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Biomedical subjects

C M Pearson

Publications and source records attributed to C M Pearson.

At least 19 recordsLinked to original sources
PubMed1997

Stroke Belt initiative: the Tennessee experience.

African Americans have a higher rate of stroke than other U.S. population groups. As part of the 11-state "Stroke Belt" region, Tennessee has the fifth highest death rate from stroke in the country. In 1993, a two-year community-based project was initiated to reduce the incidence of stroke and its associated risk factors among African Americans. Three counties, Shelby (Memphis), Davidson (Nashville), and Hamilton (Chattanooga), were selected as project sites because of their large African American populations. Specific objectives of the project were to promote risk factor awareness in African Americans, assist African American churches and community groups in developing and implementing intervention programs, and build the capacity for intervention programs within African American communities by collaborating with a variety of community organizations. This article describes the program's approach, which included using both adults and youth as mentors. In addition, it presents major accomplishments and lessons learned in project implementation.

Adolescent↗
PubMed1988

Preferential looking in clinical practice: a year's experience.

Preferential Looking (PL) is now a well established laboratory method of measuring visual acuity in preverbal children. We have evaluated the feasibility of its routine use in clinical practice. We present our methods and results obtained in 80 normal children and 36 children with visual disorder and discuss the problems encountered in applying this test.

Aging↗
PubMed1987

Analysis of transcripts homologous to acyl-CoA oxidase and enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase induced in rat liver by methylclofenapate.

Methylclofenapate is a potent peroxisome proliferating agent and liver carcinogen in rats. Animals exposed to daily oral doses (2.5 mg/kg body wt.) for a 21-day period were studied to determine the levels of mRNA homologous to peroxisomal acyl-CoA oxidase and enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase bifunctional enzyme in total liver RNA. Northern blotting revealed transcripts of approximately 3.8 and 3.3 kilobases (kb), homologous to acyl-CoA oxidase and the bifunctional enzyme, respectively. Levels of these transcripts began to rise at approximately 4 h after the initial dose of the agent, and reached maximum induction (35- and 60-fold, respectively, in excess of control levels) at 2-8 days after the start of the study. The kinetics of induction for acyl-CoA oxidase mRNA resembled those of palmitoyl-CoA oxidase activity, and the induction of mRNA preceded the expression of enzyme activity, further supporting a transcriptional control model of induction of the peroxisomal enzymes. The levels of mRNA induction for the peroxisomal enzymes were higher in the present study than those reported elsewhere for single doses of peroxisome proliferating agents and probably reflect the increased tissue levels achievable in long term carcinogenesis studies.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1987

Regulation of cell shape in the Cloudman melanoma cell line.

We show that Cloudman melanoma cells undergo rapid arborization in response to [Nle4,D-Phe7]alpha-melanocyte-stimulating hormone, a potent analogue of alpha-melanocyte stimulating hormone (alpha-MSH). The arbors were established by extension of processes and resembled dendrites. We used this system to study the regulation of cell shape. alpha-MSH is known to induce increases in cAMP levels, and agents such as forskolin and isobutylmethylxanthine that led to increased cAMP also caused arborization. However, equally dramatic arbors were formed after incubation with the protein kinase C inhibitor H-7 [1-(5-isoquinolinesulfonyl)-alpha-methyl-piperazine]. Phorbol diesters that activate protein kinase C led to cell rounding and antagonized alpha-MSH. The actions of protein kinase C cannot be rationalized in terms of indirect effects on cAMP: neither H-7 nor phorbol diesters alone altered cAMP levels, nor did they affect the increase in cAMP induced by MSH. We show also that MSH produced longer-term effects that cannot be mimicked by cAMP. Specifically, even in the continued presence of alpha-MSH, arborization was followed by morphological reversal to the unstimulated flattened configuration within 2 hr. (This did not occur with other agents that increase cAMP or with H-7.) Most importantly, whereas MSH-induced arborization occurred in the presence of cycloheximide, actinomycin D, or in enucleated cells, the reversal of arborization did not. Thus, MSH induced a program of rapid shape change that was dependent on new protein synthesis and gene transcription.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1984

Effects of hydroxyurea consistent with the inhibition of repair synthesis in ultraviolet irradiated HeLa cells.

