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1

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T-cell receptor beta-chain expression: dependence on relatively few variable region genes (1985)

M. A. Behlke ; D. G. Spinella ; H. S. Chou ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 229(4713): 566-70.

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Publication Date: 1985-08-09

Description: Fifteen independently isolated complementary DNA clones that contain T-cell receptor (TCR) V beta genes were sequenced and found to represent 11 different V beta genes. When compared with known sequences, 14 different V beta genes could be defined from a total of 25 complementary DNA's; 11 clones therefore involved repeated usage of previously identified V beta's. Based on these data, we calculate a maximum likelihood estimate of the number of expressed germline V beta genes to be 18 with an upper 95 percent confidence bound of 30 genes. Southern blot analysis has shown that most of these genes belong to single element subfamilies which show very limited interstrain polymorphism. The TCR beta-chain diversity appears to be generated from a limited V beta gene pool primarily by extensive variability at the variable-diversity-joining (V-D-J) junctional site, with no evidence for the involvement of somatic hypermutation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Behlke, M A -- Spinella, D G -- Chou, H S -- Sha, W -- Hartl, D L -- Loh, D Y -- GM07200/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 9;229(4713):566-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3875151" target="_blank"〉PubMed〈/a〉

Keywords: Alleles ; Animals ; Base Sequence ; Chromosome Mapping ; Cloning, Molecular ; Dna ; Gene Pool ; *Genetic Variation ; Humans ; Hybridomas ; Immunoglobulin Variable Region/genetics ; Mice ; Mice, Inbred BALB C/genetics ; Mice, Inbred C57BL/genetics ; Mice, Inbred Strains/genetics ; Receptors, Antigen, T-Cell/*genetics ; Species Specificity ; Spleen ; T-Lymphocytes ; Thymus Gland

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2

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Matrix-driven translocation of cells and nonliving particles (1985)

S. A. Newman ; D. A. Frenz ; J. J. Tomasek ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 228(4701): 885-9.

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Publication Date: 1985-05-17

Description: Cells of metazoan organisms produce and react to complex macromolecular microenvironments known as extracellular matrices. Assembly in vitro of native, compositionally nonuniform collagen-fibronectin matrices caused translocation of certain types of cells or polystyrene-latex beads from regions lacking fibronectin into regions containing it. The translocation process was not due to diffusion, convection, or electrostatic distribution effects, but may depend on nonequilibrium phenomena at the interface of contiguous collagen matrices formed in the presence and absence of fibronectin or particles. Extracellular matrix formation alone was sufficient to drive translocation by a biophysical process that may play a role in cellular migration during embryogenesis, as well as in other types of tissue reorganization such as inflammation, wound healing, and tumor invasion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newman, S A -- Frenz, D A -- Tomasek, J J -- Rabuzzi, D D -- HD18148/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1985 May 17;228(4701):885-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4001925" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Cartilage/cytology/embryology ; *Cell Movement/drug effects ; Chick Embryo ; Collagen/*pharmacology ; Diffusion ; Extracellular Matrix/*physiology ; Fibroblasts/cytology ; Fibronectins/*pharmacology ; Humans ; In Vitro Techniques ; Kinetics ; Microspheres ; Movement

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3

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Studies of the putative transforming protein of the type I human T-cell leukemia virus (1985)

D. J. Slamon ; M. F. Press ; L. M. Souza ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 228(4706): 1427-30.

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Publication Date: 1985-06-21

Description: The putative transforming protein of the type I human T-cell leukemia virus (HTLV-1) is a 40-kilodalton protein encoded by the X region and is termed p40XI. On the basis of both subcellular fractionation techniques and immunocytochemical analysis, it is now shown that p40XI is a nuclear protein with a relatively short half-life (120 minutes). It is synthesized de novo in considerable quantities in a human T-cell line infected with and transformed by the virus in vitro, and it is not packaged in detectable amounts in the extracellular virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Press, M F -- Souza, L M -- Murdock, D C -- Cline, M J -- Golde, D W -- Gasson, J C -- Chen, I S -- CA 32737/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 21;228(4706):1427-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990027" target="_blank"〉PubMed〈/a〉

