Staying Safe from Radiation Exposure in Cath Lab: A Review.

A successful cardiac catheterization Laboratory radiation safety program must manage patient and staff safety by reducing exposure to ionizing radiation to a level that is as low as reasonably achievable (ALARA). The first step in radiation safety is to avoid unnecessary use of ionizing radiation by justification of exposure, one of the basic principles of radiation protection. All individuals involved in fluoroscopic imaging procedures should familiarize themselves to the measures to protect themselves from exposure to unsafe doses of ionizing radiation.

Granulomatosis with Polyangiitis (Wegener Granulomatosis) with Unusual Presentation.

We came across a 32 years old male admitted in our hospital with prolonged low-grade fever, haemoptysis, leg swelling, weight loss, purpuric rashes and malaena. He received anti-TB treatment at another hospital without any improvement. He was pale with bullous and purpuric lesions over legs and feet. He also had features of consolidation over both lung fields. His CRP was 312mg/L, Urine R/M/E showed 40-50 RBC/HPF, Chest X-ray showed features of bilateral consolidation, c-ANCA-10U/L (positive); Tracheal aspirate for AFB was found to be negative. We diagnosed the case as Granulomatosis with Polyangitis (WG) and started treatment with steroid and cyclophosphamide. But the patient could not be saved probably due to delay in starting management.

Transient Loss of Vision after Coronary Angiogram - A Case Report.

A 50-year old, diabetic, hypertensive patient with post-CABG status developed complete loss of vision about one hour after coronary angiogram (CAG). Thorough ophthalmological and neurological examination as well as magnetic resonance imaging of brain especially of the occipital region revealed no abnormality. The patient had complete recovery of vision about 48 hours later. We could not document any specific cause or mechanism for the visual loss, although the selective vulnerability of occipital lobes to contrast agent toxicity (Cortical blindness) was the most likely underlying mechanism.

Testicular tumour - a review article.

Painless scrotal masses must be investigated with ultrasound imaging and tumour marker assay before being treated with radical inguinal orchidectomy. For unknown reasons, the incidence of this cancer increased in Caucasian population. The incidence of testicular germ cell tumour has doubled in past 40 years. An annual increase of 3-6% is reported in Caucasian population. But the mortality rate has been stable or decreasing due to improvement in treatment. In the past, metastatic testicular cancer was usually fatal, but recent advances in treatment, including high-dose chemotherapy and stem cell rescue, have considerably improved the prognosis. Indeed, testicular cancer is a bright spot in the oncological landscape and is now considered the model for the treatment of solid tumors. We looked into the epidemiology, presentation, classification, work up, staging, various treatment modalities and prognosis of testicular tumour in this article.

Involvement of glutathione in puberty and FSH release.

Administration of glutathione subcutaneously to immature female (age and weight matched) rats brings about a pre-ponement of puberty. A significant increase in pituitary, ovaries and uterine mass was observed in the experimental rats. Further, a considerable increase in pituitary FSH levels was also observed after intraventricular injection of glutathione in ovariectomized-steroid primed rats. Intraventricular administration of L-buthionine SR sulfoxamine produced a significant decrease in plasma FSH levels in intact male rats. These studies demonstrate the neuroendocrine role of glutathione on gonadotropins, specifically in relation to FSH release.

Altered intravenous pharmacokinetics of topotecan in rats with acute renal failure (ARF) induced by uranyl nitrate: do adenosine A1 antagonists (selective/non-selective) normalize the altered topotecan kinetics in ARF?

A series of exploratory investigations with multiple agents was carried out in normal rats and in rats with uranyl nitrate-induced acute renal failure to understand the disposition characteristics of intravenous topotecan (TPT) used as a model substrate. The disposition of TPT was unaltered in normal rats when treated with methotrexate, whereas treatment with probenecid increased the systemic exposure of TPT. In case of uranyl nitrate-induced acute renal failure (UN-ARF) rats, the systemic exposure of TPT was increased when compared with normal rats, whereas in UN-ARF rats treated with probenecid a further reduction in renal clearance of TPT was noted as compared with that of UN-ARF induced rats. Thus, TPT may be involved in the tubular secretory pathway when a passive glomerular filtration pathway for elimination was not possible. The disposition of TPT did not normalize in UN-ARF rats when treated with caffeine, a non-selective adenosine A1 receptor antagonist, whereas the selective adenosine A1 receptor antagonist (1,3-dipropyl-8-phenylxanthine, DPPX) normalized TPT pharmacokinetic disposition by improving renal function. Renal excretion studies demonstrated that CLR improved by almost fivefold following DPPX treatment in ARF rats. In addition, the qualitative stability/metabolism pattern of TPT in liver microsomes prepared from various groups of rats (normal rats, UN-ARF rats, rats treated with DPPX, and UN-ARF rats treated with DPPX) was found to be similar. In summary, using a pharmacokinetic tool as a surrogate, it has been shown that the pharmacokinetic disposition of TPT improved considerably upon treatment with DPPX, a selective adenosine A1 antagonist.

