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Biomedical subjects

F Hecht

Publications and source records attributed to F Hecht.

At least 19 recordsLinked to original sources
PubMed2001

A confirmatory factor analysis of the WISC-III in a clinical sample with cross-validation in the standardization sample.

Maximum likelihood confirmatory factor analysis was applied to the Wechsler Intelligence Scale for Children-Third Edition (WISC-III; Wechsler, 1991) data of a mixed clinical sample of 318 children. Analyses were designed to determine which of nine hypothesized oblique factor solutions could best explain intelligence as measured by the WISC-III in the clinical sample. Competing latent variable models were identified in previous studies, and results in the clinical sample were cross-validated by testing all models in the WISC-III standardization sample (n = 2200). Findings in both the clinical and standardization samples supported a five-factor model including Verbal Comprehension, Constructional Praxis, Visual Reasoning, Freedom from Distractibility, and Processing Speed factors. The Visual Reasoning factor was defined primarily by Picture Arrangement, whereas Mazes did not appear to improve model fit. Potential opportunities and pitfalls with regard to the interpretation of the proposed Visual Reasoning factor are discussed.

Adolescent↗
PubMed1998

Postexposure prophylaxis after nonoccupational HIV exposure: clinical, ethical, and policy considerations.

In the wake of recent breakthroughs in antiviral therapies and Centers for Disease Control and Prevention (CDC) recommendations advocating occupational postexposure prophylaxis (PEP), health care workers are increasingly receiving inquiries about PEP following exposures to the human immunodeficiency virus (HIV) through sex and injection drug use. The probability of HIV transmission by certain sexual or injection drug exposures is of the same order of magnitude as percutaneous occupational exposures for which the CDC recommends PEP. In such cases, if the exposure is sporadic, it seems appropriate to extrapolate from the data on occupational PEP and recommend prophylaxis. However, for individuals with continuing or low-risk exposures, we instead recommend referrals to state-of-the-art risk reduction programs. Clinicians, using local HIV seroprevalence data and their knowledge of transmission probabilities, can help exposed patients make an informed decision regarding PEP. Because of the large number of risky encounters that will not be treated prophylactically, even after significant outreach efforts, public health interventions that emphasize PEP as part of a comprehensive HIV prevention program should be confined to cities with highest HIV prevalences.

Anti-HIV Agents↗
PubMed1998

The journal "impact factor": a misnamed, misleading, misused measure.

The Institute for Scientific Information (ISI), a database publishing company that publishes Current Contents and Science Citation Index, has devised and promulgated what it terms the journal "impact factor." ISI describes this factor as a "measure of the frequency with which the 'average article' in a journal has been cited in a particular year." The factor is a ratio between citations and recent citable published items calculated by dividing the number of all current citations of items published in a journal during the preceding 2 years by the number of articles published in those 2 years by that journal. What, if anything, is wrong with the "impact factor"? There is absolutely nothing incorrect with the calculation of the ratio itself. However, the "impact factor" is misnamed and misleading. Being misnamed and misleading, the "impact factor" has been misused. It is being held out as a measure of the importance of a specific journal article and the journal in which the article appeared. By extension, the "impact factor" is also being misused to gauge the relative importance of individual researchers, research programs, and even the institution hosting the research. We recommend that the term "impact factor" be abolished and that this measure be renamed in keeping with its actual role, that merely of a time-specific "citation rate index" and nothing more. What is currently called the "impact factor" should not be misused to evaluate journals or to validate the scientific relevance of a particular researcher or research program, especially in decisions regarding employment, funding, and tenure.

Bibliometrics↗
PubMed1997

Mapping FRA11A, a folate-sensitive fragile site in human chromosome band 11q13.3.

FRA11A, a rare folate-sensitive fragile site assigned to 11q13.3, lies in an area of genomic instability associated with several diseases and amplification events. To map FRA11A, we used fluorescence in situ hybridization with yeast artificial chromosome and cosmid probes on metaphase chromosomes of patients expressing the fragile site. FRA11A was found situated centromeric to ACTN3 and telomeric to D11S913, these markers being within an interval of approximately 1 Mb in the 11q13.3 region.

Cells, Cultured↗
PubMed1995

Cytogenetics of malignant gliomas: I. The autosomes with reference to rearrangements.

Autosomal chromosome abnormalities are far from always detectable and, when detected, far from fully consistent in malignant gliomas. In 15 of 41 malignant gliomas, we found autosomal chromosome aberrations ranging from solitary trisomy to a wildly abnormal polyploid complement. The sequence of chromosome events appears to proceed from the normal to the near-diploid state (via structural and numerical changes) to near-tetraploidy (via polyploidization), and finally toward near-triploidy (via chromosome loss and additional rearrangements). Characteristic chromosome changes of trisomy 7 and monosomy 10 were repeatedly found, usually together in the same cell clones. In only one case was trisomy 7 an isolated change. We observed structural rearrangements of chromosomes 7 and 10 which may be of some use in mapping specific genes duplicated or deleted by the whole-chromosome changes of chromosomes 7 and 10. Nonrandom structural changes of other autosomes, including chromosomes 1, 5, and 11, fit with the model of malignant glioma as a process involving multiple genes. An unusual concentration of breakpoints in 12q13, juxtaposing it to at least five other regions, reflects the presence of genetic information in 12q13 important to the development of malignant gliomas.

