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Biomedical subjects

J H Winter

Publications and source records attributed to J H Winter.

At least 37 records · Page 2Linked to original sources
PubMed1988

How to deal with a hospital outbreak of Legionnaires' disease.

The outbreak of Legionnaires' disease in Glasgow Royal Infirmary is discussed together with the problems such an outbreak poses to the microbiologist. The importance of early diagnosis is stressed. The outbreak was managed by a team drawn up from various disciplines within the hospital. Frank daily reports to the press, together with regular staff meetings with staff representatives helped to allay public anxiety. The subsequent maintenance and monitoring of the wet cooling tower required for the hospital ventilation system have resulted in considerable additional work for the microbiology department but especially for the hospital engineers.

Bacteriological Techniques↗
PubMed1988

Evidence linking familial thrombosis with a defective antithrombin III gene in two British kindreds.

Using DNA probes in a structural study of the antithrombin III gene locus we found no evidence of gene deletion in two British kindreds with inherited antithrombin III deficiency. However, linkage analysis between a common DNA polymorphism and the antithrombin III deficiency trait showed that the defect lies at or close to the antithrombin III structural gene. The lod score for linkage within the larger Scottish kindred was 3.1 (theta = 0). These results are consistent with previously published data suggesting that mutation of the antithrombin III structural gene is the cause of inherited antithrombin III deficiency in some families.

Antithrombin III↗
PubMed1987

Rapid diagnosis of an outbreak of Legionnaires' disease at Glasgow Royal Infirmary.

In the last three months of 1985 there was an outbreak of legionnaires' disease at Glasgow Royal Infirmary affecting 15 patients and one surgeon; five patients died. Legionnaires' disease was first suspected when a second case of severe nosocomial pneumonia occurred in a high dependency unit. The application of the direct fluorescent antibody test to specimens obtained at bronchoscopy was responsible for the rapid diagnosis of legionnaires' disease, which led to the prescription of appropriate antibiotic treatment and the shutting down of the contaminated cooling tower, thereby containing the outbreak. It also led to a search for further cases. It is suggested that these diagnostic techniques should be included in the investigation of affected patients in an outbreak of pneumonia.

Aged↗
PubMed1986

Secondary amyloidosis in association with Aspergillus lung disease.

Three patients with amyloidosis secondary to bronchiectasis are described: in two patients bronchiectasis was secondary to allergic bronchopulmonary aspergillosis and in the third, post-tuberculous bronchiectasis was complicated by asthma and allergy to Aspergillus. We suggest that chronic Aspergillus allergy may cause amyloidosis and that some cases of amyloidosis ascribed to tuberculosis in the past may in fact have been secondary to Aspergillus allergy.

Amyloidosis↗
PubMed1986

Life-threatening respiratory failure due to a previously undescribed myopathy.

The case of a young man with a previously undescribed myopathy associated with polydactyly is reported. Although both limb girdles were affected, the major effect of the disease was upon the respiratory muscles leading to his presentation with life-threatening respiratory failure. A further feature was pronounced stiffness of the vertebral column and limb girdles, similar in some respects to the 'rigid spine syndrome'. Muscle biopsy appearances were unique but showed some similarities to both nemaline myopathy and myotonic dystrophy. Ventilatory assistance at night using a rocking bed led to a marked improvement and has enabled the patient to return to full-time employment.

Adult↗
PubMed1984

Prophylactic antithrombotic therapy with stanozolol in patients with familial antithrombin III deficiency.

Three patients with familial antithrombin III deficiency underwent a trial of prophylactic antithrombotic therapy with stanozolol. An increase in plasma fibrinolytic activity and antithrombin III was seen. Acute venous thrombosis occurred in two patients; in the first patient thrombosis was precipitated by venography but in the second no precipitating factor was found. Our experience suggests that stanozolol is not a suitable prophylactic agent in patients with familial antithrombin III deficiency.

Antithrombin III↗
PubMed1983

Preoperative antithrombin III activities and lipoprotein concentrations as predictors of venous thrombosis in patients with fracture of neck of femur.

The presence or absence of venous thrombosis was determined by the technique of autologous 111indium-labelled platelets in 64 patients following reduction and fixation of fractures of the neck of femur. Venous thrombosis was found in 41 (64%) of these patients. Compared to the thrombosis-negative group, the thrombosis-positive group had a significantly lower mean serum antithrombin, and higher mean antithrombin consumption during clotting in the immediate preoperative period. No significant differences were seen between the two groups in plasma ATIII activities, fibrinogen, alpha-2-macroglobulin, serum lipoproteins or age. Significant correlations were seen between ATIII activities and lipoprotein fractions; these are discussed.

Adult↗
PubMed1983

Frequency of venous thrombosis in patients with an exacerbation of chronic obstructive lung disease.

The presence or absence of venous thrombosis was determined in 29 patients with an acute exacerbation of chronic obstructive lung disease by the technique of autologous platelet labelling with indium-111. Deep venous thrombosis was diagnosed in 13 patients and in nine of these patients thrombosis was located proximal to the knee--that is, in areas associated with an appreciable risk of pulmonary embolism. One patient died; pulmonary emboli were found at postmortem examination. The incidence of venous thrombosis seen in this study is high enough to suggest that these patients may benefit from prophylactic antithrombotic treatment.

Aged↗
PubMed1982

Lipoprotein fractions and antithrombin III consumption during clotting.

Plasma and serum antithrombin levels were measured in functional (initial rate measurement) and immunological assays together with serum lipid levels in normal subjects and patients with coronary artery disease. Specific antithrombin activity in plasma showed a negative correlation with triglyceride levels. The consumption of antithrombin activity during blood clotting was negatively correlated with both serum total triglyceride and heparin precipitable lipoprotein and positively correlated with serum high density lipoprotein cholesterol. Different blood lipoprotein fractions may influence the activity of the antithrombin III molecule.

Adult↗