Keywords: Antigens, Polyomavirus Transforming ; Antigens, Viral, Tumor/immunology/*metabolism ; Cell Fractionation ; Cell Line ; Cell Nucleus/metabolism ; Cell Transformation, Viral ; Deltaretrovirus/*metabolism ; Half-Life ; Humans ; Immune Sera ; Precipitin Tests ; Viral Proteins/immunology/*metabolism

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4

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Induction of AIDS-like disease in macaque monkeys with T-cell tropic retrovirus STLV-III (1985)

N. L. Letvin ; M. D. Daniel ; P. K. Sehgal ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 230(4721): 71-3.

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Publication Date: 1985-10-04

Description: The T-cell tropic retrovirus of macaque monkeys STLV-III has morphologic, growth, and antigenic properties indicating that it is related to HTLV-III/LAV, the etiologic agent of the acquired immune deficiency syndrome (AIDS) in humans. Four of six rhesus monkeys died within 160 days of STLV-III inoculation with a wasting syndrome, opportunistic infections, a primary retroviral encephalitis, and immunologic abnormalities including a decrease in T4+ peripheral blood lymphocytes. These data show that an immunodeficiency syndrome can be produced experimentally in a nonhuman primate by an agent from the HTLV-III/LAV group of retroviruses. The STLV-III-macaque system will thus provide a useful model for the study of antiviral agents and vaccine development for human AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Letvin, N L -- Daniel, M D -- Sehgal, P K -- Desrosiers, R C -- Hunt, R D -- Waldron, L M -- MacKey, J J -- Schmidt, D K -- Chalifoux, L V -- King, N W -- AI 20729/AI/NIAID NIH HHS/ -- CA 34979/CA/NCI NIH HHS/ -- CA 38205/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Oct 4;230(4721):71-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2412295" target="_blank"〉PubMed〈/a〉

Keywords: Acquired Immunodeficiency Syndrome/*microbiology/pathology ; Animals ; Brain/pathology ; Deltaretrovirus ; *Disease Models, Animal ; Epitopes/analysis ; Humans ; Interleukin-2 ; Leukocyte Count ; Lymphocyte Activation ; Macaca mulatta ; Microscopy, Electron ; Pancreas/pathology ; *Retroviridae ; T-Lymphocytes/immunology

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5

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Loss of M2 muscarine receptors in the cerebral cortex in Alzheimer's disease and experimental cholinergic denervation (1985)

D. C. Mash ; D. D. Flynn ; L. T. Potter

American Association for the Advancement of Science (AAAS)

In: Science. 228(4703): 1115-7.

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Publication Date: 1985-05-31

Description: Cerebral cortex samples from patients with Alzheimer's disease and from rats after experimental cholinergic denervation of the cerebral cortex exhibited reductions in the presynaptic marker choline acetyltransferase activity and in the number of M2 muscarine receptors, with no change in the number of M1 receptors. These results are in keeping with evidence that M2 receptors function in cholinergic nerve terminals to regulate the release of acetylcholine, whereas M1 receptors are located on postsynaptic cells and facilitate cellular excitation. New M1-selective agonists and M2-selective antagonists directed at post- or presynaptic sites deserve consideration as potential agents for the treatment of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mash, D C -- Flynn, D D -- Potter, L T -- HLO-7188/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 31;228(4703):1115-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3992249" target="_blank"〉PubMed〈/a〉

Keywords: Aged ; Alzheimer Disease/*metabolism ; Animals ; Cerebral Cortex/*metabolism ; Choline O-Acetyltransferase/*metabolism ; Cholinergic Fibers/physiology ; Denervation ; Humans ; Male ; Oxotremorine ; Quinuclidinyl Benzilate ; Rats ; Rats, Inbred Strains ; Receptors, Muscarinic/*metabolism ; Synaptic Membranes/*metabolism

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6

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Ethanol withdrawal in mice precipitated and exacerbated by hyperbaric exposure (1985)

R. L. Alkana ; D. A. Finn ; G. G. Galleisky ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 229(4715): 772-4.

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Publication Date: 1985-08-23

