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T Sinclair

Publications and source records attributed to T Sinclair.

15 recordsLinked to original sources

Teaching undergraduates about familial breast cancer: comparison of a computer assisted learning (CAL) package with a traditional tutorial approach.

We have developed a computer assisted learning package for teaching clinical medical students about familial breast cancer. It explains the principles of genetic predisposition to breast cancer, the association with other cancers, the principles of family history taking and confirmation, risk assessment and possible interventions. Clinical medical students were randomised to either conventional teaching or CAL, 48 students attended the evaluation session. Students randomised to conventional teaching received a 20 min mini-lecture, those randomised to CAL completed the package with technical, but not academic support available. At the end of the intervention both groups of students completed a short written assessment of acceptability and knowledge and understanding of breast cancer genetics. There was no significant difference between the CAL and mini-lecture groups in terms of marks or acceptability. Thus CAL appears to be an acceptable and effective method of teaching clinical medical students about familial breast cancer. Although time consuming to develop, CAL can be used in a variety of settings to increase curriculum flexibility. Methods of motivating students to complete the CAL, and of providing educational support are being explored.

Breast Neoplasms↗

Priorities for adult cancer nursing research: a West Australian replication.

Two Delphi surveys have been conducted during the past 20 years to identify cancer nursing research priorities; one in the United States and one in Canada. Sir Charles Gairdner Hospital, the State Cancer Referral Centre in Western Australia, undertook a replication of this Delphi survey to identify nursing research priorities for adult cancer nursing. The aim of this replication was to identify possible changes in priorities and account for cultural difference in the healthcare systems. A total of 45 responses were received from the first Delphi round and 30 from the second. The top ten priorities identified by this sample were different from those identified in prior studies. The top ranked research topic was "What strategies would be most helpful in allowing nurses time to provide emotional support to cancer patients and carers?" These results may stimulate discussion and re-assessment of research priorities in other adult cancer care settings.

Adult↗

Developing a condition-specific measure of health for patients with dyspepsia and ulcer-related symptoms.

A patient-administered instrument for dyspepsia and symptoms suggestive of duodenal or gastric ulcer, based on the type of questions asked when taking a patient's history, was developed and tested using the following steps: literature reviews, devising the questions, testing the responses to the questions using factor analysis and internal consistency, assessing test-retest reliability, and validating the questionnaire by comparing patient responses to the SF-36 health survey questionnaire. The main sample consisted of 135 patients referred to an outpatient clinic with dyspepsia, and 152 patients in general practice who were not referred to a specialist. The final instrument produced a Cronbach's alpha of 0.72 and an intraclass correlation coefficient of 0.69. Patient scores on the dyspepsia questionnaire had small to moderate correlations with the SF-36 health survey, the largest correlation being with the SF-36 scale of pain. Patient scores were significantly related to general practitioner perceptions of symptom severity, family history of gastric ulcer disease, and whether the patient was referred. The questions asked in taking a clinical history from a patient with dyspepsia and other symptoms suggestive of ulcer disease can be used to construct a valid and reliable measure of the effect of dyspepsia on health.

Adult↗

Feasibility of monitoring patient based health outcomes in a routine hospital setting.

