Initial assessment of children's ability to climb stair guarding.

This study examined the ability of children aged between four and six years to climb stair guarding set at the minimum height for domestic handrails recommended in the guidance given in Approved Document K that supports the Building Regulations in England and Wales. The purpose was to assess the adequacy of such safety guidance. Simulated guarding was set up at an indoor play centre and behaviours examined in two groups of children. Observations were made during free play and during solicited climbing. Results indicate that the majority of children aged between four and six years can climb onto or over stair guarding unassisted. Younger children are influenced and frequently abetted by their elders in climbing, behaviour which may be replicated in the home environment. Three distinct climbing strategies are observed: the body hoisted in a semi-prone position onto the top of the guarding; the body lifted by arms above the height of the guarding enabling a kneeling position on the top of the guarding; and, the knee bent against the side of the guarding to gain the added height required to make the climb. It was noted that older or taller children tend to rely on height, leg length or each whilst climbing whereas younger children appear to depend more on strength. A re-examination of safety guidance in relation to barrier climbability by children is recommended, and has started at BRE.

Medicaid audits and the dentist.

Dental Medicaid, an essential health adjunct for many indigent people, is seen from the standpoint of a New York State dentist auditor. A few professionals may be abusing the system to the detriment of the majority. How to follow the rules and avoid costly audits.

Subcellular pathologic features of glucocorticoid-induced hepatopathy in dogs.

Dogs are particularly susceptible to development of glucocorticoid-induced hepatopathy, but the mechanisms are not well understood. We investigated the pathogenesis of glucocorticoid hepatopathy by examining sequential morphologic and biochemical changes in the liver of dogs during steroid administration. Six adult Beagles were given prednisolone acetate (4mg/kg of body weight, once daily for 24 days IM). Serum samples and percutaneous liver biopsy specimens were obtained before the start of the study (treatment day [TD] 0) and at TD 5, 10, 15, and 25. There were significant (P < 0.05) and progressive increases in serum activities of alkaline phosphatase, gamma-glutamyltransferase, and alanine transaminase. Light microscopic changes in liver biopsy specimens included progressive hepatocellular swelling and vacuolation. Electron microscopy revealed glycogen accumulation, peripheral displacement of organelles, and prominent dilatation of bile canaliculi, compared with findings at TD 0. Liver biopsy specimens taken at TD 25 had significantly (P < 0.05) increased activities of the plasma membrane enzymes, alkaline phosphatase and gamma-glutamyltransferase, and 5'-nucleotidase was significantly (P < 0.001) decreased. Subcellular fractionation on reorientating sucrose density gradients revealed high-density peaks of alkaline phosphatase and gamma-glutamyltransferase, compatible with a specific increase in the biliary canalicular component of the enzyme activities. Neutral alpha-glucosidase activity was shifted to the denser fractions, indicative of an increase in the proportion of rough to smooth endoplasmic reticulum and consistent with enhanced synthesis of plasma membrane proteins. There also was evidence for progressive increase in fragility of intracellular organelles, particularly lysosomes. These findings indicate that glucocorticoid hepatopathy in dogs is associated with progressive alterations not only to the plasma membrane, but also to other subcellular organelles.

Hepatic organelle pathology in dogs with congenital portosystemic shunts.