Description: Mice were fed an ethanol-containing liquid diet for 9 days. On removal of the diet, exposure to 12 atmospheres absolute of a mixture of helium and oxygen precipitated earlier withdrawal, increased withdrawal scores for the first 6 hours, and increased the peak withdrawal intensity compared to dependent animals exposed to control conditions. The enhanced withdrawal did not appear to reflect alterations in ethanol elimination, oxygen or helium partial pressures, body temperature, or general excitability. These results extend to chronically treated animals the evidence that hyperbaric exposure antagonizes the membrane actions of ethanol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alkana, R L -- Finn, D A -- Galleisky, G G -- Syapin, P J -- Malcolm, R D -- R01AA03972/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 23;229(4715):772-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4040651" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; *Atmospheric Pressure ; Cell Membrane/drug effects/physiology ; Ethanol/*adverse effects/pharmacology ; Humans ; Male ; Mice ; Substance Withdrawal Syndrome/*physiopathology

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Expression in Escherichia coli of open reading frame gene segments of HTLV-III (1985)

N. T. Chang ; P. K. Chanda ; A. D. Barone ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 228(4695): 93-6.

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Publication Date: 1985-04-05

Description: Human T-cell lymphotropic virus type III (HTLV-III), the causative agent of the acquired immune deficiency syndrome (AIDS), was recently isolated and its genomic structure analyzed by DNA cloning methods. In the studies reported here a combined cloning and expression system was used to identify HTLV-III encoded peptides that react immunologically with antibodies in sera from AIDS patients. Cloned HTLV-III DNA was sheared into approximately 500-base-pair fragments and inserted into an "open reading frame" expression vector, pMR100. The inserted DNA was expressed in Escherichia coli transformants as a polypeptide fused to the lambda CI protein at its amino terminus and to beta-galactosidase at its carboxyl terminus. Sera from AIDS patients containing antibodies to HTLV-III were then used to screen for immunoreactive fusion proteins. Twenty clones, each specifying a fusion protein strongly reactive with AIDS serum, were identified. DNA sequence analysis indicated that the HTLV-III fragments were derived from the open reading frame DNA segments corresponding to the gag and pol gene coding regions and also the large open reading frame region (env-lor) located near the 3' end of the viral genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, N T -- Chanda, P K -- Barone, A D -- McKinney, S -- Rhodes, D P -- Tam, S H -- Shearman, C W -- Huang, J -- Chang, T W -- Gallo, R C -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):93-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2983429" target="_blank"〉PubMed〈/a〉

Keywords: Acquired Immunodeficiency Syndrome/immunology ; Antibodies, Viral/immunology ; Cloning, Molecular ; DNA, Recombinant/metabolism ; DNA, Viral/genetics ; Deltaretrovirus/*genetics ; Electrophoresis, Polyacrylamide Gel ; Escherichia coli/genetics ; Genes, Viral ; Genetic Vectors ; Humans ; Viral Proteins/*genetics/immunology/isolation & purification ; beta-Galactosidase/metabolism

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8

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Retroviral vector-mediated gene transfer into human hematopoietic progenitor cells (1985)

H. E. Gruber ; K. D. Finley ; R. M. Hershberg ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 230(4729): 1057-61.

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Publication Date: 1985-11-29

Description: The transfer of the human gene for hypoxanthine phosphoribosyltransferase (HPRT) into human bone marrow cells was accomplished by use of a retroviral vector. The cells were infected in vitro with a replication-incompetent murine retroviral vector that carried and expressed a mutant HPRT complementary DNA. The infected cells were superinfected with a helper virus and maintained in long-term culture. The production of progeny HPRT virus by the bone marrow cells was demonstrated with a colony formation assay on cultured HPRT-deficient, ouabain-resistant murine fibroblasts. Hematopoietic progenitor cells able to form colonies of granulocytes or macrophages (or both) in semisolid medium in the presence of colony stimulating factor were present in the nonadherent cell population. Colony forming units cloned in agar and subsequently cultured in liquid medium produced progeny HPRT virus, indicating infection of this class of hematopoietic progenitor cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gruber, H E -- Finley, K D -- Hershberg, R M -- Katzman, S S -- Laikind, P K -- Seegmiller, J E -- Friedmann, T -- Yee, J K -- Jolly, D J -- AM 13622/AM/NIADDK NIH HHS/ -- GM 28223/GM/NIGMS NIH HHS/ -- HD20034/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Nov 29;230(4729):1057-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3864246" target="_blank"〉PubMed〈/a〉

