We report here a new and critical determinant of the effectiveness of hand hygiene procedures, namely the amount of residual moisture left on the hands after washing and drying. When samples of skin, food and utilities were touched with wet, undried hands, microbial numbers in the order of 68000, 31000 and 1900 respectively translocated to these representative surfaces. Bacterial numbers translocating on touch contact decreased progressively as drying with an air or cloth towel system removed residual moisture from the hands. A 10 s cloth towel-20 s air towel protocol reduced the bacterial numbers translocating to skin, food and utilities on touch contact to 140, 655 and 28 respectively and achieved a 99.8, 94 and 99% reduction in the level of bacterial translocation associated with wet hands. Careful hand drying is a critical factor determining the level of touch-contact-associated bacterial transfer after hand washing and its recognition could make a significant contribution towards improving handcare practices in clinical and public health sectors.
After different methods of hand preparation, volunteers rolled segments of sterile central venous catheter between their fingertips, and bacterial transfer was evaluated by standardized quantitative culture. The number of bacteria transferred differed between methods (P<0.001). Comparisons were made with the control group (no preparation at all; median, third quartile and maximum count=6.5, 24, 55). Bacterial transfer was greatly increased with wet hands (1227, 1932, 3254; P<0.001). It was reduced with a new rapid method, based on thorough drying with a combination of 10 s using a cloth towel followed by either 10 or 20 s with a hot-air towel (0, 3, 7 and 0, 4, 30, respectively; P=0.007 and 0.004, respectively). When asked to follow their personal routines, 10 consultant anaesthetists used a range of methods. Collectively, these were not significantly better than control (7.5, 15, 55; P=0.73), and neither was an air towel alone (2.5, 15, 80; P=0.176) nor the hospital's standard procedure (0, 1, 500; P=0.035). If hand preparation is needed, an adequate and validated method should be used, together with thorough hand drying.
The effect of diabetes mellitus vs the effect of the Ren2 gene on the glomerular pathology of (mREN-2)27 heterozygous male rats is controversial. As discrete diabetes-induced glomerular lesions may have been overlooked, we performed a detailed morphometric analysis of glomeruli in diabetic and non-diabetic heterozygous male (mREN-2)27 rats and their normotensive (non-diabetic and diabetic Sprague-Dawley) controls. Glomeruli were scored by light microscopy for nine discrete histological parameters, some of which were graded for extent and/or severity. Mesangiolysis, segmental hypocellularity, and severe tuft-to-capsule adhesions were specific to diabetes; severe mesangial matrix expansion, glomerulosclerosis, thickening of Bowman's capsule, and dilatation of the urinary space were specific to the Ren2 gene. Hyalinosis and hypercellularity were associated with both diabetes and the Ren2 gene: the effect was additive for hyalinosis and synergistic for hypercellularity. The histological parameters were then combined with two physiological indices (systolic blood pressure and proteinuria) and principle components analysis (PCA) was used to detect correlations between the variables. Four discrete patterns of pathology were identified; three were statistically associated with diabetes and/or the Ren2 gene. These findings suggest that both diabetes and the Ren2 gene make significant, albeit different, contributions to the glomerular pathology of diabetic heterozygous male (mREN-2)27 rats. Despite defining the contribution of diabetes, our work does not support the (mREN-2)27 rat as a model of diabetic nephropathy (DN). Rather, it suggests that these animals remain useful for investigating a particular and limited constellation of DN features. There are numerous rodent models of human diabetic nephropathy (DN), attesting to the uncertainty associated with many of them. 1,2 Streptozotocin (STZ), which induces hyperglycemia by selectively damaging pancreatic b cells, has been administered to genetically modified rodents to create a variety of DN models. [3][4][5][6] The validity of one of these models, the diabetic (mREN-2)27 rat, has been questioned because of the apparent overwhelming impact of its genetically mediated hypertension on renal pathology. 7 One group of investigators reported that STZ-induced diabetes in female heterozygous (mREN-2)27 rats recapitulates the proteinuria, nodular glomerulosclerosis, and progressive loss of renal function that are cardinal features of DN in human beings. 6 However, other investigators suggest that the survival and kidney pathology of male heterozygotes is determined more by hypertension than by diabetes, as the presence of diabetes in these animals seemed to exert little phenotypic effect. 7 A sexual dimorphism in hypertension is apparent from the lower blood pressure of female vs male (mREN-2)27 rats. 8 This dimorphism has been proposed to underlie the apparent gender-dependent variation in experimental outcome because the effects of diabetes might only be observed in kidneys ...
