Round the Bend: A Brief History of Mental Health Nursing in Victoria,Australia 1848 to 1950's

This paper presents a history of mental health nursing in Victoria, Australia from 1848 to the 1950's, or the asylum years to the era of the mental hospital. The research for this historical overview was conducted as part of a literature review for a mental health nursing doctoral thesis, which included an account of the evolution of the profession from asylum attendant to the present time. The literature reviewed for this project revealed a distinct lack of a coherent, chronological account of the historical development of mental health nursing in Victoria, and this paper seeks to address that knowledge gap.     

Extended hepatectomy in patients with hepatobiliary malignancies with and without preoperative portal vein embolization

HYPOTHESIS: Preoperative portal vein embolization (PVE) allows potentially curative hepatic resection without additional morbidity or mortality in patients with hepatobiliary malignancies who are marginal candidates for resection based on small liver remnant size. DESIGN: A retrospective review of a consecutive series of patients in a multi-institutional database who underwent extended hepatectomy. SETTING: University-based referral centers. PATIENTS: Forty-two patients underwent preoperative determination of the future liver remnant (FLR) volume before extended hepatectomy (> or = 5 segments) for hepatobiliary malignancy without chronic underlying liver disease. Patients were stratified by treatment with or without preoperative PVE. INTERVENTION: Preoperative percutaneous PVE. MAIN OUTCOME MEASURES: Clinical characteristics, FLR volume, operative morbidity, and survival. RESULTS: There was no difference between the groups that did and did not undergo PVE for the number of tumors, tumor size, estimated blood loss, duration of the operation, complexity of resection, or surgical margins. The FLR at presentation was significantly smaller in patients who underwent PVE than in patients who did not undergo PVE (18% vs 23%; P<.001). After PVE, FLR volumes increased significantly (P =.003); preoperative FLR volumes were similar in both groups (patients who underwent PVE, 25%; and patients who did not undergo PVE, 23%). There was no perioperative mortality and no statistical difference in the incidence of perioperative complications between those who did and those who did not undergo PVE (5 [28%] of 18 patients vs 5 [21%] of 24 patients). The overall 3-year survival was 65% and the median survival duration was equivalent in the 2 groups (40 vs 52 months for those who did vs those who did not undergo PVE). CONCLUSION: Portal vein embolization enables safe and potentially curative extended hepatectomy in a subset of patients who would otherwise be marginal candidates for resection based on a small liver remnant size.     

Down-regulation of urea transporters in the renal inner medulla of lithium-fed rats

BACKGROUND: Lithium is commonly used to treat bipolar psychiatric disorders but can cause reduced urine concentrating ability. METHODS: To test whether lithium alters UT-A1 or UT-B urea transporter protein abundance or UT-A1 phosphorylation, rats were fed a standard diet supplemented with LiCl for 10 or 25 days, and then compared to pair-fed control rats. To investigate another potential mechanism for decreased urea transport, inner medullary collecting duct (IMCD) suspensions from lithium-fed or control rats were incubated with 32P-orthophosphate to measure the phosphorylation of UT-A1. RESULTS: In lithium-fed rats (25 days), UT-A1 abundance was reduced to 50% of control rats in IM tip and to 25% in IM base, and UT-B abundance was reduced to 40% in IM base. Aquaporin-2 (AQP2) protein abundance was reduced in both IM regions. Vasopressin (100 pmol/L) increased UT-A1 phosphorylation in IMCD suspensions from control but not from lithium-fed rats; a higher vasopressin concentration (100 nmol/L) increased UT-A1 phosphorylation in control and lithium-fed rats. CONCLUSIONS: Decreases in UT-A1, UT-B, and AQP2 protein abundance, and/or vasopressin-stimulated phosphorylation of UT-A1, can contribute to the reduced urine concentrating ability that occurs in lithium-treated rats.     

A critical evaluation of a percutaneous diagnostic and treatment strategy for chylothorax after thoracic surgery.

OBJECTIVE: Because chylothorax complicating thoracic surgery is difficult to diagnose and failure of nonoperative management necessitates further surgery, we critically evaluated an evolving percutaneous strategy for diagnosing and treating chylothorax. METHODS: After thoracic surgery, 37 patients with a clinical diagnosis of chylothorax were referred for lymphangiography for definitive diagnosis and percutaneous treatment. Successful localization of the cisterna chyli by lymphangiogram facilitated percutaneous cannulation of the thoracic duct and its embolization. In patients in whom cannulation was not possible, the thoracic duct was percutaneously disrupted. RESULTS: Diagnosis: Lymphangiography was successful in 36 of the 37 patients (97%). Contrast extravasation, confirming clinical diagnosis, was present in 21 of the 36 (58%). Management: Twenty-one of 36 patients underwent 22 lymphangiographically directed percutaneous interventions: 12 embolizations and 10 disruptions. Mortality was zero, with two manageable complications. Patients without percutaneous intervention were discharged a median of 7 days (range 4-58) after first lymphangiography, 8 days (range 2-19) after percutaneous embolization, and 19 days (range 6-48) after first disruption. Eight patients had nine subsequent reoperations for chylothorax, two with negative lymphangiograms; no embolization patient required reoperation. CONCLUSIONS: There is a discrepancy between the clinical diagnosis of chylothorax after thoracic surgery and the presumed gold standard of diagnosis, contrast extravasation at lymphangiogram. Percutaneous treatment by thoracic duct embolization or disruption is safe and may obviate reoperation, but embolization of the thoracic duct is preferable to its disruption.     