Adult↗
PubMed1995

Cytogenetics of malignant gliomas. II. The sex chromosomes with reference to X isodisomy and the role of numerical X/Y changes.

Sex chromosomal monosomy with total loss of an X or Y is frequently observed in malignant gliomas. Beyond that, not much is known about the behavior of the sex chromosomes in these tumors. We noted loss of the X from 3 of 13 gliomas from women (23%) compared to loss of the Y from 16 of 28 gliomas from men (57%). There were two structural rearrangements of the Y (an inversion and a translocation with chromosome 4). Most unexpectedly, clones with sex chromosome reversal were encountered in 3 cases. These XX clones in gliomas from men are perforce the consequence of Y loss coupled with X isodisomy, a nonrandom sequence of sex chromosome changes. We examined the company kept by numerical X and Y changes in clones and found that clones with numerical sex chromosome changes had fewer autosomal abnormalities, reflecting a distinct tendency to clonal separation of sex chromosome from autosomal abnormalities. We conclude that the sex chromosome changes are not a necessary part of the neoplastic process in malignant gliomas but that they must be of biologic significance to the brain since they are highly nonrandom in frequency, type, and sequence in brain cells.

Adult↗
PubMed1995

Ring 22 chromosomes in dermatofibrosarcoma protuberans are low-level amplifiers of chromosome 17 and 22 sequences.

Ring chromosomes have been found with some regularity as solid tumors have come increasingly under cytogenetic study. The full genetic content and significance of these rings remain unclear. Dermatofibrosarcoma protuberans, a tumor of the deep dermis, consistently has supernumerary ring chromosomes, sometimes as the sole detectable cytogenetic change. Using a modified method for comparative genomic hybridization and fluorescent in situ hybridization with a panel of various probes, we found that these ring chromosomes consistently contain the chromosome 22 centromere along with interstitial sequences from chromosomes 17 and 22, specifically from regions 17q23-24 and 22q11-12. The ring chromosomes in dermatofibrosarcoma protuberans are vehicles for a particular pattern of relatively low-level genomic amplification of selected sequences.

Adult↗
PubMed1995

Chromosomes in gliomatosis cerebri.

Gliomatosis cerebri is a rare brain tumor which histologically resembles a diffuse cerebral astrocytoma. It can simultaneously infiltrate multiple sites in the cerebrum, cerebellum, brainstem, and spinal cord. This remarkable diffuseness has led to the idea that gliomatosis cerebri does not derive from a solitary focus but must arise from a broad field of glial cells. We studied the chromosomes from gliomatosis cerebri in a 12-year-old boy by conventional cytogenetics and fluorescence in situ hybridization (FISH). Aside from normal cells, we found a majority of cells with the karyotype 44,XY,del(6)(q25),del(14)(q21), der(15;21)(q10;q10),add(18)(q22),del(19)(p12),add(20)(p13),-21. A smaller proportion of cells had 88 chromosomes with a doubling of this abnormal karyotype. These findings are consistent with a clonal neoplasm stemming from a single cell. The chromosome changes we observed, with the possible exception of the chromosome 6 deletion, did not resemble those frequently found in astrocytomas. Gliomatosis cerebri may therefore belong to a separate category of brain tumors.

Brain Neoplasms↗
PubMed1994

Immunophenotyping and metastatic localization of breast cancer.

Monoclonal antibody SM 92 is involved in the immunophenotype of gastrointestinal and liver cells, SM 43 in ovarian cells, and SM 13 in lung cells. Based on a study of 61 breast adenocarcinoma patients, we found that tumors reacting with SM 92 appear associated with liver metastases, SM 43 with ovarian metastases, and SM 13 with lung metastases. These associations are highly significant. They lend some support to the concept that tumor cells that metastasize tend to go to sites where cells normally have the same surface antigens.

Antibodies, Monoclonal↗
PubMed1994

Supernumerary ring chromosomes containing chromosome 17 sequences. A specific feature of dermatofibrosarcoma protuberans?

Mystery surrounds the mechanisms by which the uncommon cutaneous tumor dermatofibrosarcoma protuberans (DP) arises and progresses. A clue may be at hand in the form of extra abnormal chromosomes (one of three ring chromosomes per case with or without other chromosome abnormalities) seen in some 10 cases, including five cases in our experience. The specificity of the rings to DP would be enhanced if the rings were found to contain a contribution from a constant chromosome. We here report fluorescence in situ hybridization (FISH) results bearing on the chromosomal content of DP rings, together with clinical, pathologic, and cytogenetic documentation of our first two cases, which were briefly reported earlier, and three new DP cases. To dissect a translocation (in our 2nd case), we probed by FISH and discovered chromosome 17 sequences in the rings in all five DP cases. Nonfluorescent bands were seen on some rings painted with a whole chromosome 17 probe, indicating the presence in these rings of foreign chromosome sequences. The complexity of the rings was underscored by the detection in only one case of chromosome 17 centromeric sequences. The situation in DP seems to have parallels to that in well-differentiated liposarcoma, another tumor of intermediate malignancy with extra abnormal marker chromosome containing contributions from a constant chromosome and variable donors. In DP the supernumerary rings are clearly specific and significant.

Adult↗