Virtual study groups: Internet-based collaborative revision for the FRANZCR examinations.

Preparation for the FRANZCR examination series is often performed cooperatively in study groups. Meeting face-to-face on a regular basis is time-consuming and distances can be prohibitive for trainees in isolated centres. We present a report of a web-based study group that used home-based broadband technologies and we discuss its efficacy and feasibility, as well as various technical issues that arose during the course of the meetings. Web-based peer revision is a useful tool that should be employed by trainees.

Hydatid cyst of the cardiac interventricular septum: report of two cases.

Cardiac hydatid cysts are rare and represent less than 2% of all hydatid cases. They can occur as part of a widespread systemic infection or as an isolated event. Cardiac hydatid cysts rarely involve the interventricular septum. Here, we present two cases of cardiac hydatid disease in which one patient had the lesion in the interventricular septum and the other in both the interventricular septum and the apex of the heart. A brief overview of the disease and the role of echocardiography, dynamic enhanced multidetector computed tomography (MDCT) and MRI imaging in establishing the diagnosis are discussed.

The security concern on internet banking adoption among Malaysian banking customers.

The existing literatures highlights that the security is the primary factor which determines the adoption of Internet banking technology. The secondary information on Internet banking development in Malaysia shows a very slow growth rate. Hence, this study aims to study the banking customers perception towards security concern and Internet banking adoption through the information collected from 150 sample respondents. The data analysis reveals that the customers have much concern about security and privacy issue in adoption of Internet banking, whether the customers are adopted Internet banking or not. Hence, it infers that to popularize Internet banking system there is a need for improvement in security and privacy issue among the banking customers.

Attenuation of oxalate-induced nephrotoxicity by eicosapentaenoate-lipoate (EPA-LA) derivative in experimental rat model.

Hyperoxaluria is one of the major risk factors for the formation of urinary calcium oxalate stones. Calcium oxalate crystals and their deposition have been implicated in inducing renal tubular damage. Lipoic acid (LA) and eicosapentaenoic acid (EPA) have been shown to ameliorate the changes associated with hyperoxaluria. This prompted us to investigate the nephroprotectant role of EPA-LA, a new derivative, in vivo in hyperoxaluric rats. Elevation in the levels of calcium, oxalate and phosphorus, the stone-forming constituents, were observed in calculogenic rats as a manifestation of crystal deposition. Tubular damage to the renal tissue was assessed byassaying the excretion of marker enzymes in the urine. Damage to the tubules was indicated by increased excretion of alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma-glutamyl transferase (gamma-GT), beta-Glucuronidase (beta-GLU) and N-Acetyl beta-D glucosaminidase (NAG). Fibrinolytic activity was found to be reduced. Administration of EPA, LA and EPA-LA reduced the tubular damage and decreased the markers of crystal deposition markedly, which was substantiated by the reduction in weight of bladder stone formed. Our results highlight that EPA-LA is the most effective drug in inhibiting stone formation and mitigating renal damage caused by oxalate toxicity, thus confirming it as a nephroprotectant. Further work in this direction is warranted to establish the therapeutic effectiveness of this new derivative.

The effect of hyperventilation and hyperoxia on cerebral venous oxygen saturation in patients with traumatic brain injury.

UNLABELLED: Eighteen head-injured patients undergoing hyperventilation were studied for changes in jugular venous oxygen saturation (SjvO2) and arteriovenous oxygen content difference (AVDO2) in response to changes in PaO2 and PaCO2. SjvO2 decreased significantly from 66% +/- 3% to 56% +/- 3% (mean +/- SD) when PaCO2 decreased from 30 to 25 mm Hg at a PaO2 of 100-150 mm Hg. SjvO2 values returned to baseline (66% +/- 2%) when PaCO2 was restored to 30 mm Hg. Repetition of the study at a PaO2 of 200-250 mm Hg produced a similar pattern. However, SjvO2 values were significantly greater with PaO2 within the range of 200-250 mm Hg (77% +/- 4% and 64% +/- 3%) than SjvO2 measured at a PaO2 of 100-150 mm Hg at PaCO2 values of both 30 and 25 mm Hg. AVDO2 also improved with a PaO2 of 200-250 mm Hg at each PaCO2 (P < 0.001). In conclusion, decreases in SjvO2 associated with decreases in PaCO2 may be offset by increasing PaO2. IMPLICATIONS: The adequacy of cerebral oxygenation can be estimated in head-injured patients by monitoring jugular bulb oxygen saturation and the arteriovenous oxygenation content difference. Increasing the partial pressure of arterial oxygen above normal offset deleterious effects of hyperventilation on jugular bulb oxygen saturation and arteriovenous oxygenation content difference in head-injured patients.

Possible involvement of prostaglandins in increases in rat plasma adrenocorticotropic hormone and corticosterone levels induced by radiation and interleukin-1 alpha alone or combined.