OBJECTIVE: To assess the feasibility of monitoring health outcomes in a routine hospital setting and the value of feedback of outcomes data to clinicians by using the SF 36 health survey questionnaire. DESIGN: Administration of the questionnaire at baseline and three months, with analysis and interpretation of health status data after adjustments for sociodemographic variables and in conjunction with clinical data. Exploration of usefulness of outcomes data to clinicians through feedback discussion sessions and by an evaluation questionnaire. SETTING: One gastroenterology outpatient department in Aberdeen Royal Hospitals Trust, Scotland. PATIENTS: All (573) patients attending the department during one month (April 1993). MAIN MEASURES: Ability to obtain patient based outcomes data and requisite clinical information and feed it back to the clinicians in a useful and accessible form. RESULTS: Questionnaires were completed by 542 (95%) patients at baseline and 450 (87%) patients at follow up. Baseline health status data and health outcomes data for the eight different aspects of health were analysed for individual patients, key groups of patients, and the total recruited patient population. Significant differences were shown between patients and the general population and between different groups of patients, and in health status over time. After adjustment for differences in sociodemography and main diagnosis patients with particularly poor scores were identified and discussed. Clinicians judged that this type of assessment could be useful for individual patients if the results were available at the time of consultation or for a well defined group of patients if used as part of a clinical trial. CONCLUSIONS: Monitoring routine outcomes is feasible and instruments to achieve this, such as the SF 36 questionnaire, have potential value in an outpatient setting. IMPLICATIONS: If data on outcomes are to provide a basis for clinical and managerial decision making, information systems will be required to collect, analyse, interpret, and feed it back regularly and in good time.

Adolescent↗

Venous ischemia in skin flaps: microcirculatory intravascular thrombosis.

Although endothelial cell injury and microcirculatory intravascular clotting have been implicated in the pathophysiology of skin-flap failure and various hematologically active drugs have been used to improve flap survival, the basic underlying pathophysiology has not been documented previously. In this study of venous ischemia in pig flaps, we focus on the accumulation and distribution of platelets and fibrinogen in the flap, on the morphologic changes in the flap microcirculation, and on changes in various coagulation factors in the venous effluent from the flap. Bilateral buttock skin flaps and latissimus dorsi myocutaneous flaps were designed and elevated on 12 pigs. All flaps had a primary ischemic insult (clamp application to the vascular pedicle) of 2 hours, followed by 2 hours of reperfusion, and then one side was subjected to a 6-hour period of secondary venous ischemia (clamp application to the dominant flap vein). In six animals, radioactively labeled autologous platelets and human fibrinogen were injected intravenously half an hour before termination of secondary venous ischemia. Flaps were weighed and counted for radioactivity. Flap biopsies and the buffy coat of venous effluent were processed for electron microscopy. In the other six animals, venous effluent was collected before secondary ischemia, upon immediate reperfusion, and at 4 and 8 hours after termination of secondary ischemia. Venous plasma levels of fibrinogen, von Willebrand factor, and antithrombin III were measured. Platelet and fibrinogen accumulation was increased in flaps with venous stasis when compared with control flaps at both time intervals studied; a twofold increase was seen prior to reperfusion, and a threefold increase was seen following 4 hours of reperfusion. Venous effluent could not be collected from buttock skin flaps because of slow reflow and clotting in the collecting system. In comparing the venous effluent of control flaps with that of venous ischemic latissimus dorsi flaps, hematocrit was significantly elevated. Blood samples collected for analysis of fibrinogen, antithrombin III, and von Willebrand factor could not be analyzed because of postcollection clotting. Electron microscopy showed extravasation of red blood cells and activated platelets, fibrin, and red blood cells in distended and partly disrupted capillaries. The venous ischemia reperfusion injury is associated with thrombosis in the microcirculation and alterations in consumption of coagulation factors. This study gives physiologic support for potential beneficial effects of treatment modalities that aim at counteracting the different components of thrombus formation.

Animals↗

Arterial ischemia in skin flaps: microcirculatory intravascular thrombosis.