Keywords: Animals ; Cells, Cultured ; Gene Expression Regulation ; *Genetic Engineering ; Genetic Vectors ; Hematopoietic Stem Cells/*physiology ; Humans ; Hypoxanthine Phosphoribosyltransferase/*genetics ; Mice ; Retroviridae/*genetics ; Transfection

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9

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Synthesis and evaluation of a prototypal artificial red cell (1985)

C. A. Hunt ; R. R. Burnette ; R. D. MacGregor ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 230(4730): 1165-8.

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Publication Date: 1985-12-06

Description: A new process allows microencapsulation of purified human hemoglobin and 2,3-diphosphoglycerate to form neohemocytes. The microcapsule membrane is composed of phospholipids and cholesterol. Neohemocytes are substantially smaller than erythrocytes, contain 15.1 grams per decaliter of hemoglobin, and have a P50 value (the partial pressure of oxygen at which the hemoglobin is half-saturated) of 24.0 torr. All rats given 50-percent exchange transfusions survived with only limited evidence of reversible toxicity. Normal serum glutamate-pyruvate-transaminase values at 1, 7, and 30 days after transfusion were consistent with minimal hepatotoxicity. The concentration of blood urea-nitrogen was elevated by 35 percent after 1 day but returned to normal by day 7. However, histopathology revealed normal kidneys on day 1 as well as on days 7 and 30. Neohemocytes cleared from the circulation of transfused rats with an apparent half-life of 5.8 hours.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hunt, C A -- Burnette, R R -- MacGregor, R D -- Strubbe, A E -- Lau, D T -- Taylor, N -- Kiwada, H -- R01-GM-24612/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1165-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4071041" target="_blank"〉PubMed〈/a〉

Keywords: Alanine Transaminase/blood ; Animals ; Aspartate Aminotransferases/blood ; Bilirubin/blood ; Blood Substitutes/adverse effects/*metabolism ; Blood Transfusion ; Blood Urea Nitrogen ; Creatinine/blood ; Disseminated Intravascular Coagulation/etiology ; Hematocrit ; Hemoglobins/metabolism ; Humans ; Microscopy, Electron ; Oxygen/metabolism ; Rats

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The role of the c-mos gene in the 8;21 translocation in human acute myeloblastic leukemia (1985)

M. O. Diaz ; M. M. Le Beau ; J. D. Rowley ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 229(4715): 767-9.

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Publication Date: 1985-08-23

Description: The human c-mos proto-oncogene is located on chromosome 8 at band q22, close to the breakpoint in the t(8;21) (q22;q22) chromosome rearrangement. This translocation is associated with acute myeloblastic leukemia, subgroup M2. The c-myc gene, another proto-oncogene, has been mapped to 8q24. The breakpoint at 8q22 separates these genes, as determined by in situ hybridization of c-mos and c-myc probes. The c-mos gene remains on the 8q-chromosome and the c-myc gene is translocated to the 21q+ chromosome. Southern blot analysis of DNA from bone marrow cells of four patients with this translocation showed no rearrangement of c-mos.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diaz, M O -- Le Beau, M M -- Rowley, J D -- Drabkin, H A -- Patterson, D -- CA 16910/CA/NCI NIH HHS/ -- CA 25568/CA/NCI NIH HHS/ -- HD 13432/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Aug 23;229(4715):767-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3860954" target="_blank"〉PubMed〈/a〉

Keywords: Chromosome Mapping ; *Chromosomes, Human, 21-22 and Y ; *Chromosomes, Human, 6-12 and X ; Humans ; Leukemia, Myeloid, Acute/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; *Translocation, Genetic

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