Diversion of portal blood in congenital portosystemic shunts (CPSS) results in liver atrophy and passage of toxins into the systemic circulation causing hepatic encephalopathy. In some dogs, there is indirect evidence for hepatic insufficiency, but histologic findings are equivocal. This study determined whether hepatocyte integrity in PSS is comprised at a subcellular level using analytical subcellular fractionation of liver biopsies. Six dogs with CPSS had hypoproteinemia (6/6), increased serum alkaline phosphatase (6/6) and alanine aminotransferase (4/6) activity, hypocholesterolemia (6/6), and decreased blood urea (2/6). Liver biopsy specimens had increased activities (mU/mg protein) of alkaline phosphatase (17.9 +/- 10.1; controls 5.1 +/- 5.3: P less than 0.01), but not of other plasma membrane enzymes. There were increased activities of endoplasmic reticular (neutral alpha-glucosidase: 1.67 +/- 0.7; controls 0.86 +/- 0.2: P less than 0.01) and lysosomal enzymes (N-acetyl-beta-glucosaminidase: 12.6 +/- 2.3; controls 6.24 +/- 2.7: P less than 0.01; alpha-mannosidase: 0.85 +/- 0.5; controls 0.39 +/- 0.3: P less than 0.05). Subcellular fractionation on reorientating sucrose density gradients showed a high-density peak of alkaline phosphatase suggestive of a specific increase in the biliary canalicular component of enzyme activity. Neutral alpha-glucosidase was shifted to denser fractions, indicative of an increase in the proportion of rough-to-smooth endoplasmic reticulum and consistent with enhanced synthesis of membranous enzymes. There was also evidence for increased fragility of intracellular organelles, particularly lysosomes. In contrast, histology showed either no abnormalities or minor degenerative changes compatible with hepatic underperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Detection of growth hormone and growth hormone-releasing hormone-related messenger RNA in rat leukocytes by the polymerase chain reaction.

To validate that growth hormone (GH) and growth hormone-releasing hormone (GHRH) can be produced by leukocytes, we have assessed the presence of GH and GHRH-related mRNA in leukocyte cultures by reverse transcription and the polymerase chain reaction. A sample of the polymerase chain reactions were size-fractionated by electrophoresis in a 0.8% agarose gel and examined with ultraviolet light after ethidium bromide staining. Single major DNA bands corresponding in length to the distance between the 5' ends of the two GH and GHRH specific primers, 603 base pairs and 260 base pairs, respectively, were obtained. The DNA bands hybridized specifically to GH- and GHRH-specific probes after Southern transfer to nitrocellulose. The identity of the GH polymerase chain reaction material was confirmed by restriction enzyme analysis. The results showed that GH and GHRH gene expression occurs in mononuclear leukocytes and support the idea that these neuroendocrine hormones may be common signal molecules between the immune and neuroendocrine systems.

Biochemical changes in the jejunal mucosa of dogs with exocrine pancreatic insufficiency following pancreatic duct ligation.

The effects of exocrine pancreatic insufficiency on the small intestinal mucosa were examined in dogs following pancreatic duct ligation. There were no significant changes either in villus architecture or enterocyte height after duct ligation, but numbers of bacteria in duodenal juice increased then subsequently decreased following treatment with exogenous pancreatic enzymes. Pancreatic insufficiency resulted in a considerable increase in the proportion of microvillar membrane proteins of molecular mass over 200 kDa from 3.3 +/- 4 per cent (mean +/- SEM) to 13.6 +/- 7.2 per cent, and this decreased to 6.9 +/- 5.2 per cent following pancreatic enzyme supplementation. However, anticipated increases in activities of maltase and sucrase were not observed following duct ligation, and there was a reduction in lactase activity which was reversed by pancreatic supplementation. Activities of marker enzymes for the other subcellular organelles showed relatively minor or no changes throughout the study. These findings are consistent with a specific role for pancreatic enzymes in the post-translational processing of intestinal microvillar membrane proteins, and suggest that reduced degradation of brush border proteins in the absence of pancreatic secretions may be masked by quantitative and qualitative changes in the intestinal microflora.

Investigation of the physical properties of dog intestinal microvillar membrane proteins by polyacrylamide gel electrophoresis: a comparison between normal dogs and dogs with exocrine pancreatic insufficiency.

Procedures have been validated for the investigation of the physical properties of canine microvillar membrane proteins by SDS-polyacrylamide gel electrophoresis. These have been used to examine mucosal samples from eight control dogs and from five dogs with naturally occurring exocrine pancreatic insufficiency (EPI) in order to evaluate the potential role of the pancreas in the normal turnover of microvillar membrane proteins in the dog. Gel scanning showed that the proportion of total membrane protein in bands corresponding to a molecular mass greater than 200 kDa was up to 20-times higher in dogs with EPI than in control dogs. In particular, a band of apparent molecular mass 218 kDa represented between 8 and 28% of membrane protein in all affected dogs, compared with only 0.5 to 1.8% in controls, and is most likely to contain single chains of both pro-maltase-glucoamylase and pro-sucrase-isomaltase. Incubation of microvillar membranes in vitro with either trypsin or canine pancreatic juice resulted in degradation of this high molecular mass band and a corresponding increase in the amount of protein in three bands representing molecular masses of 150, 133 and 106 kDa. In samples from control dogs aminopeptidase N was identified in the 133 kDa band by Western blotting and incubation with monospecific antiserum. These findings suggest that pancreatic enzymes play a major role in the normal post-translational processing of intestinal microvillar membrane proteins in the dog.