Many studies on DNA repair using established in vitro cell cultures employ conditions of low serum, nutrient deprivation, and blockade with hydroxyurea (HU) to reduce the background levels of DNA replication. There are some reports in the literature which indicate that HU inhibits DNA repair. In the present study the effects of HU on strand breaks and repair synthesis in UV irradiated Hela cells were investigated using a combined strand break and UDS assay. In conditions of low serum and arginine deprivation, HU produced effects consistent with the inhibition of the repair synthesis step in excision repair. Although the conditions used in this study are severe the results suggest that HU may have qualitatively similar effects in other studies which employ its use to detect repair synthesis.

DNA↗
PubMed1984

Resistance of mouse lymphoma L5178YAII cells to alkylation with methylmethane sulphonate resides in a late step of excision repair.

The mutant mouse lymphoma cell line (L5178YAII), resistant to X-rays, ultraviolet light and alkylating agents, was reinvestigated in an attempt to establish the nature of the mutation. These cells were compared with P388 mouse lymphoma cells, which exhibit normal sensitivity to these mutagens. A series of studies was conducted to compare DNA alkylation and strand breakage with cell survival after exposure of the two cell lines to methylmethane sulphonate. It was found that neither the degree of alkylation nor the removal of the common alkylation products was correlated with the different sensitivities observed in these cell lines. A correlation was established between cell killing and the production of long-lived strand breaks. P388 cells were found to accumulate twice as many long-lived strand breaks compared to L5178YAII cells, at equal levels of alkylation. This suggested that long-lived strand breaks were the major toxic lesions. Further experiments indicated that these long-lived strand breaks were produced by a process consistent with excision repair. Evidence is also presented that indicates that the mutation in L5178YAII cells that is responsible for their resistance may occur in ligase activity or its associated ADP-ribosyl transferase system.

Alkylation↗
PubMed1981

Adjuvant polyarthritis. V. Induction by N-acetylmuramyl-L-alanyl-D-isoglutamine, the smallest peptide subunit of bacterial peptidoglycan.

N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP), an apparently nonimmunogenic bacterial peptidoglycan-derived small peptide, was found to induce a polyarthritis the rat similar to that induced by Freund's complete adjuvant when injected in the form of an oil emulsion. An oil emulsion of its isomer, N-acetylmuramyl-L-alanyl-L-isoglutamine, which unlike MDP has no immunostimulatory activity, failed to induce the disease.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1981

Muscle adenylate deaminase deficiency. Report of six new cases.

We describe six adult patients (five men and one woman) out of 364 whose muscle biopsy specimens disclosed muscle adenylate deaminase deficiency. Two men had an associated dermatomyositis and another man had an associated progressive systemic sclerosis. Although the patients were different clinically, all complained of muscular weakness or poor exercise tolerance. The occurrence of muscle adenylate deaminase deficiency in both sexes suggests a possible autosomal mode of inheritance.

AMP Deaminase↗
PubMed1981

Role of thymus for N-acetyl muramyl-L-alanyl-D-isoglutamine-induced polyarthritis and granuloma formation in euthymic and athymic nude rats or in neonatally thymectomized rats.

A synthetic adjuvant, N-acetyl muramyl-L-alanyl-D-isoglutamine (MDP), produced extremely severe polyarthritis with almost 100% incidence in Rowett euthymic rnu/+ rats, but the same dose of MDP (100 microgram) did not produce the disease in athymic rnu/rnu rats. Five hundred micrograms of MDP or 0.2 mg of heat-killed Mycobacterium bovis BCG, however, produced mild and transient polyarthritis in nude rats with very low incidence. We have not yet succeeded in reconstituting the disease susceptibility of nude rats by using thymus cells from normal rnu/+ rats. After intradermal inoculation of 100 microgram of MDP, nude rats developed small granulomas with a little necrosis and very few multinucleated giant cells only in the regional lymph nodes, whereas, in addition to the development of polyarthritis, euthymic rnu/+ rats developed typical granuloma with massive necrosis accompanied by numerous polymorphonuclear leukocytes and sparse multinucleated giant cells in the regional lymph nodes. Thymus cell-reconstituted rnu/rnu rats developed granuloma with sparse giant cells, relatively large areas of necrosis, and many polymorphonuclear leukocytes. Neonatal thymectomy may depress adjuvant-induced arthritis in the high-responder Lewis rats and enhance the disease development in the low-responder F344 rats. These findings suggested that (i) thymus plays an important role in promoting the development of MDP-induced arthritis; (ii) MDP-induced granuloma formation does not require thymus functions; (iii) the thymus functions may however be involved in the development of massive necrosis surrounded by considerable polymorphonuclear leukocyte infiltration, the mechanisms of which remain to be determined; and (iv) there is no direct correlation between granuloma formation and development of adjuvant arthritis.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1980

Methylthioadenosine nucleosidase in normal and dystrophic human muscle.