Exposing rats to 1-10 Gy of ionizing radiation increased plasma adrenocorticotropic hormone (ACTH) and corticosterone (CORT) levels. In both irradiated and nonirradiated rats, recombinant human interleukin-1 alpha (rhIL-1 alpha; 1 hr before radiation/sham exposure) enhanced plasma ACTH and CORT levels. Indomethacin, a cyclooxygenase inhibitor, attenuated plasma ACTH and CORT levels induced by radiation. Indomethacin also attenuated ACTH and CORT levels induced by radiation and interleukin-1 alpha alone or combined. These results suggest that prostaglandins are involved in the increase in plasma ACTH and CORT levels induced by radiation and rhIL-1 alpha alone or combined.

Single-dose ethanol administration activates the hypothalamic-pituitary-adrenal axis: exploration of the mechanism of action.

Activation of the hypothalamic-pituitary-adrenal axis (HPAA) by single-dose ethanol administration, which achieved moderately high blood ethanol levels, was explored in naive rats in order to determine the mechanism of ethanol's activation of the stress axis. Adult male rats received a single dose (3.2 g/kg body weight-1 of a 12% solution of ethanol in physiological saline. The plasma concentration of immunoreactive (ir) adrenocorticotropic hormone (ACTH), beta-endorphin (BE) and corticosterone (CS) was determined by radioimmunoassay, whereas, plasma concentrations of epinephrine (E) and norepinephrine (NE) were quantified following reverse-phase liquid chromatographic separation and amperometric detection. Ethanol induced maximal plasma ACTH levels within minutes, which declined toward basal levels by 60 min, whereas, plasma concentration of CS rose rapidly and remained elevated at 60 min. Plasma ACTH and CS levels in saline-treated control animals did not vary significantly at any time point. Consistent with co-release of ACTH from corticotrophs, the plasma concentration of ir-BE increased 5-fold at 15 min and declined towards basal levels at 60 min after-ethanol challenge. Plasma E increased 10- to 20-fold as compared to saline controls or preinjection levels and returned to preinjection levels by 90 min, in a manner similar to ethanol-induced changes in proopiomelanocortin-derived peptides and CS. Removal of the adrenal medulla and thus the source of E prior to ethanol administration, did not attenuate activation of the HPAA. Passive immunoneutralization of arginine vasopressin (AVP), using a high-titer AVP antiserum and a protocol which was found to block ether-induced ACTH secretion by 40% in adult male rats, failed to even partially block ethanol-induced ACTH or CS secretion. The results of this study indicate that neither adrenal medulla-derived E nor AVP are significant regulators or coregulators of corticotroph secretions following a moderately high, single-dose, intragastric administration of ethanol.

Effect of single and repeated electroconvulsive shock on the hypothalamic-pituitary-adrenal axis and plasma catecholamines in rats.

The effects of single and repeated electroconvulsive shock (ECS) on the hypothalamic-pituitary-adrenal (HPA) axis and plasma catecholamines were studied. Rats were divided into three groups and each group received sham treatment, single ECS, or ten once-daily ECS. Jugular venous blood samples were obtained immediately before treatment and at 10, 30, 60, and 90 min following sham treatment, a single ECS or following the last of ten ECS. Plasma concentrations of corticosterone (CS), ACTH, immunoreactive beta-endorphin (ir-BE), epinephrine (E) and norepinephrine (NE) were determined. Following the single ECS plasma CS was significantly elevated at 10 and 30 min, ACTH was significantly elevated at 10, 30, and 60 min, whereas ir-BE and E peaked at 10 min and returned to basal concentration by 30 min. The concentration of plasma NE did not significantly vary at any time point. Following the tenth ECS the concentration of plasma CS revealed a significant attenuation of the increase at 10 and 30 min when compared with the CS changes observed following a single ECS. Plasma ACTH following chronic ECS was also significantly decreased in magnitude at 10, 30, and 60 min when compared with plasma ACTH levels following a single ECS. Ir-BE in plasma following ten ECS mirrored the changes following single ECS. In contrast to the attenuation of CS and ACTH following chronic ECS, the increase in peripheral catecholamines was markedly elevated after the last of ten ECS. Compared with single ECS, ten ECS produced significant increases in plasma E at 10, 30, and 60 min and at 10, 30, 60, and at 90 min for NE.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute effect of intragastric ethanol administration on plasma levels of stress hormones.

We have previously demonstrated that single-dose ethanol administration enhanced plasma levels of ACTH, beta-endorphin, corticosterone (CS) and catecholamines. Since the secretion of proopiomelanocortin-derived peptides (e.g., ACTH, beta-endorphin) can be influenced by catecholamines and vasopressin in addition to the primary physiological regulator, corticotrophin-releasing hormone, we have attempted to determine whether or not the ethanol-induced activation of the hypothalamic-pituitary-adrenal axis (HPAA) could in part be mediated via either epinephrine or vasopressin (AVP) secretion. The selective neutralization of AVP through the administration of AVP antiserum failed to block the ethanol-induced secretion of either ACTH or CS. In addition, adrenal demedullation did not significantly attenuate the ethanol-induced increase of ACTH and CS. It would appear that neither adrenal medulla-derived epinephrine nor median eminence-derived AVP mediates ethanol's activation of the HPAA.