Although endothelial cell injury and microcirculatory intravascular thrombosis have been implicated in the pathophysiology of skin-flap failure, the basic underlying pathophysiology has not been documented previously. This study focuses on the morphologic changes and the alteration in platelet, fibrinogen, antithrombin III, and von Willebrand factor levels in flaps injured by arterial ischemia and reperfusion. A thrombogenic arterial anastomosis model is compared with simple arterial clamping as methods to achieve flap ischemia. Bilateral buttock skin flaps and latissimus dorsi island flaps were elevated in 12 pigs. All flaps had a primary ischemic insult of 2 hours' duration by simple clamp application. During this interval, a thrombus-generating, microvascular anastomosis was prepared, and during a 2-hour period of reperfusion, laser Doppler and transiluminator monitoring of the vascular pedicle allowed documentation of embolic events from the thrombus-generating anastomosis. In group 1 (n = 6), the flaps were then subjected to 7 (buttock skin) and 5 (latissimus dorsi) hours of complete arterial ischemia by clamping. During the secondary ischemic period, the poor microanastomosis was resected and repaired. Radioactively labeled autologous platelets (111In) and human fibrinogen (125I) were injected intravenously half an hour before secondary reperfusion. After 4 hours of reperfusion, flap biopsies and venous effluent were collected and prepared for electron microscopic analysis. The flaps and control tissue were harvested and the radioactivity was counted. In group 2 (n = 6), flaps were subjected to 6 hours of secondary ischemia by using the same technique as in group 1. Central venous and flap venous blood was sampled at baseline as well as upon immediate secondary reperfusion and after 4 and 8 hours of reperfusion. The hematocrit, platelet count, fibrinogen, antithrombin III, and von Willebrand factor levels were determined for these intervals. Platelets and fibrinogen accumulated significantly in buttock skin flaps and in the latissimus dorsi skin and muscle components as compared with similar control tissue (p < 0.05). There was no significant difference in platelet or fibrinogen accumulation after comparing the two ischemic models. Electron microscopic studies showed occluded capillaries with activated platelets in the flaps. Control tissue showed very little capillary occlusion. Platelet count was significantly decreased both in central venous (p < 0.05) and in adventitial infolding flap venous blood (p < 0.025) during immediate reperfusion as compared with baseline. These findings confirm that microcirculatory intravascular thrombosis is implicated in skin-flap ischemia-reperfusion injury. This study provides physiologic support for treatment modalities aimed at counteracting the various components in the coagulation pathways responsible for thrombus formation.

Anastomosis, Surgical↗

Tissue plasminogen activator, plasminogen activator inhibitors, and activator-inhibitor complex in liver disease.

AIMS: To identify the relative contribution of plasminogen activators, particularly tissue plasminogen activator (t-PA) and specific plasminogen activator inhibitors (PAI-1, PAI-2), to the fibrinolytic changes associated with various types of liver disease or severe chemical and physical damage to the liver. METHODS: Platelet rich (PRP) and platelet poor plasma (PFP) from patients with alcoholic cirrhosis, primary biliary cirrhosis, hepatic malignancy, or paracetamol overdose, or who were undergoing partial hepatectomy or liver transplantation, were assayed for t-PA, PAI-1, t-PA-PAI-1 complex and PAI-2 antigen values using specific enzyme linked immunosorbent assays (ELISAs) developed in this laboratory. RESULTS: Appreciable increases in the plasma concentration of t-PA, PAI-1, and t-PA-PAI-1 were seen in patients with alcoholic cirrhosis, primary biliary cirrhosis, and hepatic malignancy. Liver damage due to paracetamol overdose and partial hepatectomy both resulted in a striking increase in plasma PAI-1 concentration, although concentrations of t-PA and t-PA-PAI-1 complex were less affected. Concentrations of t-PA, PAI-1, and t-PA-PAI-1 complex returned to near normal values after successful liver transplantation in a patient with chronic active hepatitis. PAI-2 was also detected in several patients with chronic liver disorders. CONCLUSIONS: Haemorrhage due to fibrinolytic bleeding is commonly associated with liver disease. The patients studied here all had appreciable increases in circulating t-PA antigen concentrations. This was associated with increased concentrations of PAI-1 antigen and t-PA-PAI-1 complex and the balance between activator and inhibitor did not result in systemic plasmin generation. Reduced PAI-1 activity in cirrhosis or a critical difference in the ratio of t-PA to PAI-1 concentrations may explain the enhanced plasminogen activator activity previously noted in cirrhosis but not metastatic disease. Reduced hepatic clearance of t-PA and t-PA-PAI-1 complex due to impaired liver function may account for increased concentrations of free and complexed t-PA.