Human skeletal muscle homogenate was found to contain a nucleosidase that catalyzes the hydrolysis of 5'-methylthioadenosine, a known inhibitor of many methyl transfer reactions. When the levels of methylthioadenosine nucleosidase in muscle of patients were compared with those of controls, no significant alterations in its activity were noted in patients with various forms of muscular dystrophies, polymyositis and certain denervating diseases.

Adenosine↗
PubMed1980

Adjuvant polyarthritis. IV. Induction by a synthetic adjuvant: immunologic, histopathologic, and other studies.

A solution of an apparently nonimmunogenic synthetic compound, N,N-dioctadecyl-N',N'-bis(2-hydroxyethyl) propanediamine (CP-20961), suspended in mineral oil or olive oil (50 mg/ml), induced an acute, as well as a chronic, polyarthritis when single intradermal injections (0.2 ml) were made in the tail or hindpaw of Lewis rats. The polyarthritis was morphologically almost indistinguishable from classic adjuvant arthritis induced by Freund's complete adjuvant (FCA), a disease generally thought to be the result of a delayed hypersensitivity reaction to a constituent(s) of the injected tubercle bacilli. The disease induced by CP-20961 and that induced by Freund's complete adjuvant followed the same time course and almost identical pattern of development of clinical and histopathologic features. Like the classic adjuvant arthritis, CP-20961 induced arthritis is suppressed by an immunosuppressive agent (cyclophosphamide) or an antiinflammatory drug (phenylbutazone). The alkyldiamine (CP-20961) was found to be a potent adjuvant; a dispersion or a solution of the compound in mineral oil administered intraperitoneally enhanced the development of both the cell-mediated and the humoral immune responses to EL4 cells in the rat. These findings suggest that the immunogen responsible for the development of adjuvant arthritis is endogensou, e.g., a constituent of host tissue, a viral protein, or some complex of the two.

Animals↗
PubMed1980

Muscle fructose 1,6-diphosphatase deficiency associated with an atypical central core disease.

A 25-year-old woman with a non-familial congenital nonprogressive myopathy was found to have atypical core-like lesions in type 1 muscle fibers. Typical core lesions (approximately 13 micrometers in diameter) and smaller, PAS positive (4.1 micrometers in diameter) atypical core were associated with a predominant type 1 fibre myopathy. A specific deficiency of fructose 1, 6-diphosphatase was found with normal values for nine other muscle glycolytic and mitochondrial marker enzymes. The data provide evidence for a specific muscle enzyme deficiency in a patient with atypical central core disease.

Adenosine Triphosphatases↗
PubMed1979

Catalase, superoxide dismutase, glutathione reductase and thiobarbituric acid-reactive products in normal and dystrophic human muscle.

The level of thiobarbituric acid-reactive products and the specific activities of catalase and glutathione reductase were significantly higher in muscles from patients with major forms of muscular dystrophies over those of control subjects. Superoxide dismutase activity was not altered in dystrophic muscles. These findings indicate the occurrence in human dystrophic muscles of an increased level of lipid peroxidation and the possible activation of certain enzymes that could conceivably inhibit lipid peroxidation in vivo.

Catalase↗
PubMed1979

Activity of some proteolytic enzymes in normal and dystrophic human muscle.

1. The following proteolytic enzymes were measured in muscles of control subjects and patients with muscular dystrophies and related neuromuscular diseases: an elastase-like enzyme, carboxypeptidase A, carboxypeptidase B and pyroglutamyl peptidase. 2. Elastase-like enzyme and carboxypeptidase B did not show significant alterations in various disease conditions that were examined. 3. Carboxypeptidase A was moderately elevated in dystrophic as well as other diseased muscles. 4. Pyroglutamyl peptidase was not markedly altered in any disease condition except that is was slightly lower in dystrophic muscles.

Carboxypeptidases↗