Cyclin D1 in astrocytic tumours: an immunohistochemical study

Forty-eight astrocytic tumours were stained immunohistochemically with antibodies to the cell cycle-regulating protein, cyclin D1, and to the proliferation marker MIB1 (Ki-67) using formalin fixed paraffin embedded tissue and a microwave antigen retrieval system. Cases were classified by the WHO system (1993). The labelling indices (LI) for both antibodies were compared with each other and with the tumour type. The mean labelling indices for both antibodies increased with the degree of malignancy, and a significant difference was seen between the pilocytic astrocytoma and diffuse astrocytoma together vs anaplastic astrocytoma and glioblastoma together. However, within each tumour type there was considerable variation in the labelling indices and a clear cut off value could not be demonstrated. There was a strong positive correlation between labelling indices for cyclin D1 and MIB1 in diffuse astrocytoma, but this correlation broke down increasingly in anaplastic astrocytoma and glioblastoma. There was poor correlation between cyclin D1 and MIB1 in pilocytic astrocytoma, a feature which appeared to separate them from the diffuse astrocytoma. Average labelling indices for cyclin D1 were higher than those of MIB1, which suggests that cyclin D1 positive cells represent a pool of cells from which proliferation and hence MIB1 expression can take place. In conclusion, cyclin D1 is overexpressed in astrocytic tumours, more so with increasing grade of malignancy and in a way which approximately correlates with MIB1 expression.     

Carbonic anhydrase II expression in fibrous astrocytes of the sheep

Immunohistochemical expression of carbonic anhydrase isoenzyme II (CAII) was demonstrated in a population of fibrous astrocytes in a young lamb and an adult sheep. Such cells were identified by co-expression of CAII and glial fibrillary acidic protein, nuclear morphology and their contribution of glial fibrillary acidic protein reactive processes to the glial limitans. Similar cells were not identified in neonatal lambs. As in man and mouse, CAII was also expressed in choroid plexus epithelium occurring in neonate, young and adult sheep brain. In contrast, however, to man and mouse, CAII was not expressed in sheep oligodendrocytes.     

Endothelial cell infection and thrombosis in paralysis caused by equid herpesvirus-1: Equine stroke

Summary Eight mares were infected with equid herpesvirus-1 subtype 1 isolated from a case of equine paresis. In two mares killed at 4 d.p.i. immunofluorescence showed endothelial cell infection together with thrombosis in the rete arteriosus of the nasal mucosa and also in the spinal cord of one of these mares. Circulating platelet counts in the other six mares fell as early as 2 d.p.i. and remained depressed for seven days. Circulating immune complexes started to appear at 2 d.p.i., reached maximum levels at 10 d.p.i., but were undetectable at 28 d.p.i. Three of the six remaining mares developed varying degrees of inco-ordination at 8 and 9 d.p.i. In the two inco-ordinate mares that were killed at 9 and 10 d.p.i. the haemorrhages in the spinal cord and brain were associated with extensive endothelial cell fluorescence and thrombus formation. Clinical paresis coincided with an increase in circulating complement fixing and neutralising antibodies which in all six mares were higher against the subtype 2 isolate than subtype 1.In five yearlings infected with a subtype 2 isolate of EHV-1 platelet counts remained normal and neither immune complexes nor viraemia, nor inco-ordination were detected.With 8 Figures     

Perfluorochemicals as US contrast agents for tumor imaging and hepatosplenography: preliminary clinical results

In animals, perfluorochemicals (PFCs) are effective ultrasound (US) contrast agents that produce hepatic, splenic, and tumor enhancement. The use of Fluosol-DA 20%, an emulsion of perfluorodecalin and perfluorotripropylamine, was studied in nine non-critically ill patients with cancer who had liver lesions. US studies without Fluosol were compared with studies obtained 24, 48, and 72 hours after Fluosol infusion. Vital signs and extensive laboratory analyses are performed before and after Fluosol infusion. Liver metastases from colonic, pancreatic, and gastric carcinoma exhibited rim or diffuse enhancement after a Fluosol dose of 1.6 g/kg or greater. Fluosol produced echogenic enhancement of the liver and spleen relative to kidney at a dose of 2.4 g/kg, allowing the detection of nonenhancing lesions. In addition, Fluosol at a dose of 1.6 g/kg or greater allowed detection of lesions not seen before contrast medium was administered in three of the seven patients studied. There was a mild increase in the level of serum glutamic oxaloacetic transaminase in two patients, one given 2.4 and the other 3.2 g/kg of Fluosol. Mild and transient allergic reactions without change in vital signs were experienced by two patients.     