Response of the jejunal mucosa of dogs with aerobic and anaerobic bacterial overgrowth to antibiotic therapy.

Dogs with naturally occurring aerobic or anaerobic bacterial overgrowth have been examined before and after antibiotic therapy in order to assess reversibility of damage to the jejunal mucosa. Histological changes in peroral jejunal biopsies were relatively minor before and after treatment, but sucrose density gradient centrifugation revealed specific biochemical abnormalities that responded to antibiotic therapy. Aerobic overgrowth was initially associated with a marked loss of the main brush border component of alkaline phosphatase activity; this recovered following treatment, suggesting that aerobic bacteria may cause reversible damage to the hydrophobic region of the brush border membrane. In contrast, anaerobic overgrowth was initially associated with a marked reduction in brush border density, indicative of a considerable fall in the glycoprotein-to-lipid ratio of the membrane. Density increased from 1.17 to 1.21 g/ml after antibiotic therapy, consistent with recovery from this relatively severe damage to the brush border caused by anaerobic bacteria. Reductions in soluble and peroxisomal catalase activities which could compromise mucosal protection against free radicals in dogs with aerobic overgrowth, and a loss of particulate malate dehydrogenase activity indicative of mitochondrial disruption in dogs with anaerobic overgrowth, were also reversed after treatment. These findings indicate that aerobic and anaerobic bacterial overgrowth can result in contrasting but potentially reversible damage to the jejunal mucosa which would not be detected by conventional investigative procedures.

Cardiac transplantation in patients over 50 years of age.

Sixty-two patients underwent cardiac transplantation at the University of Arizona from March 1979 to March 1985. Thirteen patients (11 men and 2 women) were over 50 years of age at the time of transplantation and 49 were under the age of 50. The mean age (+/- SEM) of the patients over 50 was 53 +/- 1 years. Eight of these patients were treated with conventional immunosuppressive therapy (azathioprine, prednisone and rabbit antithymocyte globulin) and five, beginning in January 1983, were treated with cyclosporine, prednisone and rabbit antithymocyte globulin. Early mortality (0 to 90 days) was 16% in the group over 50 versus 18% for those under 50. The late mortality (greater than 90 days) was 36 and 33%, respectively. In both groups, rejection and infection were the principal causes of death. The incidence of infection was 1.9 +/- 0.5 episodes per patient in those patients over 50 and 1.9 +/- 0.4 in those under 50. The incidence of rejection was 1.3 episodes per patient-year in patients over 50 and 1.7 episodes per patient-year in those under 50. Actuarial survival at 1 year was 72 +/- 14% in the group over 50 and 66 +/- 7% in the group under 50 years of age. These data indicate that the results of cardiac transplantation for patients over 50 do not differ significantly from those for patients under 50. Therefore, it is concluded that a rigidly defined age criterion for cardiac transplant recipients is not acceptable. Each potential recipient must be evaluated in terms of individual risk and benefit from the procedure.

The cardiac donor: a six-year experience.

