Biomedical subjects
R Hughes
Publications and source records attributed to R Hughes.
Dexamethasone treatment of rats receiving a sciatic nerve crush injury markedly diminished adherence of PC12 cells to a longitudinal section of the crushed sciatic nerve.
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A critical evaluation of the use of andragogical models in tackling social inequality in nursing education.
Issues related to inequalities within nurse education are explored by drawing on issues related to oppression and exploitation in general education, higher education and to the specific ways nurses (pre-registration and post-basic) are selected and taught. There is analysis of the way in which a holistic approach may be helpful in reducing inequalities, with specific reference being given to experiential learning and distance/open learning approaches. The role of the education system in creating and maintaining inequalities is explored in terms of rights, chances and educational outcomes.
The field of implantology--an overview.
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American Cancer Society Workshop on Adolescents and Young Adults with Cancer. Workgroup #2: Insurance and employability.
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Relationships between sensation seeking and use of caffeine, alcohol and cigarettes by New Zealand university students.
Form V of Zuckerman's Senation-Seeking Scale (SSS) was completed by a sample of psychology undergraduate students along with a questionnaire relating to their regular consumption of caffeinated and alcoholic beverages, and use of cigarettes. While there were no gender differences in the use of caffeine and cigarettes, men reported consuming nearly twice as much alcohol per week as women. Use of alcohol (but not caffeine or cigarettes) was positively related to sensation seeking in the form of thrill and adventure seeking, and boredom susceptibility for men, and disinhibition for both genders. Women generally achieved lower SSS scores than men. For both genders, caffeine use was positively related to cigarette, but not alcohol use. There were no relationships between the use of cigarettes and alcohol.
Infectious agents in reactive arthritis.
It is now clear that the deposition and persistence of bacterial antigens in the joint are significant features of reactive arthritis. It is possible that in some instances this represents persistence of live bacteria, and several studies point to the potential value of antimicrobial therapy. Searches for bacterial DNA and RNA have yielded conflicting data, however, so further developments in this area will be of great importance. It is likely that bacterial antigens interact in some way with class I major histocompatibility complex (MHC) antigens in the pathogenesis of reactive arthritis. However, with the increasing understanding of the structure and function of HLA molecules, some evidence of a classic antigen-class I MHC-CD8 T-lymphocyte interaction is now emerging. Thus far, the mechanisms that link HLA-B27 and bacterial antigens with reactive arthritis remain unclear.
Routine use of adjusted low-dose warfarin to prevent venous thromboembolism after total hip replacement.
The efficacy and safety of routine use of adjusted low-dose warfarin for twelve weeks--without sonography or venography--for the prophylaxis of deep-vein thrombosis after total hip replacement was assessed in 268 patients (134 men and 134 women) who were between the ages of forty and eighty-five years (average, sixty-one years). The patients were given warfarin orally both before and after the operation. The initial dose was usually ten milligrams on the night before the operation and five milligrams on the night after the operation. Thereafter, the dose was adjusted to keep the prothrombin time between fourteen and sixteen seconds. The control time was ten to twelve seconds. The partial thromboplastin time was also measured, and the dose of warfarin was reduced if the value was more than fifty seconds. All 268 patients continued to take low-dose warfarin for twelve weeks after the operation. There were 170 primary and ninety-eight revisional total hip-replacement operations. Thirty-four patients (13 per cent) had a history of thromboembolic disease or venous stasis in a lower limb. Neither phlebography nor sonography was done routinely. All of the patients were followed for six months after the operation. There were no fatal pulmonary emboli during the period of the study and no known pulmonary emboli after any patient was discharged from the hospital. Two non-fatal pulmonary emboli were identified, both during hospitalization. Ten patients (4 per cent) had an episode of major bleeding--a wound hematoma in nine and a gastrointestinal hemorrhage in one--during hospitalization.(ABSTRACT TRUNCATED AT 250 WORDS)
Reduction in factor VII, fibrinogen and plasminogen activator inhibitor-1 activity after surgical treatment of morbid obesity.