Enzyme-Linked Immunosorbent Assay↗

Declining prevalence of hydrocephalus.

Data from the Glasgow Register of Congenital Anomalies were used to compare the recent prevalence of primary hydrocephalus with that of anencephalus and spina bifida. Between 1974 and 1985, the prevalence rates of all three conditions declined significantly and virtually in parallel, a phenomenon suggestive of a common aetiology.

Anencephaly↗

Trauma center verification.

Sanctioned trauma center designation began in the late 1970's to improve hospital capabilities to care for injured patients. Guided by criteria established by the American College of Surgeons Committee on Trauma and led by surgeons dedicated to improving trauma care, many states focused early on the quality of care issue only to later struggle with the political consequences that followed the designation process. Institutional commitment to trauma care was often stated but seldom measured. Unlike the designation process with its strong emphasis on capabilities assessment, the verification process focused on performance documentation. Confirmation was sought in response time of key personnel, completeness of registry database, and trauma death audits. Trauma Committee minutes were reviewed and prehospital personnel interviewed to confirm institutional involvement in paramedic education and overall EMS system design. Other areas of documentation included trauma education at all levels, research, nursing audits, and outreach programs. We conclude that trauma center designation and verification are both essential and complementary. Effective trauma system performance requires trauma center designation plus a verification process to confirm institutional commitment of these resources for optimal care of the injured patient.

Accreditation↗

T-suppressor cell chronic lymphocytic leukemia. Phenotypic characterization by monoclonal antibodies.

A patient with long standing seropositive rheumatoid arthritis developed lymphocytosis which phenotypically involved the cytotoxic/suppressor T-lymphocyte population. There are 10 reported instances of this new disease entity described as "chronic T-cell lymphocytosis with neutropenia" or "chronic suppressor T-cell lymphocytic leukemia." The disease is characterized by hepatosplenomegaly, neutropenia, and the frequent presence of rheumatoid factor without clinical evidence of rheumatoid arthritis. Splenectomy in our patient, as well as in other instances where undertaken, has been ineffective in alleviating the neutropenia. The peripheral blood lymphocytes in our patient were OKT-3+, OKT-5+, OKT-8+, OKT-11+, cALL-, OKT-6-, TdT-. They possessed ADCC but no NK activity and did not suppress PWM-induced B-cell differentiation in spite of the presence of Fc receptor for IgG. Since the lymphocytosis of OKT-8+ cells appears to be clonal, it is suggested that the disease be designated chronic suppressor T-cell lymphocytic leukemia.

Antibodies, Monoclonal↗

Rosette and blastogenesis inhibition by plasma from Hodgkin's disease and other malignancies. Positive correlation in State I and II Hodgkin's disease.

The simultaneous presence of both rosette- and mitogen-induced blastogenesis inhibitors was measured in the plasma from 29 patients with active Hodgkin's disease, 21 patients with advanced lung cancer, nine patients with diffuse histiocytic lymphoma, 25 patients with non-Hodgkin's lymphoma, and 17 patients with a variety of solid tumors. Only patients with active Hodgkin's disease consistently demonstrated factors which interfered with both rosetting and mitogenesis when normal allogeneic cells were utilized. While a similar proportion of patients with early and late Hodgkin's disease possessed plasma which could inhibit both tests, a significant correlation between these tests was observed only in Stage I and II disease. Varying degrees of inhibition of these tests was also observed when plasmas from patients with other malignancies were tested. Both lung cancer and histiocytic lymphoma plasma contained a factor which was capable of significantly inhibiting in the rosette assay when compared to normal human serum. Plasma from these patients also demonstrated inhibition of blastogenesis, but unlike Hodgkin's disease, no correlation between these activities could be demonstrated. Neither patients with diffuse or nodular lymphocytic lymphoma nor patients with solid tumors had significant plasma inhibition in either assay.

Hodgkin Disease↗