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Biomedical subjects

F Hecht

Publications and source records attributed to F Hecht.

At least 235 records · Page 13Linked to original sources
PubMed1981

Amniocyte clones for prenatal cytogenetics.

Amniotic fluid cells were processed in situ on coverslips in 1,429 consecutive cases from Colorado and Arizona. Two true chromosome mosaics were differentiated from 39 pseudomosaics with clarity by the method described here in detail. The culture failure rate was 1--2% and the error rate was 0% in both laboratories. The time in culture prior to the initial harvest for the last 329 cases was 8.7 days.

Amniotic Fluid↗
PubMed1981

Ataxia-pancytopenia: syndrome of cerebellar ataxia, hypoplastic anemia, monosomy 7, and acute myelogenous leukemia.

In a family with ataxia and pancytopenia, the proband had cerebellar ataxia, developed hypoplastic anemia at age 3 years, and died of acute myelomonocytic leukemia at age 7. Serial cytogenetic studies of the proband's hypoplastic bone marrow over a 25-month period revealed progressive expansion of a clone of cells with C(6 - 12 + X) monosomy from 33% to 94% of metaphases. The missing chromosome by banding was deduced to be No.7. No increased sensitivity of the patient's cells was found in response to ultraviolet or ionizing radiation or to mitomycin C. Cerebellar atrophy was confirmed at autopsy. Family studies revealed cerebellar ataxia in the proband's father and all four siblings. Two brothers, including one with C-monosomy, died with hypoplastic anemia and another brother died with acute myelocytic leukemia. The only surviving sibling is a 19-year-old sister who has unexplained anemia, decreased mitotic activity in bone marrow, and slow progressive cerebellar ataxia. The name ataxia-pancytopenia syndrome is proposed to encourage study of additional patients with this disorder, which predisposes to pancytopenia and acute leukemia.

Adult↗
PubMed1980

Mechanisms of Giemsa banding. II. Giemsa components and other variables in G-banding.

We investigated the capability of individual thiazins in Giemsa mixture (methylene blue and azures A, B, and C) and of two related dyes (toluidine blue and thionin) to produce G-banding. We further tested the effects of variations of buffer composition and concentration, dye concentration, and staining time. G-banding was produced by all of the dyes at low concentrations, although differences were noted. Overall, methylene blue and azure B produced the best banding, azures A, C, and toluidine blue produced moderately good banding, and thionin produced poor banding. This order did not appear to be altered essentially by different treatments. The optimal conditions for G-banding for all dyes and treatments included the use of (1) 0.025-0.05 M phosphate buffer, (2) dye concentrations of 0.002%--0.005%, and (3) staining times of 6--15 min.

Azure Stains↗
PubMed1980

The use of sequential silver and quinacrine staining to determine the parental origin and breakpoints of a ring-22 human chromosome.

We delineated a G-ring syndrome in 1968 and suggested it was due to a ring-22 (Weleber et al. 1969). We confirmed in 1972 that the ring was derived from chromosome 22 (Magenis et al. 1973). The present report constitutes a new case of the ring-22 syndrome with clinical findings virtually identical to those we described earlier. By sequential staining techniques with silver and quinacrine, it was possible to determine the parental origin of the ring (maternal) and to estimate the breakpoints in the chromosome 22 (22p12 and 22q13) leading to the ring configuration. The clinical abnormalities are due to terminal deletion of 22q distal to the breakpoint in band 22q13. The silver technique, especially in sequence with other stains, provides new and useful data concerning the origin and precise cytology of this, one of the tiniest rings known in humans.

Abnormalities, Multiple↗