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  • Articles  (2,057)
  • Medicine  (2,057)
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  • Articles  (2,057)
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  • 1
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    Evaluation of alternating chemotherapy and sites and extent of disease in extensive small cell lung cancer (1981)
    Wiley
    Details
    Publication Date: 1981-11-15
    Print ISSN: 0008-543X
    Electronic ISSN: 1097-0142
    Topics: Biology , Medicine
    Published by Wiley on behalf of American Cancer Society.
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    PAPER CURRENT
  • 2
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    Cryptic transmission of SARS-CoV-2 in Washington state (2020)
    American Association for the Advancement of Science
    Details
    Publication Date: 2020-10-30
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science
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    PAPER CURRENT
  • 3
    Electronic Resource
    Electronic Resource
    Respiratory adaptations of a fossorial mammal, the pocket gopher (Thomomys bottae) (1972)
    Springer
    Journal of comparative physiology 78 (1972), S. 121-137 
    Details
    ISSN: 1432-1351
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary 1. Fossorial rodent burrows exhibit relatively stable environmental conditions with regard to light, y. However, vastly different concentrations of CO2 and O2 are encountered in these burrows. Field observations of shallow pocket gopher burrows (Thomomys bottae) reveal CO2 concentrations to 3.8%, and O2 concentrations from 15.5% to 20.5% (Darden, 1970). Values similar to these have been reported for another genus of gopher,Geomys, by Kennerly (1964) and McNab (1966). 2. The sensitivity of the respiratory control mechanisms of the pocket gopher (T. bottae) O2 was tested and expressed as percent increase in minute volume as a function of the level of inspired CO2 (2% to 8%). The CO3 response curve is markedves for other terrestrial and diving mammals (Figs. 1 and 3). 3. Except for a reduction in slope, the respiratory response to CO2 of gophers can be described as similar to that recorded for humans. Carbon dioxide stimulates both increased ventilatory frequency and tidal volume in a near linear fashion. Individual difference in CO2 sensitivity among gophers was demonstrated (Table 2). 4. The level of alveolar CO2 (P A,CO2) in anesthetized pocket gophers is not significantly altered from values normally observed in man at sea level (Table 4). The reduced ventilatory response is due to a reduction in the slope of the response curve. The possible causes for the decreased sensitivity are discussed. 5. Comparisons of predicted and observed values of tidal volume (V T), rate of ventilation (f), minute volume ( $$\dot V_{\min } $$ ) and respiratory dead space (V D) were made (Table 3). Of these,V D and f and consequently $$\dot V_{\min } $$ were smaller than expected. The reduced value ofV D offsets the low $$\dot V_{\min } $$ and thus alveolar ventilation ( $$\dot V_A $$ ) is only slightly lower than expected. The possible biological significance of the alterations in f andV D are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00693609
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  • 4
    Electronic Resource
    Electronic Resource
    Expression of Ly-6A/E alloantigens in thymocyte and T-lymphocyte subsets: variability related to the Ly-6 a and Ly-6 b haplotypes (1989)
    Springer
    Immunogenetics 29 (1989), S. 98-107 
    Details
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We have studied the cellular basis for differential expression of the Ly-6A/E alloantigen on T cells obtained from mice of the Ly-6 a (10–20% Ly-6A/E +) and Ly-6 b (50–60% Ly-6A/E +) haplotypes. During T-cell ontogeny only a small fraction (〈 12 %) of thymocytes expressed Ly-6A/E. By 4 weeks of age adult levels of Ly-6A/E bearing lymphocytes were seen in peripheral lymphoid tissue. Immunohistochemical studies of the thymus revealed that Ly-6A/E+ cells were located predominantly in the medulla with small clusters of Ly-6A/E+ cells throughout the cortex. Consistent with this result, phenotypic studies showed that in the adult thymus the majority of Ly-6A/E expression was on mature CD4+ CD8− and CD4− CD8+ cortisone-resistant and precursor CD4− CD8− thymocytes. However, a much higher percentage of CD4+ CD8− and CD4− CD8− thymocytes as well as CD4+ CD8− peripheral T cells expressed Ly-6A/E from Ly-6 b mice. Furthermore, although gamma interferon induced increased Ly-6A/E expression in certain thymocyte and T-cell subsets, this induction functioned preferentially for cells obtained from Ly-6 b mice. Studies using F1 hybrid mice (Ly-6 a × Ly-6 b) indicated that the “basal” level of Ly-6A/E expression on these subsets appeared to be under codominant genetic control, whereas gamma interferon-induced regulation of Ly-6A/E expression appeared to be under dominant genetic control. Collectively, these results suggest that the expression of Ly-6A/E on a particular T-cell subset is established in the thymus and is a stable characteristic of each haplotype. In addition, the low levels of Ly-6A/E expression for the Ly-6 a haplotype appear to be partially due to the inability of the majority of resting CD4+ T cells to express Ly-6A/E and to the relatively poor induction of this protein by gamma interferon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00395857