The aim of this study was to determine the effects of the surgical treatment of morbid obesity on some aspects of haemostatic and fibrinolytic function. Measurement of haemostatic and fibrinolytic factors was performed before and again 6 and 12 months after operation in 19 patients suffering from morbid obesity. Surgical treatment resulted in a mean decrease in body weight of 50 kg at 6 months and 64 kg at 12 months. Weight loss was accompanied at 12 months by significant reductions in median (interquartile range) concentrations of serum cholesterol from 5.3 (4.5-6.2) mmol/l to 3.6 (2.9-4.6) mmol/l; factor VII from 113 (92-145)% of normal to 99 (85-107)%; of fibrinogen from 3.5 (3-9.3) g/l to 2.8 (2.4-3.8) g/l; and of plasminogen activator inhibitor-1 (PAI-1) activity from 21 (11-30) IU/ml to 6.3 (5-10) IU/ml. The decrease in PAI-1 activity probably accounted for a significant reduction in euglobulin clot lysis time. Tissue plasminogen activator activity was undetectable in most patients pre-operatively but increased slightly after 1 year to 110 (100-204) mIU/ml. There were no significant changes in plasma levels of KCCT, factor VIII, von Willebrand factor antigen, alpha-2-antiplasmin, antithrombin III, protein C antigen, beta thromboglobulin, platelet factor 4, fibrinopeptide A or platelet count. These findings provide support for the hypothesis that the surgical treatment of morbid obesity may have a long-term beneficial effect on mortality from cardiovascular and thromboembolic disease.
Intracranial aneurysms in autosomal dominant polycystic kidney disease.
BACKGROUND AND METHODS: Intracranial aneurysms are a feature of autosomal dominant polycystic kidney disease, but their prevalence is uncertain. We studied 92 subjects with autosomal dominant polycystic kidney disease who had no symptoms or signs of any neurologic disorder. To determine the prevalence of intracranial aneurysms, we performed high-resolution computed tomography (CT) in 60 subjects, four-vessel cerebral angiography in 21, and both procedures in 11. RESULTS: Four of the 88 subjects in whom the radiologic studies were successfully completed had intracranial aneurysms (4 percent; 95 percent confidence interval, 0.1 to 9 percent), as compared with the prevalence of 1 percent reported for an angiographic study of the general population. Three of the four subjects had multiple aneurysms. Seven subjects for whom the results of CT studies were suspicious underwent cerebral angiography: two had aneurysms, and five had normal vascular structures that accounted for the suspicious results of tomography. Four subjects who had normal CT imaging studies also had normal angiographic examinations. Eight of the 32 subjects who underwent angiography (25 percent) had transient complications, as compared with 22 of 220 control subjects (10 percent) who did not have polycystic kidney disease (P less than 0.05). We could not identify any risk factor in these subjects that was related to the occurrence of aneurysm. CONCLUSIONS: Asymptomatic intracranial aneurysms appear to be more frequent in people with polycystic kidney disease than in the general population, although our 95 percent confidence interval includes the possibility of no difference. Because cerebral angiography is associated with increased morbidity in people with polycystic kidney disease, we recommend high-resolution CT as a screening test.
Subacute idiopathic demyelinating polyradiculoneuropathy.
Seven cases of subacute idiopathic demyelinating polyradiculoneuropathy had a monophasic illness characterized by progressive weakness of all four limbs that evolved during 4 to 8 weeks. Neurophysiological investigations implied demyelination in all seven cases. In two patients, sural nerve biopsy specimens that were taken showed macrophage-associated demyelination. All patients made substantial or complete recoveries with oral prednisolone (four cases) or without treatment (three cases). None of the patients required ventilation or had autonomic complications. These cases provide a link between the acute idiopathic demyelinating form of Guillain-Barré syndrome and chronic idiopathic demyelinating polyradiculoneuropathy.
Sural nerve biopsies in Guillain-Barre syndrome: axonal degeneration and macrophage-associated demyelination and absence of cytomegalovirus genome.
