No description available.

The liver is a target tissue for Vitamin A toxicity. High doses of Vitamin A have been shown to produce hepatomegaly, portal hypertension, fatty liver, and hepatic degeneration and fibrosis. Of concern to us was the potential interactions of Vitamin A with other known or potential hepatotoxicants. Male SD rats (18o-200 gm) were given Vitamin A (retinol, 250,000 IU/Kg) daily for 7 days by oral gavage. 24 hr after the last dose of Vitamin A, they were then challenged with CCl₄ (0.15 ml/Kg, ip). Ethane, as a marker of lipid peroxidation, was measured during the first 2 hr and hepatic injury was assessed at 24 hr after CCl₄. There was approximately 5-fold increase in ethane exhalation and 17-fold increase in Plasma GPT activity in Vitamin A/CCl₄ group. There was also increase in the incidence of hepatocellular necrosis. Vitamin A pretreatment did not increase the metabolism of 14CCl₄ as examined by the amount of exhaled ¹⁴CO₂, and the covalent binding of ¹⁴C-equivalents to liver lipids and proteins. In addition, liver levels of Vitamin E or GSH were not changed by Vitamin A. Electron microscopic analysis of livers from Vitamin A treated rats revealed activated Kupffer cells. To determine if the Kupffer cells were functionally more active, the clearance of intravenously administered colloidal carbon from the blood of Vitamin A treated rats was compared to that of control rats. It was found that Vitamin A treated rats cleared carbon particles three times faster than that of controls. Therefore, we hypothesized that Vitamin A activation of Kupffer cells may be the mechanism of potentiation of liver injury. When stimulated, these activated cells could release active oxygen species which could promote peroxidation of hepatocyte membranes and potentiate CCl₄-induced liver injury. To test this hypothesis animals were treated with superoxide dismutase or catalase to catalyze the degradation of active oxygen species; or with methyl palmitate to deactivate Kupffer cells. Superoxide dismutase, catalase or methyl palmitate completely inhibited the Vitamin A potentiation of CCl₄ induced liver injury, but did not alter the toxicity of CCl₄ in non-Vitamin A treated rats. In addition, these agents inhibited the enhanced lipid peroxidation observed in Vitamin A treated rats administered CCl₄. Therefore, we conclude that the Vitamin A potentiation of CCl₄ induced liver injury results from Vitamin A's ability to activate Kupffer cells. Upon minimal hepatocellular injury produced by CCl₄, these activated Kupffer cells are stimulated to release activated oxygen species. It is these reactive intermediates that induce the enhanced lipid peroxidation that results in the potentiated response.

Cyclosporin A (CsA) was incubated at concentrations of 5.0 x 10⁻⁶ M for 72 hours, and at concentrations of 1.0 and 0.5 x 10⁻⁶ M for 30 days with kangaroo rat proximal tubular epithelial cells (PtK₂) in order to evaluate its effects on the cytoskeleton. Alterations in the cytoskeleton were assessed by indirect immunofluorescence of viable cells, and by two dimensional electrophoresis of a high salt extract from the cells. There is a selective alteration of the cytokeratin intermediate filament organization in both the short term (5 x 10⁻⁶ M, 72 hr) and long term (1 and 0.5 x 10⁻⁶ M, 30 days) exposures. There are either peri-nuclear rings formed or the formation of a single aggregate clump of the cytokeratins within the cytoplasm. Other components of the cytoskeleton, the microtubules and the microfilaments remain unaffected at both short term and long term exposures. Along with this cytokeratin alteration in CsA exposed cells is the decrease or elimination of an acidic triplet of cytokeratin protein monomers, human equivalent K15 (50 kd), K16 (48 kd), K17 (46 kd). This may be related to CsA-associated nephrotoxicity.

No description available.

No description available.

Being involved in soccer in Rwanda at both national and international level exposes soccer players to the risk of injury. The aim of this study was to identify common soccer injuries among the 1st and 2nd division soccer teams in Rwanda and to establish the need for physiotherapy intervention. This deals with the first two stages of injury prevention, which included identification and description of the extent of the problem and the identification of factors and mechanisms that play a part in the occurrence of injuries.

This thesis includes a review of scientific studies of tree injuries following mechanized thinning. Interviews have been made with drivers of single grip harvesters and forwarders in forest thinning and a number of essential factors have been identified as the most important to take into account in order to minimize and/orprevent injuries to stems and roots of remaining trees.