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  • 5
    Electronic Resource
    Electronic Resource
    Neuritogenic Lewis rat T cells use Tcrb chains that include a new Tcrb-V8 family member (1994)
    Springer
    Immunogenetics 40 (1994), S. 266-270 
    Details
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The P2 protein obtained from Schwann cells induces a population of T cells which, upon adoptive transfer, causes the disease experimental allergic neuritis (EAN), an animal model for Guillain-Barre syndrome. In this report, a truncated peptide, FR22, derived from a previously reported neuritogenic T-cell determinant, was used to generate from Lewis rats T cells that were shown to cause EAN. Since our previous studies showed that Tcrb-V8 was used by a majority of T-cell hybridomas specific for the neuritogenic peptide P26, which contains the FR22 sequence, we sequenced the Tcrb-V8 + mRNA from FR22-specific T-cell lines, and compared the sequences obtained with those obtained from similarly generated myelin basic protein (MBP) 68–88-specific Lewis rat T-cell lines. We found that in the EAN lines, several members of the Tcrb-V8 family were used, including a new family member, Tcrb-V8E. This was more diverse than the MBP-68–88-specific response in which only a single Tcrb-V8 family member was used. Also, in the EAN lines, the beta chain sequences did not show the same conserved junctional regions seen in the MBP lines. Thus, T-cell receptor beta chain usage in the response to this dominant neuritogenic peptide appears to be less restricted than the response to the dominant encephalitogenic determinant of MBP both in V region usage and in CDR3 usage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00189971
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  • 6
    Electronic Resource
    Electronic Resource
    Genomic organization and 5′ regulatory region of the mouse IL-2 receptor β-chain gene (IL-2Rb) (2000)
    Springer
    Immunogenetics 51 (2000), S. 508-512 
    Details
    ISSN: 1432-1211
    Keywords: Key words Interleukin-2 receptor ; Promoter ; regions ; Transcription factors ; Sequence homology ; Nucleic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002510050653
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  • 7
    Electronic Resource
    Electronic Resource
    Physical location of the human immunoglobulin lambda-like genes, 14.1, 16.1, and 16.2 (1993)
    Springer
    Immunogenetics 38 (1993), S. 387-399 
    Details
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The human immunoglobulin lambda-like (IGLL) genes, which are homologous to the human immunoglobulin lambda (IGL) light chain genes, are expressed only in pre-B cells and are involved in B cell development. Three IGLL genes, 14.1, 16.1, and 16.2 are present in humans as opposed to one, λ5 (Igll), found in the mouse. To precisely map the location of the human IGLL genes in relation to each other and to the human IGL gene locus, at 22q11.1–2, a somatic cell hybrid panel and pulsed field gel electrophoresis (PFGE) were used. Hybridization with a λ-like gene-specific DNA probe to somatic cell hybrids revealed that these genes reside on 22q11.2 between the breakpoint cluster region (BCR) and the Ewing sarcoma breakpoint at 22q12 and that gene 16.1 was located distal to genes 14.1 and 16.2. Gene 14.1 was found by PFGE to be proximal to 16.2 by at least 30 kilobases (kb). A 210 kb Not I fragment containing genes 14.1 and 16.2 is adjacent to a 400 kb Not I fragment containing the BCR locus, which is just distal to the IGL-C (IGL constant region) genes. We have determined that the IGLL genes 14.1 and 16.2 are approximately 670 kb and 690 to 830 kb distal, respectively, to the 3′-most IGL-C gene in the IGL gene locus, IGL-C7. We thus show the first physical linkage of the IGL and the IGLL genes, 14.1 and 16.2. We discuss the relevance of methylation patterns and CpG islands to expression, and the evolutionary significance of the IGLL gene duplications. Consistent with the GenBank nomenclature, these human IGLL genes will be referred to as IGLL1 (14.1), IGLL2 (16.2), and IGLL3 (16.1), reflecting their position on chromosome 22, as established by this report.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00184519
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  • 8
    Electronic Resource
    Electronic Resource
    Molecular analyses of a Lesch-Nyhan syndrome mutation (hprt Montreal) by use of T-lymphocyte cultures (1990)
    Springer
