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Biomedical subjects

J Lenz

Publications and source records attributed to J Lenz.

At least 73 records · Page 4Linked to original sources
PubMed1989

Blood/injury fear, fainting and avoidance of medically-related situations: a family correspondence study.

The relationship of mutilation fear and fainting was examined in 204 students, (103 fainters and 101 non-fainters) by administering a series of questionnaires and a structured interview concerning the history, effects and circumstances of their fear and fainting. Two hundred and sixty of their parents completed the same scales along with a self-report version of the structured interview. Subjects were classified according to their fainting status and level of fear based on Mutilation Questionnaire scores, as phobic, fearful, and non-fearful fainters, and fearful non-fainters. Phobic and fearful fainters avoided significantly more medical and related situations due to their fear and fainting than fearful non-fainters and non-fearful fainters. Medical avoidance was best predicted by a linear combination of subjects' estimated probability of future fainting and number of past faint episodes. More females reported fainting and females reported greater fear, but they did not differ from males in fear-motivated avoidance of medical situations. A significant parent-child correspondence was found for fainting, but not for fear nor for avoidances. Implications of these findings for fear and fainting acquisition and its relation to avoidance were discussed.

Adolescent↗
PubMed1989

Identification of the SL3-3 virus enhancer core as a T-lymphoma cell-specific element.

Transient expression assays were used to determine the sequences within the long terminal repeat (LTR) that define the high activity in T-lymphoma cells of the leukemogenic SL3-3 virus in comparison with that of the nonleukemogenic Akv virus. Each of these viruses contains sequences related to the consensus element, the enhancer core. The SL3-3 and Akv enhancer cores differ at a single base pair. Substitution of the Akv core element into the SL3-3 LTR decreased expression in T-lymphoma cells but not in other cell types. Likewise, substitution of the SL3-3 core sequence into the Akv LTR increased expression in T-lymphoma cells but not in other types of hematopoietic cells. These data indicate that the SL3-3 enhancer core sequence functions better than that of Akv in T-lymphoma cells, but in other hematopoietic cell types the two are approximately equivalent. Competition DNA-protein binding assays were used to assess what nuclear factors from T-lymphoma lines and non-T lines bound to the SL3-3 and Akv core elements. Factors were detected that bound specifically to either the SL3-3 or Akv core but not to the other. Another factor was detected that bound equally well to both. However, none of these factors was specific to T-lymphoma cells.

Animals↗
PubMed1989

Differences in activities of murine retroviral long terminal repeats in cytotoxic T lymphocytes and T-lymphoma cells.

Transcriptional activities of the long terminal repeats (LTRs) of various murine leukemia viruses were tested in the cytotoxic T-cell lines CTLL-1 and CTLL-2. In contrast to T-lymphoma cells, in which the LTRs of T-lymphomagenic virus SL3-3 and Moloney murine leukemia virus are more active than those of other viruses, transcriptional activity in these mature, interleukin-2-dependent cells is not correlated with the specificity of viral leukemogenicity. Several approaches were used to investigate the molecular basis for LTR activity differences in lymphoma cells and mature cytotoxic T cells. Deletion analysis of the Moloney virus LTR showed that the direct repeats associated with enhancer activity have, at most, a slight effect on expression in CTLL-1 cells, whereas they stimulate expression six- to eightfold in T-lymphoma cells. This suggests that the mature T-cell line lacks one or more factors present in T-lymphoma cells that function to augment transcription from the Moloney murine leukemia virus LTR. We also used recombinant viral LTRs to investigate the role of the enhancer core element of SL3-3 in CTLL-1 and CTLL-2 cells. A one-base-pair difference between the core sequences of SL3-3 and nonleukemogenic Akv virus, which is important for SL3-3 activity in T-lymphoma cells, had no effect in these cells. The inability to distinguish the single-base-pair difference in expression assays was correlated with the absence of binding of a cellular factor, S-CBF, to the SL3-3 enhancer core in extracts of CTLL-1 and CTLL-2 nuclei. These studies may have implications for identification of the target cells for viral leukemogenesis, as well as for tracing of changes in the transcriptional machinery during T-lymphocyte differentiation.

