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Biomedical subjects

L Daniel

Publications and source records attributed to L Daniel.

14 recordsLinked to original sources
PubMed1991

Studies on the respiratory health of primary school children in urban communities of Hong Kong.

The first stage of a 2-year survey of respiratory morbidity in primary school children was conducted in two districts of Hong Kong in April/May 1989. One group (2009) of children was from Kwai Tsing District, which had high levels of exhaust emission from factories. The other group (1837) was from Southern District where atmospheric pollution was considered to be relatively low. After adjustment for gender, age, socioeconomic factors, child smoking and exposure to parental smoking, the prevalence ratios of sore throat, evening cough, cough for more than 3 months, morning phlegm and wheezing were found to be significantly higher in Kwai Tsing. The difference between the districts is likely to be related to the environmental air quality. The study, which is continuing, will provide the basis for an evaluation of the impact of new low sulphur fuel regulations introduced in July 1990.

Acute Disease↗
PubMed1991

Plasma atrial natriuretic factor concentrations in a canine model of right heart pressure overload.

Two studies were carried out in order to evaluate the plasma atrial natriuretic factor (ANF) concentrations, as well as hemodynamic and renal profiles in a chronic canine model of right heart pressure overload induced by pulmonary artery (PA) banding. In study I (n = 6), the animals were submitted to a gradual increase in pressure to clarify whether an increase in pressure or atrial distension was the main stimulus to ANF secretion. In study II (n = 6), right heart pressure overload was produced more rapidly, resulting in fluid retention and weight gain, thereby completing the model of right heart failure, and allowing an evaluation of the mechanisms involved in ANF resistance. In study I there were significant increases in right atrial pressure over baseline at 20 weeks, ANF levels at 24 weeks and right atrial area at 28 weeks following PA banding. In study II right heart pressures and ANF levels were higher than baseline at 12 weeks (p less than 0.0001), and fluid retention developed between 12-24 weeks in all dogs. The results suggest that increased right heart pressure, rather than atrial size, is a primary stimulus to ANF secretion in chronic right heart pressure overload. Despite the increases in right atrial pressure, clinical fluid retention occurred only with elevations of renin and aldosterone.

Aldosterone↗
PubMed1990

Relationship of bcr breakpoint to chronic phase duration, survival, and blast crisis lineage in chronic myelogenous leukemia patients presenting in early chronic phase.

Strong evidence implicates fusion of control elements and 5' sequences of the bcr gene of chromosome 22 with 3' sequences of the c-abl gene of chromosome 9 in the pathogenesis of Ph-positive and certain cases of Ph-negative chronic myelogenous leukemia (CML). Since this fusion gene gives rise to a chimeric tyrosine protein kinase with transforming potential, and since the bcr exon contribution to this chimeric protein is variable, the question has arisen as to whether bcr breakpoint location and bcr exon contribution could influence the clinical course of CML. Prior studies have yielded conflicting results on this point. Here we have looked, in a manner approximating a prospective analysis, at the relation of bcr breakpoint localization to the duration of chronic phase, total survival, and blast crisis phenotype in 81 patients presenting in the chronic phase of CML. We have found no significant differences in chronic phase duration or total survival among patients with breakpoints in the three major subregions of a breakpoint cluster region within the bcr gene. These findings indicate that chronic phase duration and total survival cannot be predicted from bcr breakpoint for CML patients presenting in chronic phase and suggest that unknown oncogenic events determining the onset of blast crisis are the prime determinants of prognosis. Combined analysis of blast crisis cell lineage in our patients and patients presented in a previous study has revealed an overall ratio of myeloid:lymphoid (M:L) crisis of 3.4:1, but a striking predominance of myeloid crisis in patients with breakpoints in subregion 2 (M:L of 9:1), and a lower than expected M:L ratio (1.6:1) among patients with breakpoints in subregion 3 (P for subregion 2 versus 3 = .012; subregions 0,1,2 versus 3 = .012; subregions 0,1,3 versus 2 = .032). The molecular basis for this divergence from the anticipated M:L ratio in patients with breakpoints in bcr subregions 2 and 3 is unknown.

Adult↗
PubMed1990

Localization of the von Hippel-Lindau disease gene to a small region of chromosome 3.

We studied 25 families with von Hippel-Lindau disease (VHL) to locate VHL more precisely on chromosome 3. We found that VHL was linked to RAF1, confirming previous observations, and to two polymorphic DNA markers, D3S18 and D3S191. Multipoint linkage analysis indicated that the most likely location for VHL was in the interval between RAF1 and D3S18. D3S18 was located at 3p26. Genetic heterogeneity was not detected in this panel of von Hippel-Lindau disease families. The polymorphic markers RAF1, D3S18, and D3S191 should be useful in identifying asymptomatic gene carriers in VHL families and in guiding efforts at gene isolation.

Chromosome Mapping↗
PubMed1988

Integration of bovine leukaemia virus in the ovine genome.

Circulating lymphocytes and tumour cells from 12 sheep experimentally infected with bovine leukaemia virus (BLV), for periods of time varying from 9 to 48 weeks, were analysed for evidence of integrated and unintegrated provirus. Hybridization analysis demonstrated that the provirus was integrated at one or two sites in all cases. Integration was observed at different sites in the animals studied and there was no evidence of unintegrated virus molecules in infected sheep lymphocytes or tumour cells. The data obtained support a monoclonal origin of different tumours in the same sheep.

Animals↗
PubMed1987

Polymorphism of the human c-abl gene: relation to incidence and course of chronic myelogenous leukemia.

Abnormalities in structure and expression of the proto-oncogene c-abl have been implicated in the genesis of chronic myelogenous leukemia (CML). We studied leukemic cell DNA from 42 CML patients for evidence of rearrangement and/or amplification of c-abl analogous to that described in the CML cell line K562. Using the enzymes Bgl II, Pst I, Xba I, seven patients demonstrated an atypical Southern blot pattern similar to that found in K562. Analysis of DNA from normal controls and skin fibroblast from one of the seven patients established that the atypical blot pattern was due to a restriction fragment length polymorphism rather than a gene rearrangement. Further analysis revealed that c-abl exists as two alleles, A and B, yielding three genotypes: AA, AB and BB. Inheritance was Mendelian. With respect to allele A, allele B contains a deletion of about 1 kb lying in a intronic region in close proximity to highly repetitive Alu sequences and the sequence coding for phosphotyrosine of the c-abl protein. K562 and the seven patients with similar Southern patterns were identified as AB heterozygotes. In K562, only the A allele was amplified. The frequencies of AA and AB genotypes in 37 Caucasian CML patients were 81.1% and 18.9% and in 57 unrelated normal Caucasian controls 87.7% and 12.3%, not significantly different. The BB genotype was identified in less than 1% of Caucasians. Of note, five AB patients who developed a terminal blast crisis demonstrated a 4:1 lymphoid:myeloid crisis ratio in contrast to a 2:7 lymphoid:myeloid crisis ration in nine AA patients and a similar ratio in mixed AA and AB historical controls. Otherwise, CML patients with AA and AB genotypes manifested similar clinical parameters. No patients demonstrated amplification of c-abl and analysis of four AB patients for loss of one c-abl allele during the course of their disease was negative. Thus, amplification of c-abl and loss of one c-abl allele are both infrequent in CML and do not play a significant role in the course of the disease.

Blast Crisis↗