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Biomedical subjects

J Palermo

Publications and source records attributed to J Palermo.

9 recordsLinked to original sources
PubMed2000

Regional differences in cardiovascular mortality in Minnesota.

Cardiovascular disease is the leading cause of death in the United States. Initial results from our health survey in the Red River Valley of Minnesota suggested elevated cardiovascular mortality in men and women in younger age groups there compared with the rest of the state. Similarly, earlier published longitudinal studies of cardiovascular mortality in Minnesota revealed increased cardiovascular mortality in counties west of a diagonal line drawn through the tip of the arrowhead region (northeast Minnesota) to the southwest corner of the state. In this study we examined cardiovascular mortality by geographic region with respect to economic factors, residence patterns, and ethnic group. Since these regions vary in geology and major land use, environmental factors were considered as well. Our present data show a significant elevation in cardiovascular mortality from 1987-1997 in men and women aged 25-59 in northwest and northeast Minnesota counties compared with central-metro counties. In contrast, south-central Minnesota shows a rate of cardiovascular mortality for that age group similar to that seen in the central-metro region. The increase in cardiovascular deaths from myocardial infarct in the younger groups in the more rural, less affluent areas of northwest Minnesota is nearly two times higher than in the central-metro counties. Genetic factors may play a role in the increased mortality recorded for northeast Minnesota. Environmental contaminants such as pesticides are additional considerations. Finally, our data suggest the need to address long-standing regional cardiovascular mortality differences and rural health care access in Minnesota.

Adult↗
PubMed1999

Altered kinetics of contraction of mouse atrial myocytes expressing ventricular myosin regulatory light chain.

To investigate the role of myosin regulatory light chain isoforms as a determinant of the kinetics of cardiac contraction, unloaded shortening velocity was determined by the slack-test method in skinned wild-type murine atrial cells and transgenic cells expressing ventricular regulatory light chain (MLC2v). Transgenic mice were generated using a 4.5-kb fragment of the murine alpha-myosin heavy chain promoter to drive high levels of MLC2v expression in the atrium. Velocity of unloaded shortening was determined at 15 degrees C in maximally activating Ca2+ solution (pCa 4.5) containing (in mmol/l) 7 EGTA, 1 free Mg2+, 4 MgATP, 14.5 creatine phosphate, and 20 imidazole (ionic strength 180 mmol/l, pH 7.0). Compared with the wild type (n = 10), the unloaded shortening velocity of MLC2v-expressing transgenic murine atrial cells (n = 10) was significantly greater (3.88 +/- 1.19 vs. 2.51 +/- 1.08 muscle lengths/s, P < 0.05). These results provide evidence that myosin light chain 2 regulates cross-bridge cycling rate. The faster rate of cycling in the presence of MLC2v suggests that the MLC2v isoform may contribute to the greater power-generating capabilities of the ventricle compared with the atrium.

Animals↗
PubMed1998

Effects of total replacement of atrial myosin light chain-2 with the ventricular isoform in atrial myocytes of transgenic mice.

BACKGROUND: In contrast to their well-known and critical role in excitation-contraction coupling of vascular smooth muscle, the effects of the myosin light chains on cardiomyocyte mechanics are poorly understood. Accordingly, we designed the present experiment to define the cardiac chamber-specific functional effects of the ventricular isoform of the regulatory myosin light chain (MLC2v). METHODS AND RESULTS: Postnatal transgenic cardiac-specific overexpression of MLC2v was achieved by use of the alpha-myosin heavy chain promoter. Enzymatically disaggregated atrial and ventricular mouse myocytes were field-stimulated at multiple frequencies, and mechanical properties and calcium kinetics were studied by use of video edge detection and FURA 2-AM, respectively. MLC2v overexpression resulted in complete replacement of the atrial with the ventricular isoform of the regulatory myosin light chain at the steady-state mRNA and protein levels in the atria of transgenic mice. Mechanical properties of transgenic atrial myocytes were enhanced to the level of ventricular myocytes of control animals in association with modest decreases in the amplitude of the calcium transient. CONCLUSIONS: MLC2v modulates chamber-specific contractility by enhanced calcium sensitivity and/or improved cross-bridge cycling of the thin and thick filaments of the cardiomyocyte.