From March 1, 1979, to March 1, 1985, the University of Arizona received 223 cardiac donor referrals. Sixty-two were accepted: 15 local, 23 regional (less than 370 km or 200 nautical miles), and 24 distant (370 to 1556 km or 200 to 840 nautical miles). Thirty-eight donor deaths were due to motor vehicle accidents, 10 to gunshot wounds, 6 to cerebral disease, and 8 to other closed-head lesions. The mean time from injury to brain death was 65 +/- 5 hours (+/- standard error of the mean [SEM]) and from brain death to organ donation, 12 +/- 3 hours. The mean ischemic time for the donor hearts ranged from 30 to 233 minutes (mean +/- SEM, 128 +/- 7 minutes). Fifty patients, otherwise acceptable, were refused as cardiac donors because an ABO-compatible recipient was not available. Two regionally procured hearts failed at operation, 1 because of unrecognized donor sepsis and 1 from a patient on large-dose inotropic support. Although there was no difference in myocardial function, median survival with follow-up through June 30, 1985, of patients receiving locally, regionally, and distantly procured organs was 59 months, 18 months, and 21 months, respectively. Cumulative proportion 1-year survival was 93%, 56%, and 61%, respectively. The 2-year survival was 85% for patients given locally procured hearts, 43% for those with regionally procured hearts, and 38% for those with a heart from a distant donor. Survival curves showed significantly longer survival for locally procured organs than regionally or distantly procured organs (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Returning to work after heart transplantation.

This study was designed to identify the determinants of postoperative work status among 47 heart transplantation patients at the University of Arizona Medical Center and to focus attention on those actions or policies that increase the probability that a patient will return to work within 6 months after transplantation. Issues regarding work status, disability, and early retirement have become increasingly salient. Case study methods were employed to assign each of the patients to one of four categories, which together form a typology of postoperative work status. Analysis of the patients identified four major variables of work status: age, length of disability before transplantation, control over working conditions including job redefinition/discrimination, and type of health insurance including cost of medication. Although these variables are interdependent, each also has an independent effect on postoperative outcome. The study concludes that although age and length of disability before transplantation cannot be directly affected, both control over working conditions and types of insurance are amenable to intervention.

Pericardiectomy for effusive constrictive pericarditis after heart transplantation.

The following is a case report of an unusual complication after heart transplantation. The patient was a 37-year-old man who underwent heart transplantation because of idiopathic cardiomyopathy. His postoperative course was complicated by cardiac tamponade, coagulopathy, and chronic constrictive pericarditis. After transplantation, he underwent three subsequent open-chest procedures: the first for tamponade, the second for Serratia mediastinitis, and the third for a pericardiectomy for constrictive pericarditis. Although constrictive pericarditis and pericardiectomy have been described following coronary bypass surgery and valve replacement, they have not yet been reported in a heart transplant recipient.

Cyclosporine: an immunosuppressive panacea?

Between March 29, 1979, and March 1, 1985, 62 heart transplants were done in 61 patients at the University Medical Center, University of Arizona. There were two treatment groups with nearly equal numbers in each; conventional immunosuppression (1979 to 1982) and cyclosporine (1982 to the present). Comparison of actuarial survival, number of rejection episodes, number of fatal rejection episodes, number of infections, and number of "other complications" failed to reveal any significant difference between the two groups. The cyclosporine-treated patients had a documented increase in blood urea nitrogen and serum creatinine accompanied by an increase in diastolic blood pressure. The length of hospital stay of the cyclosporine group was approximately one half of that of the conventionally treated patients, and they required fewer rehospitalizations. The cost for initial hospitalization was not significantly different between the two groups. Therefore, in 1979 dollars, the cost for cyclosporine-treated patients has decreased. This difference in cost was only minimally diminished by the difference in expenditure for outpatient pharmaceuticals, which was four times higher in the cyclosporine group. We believe that cyclosporine is a potent immunosuppressive agent but that it has toxic, possibly irreversible effects on the kidney. In view of the minimal differences that we were able to demonstrate in survival rejection and infection, it seems prudent to reduce or modify present doses of cyclosporine in an attempt to avoid irreversible renal damage.

The impact of transcutaneous electrical nerve stimulation on the postcesarean patient.

Nurses need to be actively involved in current research on TENS therapy. A thorough in-service training program for all nurses involved in the TENS program must be developed in order for nurses to knowledgeably assist their patients in maximal adaptation to TENS therapy. Transcutaneous electrical nerve stimulation therapy is not a panacea in postpartal pain management. It can be argued that TENS is another extension of technology interfering with the original natural simplicity of the birthing process; however, further research in the technique needs to be conducted before TENS can be rejected as such. Ultimately, the goal of postpartal care for the cesarean-birth family is to allow the parents to enjoy the birth experience without the dangers of the past and the, at times, unnecessary interference of the present. TENS therapy may be a means toward that end.