Cholesterol emboli to the kidney: an immunoperoxidase study.

Cholesterol emboli (CE) are an increasingly recognised cause of renal impairment in the elderly population, especially following diagnostic vascular procedures and aortic surgery. They can present as part of a multisystem disease which can mimic many conditions, depending on the site of the emboli. As a pathological entity, it was described by Florey in 1945. Relatively few cases have been reported in the literature. At this stage there is no accepted treatment protocol for CE induced renal failure. Little is known about the precise nature of the cells involved in the proliferating tissue surrounding CE in the kidney. To date, all studies on CE have involved routine Haematoxylin and Eosin (H&E) stains. By studying the cellular interactions, hopefully this will contribute further to our understanding of CE in the kidney. Nine (n = 9) out of 1150 consecutive renal biopsies over a six year period were analysed. Standard three- and four-layered peroxidase-antiperoxidase techniques were employed. A panel of antibodies to specific cells were used. The particular cells analysed were the myofibroblast, smooth muscle, endothelium, macrophage, neutrophil, T cell and B cell. All vessels in the biopsy specimen containing CE were analysed. T cell, B cell, macrophage and neutrophil infiltrates were counted and expressed as cells/mm2 using a 0.022 mm2 graticule under 400 (10x40) magnification. The vessel and perivascular space were analysed. The myofibroblast, smooth muscle and endothelial cell proliferation were graded semiquantitatively. Vessels without evidence of CE were used as controls. The data were subjected to statistical analysis using the unpaired non-parametric Mann-Whitney Two Sample test. P values <0.05 were accepted as significant. Histological sections demonstrated the host response in the vessel to CE involve a significant response including the myofibroblast, endothelium, T cell and macrophage. The B cell response was absent and the smooth muscle cell response was not significantly different. The perivascular responses were not different for the cells studied. This study has characterised the host response to CE in the human kidney by demonstrating the presence of the myofibroblast, macrophage T cell and endothelial cell response. The myofibroblast is a cell which is increasingly being recognised in the host response of both granulation tissue and pathological tissue. The population at risk for CE is growing and the disease is increasingly iatrogenic in origin. Currently our only treatment is prevention.

Angle grinder injuries: a cause of serious head and neck trauma.

Over the past 12 months, the Victorian Trauma Centre at the Alfred Hospital, Melbourne, has dealt with serious head and neck injuries associated with angle grinder use. Three cases are presented, documenting the circumstances and severity of these injuries and subsequent management. Angle grinder injuries are a source of serious morbidity and mortality, much of which is preventable.

Source of inhibin in ovine fetal plasma and amniotic fluid during late gestation: half-life of fetal inhibin.

Immunoactive inhibin (ir-inhibin) concentrations were determined in chronically catheterized sheep between 120 and 145 days gestation. Maternal plasma ir-inhibin concentrations remained basal (0.19 +/- 0.05 ng/ml) throughout the period of study. Immunoactive inhibin concentrations in male and female fetal plasma were elevated above those observed in maternal plasma, with the concentrations in plasma of male fetuses (7.38 +/- 0.04 ng/ml) being significantly greater (p < 0.001) than those in female fetuses (1.07 +/- 0.14 ng/ml). The concentrations of ir-inhibin in amniotic fluid of ewes bearing male fetuses (10.93 +/- 1.55 ng/ml) were significantly greater than in ewes bearing female fetuses (2.81 +/- 0.32 ng/ml; p < 0.05) but not significantly different from the concentrations in male fetal plasma. Immunoactive inhibin concentrations decreased following surgery in gonadectomized fetuses, to 3.25 +/- 0.99 ng/ml within 6 h, and remained at a mean value of 0.75 +/- 0.38 ng/ml from 24 h after gonadectomy. The half-life of circulating inhibin in fetal plasma, estimated from the decay curve during the first 6 h after surgery, was 3.94 +/- 0.88 h. There was a significant (p < 0.05) decrease in the concentration of ir-inhibin in amniotic fluid after gonadectomy; however, this decrease occurred gradually over 7 days, and ir-inhibin concentrations did not fall to those concentrations observed in fetal circulation at any time after gonadectomy. It is concluded that the major source of circulating ir-inhibin in male fetal plasma, but not in amniotic fluid, is the gonads.

Inhibin and follistatin concentrations in fetal tissues and fluids during gestation in sheep: evidence for activin in amniotic fluid.

The concentrations of inhibin and follistatin in amniotic fluid and in tissue extracts from the placenta, gonads and adrenals of fetal sheep were measured using radioimmunoassays. These tissue extracts were from whole fetuses from days 16 to 45 and from the individual organs from day 46 to 145 (term) and were assayed at multiple dilutions. The capacity of these extracts to alter FSH production of rat anterior pituitary cells in culture was also assessed at multiple dilutions. Immunoactive inhibin concentrations in amniotic fluid from both sexes increased during gestation and levels were significantly greater in males than females. Peak concentrations of immunoreactive inhibin of 11.2 +/- 1.9 ng/ml were found in males at 116-125 days of gestation. Follistatin concentrations did not change throughout gestation and no significant difference was noted between sexes. Mean follistatin levels throughout gestation were 3.0 +/- 0.9 ng/ml for males and 3.7 +/- 0.9 ng/ml for females. Despite the potential for FSH inhibition by inhibin and follistatin, amniotic fluid from both sexes at all stages of gestation stimulated FSH secretion in the pituitary cell bioassays, suggesting the presence of activin which was confirmed by the measurement of immunoactive activin (13.3 +/- 2.5 ng/ml) in a specific radioimmunoassay. Maximum concentrations of immunoactive and bioactive inhibin in placental extracts were observed in late gestation (2.2 +/- 0.6 and 3.8 +/- 1.6 ng/g respectively) and there was no significant difference between sexes. Follistatin concentrations in placental cotyledons ranged from 11.5 to 27.1 ng/g with no significant difference between sexes. In view of the higher follistatin concentrations compared with inhibin, it is likely that the capacity of placental extracts to suppress FSH production by pituitary cells in culture is due predominantly to follistatin. Immunoactive inhibin was observed in high concentrations in the fetal testis throughout gestation; with concentrations increasing to a maximum of 1993.0 +/- 519.7 ng/g at 126-135 days of gestation with a ratio of bioactive: immunoactive inhibin of 1:20. Although bioactive and immunoactive inhibin was also observed in fetal ovaries and adrenals from both male and female fetuses, concentrations were lower than those observed in fetal testes. Follistatin concentrations in the fetal testis were elevated between 70 and 95 days (97.6 ng/g) and then declined. Similar concentrations were found in the adrenal glands of both sexes (males 83.5-103.3 ng/g: females 55.3-95.8 ng/g).(ABSTRACT TRUNCATED AT 400 WORDS)