This work used <i>Pax6</i>^+/- mice as a model for Pax6-realted corneal diseases and assessed the roles of oxidative stress and epithelial injury in the aetiology of ARK. Histological investigation revealed epithelial lesions in <i>Pax</i>6^+/- corneas. Proteomic analysis demonstrated reduced levels of protective enzymes, transketolase, aldehyde dehydrogenase 3A1 and glutathione S-transferase α4, and cytoskeletal proteins. Keratin 5 and 12 in <i>Pax</i>6^+/- adult mouse corneas. These physical/structural and chemical defects imply that <i>Pax</i>6^+/- corneas may be in a chronic ‘stressed and wounded’ state. Using a DNPH/protein oxidation assay, <i>Pax</i>6^+/- corneal protein oxidation was found to be consistently higher than that in <i>wild-type</i> (WT), and to get worse with age, in parallel with the development of corneal opacity. H₂O₂ was used to induce oxidative stress in mouse corneas and this was found to activate the Ca²⁺ (protein kinase C/ phospholipase C) → p38/p42/p44 mitogen activated kinase signalling pathway. Oxidative stress-induced Pax6 exclusion form cell nucleus led to abnormal expression of non-corneal epithelial markers, indicating a metaplasia process that may cause normally transparent epithelial cells to become opaque. This report for the first time describes cytoskeleton architectures <i>in vivo</i> using flat-mount mouse corneal epithelial by fluorescent staining and confocal microscopy, which is potentially applicable to studies interested in cytoskeleton <i>in vivo</i>. Keratin, desmoplakin and actin cytoskeletal structures were found to be heterogeneous and defective in <i>Pax</i>6^+/- cells. Twenty-one hours after wounding WT corneal epithelia <i>in vivo</i>, healing cells developed desmoplakin and actin structural features, intercellular gaps, interdigitated filopodia-like processes and vesicles similar to the unscratched <i>Pax</i>6^+/- corneal epithelia. These data support the hypothesis of a ‘chronic wounded’ state in apparently uninjured <i>Pax</i>6^+/- corneal epithelia and reveal the cytoskeletal origins of poor adhesion and cellular structure.

This thesis examines the administrative separation process and attrition documentation as well as the characteristics of recruits who attrite from the U.S. Navy's Recruit Training Command (RTC). A random sample of 754 "retained files" from Customer Service Desk RTC was examined for attrition documentation and the information obtained was compared with attrition documentation contained in the Corporate Enterprise Training Activity Resource System (CETARS). The comparison is used to determine the accuracy of CETARS in documenting the reasons for medical and psychiatric attrition and its relationship to Separation Program Codes (SPD) listed on the DD 214 discharge form. The results indicate that CETARS is 95.2 percent accurate in documenting medical reasons for attrition and 94.2 percent accurate for psychiatric reasons. It was unclear whether a relationship existed between SPD codes and CETARS in documenting attrition. The specific reasons for psychiatric attrition include the following: Personality Disorder, Adjustment Disorder, Borderline Personality Disorder, and Attention Deficit Hyperactivity Disorder. In addition to the analysis of attrition documentation, we analyzed data on 216,028 recruits entering RTC between fiscal year 2000 and 2004 to determine the predictors of non-psychiatric attrites versus psychiatric attrites. Logit regression found that the predictors of both types of attrition were similar.

Dissertation submitted in partial compliance with the requirements for the Master's Degree in Technology: Chiropractic, Durban Institute of Technology, 2005. / Damage to the proprioceptive organs, as well as lack of proprioceptive retraining, after an inversion ankle sprain, has been shown to contribute to the problem of recurring ankle joint injuries, which has the highest incidence of sports related injuries. The proprioceptive organs are important as afferent pathways in reflexes and for the adjustment of posture and muscle tone (Miller and Narson, 1995 and Jerosch and Bischof, 1996). Manipulation is thought to cause a change in the afferent pathways of the manipulated joints and it is proposed that this change may restore normal proprioceptive input, in a previously injured joint (Wyke, 1981 and Slosberg 1988). This however is unproven as indicated in a study by Lephart and Fu, (1995), where techniques to improve proprioception remain untested and according to Brynin and Farrar (1995), screening for proprioceptive and neuromuscular co-ordination should be carried out as part of a chiropractor's physical examination and injury evaluation. This was a qualitative pre-post clinical study. Forty (40) subjects between the ages of 25 and 45, who had been diagnosed with chronic ankle instability syndrome, were recruited. The only treatment they received was a single mortise separation adjustment and all participants received the same treatment. Clinical outcomes were measured before and after the adjustment on both ankles using a Dualer Electronic Inclinometer and algometer. Only the affected ankle received an adjustment, but both ankles were measured. The participants were evaluated by the examiner at an initial consultation during which diagnosis of chronic ankle instability syndrome was made based on case history, physical examination and foot and ankle regional examination. Participants presented with at least four of the following (Kessler and Hertling 1983) / M