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Biomedical subjects

C M Litwin

Publications and source records attributed to C M Litwin.

44 records · Page 3Linked to original sources
PubMed1991

Molecular epidemiology of Shigella infections: plasmid profiles, serotype correlation, and restriction endonuclease analysis.

Plasmid isolation was used to refine the epidemiologic analysis for 168 shigellosis cases in Pima County, Ariz. Plasmids of less than 20 kb were used for comparison of plasmid profiles. Plasmid patterns for each species were distinct. A total of 57 of 74 (77%) Shigella flexneri strains could be placed into seven plasmid patterns, 70 of 79 (89%) Shigella sonnei strains could be placed into seven patterns, 12 Shigella boydii strains could be placed into six patterns, and each of 3 Shigella dysenteriae strains differed. There was a correlation between plasmid patterns and serotypes for S. flexneri, and multiple plasmid patterns were found in serotypes 1, 2, and 6, offering a refinement beyond serotyping. In previous studies we found an association between Mexican travel and an S. sonnei 5.1-kb plasmid. When this plasmid was used as a probe, strong homology was seen with numerous small plasmids in all Shigella species: restriction endonuclease analysis revealed a 1.1-kb AvaI-AvaII fragment common to various plasmids of S. sonnei. S. flexneri, and S. boydii independent of species. Of 34 Pima County Shigella isolates from the mid-1970s. 8 showed plasmid patterns similar to those of the recent isolates. Some plasmids from S. sonnei, S. flexneri, and S. boydii strains isolated in the 1970s also contained the AvaI-AvaII fragment. The conservation of this specific fragment in our population for more than 12 years suggests that it may contain genes important in virulence or survival.

Arizona↗
PubMed1991

Contractility and stiffness of noninfarcted myocardium after coronary ligation in rats. Effects of chronic angiotensin converting enzyme inhibition.

BACKGROUND: Previous studies have shown that global left ventricular function is depressed after myocardial infarction. However, little is known about the effects of myocardial infarction on contractility and the passive-elastic properties of residual myocardium. METHODS AND RESULTS: We evaluated isometric function and passive myocardial stiffness in isolated, noninfarcted left ventricular papillary muscle from rats 6 weeks after sham operation or myocardial infarction. Maximal developed tension and peak rate of tension rise (+dT/dt) were significantly decreased in untreated rats with large myocardial infarction compared with controls (3.3 +/- 1.1 versus 4.3 +/- 0.6 g/mm2 and 49.5 +/- 17.5 versus 72.5 +/- 10.5 g/mm2/sec, respectively). Time to peak tension was prolonged (120 +/- 8 versus 102 +/- 4 msec) and myocardial stiffness was increased in untreated myocardial infarction rats compared with controls (35.2 +/- 4.9 versus 24.2 +/- 3.7). Rats with smaller myocardial infarctions differed from controls only with respect to a prolongation of time to peak tension. Papillary muscle myocyte cross-sectional area was increased by 44% (p less than 0.05), and myocardial hydroxyproline content was increased by 160% (p less than 0.05) in rats with large myocardial infarctions compared with controls. To determine whether treatment that improves left ventricular function after myocardial infarction also improves myocardial function, rats were treated with captopril beginning 3 weeks after myocardial infarction and continuing for 3 weeks. Treatment with captopril attenuated the prolongation in time to peak tension in the myocardial infarction rats; however, developed tension, +dT/dt, and muscle stiffness remained abnormal. Compared with untreated myocardial infarction rats, captopril-treated myocardial infarction rats had a 9% decrease in myocyte cross-sectional area (p = 0.1) but a persistent increase in myocardial collagen content. In summary, large myocardial infarction in rats causes contractile dysfunction, increased stiffness, myocyte hypertrophy, and increased collagen content in the residual noninfarcted myocardium. Treatment with captopril alters the process of cardiac remodeling and hypertrophy and improves one parameter of contractility in noninfarcted myocardium; however, myocardial collagen content and myocardial stiffness remain abnormal. CONCLUSIONS: These findings suggest that angiotensin converting enzyme inhibition in the rat infarct model of heart failure improves global cardiac performance via combined effects on myocardial function and the peripheral circulation.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Induction of myocardial hypertrophy after coronary ligation in rats decreases ventricular dilatation and improves systolic function.

BACKGROUND: Previous studies have shown that hypertrophy of surviving myocytes after myocardial infarction (MI) is limited. Progressive ventricular dilatation after MI may occur when compensatory hypertrophy cannot restore left ventricular (LV) wall stress to normal. METHODS AND RESULTS: To test whether induction of additional myocyte hypertrophy might prevent pathological LV remodeling after large MI, we administered 2-tetradecylglycidic acid (TDGA) 20 mg/kg/day to sham-operated (n = 12) and MI (n = 10) rats for 10 days, beginning the third day after infarction. We have previously shown that chronic inhibition of long-chain fatty acid oxidation with TDGA in rats results in myocardial hypertrophy without any apparent impairment of LV systolic function. When compared with untreated MI rats (n = 9), we found that TDGA-treated MI rats had increases in LV weight/body wt, myocyte cross-sectional area, and peak developed LV pressure during abrupt aortic occlusion. MI rats treated with TDGA had lower LV end-diastolic pressures and smaller end-diastolic volumes, whereas stroke volume was maintained. The ex vivo passive LV pressure-volume relation was shifted toward the pressure axis compared with untreated infarct rats. In sham-operated rats, TDGA caused increases in LV weight/body wt, myocyte size, peak developed LV pressure, cardiac index, and stroke volume index, and a shift of the passive LV pressure-volume relation toward the pressure axis. CONCLUSIONS: Induction of myocardial hypertrophy with an inhibitor of long-chain fatty acid oxidation retarded the process of LV dilatation and produced beneficial effects on systolic function after large myocardial infarction. These data support the hypothesis that inadequate hypertrophy of residual myocardium after infarction may contribute to LV dilatation and the development of congestive heart failure.