Nipple development and pup-induced prolactin release in male rats treated prenatally with the antiandrogen flutamide

While maternal female rats display increases in circulating prolactin (PRL) concentrations in response to pup exposure, parental male rats fail to show such an increase. One possible explanation for the lack of an acute PRL response in parental male rats is that males do not have nipples and therefore do not receive stimuli from the pups comparable to those experienced by parental female rats. To examine the contribution of nipple presence and possible stimulation, i.e. suckling, in this sexually differentiated endocrine response, male rats were exposed from days 12-15 of gestation to the antiandrogen flutamide. As adults, flutamide-exposed males had nipples. These males and a group of control males were castrated in adulthood and treated with a 21-day hormone regimen (estradiol and progesterone) that effectively stimulates parental behavior in adult rats. Following hormone treatment, mammary tissue from one set of flutamide-treated males was examined histologically to assess nipple and mammary gland development and responsiveness of these tissues to hormonal stimulation. Additional sets of flutamide-treated and control animals were tested for parental behavior. These latter animals were implanted with indwelling atrial cannulae on day 4 of parental behavior and subsequently bled on day 6 in the absence of young and on day 8 after presentation of young. PRL concentrations did not change in either the flutamide-treated or control parental males bled in the presence or absence of young.(ABSTRACT TRUNCATED AT 250 WORDS)     

Domperidone induces a probenecid-sensitive rise in immunoreactive prolactin in cerebroventricular perfusates in female rats.

The present study examined immunoreactive prolactin (ir-PRL) access into the cerebrospinal fluid (CSF) by monitoring ir-PRL levels in the blood and cerebroventricular perfusates of ovariectomized (ovx) rats treated with the dopamine antagonist, domperidone (DOMP). In Expt. 1 PRL plasma levels were measured in rats treated with DOMP i.p. (2.5, 5.0 and 10.0 mg/kg). All doses of DOMP significantly increased PRL plasma levels. In Expt. 2 animals were treated i.p. with DOMP (10 mg/kg) or DOMP plus the active transport blocking agent, probenecid (PROB; 250 mg/kg). Plasma PRL and ir-PRL in cerebroventricular perfusates were measured in separate sets of animals using catheters and a push-pull perfusion system, respectively. DOMP induced an increase in plasma PRL that was followed 30-40 min later by a rise in ventricular perfusates ir-PRL levels. PROB treatment induced a greater increase in plasma PRL levels in DOMP-treated animals, but delayed the DOMP-induced increase in ir-PRL ventricular perfusate ir-PRL levels. The delay in the rise of ir-PRL in ventricular perfusates observed in rats treated with DOMP plus PROB may be due to a PROB's interference with the transport of PRL from the blood into CSF. These results suggest that under some conditions ir-PRL in CSF originates from the pituitary.     

Classical and anaplastic seminoma: difference in survival

Classical and anaplastic seminoma are traditionally treated with radiation therapy and are said to have the same prognosis. A retrospective study was undertaken of 90 seminoma patients treated with radiation therapy between 1961 and 1985. The classical group consisted of 71 patients of whom 50 had stage I and 21 had stage II disease. The anaplastic group consisted of 19 patients of whom ten had stage I and nine had stage II disease. The median follow-up time was 64 months for the entire group. The 10-year relapse-free survival rate for the classical group was 94% and for the anaplastic group was 70% (P less than .05). For patients with classical stage I disease, the relapse-free actuarial survival rate was 98%; for patients with anaplastic stage I disease, it was 64% (P less than .02). For the classical stage II disease group, the relapse-free actuarial survival rate was 84% and for the anaplastic stage II disease group, 75% (P less than .70). Four patients in the classical group (6%) had relapses; of these, one patient had local recurrence of tumor, and three had distant metastases. In the anaplastic group, four patients (21%) had relapses; two patients had local recurrence of tumor, and two had distant metastases. Therefore the data suggest a difference in survival and relapse rates between classical and anaplastic seminoma.     

Hemorrhagic shock-induced bacterial translocation is reduced by xanthine oxidase inhibition or inactivation

Experiments were performed to determine whether bacterial translocation (BT) after hemorrhagic shock is due to a reperfusion injury mediated by xanthine oxidase-derived oxidants. Rats were subjected to 30 minutes of shock (30 mm Hg) followed by reinfusion of shed blood. Twenty-four hours after hemorrhage and reinfusion, the mesenteric lymph node, liver, and spleen were harvested from each animal for bacterial culture, and the ileum and cecum were examined histologically. Sham-shocked (control) rats were instrumented, but blood was not withdrawn. The incidence of BT was higher in the shocked rats (61%) than in the sham-shocked animals (7%) (p less than 0.01). Allopurinol (50 mg/kg, administered orally), a competitive inhibitor of xanthine oxidase, reduced the incidence of shock-induced BT to 14% (p = 0.02). Similarly, rats fed a tungsten-supplemented molybdenum-free diet, which inactivates xanthine oxidase, reduced shock-induced BT to 10% (p = 0.02). The histologic damage cause by hemorrhagic shock was prevented by blocking xanthine oxidase activity. Thus hemorrhagic shock-induced bacterial translocation from the gut appears to be mediated by oxidants generated by activation of the xanthine oxidase system.