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Biomedical subjects

M Potter

Publications and source records attributed to M Potter.

At least 19 recordsLinked to original sources
PubMed1992

Pathogenetic mechanisms in B-cell non-Hodgkin's lymphomas in humans.

A very large proportion of non-Hodgkin's lymphoma in the United States are of B-cell origin. This group of tumors includes a variety of different pathological and clinical types. Chromosomal rearrangements play an important role in the pathogenesis of many of these tumors. In B-cells these translocation processes appear to develop as illegitimate products of physiological V-(D)-J or heavy chain switch rearrangements. The biology of the well-known chromosomal translocations is discussed. Additional biological factors in lymphomagenesis (aging, immunodeficiency, role of antigenic stimulation, and genetically determined susceptibility) are discussed.

Humans↗
PubMed1992

A fatal neonatal case of medium-chain acyl-coenzyme A dehydrogenase deficiency with homozygous A-->G985 transition.

A term neonate became lethargic and hypotonic at 46 hours of age and died 10 hours later despite supportive therapy. Urinary organic acids indicated medium-chain acyl-coenzyme A dehydrogenase deficiency, and DNA studies confirmed this disorder. Neonatal symptoms in this enzyme deficiency have rarely been reported, and recent reviews have ignored or discounted this presentation.

Acyl-CoA Dehydrogenase↗
PubMed1992

Plasmacytomagenesis in mice: model of neoplastic development dependent upon chromosomal translocations.

Three model systems of plasmacytomagenesis that are associated with mutations that affect c-myc transcription were discussed. Plasmacytoma induction by chronic peritoneal irritation induced by non-metabolized paraffin oils or plastic objects is strongly influenced by the immune status of the host. BALB/cAn mice must be exposed to natural environmental antigens to develop a high incidence of plasmacytomas. This may be related to T-cell priming. BALB/cAn mice raised under strict SPF conditions are refractory to plasmacytoma induction by pristane. The genotype of the mouse plays an important role in the chronic peritoneal irritation model of plasmacytomagenesis in mice. Only a few of the standard inbred strains are susceptible, notably BALB/cAn and NZB/B1. The genetic basis of susceptibility and resistance has been studied in crosses and congenic strains involving the susceptible BALB/cAn and resistant DBA/2 strains. While several genes play a role in determining resistance at least one resistance gene located on the distal end of Chr 4 reduces the incidence by at least 50% as determined in the BALB/cAn.DBA/2 Fv-1n/n congenic strain. The action of susceptibility and resistance genes is not known; hypothetically these genes could play a role in plasmacytomagenesis by increasing the probabilities of illegitimate exchanges between genes or by influencing the formation of mutations in genes that regulate mitotic cycling. Plasmacytomas appear to develop in the chronic inflammatory tissues induced by these agents. Fundamental unanswered questions are whether these inflammatory tissues provide products such as oxidants in vivo that damage DNA and promote mutagenesis. In the mouse there is a resident self-renewing B cell population that is CD5+. These B cells, which are known to be precursors of normal lamina propria IgA-secreting plasma cells, are directly in contact with the chronic inflammatory process induced by pristane; they may be targets in plasmacytomagenesis. The plasmacytomas that develop by the peritoneal mode of induction all have chromosomal translocations that directly or indirectly activate c-myc. The predominant MACTR found in 90% of these tumors is T(12;15) in which a heavy-chain switch region sequence is joined to the 5' region of c-myc. The evidence strongly suggests that the translocation develops in a late mature B cell that is in the process of isotype switching. An unanswered question is whether the switching associated T(12;15) takes place in a B cell that is exposed to the inflammatory microenvironment.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

A nursing camp--a multi-agency cooperative effort.

A summer nursing camp for junior and senior high school youth, planned and implemented by a multi-agency advisory group, demonstrates one way to attract future nurses into the profession. To effectively solve the problem of the nurse shortage, the efforts of nurse administrators in education and practice must be coordinated.

Adolescent↗
PubMed1992

A retrovirus that expresses v-abl and c-myc oncogenes rapidly induces plasmacytomas.

ABL-MYC, a murine retrovirus that encodes the v-abl and c-myc oncogenes, was constructed from Abelson murine leukemia virus (A-MuLV) in order to assess the biological consequences of co-expression of these genes in lymphoid cells. When inoculated into mice this retrovirus induced plasmacytomas in up to 100% of infected mice and less frequently induced pre-B lymphomas. Both tumor types contained genome-length proviruses in one or a few chromosomal locations, were mono- or oligoclonal as judged by immunoglobulin gene rearrangement and had unrearranged endogenous c-myc loci. The type of tumor induced depended upon the age and strain of mouse, and whether helper virus was present in the inoculated virus pool. ABL-MYC induced plasmacytomas with or without helper virus, with or without pretreatment of the mice with pristane, and in strains of mice resistant to pristane-induced plasmacytomas. Pristane treatment prior to ABL-MYC infection shortened the latent period of plasmacytomagenesis and produced mostly IgM-secreting tumors rather than IgA-secreting tumors, which predominantly arose in the absence of pristane. Control viruses for ABL-MYC with either a deletion in v-abl or a frameshift mutation in c-myc caused predominantly monocyte/macrophage tumors and pre-B-cell lymphomas respectively. Histopathological analysis of ABL-MYC-infected mice showed foci of transformed plasma cells as early as 14 days after infection. These results indicate that v-abl and c-myc act synergistically to transform mature B cells with high efficiency.