Urea excretion in white rats and kangaroo rats as influenced by excitement and by diet

Reprinted from The American Journal of Physiology, Vol. 181, No.1, April, 1955.     

The influence of non‐HLA antibodies directed against angiotensin II type 1 receptor (AT1R) on early renal transplant outcomes

Non‐HLA antibodies (Abs) targeting vascular receptors are thought to have an impact on renal transplant injury. Anti‐angiotensin II type 1‐receptor‐activating antibodies (anti‐AT1R) have been mentioned to stimulate a severe vascular rejection, but the pretransplant screening has not been introduced yet. The aim of our study was to assess the incidence and importance of anti‐AT1R antibodies and their influence on renal transplant in the 1st year of observation. We prospectively evaluated the presence of anti‐AT1R antibodies in 117 consecutive renal transplant recipients in pre‐ and post‐transplant screening. Anti‐AT1R antibodies were observed in 27/117 (23%) of the analyzed recipients already before transplantation. The function of renal transplant was considerably worse in anti‐AT1R(+) group. The patients with anti‐AT1R Abs >9 U/ml lost their graft more often. Biopsy‐proven AR was described in 4/27 (15%) pts in the anti‐AT1R(+) group and 13/90 (14.4%) in the anti‐AT1R(?) group, but more severe cases of Banff IIB or antibody‐mediated rejection (AMR) were more often observed in anti‐AT1R (+) 4/27 (15%) vs. 1/90 (1.1%) in anti‐AT1R(+) (P = 0.009). Patients with anti‐AT1R Abs level >9 U/ml run a higher risk of graft failure independently of classical immunological risk factors. The recipients with anti‐AT1R Abs developed more severe acute rejections described as IIB or AMR in Banff classification. More recipients among the anti‐AT1R‐positive ones lost the graft. Our study suggests monitoring of anti‐AT1R Abs before renal transplantation for assessment of immunologic risk profiles and the identification of patients highly susceptible to immunologic events, graft failure, and graft loss.     

Heart ventricular activation in VAT difference maps from children with chronic kidney disease

Children with chronic kidney disease (CKD) are affected by cardiovascular complications, including disturbances in the intraventricular conduction system. Body surface potential mapping (BSPM) is a non-invasive method of assessing the cardioelectrical field. Our aim was to investigate conduction disturbances in young CKD patients using ventricular activation time (VAT) maps. Our study comprised 22 CKD children (mean age: 13.1 ± 2.5 years) treated conservatively and 29 control patients. For each child 12-lead electrocardiogram (ECG) readings were taken, and blood pressure and serum concentrations of iPTH, Pi, t-Ca, creatinine, Fe⁺³, ferritin, and Hb, as well as eGFR were measured. All children underwent registration in the 87-lead BSPM system, and group-mean VAT maps and a difference map, which presents statistically significant differences between the groups, were created. The VAT map distribution in CKD patients revealed abnormalities specific to left anterior fascicle block. The difference map displays the areas of intergroup VAT changes, which are of discriminative value in detecting intraventricular conduction disturbances. Intraventricular conduction impairments in the left bundle branch may occur in children with CKD. BSPM enables conduction disturbances in CKD children to be detected earlier than using 12-lead ECG. The difference map derived from the group-mean isochrone maps precisely localizes the sites of disturbed conduction in the heart intraventricular conduction system.     

Molecular approaches to urea transporters

Urea plays a critical role in the urine-concentrating mechanism in the inner medulla. Physiologic data provided evidence that urea transport in red blood cells and kidney inner medulla was mediated by specific urea transporter proteins. Molecular approaches during the past decade resulted in the cloning of two gene families for facilitated urea transporters, UT-A and UT-B, encoding several urea transporter cDNA isoforms in humans, rodents, and several nonmammalian species. Polyclonal antibodies have been generated to the cloned urea transporter proteins, and the use of these antibodies in integrative animal studies has resulted in several novel findings, including: (1) the surprising finding that UT-A1 protein abundance and urea transport are increased in the inner medulla during conditions in which urine concentrating ability is reduced; (2) vasopressin increases UT-A1 phosphorylation in rat inner medullary collecting duct; (3) UT-A protein abundance is upregulated in uremia in both liver and heart; and (4) UT-B is expressed in many nonrenal tissues and endothelial cells. This review will summarize the knowledge gained from using molecular approaches to perform integrative studies into urea transporter protein regulation, both in normal animals and in animal models of human diseases, including studies of uremic rats in which urea transporter protein is upregulated in liver and heart.