectable RNA polymerase activity. Removal of the “halo” by trypsin resulted in virions which possessed RNA polymerase activity and relatively high infectivity.Preparations of particles with and without the “halo” were similar in percent DNA, protein per OD₂₆₀, number of particles per OD₂₆₀, and RNA polymerase activity. Particles without the “halo,” however, were less dense (1.262 g/cm³) in CsCl than those with the “halo” (1.282 g/cm³) and 15–45 times more infective.Parallel studies of “nonhaloed” Amsacta virions (trypsin-treated) and vaccinia virions showed that both viruses contained similar amounts of protein per OD₂₆₀, but Amsacta virions contained only 36% of the DNA found in vaccinia.     

Induction of PGE2 by estradiol mediates developmental masculinization of sex behavior

Adult male sexual behavior in mammals requires the neuronal organizing effects of gonadal steroids during a sensitive perinatal period. During development, estradiol differentiates the rat preoptic area (POA), an essential brain region in the male copulatory circuit. Here we report that increases in prostaglandin-E(2) (PGE(2)), resulting from changes in cyclooxygenase-2 (COX-2) regulation induced by perinatal exposure to estradiol, are necessary and sufficient to organize the crucial neural substrate that mediates male sexual behavior. Briefly preventing prostaglandin synthesis in newborn males with the COX inhibitor indomethacin permanently downregulates markers of dendritic spines in the POA and severely impairs male sexual behavior. Developmental exposure to the COX inhibitor aspirin results in mild impairment of sexual behavior. Conversely, administration of PGE(2) to newborn females masculinizes the POA and leads to male sex behavior in adults, thereby highlighting the pathway of steroid-independent brain masculinization. Our findings show that PGE(2) functions as a downstream effector of estradiol to permanently masculinize the brain.     

A differential effect of C5a and C5a des Arg in the induction of pulmonary inflammation.

Earlier studies have shown that C5 fragments induce an inflammatory reaction when instilled into the rabbit lung. Because C5a is rapidly converted to C5a des Arg in vivo, experiments were performed to determine which fragment was most effective in producing pulmonary inflammation in this animal model. C5a des Arg consistently produced marked inflammation. This was characterized by neutrophil accumulation, edema, hemorrhage, fibrin formation, and damage to alveolar epithelium. The time course of the inflammatory reaction initiated by C5a des Arg showed pulmonary vascular sequestration of neutrophils with no intra-alveolar migration at 30 minutes after injection. By 2 hours, interstitial and alveolar neutrophils were numerous, with the accumulation of neutrophils in the alveoli increasing to a maximum at 6 hours. At 24 and 48 hours, the predominant cells were mononuclear (macrophages). By 120 hours, the lesions were resolving. In contrast, at all doses examined, a similar instillation of C5a induced either no inflammation or a milder, more focal response than C5a des Arg. This inability of C5a to initiate inflammation was not apparently due to the generation of inhibitors, since mixtures of C5a and C5a des Arg were phlogistic. A prolonged, intrapulmonary infusion of C5a (20 minutes), in contrast to a bolus instillation (1 minute), did initiate an inflammatory response, which may reflect the conversion of the C5a to C5a des Arg in the lung. This study points out the inflammatory potential of products of complement activation, particularly of the C5 fragment C5a des Arg, when applied to the airway side of the lungs. This inflammatory response raises the possibility that cleavage of intrapulmonary C5 may play an important role in the initiation of pulmonary inflammation.     

Effects of N-methyl-thiotetrazole cephalosporin on haemostasis in patients with reduced serum vitamin K1 concentrations.

Two patients with low random serum vitamin K1 concentrations but with normal prothrombin times and normal biological assays of the vitamin K dependent coagulation proteins were treated with an N-methyl-thiotetrazole cephalosporin (cefotetan) postoperatively. Four to six days later both patients developed a prolonged prothrombin time and a noticeable and specific lowering of the clotting activities of factors II, VII, IX and X, though the serum vitamin K1 concentrations remained unchanged. Crossed immunoelectrophoresis of prothrombin showed the appearance of a second peak corresponding to descarboxyprothrombin (PIVKA II). These abnormalities corrected after vitamin K administration. These data are consistent with the hypothesis that cephalosporins with an N-methyl-thiotetrazole side chain inhibit the hepatic utilisation of vitamin K but that this only causes hypoprothrombinaemia when liver reserves of vitamin K are low.