Animals↗
PubMed1996

Transgenic remodeling of the contractile apparatus in the mammalian heart.

The structure-function relationships of the sarcomeric proteins in the mammalian cardiac compartment remain ill-defined because of the lack of a suitable model in which they can be readily manipulated or exchanged in vivo. To establish the validity of the transgenic paradigm for remodeling the mammalian heart, the murine alpha -cardiac myosin heavy chain gene promoter was used to express a ventricular myosin light chain-2 transgene (MLC2v) in both the atria and ventricles of the adult animal. Expression resulted in high levels of the transgene's transcript in both compartments. In the ventricle, the transgene was expressed against the background expression of the normal isoform. In the atrium, the transgene's expression would be ectopic, in that normally, MLC2v expression is restricted to the ventricle. Ectopic expression of the transgene in the atria resulted in a complete replacement of the atrial myosin light chain-2 protein isoform, although the endogenous isoform's steady state transcript levels were unchanged. In contrast, ventricular expression of the transgene had no effect at the protein level, despite an eightfold increase in MLC2v transcript levels. The data show that sarcomeric protein stoichiometry is maintained rigorously via posttransciptional regulation and that protein replacement can be achieved through a single transgenic manipulation.

Animals↗
PubMed1995

Remodeling the mammalian heart using transgenesis.

Our objective was to test the hypothesis that, via transgenesis, one can modify the contractile protein complement of the mouse heart. Using a promoter derived from the mouse myosin heavy chain gene (alpha-MyHC), we attempted to remodel the mouse myocardium by ectopically expressing a ventricular form of the myosin light chain 2 (MLC2v) in the atrium. The ability of the heart to maintain contractile isoform stoichiometry was tested by overexpressing the cDNA in both the atria and ventricle. The promoter drove high levels of transgene expression in both cardiac compartments and was controlled in an appropriate manner during development. The data show that ectopic overexpression of a contractile protein isoform can lead to compartment specific replacement. However, if the transgene encodes the isoform that is normally present (e.g., MLC2v expressed in the ventricle), the protein levels remain unaffected, although the transgenic transcript accumulates to very high levels. The basic function and the physiologic or pathophysiologic significance of differential MLC2 isoform content was examined. Using the whole working heart preparation, we show that an MLC2a --> MLC2v shift in the atrium severely affects contractile function and performance.

Amino Acid Sequence↗
PubMed1992

Structural and developmental analysis of two linked myosin heavy chain genes.

We have identified at the molecular level two murine myosin heavy chain (MHC) genes which encode adult skeletal isoforms. As is the case for the murine cardiac MHC genes, the genes are closely linked, head to tail. To identify the isoform encoded by each gene, we located and sequenced the 3' termini and assessed the genes' temporal and tissue-specific expression patterns using probes specific for the 3' untranslated regions. These analyses indicate that the myosin encoded by the gene located 5' in the linked pair is the murine 2A isoform. The isoform encoded by the 3'-most gene of the linked pair appears to encode an additional isoform that is expressed in a number of adult skeletal muscles. The pattern of expression of the 3'-most gene indicates that it is tightly controlled developmentally. Transcripts from this gene, when compared to those from the MHC2A and beta-MHC genes, are the predominant MHC transcripts found in the diaphragm, tongue, soleus, and masseter, indicating that it encodes a major skeletal MHC isoform.

Animals↗
PubMed1978

AMTEC: a cooperative effort in medical technology education.

A committee in the St. Louis Metropolitan area has been established to promote communication and cooperation among the area's existing hospital-based programs in medical technology. Area Medical Technology Education Coordinators (AMTEC) was established three years ago primarily to facilitate the administrative functions of medical technology education and to serve as an instrument for the exchange of ideas. Its primary undertaking has been the central processing of applications to the area programs, as an aid in the admission process. In addition, a continuing education program sponsored by the committee has been established, and various "curriculum sharing" activities have been sponsored for the students enrolled in the schools. Future plans for the committee include sponsoring an on-going evaluation process of graduates by employers, and establishing a criterion-referenced question pool. The authors describe the experiences of the committee to date and plans for the implementation of future goals.

Medical Laboratory Science↗
PubMedDate not supplied

Decontaminating agents.

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Anti-Infective Agents↗