Cell Line↗
PubMed1989

Absence of mouse mammary tumor virus proviral amplification in chemically induced lymphomas of RF/J mice.

RF/J mice are susceptible to the induction of thymic lymphomas by the carcinogens 3-methylcholanthrene and N-methyl-N-nitrosourea. Given the association of mouse mammary tumor virus (MMTV) with certain thymomas, we examined genomic DNA from chemically induced lymphomas of RF/J mice for new MMTV proviruses. Of 13 tissue culture lines derived from 3-methylcholanthrene-induced tumors, 5 had acquired new proviruses. MMTV amplification coincided with the appearance of viral mRNAs and proteins. However, no primary tumors or animal-passaged tumors contained new proviruses. These observations indicate that MMTV does not have a role in the tumor induction process, although it may become activated and amplified in tissue culture lines derived from tumors.

Animals↗
PubMed1987

Correlation of leukemogenic potential of murine retroviruses with transcriptional tissue preference of the viral long terminal repeats.

Recombination studies have established that retroviral long terminal repeats (LTRs) are important genetic determinants of the viral capacity to induce hematopoietic tumors and to specify the type of cell making up the tumor. Plasmids containing LTRs of several murine leukemia viruses linked to the chloramphenicol acetyltransferase gene were tested in transient assays to measure relative rates of transcriptional activity in different types of hematopoietic cells. LTRs of the thymomagenic viruses SL3-3, Moloney leukemia virus, and a Moloney mink cell focus-forming virus all expressed to higher levels than other LTRs in T-lymphocyte cell lines. Conversely, the LTRs of Friend leukemia virus and a polycythemic spleen focus-forming virus expressed to higher levels than other LTRs in erythroleukemia cells. The LTR of nonleukemogenic Akv virus induced a relatively low level of activity compared with the others in all cells tested. Thus the relative level of LTR-driven expression in various types of cells corresponds to the type of tumor caused by the intact virus in vivo. These results provide direct evidence that the tissue specificity of the transcriptional activity of LTRs plays a critical role in determining the target cell for retroviral oncogenesis.

Animals↗
PubMed1985

Retroviral insertional mutagenesis of a target allele in a heterozygous murine cell line.

A clonal murine cell line that is heterozygous at the beta 2-microglobulin locus (B2m) was obtained by Abelson murine leukemia virus (Ab-MuLV) transformation of liver cells from (C57BL/6 X BALB/c) F1 fetuses. To obtain proviral insertional mutants, we superinfected a subclone of these cells, which does not express the env surface protein of the Moloney leukemia virus (Mo-MuLV, the helper virus that was used to transmit the defective Ab-MuLV genome during transformation), with Mo-MuLV. Mutant clones that fail to express the C57BL/6 allele of B2m (B2mb) were then immunoselected by using a monoclonal antibody that specifically recognizes the B2mb gene product and not that of the B2ma allele. Of 22 independent clones obtained, one contains a proviral insertion that is near or in the first exon of the B2mb gene. Surprisingly, the insertion is of the Ab-MuLV genome and not of replication-competent Mo-MuLV. This indicates that superinfection with Mo-MuLV "rescued" the defective Ab-MuLV genome, which then inserted into the B2mb gene. We conclude that when an allele-specific selection procedure exists, proviral insertion is a potential method for obtaining mutations in heterozygous mammalian cells. This approach may thereby provide a method for molecular cloning of such selectable genes, using a retroviral hybridization probe.

Abelson murine leukemia virus↗
PubMed1985

Tissue selectivity of murine leukemia virus infection is determined by long terminal repeat sequences.

Here we show that the tissue specificity of murine retrovirus infections is determined by the long terminal repeat (LTR) of an otherwise isogenic set of viruses. The isogenic viruses used for this study contain the coding gag, pol, and env genes of the avirulent Akv virus. Recombinant viruses that contain the LTR of a virus that induces T-cell leukemia lymphoma preferentially infect T lymphocytes. Viruses that carry the LTR of a virus that induces erythroleukemia preferentially infect non-T lymphoblastoid cell lines in the marrow and spleen. The Akv virus itself displays no tissue preference for hematopoietic cells. These experiments suggest that retroviruses that carry appropriate enhancer-promoters can be used to infect selectively specific target cells in animals.

Animals↗