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Biomedical subjects

J M Hopkin

Publications and source records attributed to J M Hopkin.

At least 91 records · Page 5Linked to original sources
PubMed1990

A sequential ultrastructural study of rat lungs infected with Pneumocystis carinii to investigate the appearances of the organism, its relationships and its effects on pneumocytes.

A sequential study of the lungs of rats infected with Pneumocystis carinii is reported. The aim was to investigate variations in the appearance of the organism from the inception of infection until the death of the host and, during this period, the relationships of the organism with one another and changes occurring within pneumocytes. Trophozoites predominated at all stages of infection and were those first recognized but no clear role for the filopodia was evident. Organisms were related with both Type I and Type II pneumocytes but were not found within these cells. There was no obvious method of linkage to pneumocytes and the way in which lung damage is caused is unclear. However, from analogy with similar pulmonary disorders, lung damage probably involves a number of factors.

Animals↗
PubMed1989

Linkage between immunoglobulin E responses underlying asthma and rhinitis and chromosome 11q.

Family studies of IgE responses to common inhaled antigens have suggested dominant inheritance of atopy. Molecular genetic linkage analysis was used to confirm this proposal. In seven families the transmission of atopy was linked, with a maximum lod score of 5.58, to a DNA polymorphism defined by p lambda MS.51, which confirms dominant inheritance and assigns the gene locus to chromosome 11.

Asthma↗
PubMed1989

Diagnosis of Pneumocystis carinii pneumonia.

Pneumocystis carinii is the prime opportunistic pathogen of our time, the leading cause of fatal pneumonia in the increasing number of immunosuppressed subjects encountered on oncology and transplant programmes' and in subjects with the acquired immuno-deficiency syndrome (AIDS).

Journal Article↗
PubMed1988

Dominant inheritance of atopic immunoglobulin-E responsiveness.

The familial occurrence of atopy, defined by skin prick test responses and serum immunoglobulin-E (IgE) titres to common inhaled allergens, was studied in 239 members of 40 nuclear and 3 extended families. 90% of the atopic children in the nuclear families had at least one demonstrably atopic parent. In each extended family, atopy was vertically transmitted, and 31 of 47 (66%) offspring of marriages between atopic and unaffected parents were atopic. Of the designated atopic subjects, 83% admitted to symptoms suggesting atopic disease but only 30% regarded themselves as having any such disorder. It is suggested that atopy, the propensity to produce IgE in response to common, usually inhaled, allergens, is inherited as an autosomal dominant character but that its clinical expression depends on interaction with other factors.

Adolescent↗
PubMed1984

Sister chromatid exchange induction by cigarette smoke.

This paper presents evidence that cigarette smoke condensate (CSC) is a potent inducer of sister chromatid exchanges (SCEs) in cultured human lymphocytes; that benzo(a)pyrene (BP) contributes very little to this activity; that smokers have higher SCE rates than nonsmokers; that smokers with untreated lung cancer have consistently higher basal and CSC-induced SCE rates than their matched heavy smoking controls; and that, on a weight-for-weight basis, CSCs from different tar categories of cigarettes induce similar numbers of SCEs. These results are in keeping with the evidence that many smokers die of lung cancer, and that the basis of malignant transformation may be an alteration in cellular DNA. The results raise questions about possible innate differences in individuals' responses to cigarette smoke, and about the "safeness" of lower tar cigarettes.

Adult↗
PubMed1984

Cellular effects of smoke from "safer" cigarettes.

Mutagenicity and cytotoxicity are basic cellular effects of cigarette smoke which underlie the development of lung cancer and chronic obstructive airways disease. This study reports that, on a weight-for-weight basis, cigarette smoke condensates from low, middle and high tar cigarettes produce similar mutagenic effects detected by induced sister chromatid exchanges and similar cytotoxic effects detected by vital dye exclusion in human leucocytes. These findings, taken with the strong evidence that smokers extract more smoke from lower tar cigarettes to compensate for low nicotine yields, suggest that the health dangers associated with smoking these "safer" products are underestimated.

Adult↗
PubMed1984

Pulmonary infiltrates in immunocompromised patients: diagnosis by cytological examination of bronchoalveolar lavage fluid.

Thirty pulmonary infiltrates in 26 patients were investigated by bronchoalveolar lavage. Sixteen of the patients were on therapeutic immunosuppression for renal disease or transplant and 10 had leukaemia, lymphoma, or allied conditions. A rapid specific diagnosis was made in 21 (70%) episodes by cytological examination of the fluid and in 28 (93%) by a combination of cytology and microbiology. No complications from haemorrhage or pneumothorax ensued. Pneumonia due to Pneumocystis carinii was the most common diagnosis (27%), but opportunistic infections from cytomegalovirus, candida, aspergillus, zygomycetes, and acid fast bacilli were also identified by cytology. Two episodes were caused by occult pulmonary haemorrhage and five patients had malignant infiltration of the lung from leukaemia, myeloma, Hodgkin's disease, and lymphoplasmacytoid lymphoma. In two of these there was also evidence of infection. In seven cases with non-diagnostic cytology infections due to Staphylococcus aureus, Pseudomonas aeruginosa, pneumococcus, micrococcus, and Aspergillus fumigatus were identified on culture. In two patients (7%) no specific diagnosis was established by lavage: one had serological evidence of legionella infection and the second had P aeruginosa septicaemia. Twelve (75%) of the renal patients and six (60%) of those with leukaemia, lymphoma, and allied conditions recovered.

Anemia, Aplastic↗
PubMed1983

Rapid diagnosis of obscure pneumonia in immunosuppressed renal patients by cytology of alveolar lavage fluid.

16 episodes of pneumonia of obscure origin in 15 immunosuppressed renal patients were investigated without complication by fibreoptic bronchoscopy with alveolar lavage under local anaesthesia. Cytological examination and culture of lavage fluid produced a rapid definitive diagnosis in 15 episodes of pneumonia caused by infections with Pneumocystis, fungi, tuberculosis and staphylococci, or by pulmonary haemorrhage. This led to successful treatment of 10 of the 13 infective episodes.

Adult↗
PubMed1981

Variation in response to cytotoxicity of cigarette smoke.

The cytotoxic effect of cigarette smoke condensate on human polymorphs was investigated in vitro by the method of vital dye exclusion. Exposure to 1/800 of the smoke from one high-tar cigarette killed a detectable proportion of a population of 10(6) cells. The response among the cells from 40 healthy people varied widely, the percentage of dead cells ranging from 3% to 66% and from 17% to 87% at exposure levels of 125 micrograms and 250 micrograms cigarette smoke condensate respectively. Differences in individuals' responses were reproducible and unrelated to age or sex or smoking habit. The cells from 10 patients with irreversible obstructive airways disease and probable emphysema were significantly more sensitive than those from 10 patients with no respiratory disability matched for age and smoking habits. Genetically influenced variation in cellular response to cytotoxicity may be an important determinant of the risk of developing emphysema among smokers.

Adult↗
PubMed1980

Failure of propranolol and metoprolol to alter ventilatory responses to carbon dioxide and exercise.

Neither propranolol (80 mg) nor metoprolol (100 mg) give orally to eight normal subjects altered mean ventilatory responses to carbon dioxide or to moderate graded exercise. Incremental doses of the drugs to totals of 320 mg propranolol and 400 mg metoprolol also did not effect these ventilatory responses. Both drugs markedly decreased the heart rate response to exercise. Neither propranolol nor metoprolol are likely to cause CO2 retention by an effect on the ventilatory responses to inhaled carbon dioxide or to exercise.

Adult↗