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Biomedical subjects

M Contreras

Publications and source records attributed to M Contreras.

At least 253 records · Page 14Linked to original sources
PubMed1982

Tuberculosis--a review of 498 recent admissions to hospital.

To document the changing clinical spectrum of tuberculosis among inpatients, 498 consecutive admissions to the tuberculosis unit of West Park Hospital, Toronto between January 1977 and March 1980 were reviewed. The results were compared with those of a study at this hospital two decades earlier. The recent patients were older, had a shorter stay in hospital, were more often alcoholic and more often had nontuberculous mycobacterial pulmonary disease.

Aged↗
PubMed1982

Linkage of autosomal dominant type I hereditary motor and sensory neuropathy to the Duffy locus on chromosome 1.

Data from English families confirms the probable linkage of the loci for autosomal dominant type I hereditary motor and sensory neuropathy (HMSN) and the Duffy blood group. The locus for autosomal dominant type I HMSN is in chromosome 1 near the centromere, about 15 centimorgans from the Duffy locus. The linkage between type I HMSN and the Duffy locus and the two recombinants found between Duffy and type II HMSN support the hypothesis that there are at least two genetic variants of autosomal dominant HMSN.

Adult↗
PubMed1982

Intramuscular and intravenous albuterol in the treatment of asthma.

The efficacy and side effects of intravenous and intramuscular albuterol were determined in 13 adult asthmatic patients whose airway responsiveness had previously been evaluated with inhaled albuterol. In each patient, a single dose of intramuscular or intravenous albuterol was given at the same time on separate days. There was no significant difference in bronchodilator effect between the two routes of administration; both were effective. By 15 minutes after injection, both had produced an increase in FEV1 (mean, 0.32 liter), but both were associated with transient increases in heart rate (mean, 8 beats/min, P less than 0.01). It is concluded that minimal cardiovascular side effects can be achieved with either parenteral form of albuterol.

Adult↗
PubMed1981

Failure to augment primary Rh immunization using a small dose of "passive" IgG anti-Rh.

The immune response to the i.v. injection of 1 ml of D-positive (ccDEE, presumably cDE/cDE) red cells was studied in 12 D-negative (ccddee) subjects who received a simultaneous i.m. injection of 5 microgram anti-D (the test group) and in a further 12 D-negative subjects who were not given anti-D (the control group). In all cases the red cells were labelled with 51Cr. Further injections of 1 ml of red cells were given at 7 and 12 months to subjects who had not made serologically detectable anti-D. In the test group the rate of clearance of the first injection of red cells was very variable, 99% of the cells being cleared in a period ranging from 3 to 20 d. Within 6-10 weeks of the first injection four subjects had produced anti-D; four more subjects produced anti-D after the second injection of red cells. In the control group Cr red cell survival following the first injection was normal in six cases and curtailed in the remaining six. Of the latter, four produced anti-D within 4-10 weeks of the first injection and two produced anti-D only after the second or third injection of red cells. Amongst the subjects who produced anti-D after the first injection of red cells antibody levels were lower in the test group than in the control group, indicating that the injection of 5 microgram of anti-D with 1 ml red cells had not augmented the immune response and might have partially suppressed it.

Aged↗
PubMed1979

The incidence of antibodies to low frequency antigens (LFA) in plasmapheresis donors with hyperimmune Rh antisera.

Over 50% of plasmas from plasmapheresis donors hyperimmunized for Rh antibodies were found to contain antibodies to low frequency red cell antigens (LFA). The majority of these plasmas contained antibodies to more than one LFA. On the other hand, the incidence of these antibodies in immune plasma from control plasmapheresis donors was markedly lower. The significance of the high incidence of these antibodies in grouping reagents is discussed.

Antibodies↗
PubMed1979

Homozygous.D.

A homozygote for the Rh complex .D. associated with the rare Evans antigen was identified and her family tested: .D./.D. can be clearly distinguished serologically from -D-/-D-. The immune antibody in the serum of the propositus reacts with all cells tested except homozygous -D-, CwD-, cD- and Rhnull cells.

Female↗
PubMed1978

The Rh antigen Evans.

Two families are described which clearly show that the low frequency antigen Evans is a part of the Rh system, in which it defines a 'new' gene complex.

Female↗
PubMed1978

Further data on the Pta antigen.

The second Pt(a+) family is described. Pta is shown to segregate independently from several genetic markers.

ABO Blood-Group System↗
PubMed1978

The Redelberger antigen Rba.

A new low frequency antigen, Rba, has been found in three blood donors. Studies on their families show that the antigen is inherited as a Mendelian autosomal dominant character. Rba segregates independently from ABO, MNSs P1, Rh, Kell, Duffy, Kidd, ACP1 and PGM1. Anti-Rba is not common in sera containing multiple antibodies ot low frequency antigens.

Antibodies↗
PubMed1977

Anti-Lu14: a Lutheran antibody defining the product of an allele at the Lu8 blood group locus.

A 'new' Lutheran-related antibody, named anti-Lu14, reacts with approximately 2.4% of random bloods. Red cells of the rare Lu:-8 phenotype are Lu:14. The data indicate, with a high probability, that the Lu 14 antigen is a product of an allele of Lu8 and that Lu14 and Lu8 comprise a third pair of alleles at the Lutheran locus. Red cells of the original Sw (a+) propositus are Lu:14. By coincidence, he has inherited two low-incidence genes. This observation may explain the discrepancy in different families concerning a possible relationship between Swa and Lutheran. Pedigree information now suggests that Swa is not a Lutheran gene.

Alleles↗