    Human genetics 〈Berlin〉 85 (1990), S. 111-116 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The frequency of hprt mutants in peripheral blood T-lymphocytes of two putative Lesch-Nyhan individuals and their parents was determined by a cell cloning assay to quantify the frequency of thioguanine-resistant mutants. The results confirmed the Lesch-Nyhan diagnosis and demonstrated that the mother has an elevated mutant frequency consistent with being heterozygous for an hprt mutation. Mass cultures of T-lymphocytes from both the children and their mother, as well as cultures of hprt mutant clones from the mother, were employed as sources of mRNA for cDNA sequence analysis. These hprt mutants show a single base substitution (T→C transition) at position 170 (exon 3). The predicted amino acid change is the substitution of threonine for methionine56. We have designated this new Lesch-Nyhan mutation hprt Montreal. The use of T-lymphocyte cultures allows rapid sequence analyses of hprt mutations, as well as family studies to define the origin of a particular mutation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00276334
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  • 9
    Electronic Resource
    Electronic Resource
    Arg538 to Cys mutation in a CpG dinucleotide of the human biotinidase gene is the second most common cause of profound biotinidase deficiency in symptomatic children (1997)
    Springer
    Human genetics 〈Berlin〉 99 (1997), S. 506-512 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Biotinidase deficiency is an autosomal recessively inherited disorder in the recycling of the vitamin biotin. The most common mutation that causes profound biotinidase deficiency in symptomatic individuals is a deletion/insertion (G98:d7i3) that occurs in exon B of the biotinidase gene. We now report the second most common mutation, a C-to-T substitution (position 1612) in a CpG dinucleotide in exon D of the biotinidase gene. This mutation results in the substitution of a cysteine for arginine538 (designated R538C) and was found in 10 of 30 symptomatic children with profound biotinidase deficiency, 5 of whom also have the G98:d7i3 mutation. This mutation was not found in DNA samples from 32 individuals with normal biotinidase activity, but was found in one individual with enzyme activity in the heterozygous range. This mutation was not detected in 371 randomly selected, normal individuals using allele-specific oligonucleotide hybridization analysis. Aberrant biotinidase protein was not detectable in extracts of fibroblasts from a child who is homozygous for the R538C mutation, but was present in less than normal concentration in identical extracts treated with β-mercaptoethanol. Because there is no detectable biotinidase protein in sera of children who are homozygous for the R538C mutation and in combination with the deletion/insertion mutation, the R538C mutation likely results in inappropriate intra- or intermolecular disulfide bond formation, more rapid degradation of the aberrant enzyme, and failure to secrete the residual aberrant enzyme from the cells into blood.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004390050397
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  • 10
    Electronic Resource
    Electronic Resource
    C4 urernic variant: An acquired C4 allotype (1985)
    Springer
    Immunogenetics 22 (1985), S. 553-562 
    Details
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The major histocompatibility complex (MHC)-linked complotype region includes alleles for B, C2, and C4 loci. These loci are closely linked to each other and to HLA-DR on chromosome 6. The duplicated C4 loci,, C4A and B, are especially polymorphic. In seven patients with renal insufficiency, we observed a C4 variant with electrophoretic mobility between C4B2 and C4B3. Four of these patients were detected during a study of MHC markers in mernbranoproliferative glomerulonephritis. Complete complotype and HLA data from families of five of the seven patients demonstrated that the variant was not inherited. The pattern was revealed by immunofixation electrophoresis and also by C4-specific hemolytic overlay. In serial plasma specimens taken from one patient, the C4 variant appeared only after the patient became uremic. However, the variant could not be produced in normal plasma after incubation with C4-depleted uremic plasma. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reducing conditions of immunoprecipitated C4 from these patients showed C4A and C4B α chains of normal molecular mass; incompletely processed forms of C4 were not observed. We believe that this variant is probably acquired in the presence of uremia and may represent the C4B2.9 allele found by Wank and co-workers in many patients with glomerulonephritis. Family studies are mandatory to distinguish genetic variants from acquired alterations in the C4 phenotype.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00430303
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