Objective To determine the level of bacterial contamination associated with touch contact of a connector set during peritoneal dialysis (PD). Design The experiment utilized a laboratory-based simulation of a bag exchange procedure. Deliberatetouch contamination of the connector set spike was followed by quantitative recovery of micro-organisms from the connector and, in some cases, the dialysis bag. Subjects Patients undergoing PD were used as the “test” group. Departmental secretarial and laboratory staff served as the comparative control group. Setting The patients were voluntary subjects from a PD outpatients unit and were tested in their own homes. Outcome The numbers of micro-organisms contaminating a connector set and entering the dialysis bag during a touch-contamination event were determined. Additionally we identified hand hygiene and, in particular, the care taken to dry the hands after washing as being highly relevant to microbial touch-contamination levels. Patient hand disinfection, as practised in most PD units, effectively reduced touch contamination to low levels. Results Touch contamination of a connector set with unprepared hands led to fewer than 100 micro-organisms translocating from fingers to the spike. If the hands were washed but not dried before touch contact was made, up to 4500 micro-organisms trans located to the connector set spike. Air-towel drying of washed hands before touch contact reduced the translocating numbers by 95% -99%. Hand disinfection, as routinely practiced by PD patients, reduced the bacterial numbers reaching the peritoneal cavity after touch contamination to <5. The range of micro-organisms isolated from the fingers of PD patients using hand disinfectants on a regular basis showed considerably more diversity than the control group. Conclusion Hand care prior to bag exchange has a major effect on touch-contamination levels. Accidental touch contact of connecting devices by unprepared hands using a PD-bag exchange procedure leads to the translocation of 500 micro-organisms or fewer to the connector device. If the hands are wet at the time of contact the number translocating can be as high as 4500. Hand drying with an air towel before touch contact reduces the numbers translocating by 95% -99%. Hand disinfection procedures carried out prior to bag exchange minimizes touch-contamination levels.
Hill JV, Findon G, Appelhoff RJ, Endre ZH. Renal autoregulation and passive pressure-flow relationships in diabetes and hypertension. Am J Physiol Renal Physiol 299: F837-F844, 2010. First published July 21, 2010 doi:10.1152/ajprenal.00727.2009.-We investigated renal hemodynamics in isolated, perfused kidneys from rat models of diabetes and hypertension. Autoregulation and passive vascular responses were measured using stepped pressure ramps in the presence of angiotensin II (pEC50) or papaverine (0.1 mM), respectively. Male diabetic heterozygote m(Ren2)27 rats were compared with three male control groups: nondiabetic, normotensive Sprague-Dawley (SD) rats; nondiabetic, hypertensive heterozygote m(Ren2)27 rats; and diabetic, normotensive SD rats. Kidney function (proteinuria, creatinine clearance) was monitored before induction and at monthly intervals. Vascular function was measured in vitro in rats of induction age (6 -8 wk) and at 2 and 4 mo postinduction. Renal flow correlated with age, but not diabetes or the Ren2 gene. Kidney weight-specific and body weightspecific renal flow differed between diabetic and nondiabetic rats because diabetic rats had higher kidney but lower body weights. Kidneys from all groups showed effective autoregulation in the presence of angiotensin II. The autoregulatory pressure threshold of m(Ren2)27 rats was higher, and the autoregulation pressure range was wider, compared with SD rats. When vascular smooth muscle activity was blocked with papaverine, pressure-flow responses differed between groups and with time. The m(Ren2)27 rat groups showed higher renal vascular resistance at lower pressures, suggesting greater vascular stiffness. In contrast, diabetic SD rat kidneys demonstrated reduced vessel stiffness. Flow was impaired in diabetic m(Ren2)27 rats at 4 mo, and this correlated with a decline in creatinine clearance. The results suggest that the characteristic late decline in renal filtration function in diabetes-and hypertension-related renal disease follows changes in renal vascular compliance. change in vascular conductance; vascular remodeling DIABETIC NEPHROPATHY (DN) is the most common cause of end-stage renal failure (ESRF) in the Western world (24). Clinical progression of DN follows a relatively well-defined course characterized by early microalbuminuria, renal hyperfiltration and hyperperfusion, and increased capillary permeability to macromolecules. DN occurs late in diabetes, generally becoming apparent 15-25 yr after onset (8). However, glomerular basement membrane thickening begins less than 2 yr after onset of diabetes and is followed by mesangial matrix expansion. The final stage leading to ESRF is a progressive decline in glomerular filtration rate (GFR) (8,24).Progressive deterioration of renal function is commonly due to diabetes and hypertension, both separately and together. The causes of hypertension are multifactorial and diabetes is characterized by multiple potential mediators of progressive renal injury, including hyperglycemia, hypertension, endothe...
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