Animals↗
PubMed1990

Molecular epidemiology of Shigella sonnei in Pima County, Arizona: evidence for a Mexico-related plasmid.

In 1984, the incidence of shigellosis was 32.4 per 100,000 population in Pima County, Arizona. To investigate sources, Shigella isolates and epidemiologic data were collected for 79 cases of infection with Shigella sonnei, the most common species. Since S. sonnei has a single serotype, plasmid isolation was attempted to refine the epidemiologic analysis. There were seven plasmid patterns containing 17, 13, 4, 22, 9, 2, and 3 isolates. Twelve of 17 isolates associated with recent travel to Mexico were in a group distinguished by a 5.1-kilobase (kb) plasmid. This plasmid was used to probe Southern blots of plasmids from strains of all groups. The Mexico-related plasmid probe hybridized to all the 5.1-kb plasmids and to 5.5- and 7.4-kb plasmids from three other groups. Of the 79 isolates, 50 contained plasmids homologous to the Mexico-related plasmid probe, suggesting association with travel to Mexico.

Arizona↗
PubMedDate not supplied

Hymenoptera sensitivity occurring in families.

A total of 248 patients with systemic reactions to Hymenoptera envenomation were studied. There were 138 adults and 110 children. Twenty-eight of these 248 (11.3%) had family members with histories consistent with Hymenoptera anaphylaxis. These included five mothers and sons, two sister pairs, three pairs of sister-brother, one pair brother-brother, and one pair father-daughter. In one extended family, a father, mother, son, and mother's sister had Hymenoptera sensitivity. Ninety-six consecutive allergic patients without Hymenoptera sensitivity served as controls, and of these, 3.1% had family members with Hymenoptera sensitivity. The occurrence of Hymenoptera sensitivity in families of patients with Hymenoptera sensitivity is statistically different from our controls (11.3% vs 3.1%, p = 0.0195). There appears to be a hereditary aspect for Hymenoptera sting sensitivity.

Adolescent↗
PubMedDate not supplied

Anaphylaxis to the ingestion and inhalation of Tenebrio molitor (mealworm) and Zophobas morio (superworm).

It has been well documented, worldwide, that inhalation and/or contact with airborne particulate insect products has resulted in sensitivity to insect proteins and is manifested by such common entities as dermatitis, conjunctivitis, rhinitis, and asthma. However, the deliberate ingestion of a variety of insects (undertaken to prove their edibility and nutrient value) resulted in subsequent sensitization of some individuals. Such an outcome has not previously been reported in the literature. The objective was to document the anaphylactic reaction to the purposeful ingestion of mealworm in an individual known to be sensitized to the inhalation of beetle larvae. We used the occasion of the Centennial Celebration of The New York Entomological Society to expose members and guests of the Society to the ingestion of various insects. The subjects of the study consisted of: 1) Three members were adversely affected; 2) One individual with Baker's asthma; and 3) A number of controls with no known hypersensitivity to insect products. The investigation was undertaken by food challenges, inhalation challenges, skin testing to the individual insect allergens, a) Tenebrio molitor (TM), b) Zophobas morio (ZM), c) Blattella germanica (BG), skin testing to common indoors and outdoor allergens, and direct bind ELISA and ELISA inhibition. One individual manifesting hypersensitivity both by ingestion and inhalation to mealworm was identified. This sensitivity was documented clinically as well as by objective testing.

Anaphylaxis↗
PubMedDate not supplied

Variations of pollen and mold concentrations in 1998 during the strong El Niño event of 1997-1998 and their impact on clinical exacerbations of allergic rhinitis, asthma, and sinusitis.

Previous studies of pollen and mold dispersal have not correlated meteorological phenomena with clinical exacerbations of asthma, allergic rhinitis, and sinusitis. We utilized the resources of 11 New England Society of Allergy (NESA) pollen collectors, a certified palynologist, over a dozen weather stations for meteorological data, and 10 emergency rooms to explore the effects of the strong "El Niño" of 1997-1998 on our region during the 1998 pollen season. There was a marked increase in the number of clinical exacerbations of asthma, allergic rhinitis, and sinusitis in April, May, and June of 1998. Several emergency rooms reported a greater increase in visits for sinusitis as compared to asthma. In addition, maximum mold counts occurred two to three months earlier than in 1997. Maximum pollen counts were also higher than in 1997, and occurred two to four weeks earlier for most tree pollen types.

Air Pollution↗