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Biomedical subjects

L B Russell

Publications and source records attributed to L B Russell.

At least 163 records · Page 9Linked to original sources
PubMed1975

The effects of inflation on federal health spending.

This paper examines the effects of inflation on the expenditures made by federal health programs, in total and by functional category. Over the period 1969-74, a total increase of more than 90 per cent in federal dollars was required to support real growth of 44 per cent. Federally financed service programs, like Medicare and Medicaid, and health manpower training programs made particularly large gains, while construction support for health care facilities lost substantially in real terms. Health research and prevention and control programs made more moderate real gains-25 and 29 per cent, respectively, over the period. Comparison of inflation rates in the health sector and in the economy generally suggest that there are important inflationary forces specific to that sector; policies to stem general inflation cannot be expected to solve the problem of health sector inflation.

Costs and Cost Analysis↗
PubMed1974

Translocations, the predominant cause of total sterility in sons of mice treated with mutagens.

Histological and cytological analyses of the testes were carried out in 42 sterile sons of males treated in the spermatozoal or spermatid stage with 250 mg/kg ethyl methanesulfonate (EMS) alone or after prefeeding with butylated hydroxytoluene (BHT); or treated with 200 R X-rays. Of the 42 sterile males, 17 had some mature spermatids, nine were blocked at diakinesis, 15 were blocked in pachytene, and one lacked spermatogenic cells altogether, having Sertoli cells only. Mitotic (spermatogonial) metaphases could therefore be analyzed in 41 of the males and meiotic configurations in 26.-(1) None of the males showed abnormalities in chromosome number, such as monosomy, trisomy, or mosaicism for either of these conditions. Certain classes of chromosome abnormalities that have been found associated with male sterility in other investigations, namely trisomies, XXY's, and X-autosome translocations, are not expected from treatment of 19A + Y cells when F(1) males are studied. (2) A very high percentage of the sterile males carried translocations. Direct meiotic evidence for this was found in 22 of the animals. In addition, 11 of the 16 that were blocked (or virtually blocked) in pachytene, and thus could be analyzed in mitosis only, consistently showed one abnormally short chromosome (or, one short plus one long), which presumably had resulted from unequal exchange (or sizable deficiency). Of the meiotically detected translocation males, 1 carried a T(A;Y), 17 had single autosomal translocations, and 4 had multiple autosomal rearrangements involving three, four, four, and six breaks, respectively. In addition, three males showed failure of X-Y pairing. (3) Translocations that cause sterility, rather than partial sterility, in males appear to be those in which at least one of the breaks occurs close to one end of a chromosome. The mitotic and meiotic evidences for this were found to be correlated. (4) It is proposed that many cases of induced F(1) male sterility may be the result of position effects produced when paracentromeric regions are translocated to euchromatic regions of certain other chromosomes. Since many translocations that produce partial sterility in the female cause complete sterility in the male, the male must be assumed to be more susceptible to disturbances of fertility by the postulated mechanism. (5) There is evidence that EMS, especially in the lower dose range, more often breaks chromosomes near one of their ends than does X-irradiation.

Animals↗
PubMed1968

Mutant Sl alleles of mice affect susceptibility to Friend spleen focus-forming virus.

Mice of genotypes S1/S1(d), S1/+, and S1(d)/+ (but not S1(T)/S1(T) or S1(T)/+) were resistant to spleen focucs-forming virus. The "environment" in which hemopoietic target cells for this virus develop was not conducive for infection or focus formation, or both, but the target cells were not altered directly. The same genes appear to regulate hemopoiesis and leukemogenic transformation.

Alleles↗
PubMedDate not supplied

Recommendations for reporting cost-effectiveness analyses. Panel on Cost-Effectiveness in Health and Medicine.

OBJECTIVE: This article, the third in a 3-part series, describes recommendations for the reporting of cost-effective analyses (CEAs) intended to improve the quality and accessibility of CEA reports. PARTICIPANTS: The Panel on Cost-Effectiveness in Health and Medicine, a nonfederal panel with expertise in CEA, clinical medicine, ethics, and health outcomes measurement, convened by the US Public Health Service. EVIDENCE: The panel reviewed the theoretical foundations of CEA, current practices, alternative methods, published critiques of CEAs, and criticisms of general CEA methods and reporting practices. CONSENSUS PROCESS: The panel developed recommendations through 2 1/2 years of discussions. Comments on preliminary drafts were solicited from federal government methodologists, health agency officials, and academic methodologists. CONCLUSIONS: These recommendations are proposed to enhance the transparency of study methods, assist analysts in providing complete information, and facilitate the presentation of comparable cost-effectiveness results across studies. Adherence to reporting conventions and attention to providing information required to understand and interpret study results will improve the relevance and accessibility of CEAs.

Cost-Benefit Analysis↗
PubMedDate not supplied

A report of the U.S. Environmental Protection Agency Gene-Tox Program. Evaluation of mutagenicity assays for purposes of genetic risk assessment.

For the vast majority of chemicals, mammalian germ-line (MG) mutation data do not exist. The question was examined of how best to utilize results of non-MG genotoxicity assays that are included in the Gene-Tox data base to provide information of the likelihood that genetic damage might be induced in and transmitted by the reproductive cells of exposed human beings. Two approaches were used to assess the relative value of different assays for genetic hazard identification. (1) Test results were weighted according to parameters by which conditions of an assay resemble those encountered in the potential induction of transmitted genetic damage in mammals. For this purpose, 35 assays were grouped into 16 categories that were assigned weights ranging from 1 to 15; there were 2367 chemicals in the data base. This system was evaluated by comparing the sum of weighted test results for each chemical with the outcome of MG-standard (MGst) tests where such had been reported. (MGst tests used were the specific-locus and heritable-translocation assays [SLT and HTT] for gene mutations and chromosome aberrations, respectively.) The weighting system produced a few false positives with respect to the MGst results. It produced no false negatives, but the available evidence is limited by the circumstance that MGst test have evidently been preferentially performed with chemicals that had already been shown to be positive in several other assays. (2) Findings from each MGst test were compared with those from each of the other assays in turn, provided that at least 10 chemicals had been tested in both of the assays. There were 11 such comparisons involving the SLT, and 14 such comparisons involving the HTT. The observed concordance was above random expectation in several comparisons, particularly those involving certain mammalian in vivo tests, but in only one case (HTT vs. unscheduled DNA synthesis in the testis) did the degree of elevation approach statistical significance.

Animals↗
PubMedDate not supplied

Induced mouse chromosomal rearrangements as tools for identifying critical developmental genes and pathways.

Due to the rapid advances that have been made in molecular and genetic technology during the past decade, the genes associated with a large number of human hereditary diseases have been isolated and analyzed in detail. These cloned genes provide new tools for research geared toward a better understanding of normal human development, and also of the many ways that basic, essential morphologic pathways can be disturbed. Chromosomal rearrangements, especially deletions and translocations, have been especially beneficial in the mapping and isolation of human disease genes because of their visibility on both the cytogenetic and molecular levels. However, these useful types of mutations occur with low frequency in the human population. Chromosomal rearrangements can be induced relatively easily in mice, and several large, independent collections of translocation and deletion mutants have been generated in the course of risk-assessment and mutagenesis studies over the past several decades. Combined with new molecular technologies, these collections of mutant animals provide a means of gaining ready access to genes associated with developmental defects including craniofacial abnormalities, hydrocephaly, skeletal deformities, and complex neurologic disorders. As an illustration of this approach, we briefly review our progress in the study of three mutations associated with defects in palate development, juvenile growth, fitness and sterility, and neurologic development in mice, respectively.

Animals↗