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Biomedical subjects

M Ma

Publications and source records attributed to M Ma.

At least 145 records · Page 8Linked to original sources
PubMed1987

Hb F-Xin-Su or A gamma I73(E17)Asp----His: a new slow-moving fetal hemoglobin variant.

A slow-moving gamma chain variant was discovered in the cord blood of an infant born to parents of the Han nationality from Jiangsu. The variant, which migrated electrophoretically at alkaline pH between Hb A and Hb D, was characterized by an Asp----His substitution at gamma 73, while residues gamma 75 and gamma 136 were occupied by Ile and Ala, respectively. As the A gamma T-chain was also present, this baby has two types of abnormal gamma-chain. The variant was named Hb F-Xin-Su.

Amino Acid Sequence↗
PubMed1986

Adverse reactions associated with pentamidine isethionate in AIDS patients: recommendations for monitoring therapy.

Since pentamidine has become commercially available, there is renewed interest in using it as the initial treatment for Pneumocystis carinii pneumonia (PCP) in AIDS patients. We reviewed the use of pentamidine in 24 patients with PCP to gain information on the prevalence and severity of adverse effects from this drug. Twenty out of twenty-four patients (83 percent) experienced some kind of adverse effect. Hepatic abnormalities (58 percent), nausea and vomiting (46 percent), hypoglycemia (33 percent), azotemia (25 percent), and pain at the injection site (25 percent) were the most frequently seen effects. We recommend monitoring guidelines to be applied during pentamidine therapy based on the observed frequency of specific side effects.

Acquired Immunodeficiency Syndrome↗
PubMed1975

A transforming marker that produces merodiploids with high efficiency and stable transformants with low efficiency in Streptococcus.

A mutation (ery-r8) conferring a high level of resistance to erythromycin in the Challis strain of Streptoccus sanguis can be transferred to wild-type erythromycin-sensitive recipients via single molecules of donor DNA. The transformants thus produced are of two types: (1) cells slightly more resistant to erythromycin than wild-type and capable of segregating (at a frequency of 2 X 10(-4)/bacterium/generation) either wild-type or highly-resistant cells like the original donor type; (2) cells phenotypically and genotypically identical to the original donor type. The unstable diploids (ery-r8/+) occur with a frequency equivalent to that obtained with high-efficiency (HE) markers, whereas the stable donor-type (ery-r8) transformants occur with about five hundred times lower frequency. Penetration of the wild-type recipient by more than one molecule of DNA bearing the ery-r8 marker increases by as much as seven times the incidence of stable transformants. UV-irradiation of molecules bearing the ery-r8 marker diminishes their ability to cooperate in producing a stable transformant, although the UV sensitivity of stable transformant production by a single DNA molecule is not different from that of diploid production. Hence, stable transformants do not appear to be produced by a process typical of low efficiency (LE) markers, which are generally highly sensitive to ultraviolet irradiation. Moreover, stable ery-r8 transformants are produced with equally low frequencies in strains of S. pneumoniae that discriminate (hex+) and fail to discriminate (hex--) between HE and LE markers. We postulate that all transformations by the ery-r8 marker result in ery-r8/+ diploids, and that segregation results in the infrequent stable transformants of the original donor type. This hypothesis is supported by the observations that rifampin treatment of ery-r8/+ populations increases the frequency of segregation and similar treatment of wild-type recipients under-going transformation by the ery-r8 marker increases the frequency of stable transformants.--In producing the ery-r8/+ transformant the r8 allele is integrated close to the site of its wild-type homolog, since single molecules of DNA from this transformant can be shown to carry both alleles. Segregation of either the ery-r8 or + allele is not detectably enhanced by acridine orange or thymidine deprivation.--The ery-r8 marker occurs close to a site of mutation (ery-r2) which confers erythromycin resistance upon ribosomes. When the r2 and r8 markers are jointly transferred, ery-r2-r8/+ genomes are produced in which the r2 marker is stably integrated but the r8 marker is unstably adjoined to its wild-type homolog. Thus, the duplicated region can be quite short. When the ery-r8 marker is stably integrated, the region of the marker is refractory to subsequent transformation. Markers with properties like ery-r8 are not particularly rare, being found with a frequency of about 4% among spontaneous mutations to erythromycin resistance.

Diploidy↗