1,720,961 research outputs found
Ventricular myosin and creatine-kinase isoenzymes in hypertensive rats treated with captopril.
No full textHypertension. 1989 Nov;14(5):556-62.
Ventricular myosin and creatine-kinase isoenzymes in hypertensive rats treated with captopril.
Pauletto P, Nascimben L, Piccolo D, Secchiero S, Vescovo G, Scannapieco G, Dalla Libera L, Carraro U, Pessina AC, Dal Palù C.
Source
Institute of Clinica Medica I, University of Padova, Italy.
Abstract
In the myocardium, myosin and creatine kinase isoforms possess different capacities for using O2 and energy-rich phosphates. We studied electrophoretically the distribution of these isoforms in 19 hypertensive rats (two-kidney, one clip model of hypertension) and in age-matched controls. After 6 weeks of hypertension, seven rats were treated with captopril (2 mg/kg daily) for 4 weeks, six were left hypertensive for another 4 weeks, and the remaining rats were killed under ether anesthesia. In the latter, ventricular mass was significantly higher than in controls; V3 isomyosin was 32.3 +/- 6.8% versus 0%, and both creatine kinase-MB and -BB were increased at the expense of creatine kinase-MM (creatine kinase-MB = 29 +/- 2.8% vs. 14.7 +/- 1.8%, p less than 0.001; creatine kinase-BB = 3.1 +/- 0.6% vs. 1.7 +/- 0.8%, p less than 0.001). After 10 weeks of hypertension, ventricular mass, V3 isomyosin, and both creatine kinase-MB and -BB isoforms were found to be persistently higher than in controls. At the same time, captopril-treated rats showed reduced but not normalized blood pressure levels, normalized ventricular mass, and prevalence of the V1 isomyosin (56.9 +/- 22% vs. 47.9 +/- 23.8% in normotensive controls, p = NS). However, higher levels of creatine kinase-MB and -BB were still found in these rats in comparison with the normotensive controls (creatine kinase-MB = 22.4 +/- 5.4% vs. 15.8 +/- 2.8%, p less than 0.025; creatine kinase-BB = 2.3 +/- 0.1% vs. 1.8 +/- 0.3%, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
PMID:
2680963
[PubMed - indexed for MEDLINE]
Free full tex
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Usefulness of the 12-lead standard electrocardiogram in assessing myocardial infarct size.
No full textThe value of the electrocardiogram in assessing infarct size was studied using serial estimates of serum creatine phosphokinase (CPK) in serum and serial 12-lead electrocardiograms in patients admitted to a coronary care unit with acute myocardial infarction. Sum of the ST segment deviations from the isoelectric line (sigma ST12) and sum of the conventional scores of Q waves amplitude (sigma Q12) were obtained from each electrocardiogram, and then the time-course of these parameters was considered. The correlation between maximum sigma Q12 and CPK-peak in anterior infarcts, was highly significant (r = 0.733; P less than 0.001). Maximum sigma ST12, measured upon admission or immediately thereafter in patients hospitalized within 4 hours from the onset of chest pain, was found to correlate significantly with CPK-peak (r = 0.675, P less than 0.001 for the whole group; r = 0.758, P less than 0.01 for patients with inferior infarcts). Time-course of sigma ST12 and CPK showed 4 different patterns. Among them, type 1 ("rapid necrosis") showed the most significant correlations (maximum sigma ST12 within 4 hours from symptoms versus CPK-peak: r = 0.909, P less than 0.001; maximum sigma Q12 versus CPK-peak in anterior infarcts: r = 0.782, P less than 0,05; and maximum sigma ST12 within 4 hours from the onset of pain versus sigma Q12 in patients with anterior infarcts: r = 0.863, P less than 0,05). There was no correlation between sigma ST12 at any other time and CPK-peak: this observation is in accordance with the presence of a rapid decrease in the mean sigma ST12 after the first 3-4 hours from the beginning of symptoms. This study shows that the analysis of ST segment deviations and of Q waves development in the standard electrocardiogram provides useful information on the size of acute myocardial infarction as reflected by the peak value of serum CPK
Enalapril treatment increases cardiac performance and energy reserve via the creatine kinase reaction in myocardium of Syrian myopathic hamsters with advanced heart failure.
No full textVariations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Defective DNA replication impairs mitochondrial biogenesis in human failing hearts
No full textMitochondrial dysfunction plays a pivotal role in the development of heart failure. Animal studies suggest that impaired mitochondrial biogenesis attributable to downregulation of the peroxisome proliferator-activated receptor gamma coactivator (PGC)-1 transcriptional pathway is integral of mitochondrial dysfunction in heart failure.
OBJECTIVE:
The study sought to define mechanisms underlying the impaired mitochondrial biogenesis and function in human heart failure.
METHODS AND RESULTS:
We collected left ventricular tissue from end-stage heart failure patients and from nonfailing hearts (n=23, and 19, respectively). The mitochondrial DNA (mtDNA) content was decreased by >40% in the failing hearts, after normalization for a moderate decrease in citrate synthase activity (P<0.05). This was accompanied by reductions in mtDNA-encoded proteins (by 25% to 80%) at both mRNA and protein level (P<0.05). The mRNA levels of PGC-1alpha/beta and PRC (PGC-1-related coactivator) were unchanged, whereas PGC-1alpha protein increased by 58% in the failing hearts. Among the PGC-1 coactivating targets, the expression of estrogen-related receptor alpha and its downstream genes decreased by up to 50% (P<0.05), whereas peroxisome proliferator-activated receptor alpha and its downstream gene expression were unchanged in the failing hearts. The formation of D-loop in the mtDNA was normal but D-loop extension, which dictates the replication process of mtDNA, was decreased by 75% in the failing hearts. Furthermore, DNA oxidative damage was increased by 50% in the failing hearts.
CONCLUSIONS:
Mitochondrial biogenesis is severely impaired as evidenced by reduced mtDNA replication and depletion of mtDNA in the human failing heart. These defects are independent of the downregulation of the PGC-1 expression suggesting novel mechanisms for mitochondrial dysfunction in heart failure
- …