Animals↗
PubMed1992

Perspectives on the origins of multiple myeloma and plasmacytomas in mice.

The natural history of multiple myeloma and related human plasma cell tumors is compared to the process of plasmacytomagenesis in mice. Intriguing new findings are beginning to give a more complete picture of the evolution of these tumors. Mouse plasmacytomas consistently develop chromosomal translocations that dysregulate c-myc, but consistent oncogenic mutations have not yet been defined in multiple myeloma.

Animals↗
PubMed1992

A 38-year-old female trauma victim of a car bomb.

This case profoundly affected prehospital and hospital care providers alike. Most Midwestern areas have small cities and towns, and most of our trauma results from accidents, not deliberate, senseless human acts. There is a quality of life in our community that does not involve doing things like this to others. If our staff was this affected, it is sobering to think of the profound adjustment required of the victim.

Adult↗
PubMed1991

Specific pathogen-free BALB/cAn mice are refractory to plasmacytoma induction by pristane.

Forty to sixty percent of conventionally (CON) raised BALB/cAnPt (BALB/c) mice develop plasmacytomas (PCT) when injected with three 0.5 ml i.p. injections of pristane. When CON-BALB/c mice were converted to specific pathogen free (SPF) status by foster nursing caesarean delivered term mice on C3H/HeN SPF mothers and maintained under strict SPF conditions, less than 5% of the mice developed pristane-induced PCT. FACS analysis of the cellular composition of oil granulomatous tissue revealed a dramatic influx of CD4+ cells in CON mice that was significantly reduced in SPF mice. Moreover, while both CON and SPF mice had similar patterns of gut flora colonization, only CON-BALB/c mice had occasional circulating antibodies to mouse hepatitis virus and Sendai viruses. Maintenance in strict SPF conditions, therefore, results in a prolonged state of relative Ag deprivation and a failure to continuously activate new T and B cell populations. The results suggest that PCT formation depends on exogenous antigenic stimulation and that the presence of minimal gut flora is insufficient to render these mice susceptible to PCT induction.

Animals↗
PubMed1991

Chronic multifocal osteomyelitis, a new recessive mutation on chromosome 18 of the mouse.

Mice with tail kinks and deformities in their lower extremities were observed in a litter of C.D2-Qa-2+N6F15 mice. A mutant line that exhibits this phenotype in 100% of its offspring was established by subsequent breeding. The abnormalities resembled to some degree those found in a human syndrome termed chronic recurrent multifocal osteomyelitis (CRMO). Accordingly, we name the new mutation chronic multifocal osteomyelitis (cmo). Breeding analysis showed that the defect was determined by a single autosomal recessive gene. Restriction fragment length polymorphism (RFLP) analysis of progeny from a backcross between Mus musculus domesticus (CLA) and C.D2-Qa-(2+)-cmo/cmo indicated that the cmo gene resides on mouse Chromosome 18.

Animals↗
PubMed1991

Alcohol abuse by patients undergoing methadone treatment programmes.

To study the prevalence of problem drinking among patients undergoing methadone treatment programmes, 170 patients were assessed using the self-administered alcohol screening test (mSAAST). Fifty-three (31.9%) patients scored 7 or more on the mSAAST, indicating actual or potential drinking problems. There was a slight tendency for these to be male. Patients who abused alcohol also tended to use benzodiazepines irrespective of sex. The results of the study seem to indicate that the prevalence of dual alcohol and opiate use is high amongst patients attending drug dependency units. Furthermore comprehensive research is required in order to plan effective treatment for these dual addicted patients.

Adult↗
PubMed1991

DNA repair in the c-myc proto-oncogene locus: possible involvement in susceptibility or resistance to plasmacytoma induction in BALB/c mice.

This report describes an unexpected difference in the efficiency of removal of UV-induced DNA damage in the c-myc locus in splenic B lymphoblasts from two inbred strains of mice. In cells from plasmacytoma-resistant DBA/2N mice, 35% of UV-induced damage in the regulatory and 5' flank of c-myc is removed by 12 h. However, in cells from plasmacytoma-susceptible BALB/cAn mice, damage is not removed from this region. In the protein-encoding region and 3' flank of c-myc as well as in two dihydrofolate reductase gene fragments, UV damage is repaired with similar efficiency in B lymphoblasts from both strains of mice. Furthermore, in the protein-encoding portion and 3' flank of c-myc, damage is selectively removed from only the transcribed strand. No repair is detected in the nontranscribed strand. In contrast, DNA repair in the 5' flank of c-myc is not strand specific; in DNA from DBA/2N cells, UV damage is rapidly removed from both the transcribed and nontranscribed strands. In BALB/cAn cells no repair was detected in either strand in the 5'flank, consistent with the results with double-stranded, nick-translated probes to this region of c-myc. In addition to the repair studies, we have detected post-UV-damage formation: in most of the genes studied, we find that additional T4 endonuclease-sensitive sites are formed in the DNA 2 h after irradiation. Our findings provide new insights into the details of gene-specific and strand-specific DNA repair and suggest that there may be close links between DNA repair and B-cell neoplastic development.

Animals↗