Acute and short-term effects of intraventricular injection of somatostatin and LHRH on glutamate and GABA levels in rat brain.

Glutamate and GABA content in different regions of adult female rat brain were determined at 10 and 30 min following intraventricular injection of LHRH or somatostatin. Cerebral cortex, cerebellar and hypothalamic glutamate levels were significantly elevated at 30 min following injection of 1 micrograms somatostatin, whereas hypothalamic glutamate levels were elevated at 10 min following a 0.5 micrograms dose. LHRH at a dose of 1 micrograms elevated cerebellar and brain stem glutamate levels at 10 and 30 min, whereas a 0.5 micrograms dose significantly elevated cerebral cortex, cerebellar and hypothalamic glutamate levels at 30 min. Third ventricular injection of 1 micrograms somatostatin produced a significant decrease in hypothalamic GABA levels at 10 and 30 min, whereas a 0.5-microgram dose decreased brain stem GABA levels at 10 min. LHRH at a dose of 0.1 microgram significantly increased cerebral cortex and cerebellar GABA levels at 10 min and brain stem GABA levels at 10 and 30 min following injection. Intraventricular injection of LHRH at a dose of 0.5 microgram significantly elevated cerebral cortex, cerebellar and brain stem GABA levels at 30 min. Hypothalamic GABA levels were elevated at 10 and 30 min following 0.5 and 1 microgram intraventricular LHRH injection. The implications of these results are discussed in relation to probable interaction between these neuroactive amino acids and neuropeptides in the rat brain.

Glutathione and gamma-glutamyl transpeptidase in the adult female rat brain after intraventricular injection of LHRH and somatostatin.

Glutathione content and glutamyl transpeptidase activity in different regions of adult female rat brain were determined at 10 and 30 min following intraventricular injection of LHRH and somatostatin. Hypothalamic glutathione levels were significantly elevated at 10 and 30 min after a single injection of a 0.1 micrograms dose of LHRH. On the contrary, glutathione levels significantly decreased in the hypothalamus, cerebral cortex and cerebellum at 10 and 30 min after 0.5 or 1 microgram dose. However, significant decrease in brain stem glutathione was evident at 30 min after 0.5 microgram and 10 min after the 1 microgram dose. Somatostatin at doses of 0.5 microgram and 1 microgram significantly decreased glutathione levels in all four brain regions both at 10 and 30 min following injection into the 3rd ventricle. Gamma-glutamyl transpeptidase activity in the hypothalamus and cerebral cortex was significantly elevated after intraventricular injection of LHRH. However, a significant increase in gamma-glutamyl transpeptidase activity in cerebellum and brain stem was seen only with 0.5 and 1 micrograms doses of LHRH. Somatostatin also significantly increased gamma-glutamyl transpeptidase activity in hypothalamus, cerebral cortex, brain stem and cerebellum. The decrease in glutathione levels with corresponding increase in gamma-glutamyl transpeptidase activity after intraventricular administration of LHRH and somatostatin suggests a possible interaction between glutathione and hypothalamic peptides.

Glutathione distribution in rat brain at different ages and the effect of intraventricular glutathione on gonadotropin levels in ovariectomized steroid-primed rats.

Glutathione levels were estimated in different regions of the brain of 21-, 30-, 40-, 42-, 45-day-old and adult female rats. Glutathione content in the cerebral cortex, cerebellum and the brain stem remained almost the same beginning from day 21 to sexually mature adult rats. There is a significant increase in hypothalamic glutathione content reaching a peak at puberty (42 days) and thereafter decreasing to the adult levels. Plasma gonadotropin levels were evaluated at 5 and 15 min after third ventricular injection of 15 and 30 microgram doses of glutathione in ovariectomized steroid-primed rats. Intraventricular injection of either 15 or 30 micrograms dose of glutathione significantly elevated plasma FSH levels. The 15 micrograms dose of glutathione significantly decreased plasma LH levels whereas 30 micrograms dose had no effect. Lower dose of glutathione inhibits LH release and stimulates FSH release whereas the higher dose of glutathione specifically elevates FSH levels without any change in LH levels suggesting a selective FSH releasing action of glutathione.