T-cell infiltration was detected by immunohistochemistry in only 2 of 10 sural nerve biopsies from patients with Guillain-Barré syndrome (GBS). The number of endoneurial macrophages, identified by the monoclonal antibody MAC 387, was increased, compared with the number in 10 cases of axonal neuropathy. Macrophage-associated demyelination was identified in 7 and axonal degeneration in 8 cases. Cytomegalovirus (CMV) genome was not detected with the polymerase chain reaction.
Reactive arthritis: the role of bacterial antigens in inflammatory arthritis.
For more than 100 years it has been suspected that bacteria or products derived from them are deposited in joints and cause arthritis without suppuration. Over this time a vast amount of evidence, much of which is still unchallenged, has accumulated to demonstrate that whole bacteria and subcellular bacterial elements do pass, under certain circumstances, from sites of mucosal colonization or infection into the circulation and thence into joints. Similarly, experimental studies have demonstrated that the deposition of both inert material and bacterial components within synovium is sometimes, but not always, associated with the development and persistence of synovitis. In human reactive arthritis aseptic synovitis follows localized bacterial infection in the gut or genitourinary tract. A genetic predisposition, associated with the HLA B27 antigen, is recognized, and interaction between class I HLA determinants and bacteria-derived antigens may underlie the development of arthritis. Although much remains to be learned about the dissemination of antigens from the primary site of infection in reactive arthritis, strong evidence implicates the deposition of antigenic elements of Chlamydia, Yersinia, Salmonella and perhaps other micro-organisms within the synovium. Immunological findings support the notion that such antigens are being presented within the joint and participating in the induction and/or maintenance of synovitis. It is not yet clear whether such bacteria are complete or viable or whether persistence at an extra-articular site is important to the persistence of arthritis. The possibility that reactive arthritis, and perhaps other forms of seronegative arthritis also, is caused and perpetuated by bacterial antigens within the joint poses new questions about the role of HLA B27 in pathogenesis. It also raises important and exciting issues regarding treatment. Already, studies of antimicrobial therapy have yielded encouraging initial findings, and it is now possible to design and evaluate therapies aimed at blocking specific antigen recognition within the joint.
Nonlinearity of human arterial pulse wave transmission.
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Synovial T lymphocyte-specific immune response to Chlamydia trachomatis in Reiter's disease.
We studied the lymphocyte proliferative response to Chlamydia trachomatis in Reiter's syndrome (RS) compared with that in other rheumatic diseases. RS patients showed significantly increased C trachomatis-specific synovial fluid (SF) T cell proliferation. Proliferating cells were found in both CD4+ and CD8+ T cell subsets. The SF lymphocyte proliferative response to C trachomatis in RS was inhibited by anti-class I and class II major histocompatibility complex monoclonal antibodies, while the response to tuberculin purified protein derivative was inhibited only by anti-class II monoclonal antibodies. T cell receptor gamma/delta-bearing T cells were not consistently increased in RS SF compared with peripheral blood, nor did such cells consistently expand upon in vitro culture with C trachomatis. Finally, there was no correlation between the cellular immune response and levels of antibody to C trachomatis antigens. Our results indicate that a specific T cell response to C trachomatis within the joint plays a role in the pathogenesis of RS.
Temperature, time-of-night of testing, and responsiveness to stimuli presented while sleeping.
The present study examined how time-of-night of testing and body temperature related to responsiveness to stimuli presented in sleep. Nine males slept for two nonconsecutive nights in the sleep laboratory. On Night 1, tympanic temperature was assessed at 30-min intervals. On Night 2, responsiveness was assessed with an incremental series of tones (5dB steps) presented in sleep stages 2, 3/4, and REM throughout the night (0030-0800 h). Subjects were instructed and given practice prior to sleep to make a microswitch closure to the tones. Results showed a curvilinear pattern of responsiveness across the night in that the intensity of tones required for a response increased until about 0530 h, then decreased thereafter. This pattern of responsiveness was positively related to the circadian rhythm of body temperature. A close correspondence was also found between the temperature trough and the performance trough (both occurred at about 0530 h). A greater emphasis on circadian factors may help understand previously reported but contradictory findings. The present results also suggest that measures of responsiveness follow a circadian pattern regardless of the sleep/wake state.