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Biomedical subjects

M Zajac

Publications and source records attributed to M Zajac.

At least 19 recordsLinked to original sources
PubMed2006

[EBV quantification in children after allogeneic hematopoietic stem cell transplantation].

BACKGROUND: Patients undergoing allogeneic hematopoietic stem cell transplantation (AHSCT) are endangered by developing Epstein-Barr virus-related post-transplant lymfoprolipherative disease (EBV-LPD). The aims of the study were to retrospectively characterise the viral loads in four patients who died of this complication, and to test possible risk factors for EBV reactivation in a prospectively observed cohort of children after AHSCT. METHODS AND RESULTS: Serial DNA samples extracted from whole blood from four patients who died of post-transplant EBV-LPD in year 2000 were retrospectively analysed for EBV load using quantitative real-time PCR. First detection of EBV activation preceded death by 24-91 days. All four patients exceeded a viral load of one million EBV copies per 100,000 human genome equivalents. A cohort of 72 children undergoing AHSCT between 2001-2004 was prospectively followed-on using the same quantification method from regularly obtained samples of whole blood, and clinical and laboratory data were recorded on a weekly basis, totalling at 3,896 person-weeks of observation. Approximately one half of the cohort experienced at least one episode of EBV reactivation during the first 100 days after AHSCT, four of the episodes being accompanied with viral loads higher than our provisional threshold of 10,000 copies per 100,000 human genome equivalents. Three of the four patients developed EBV-LPD and were successfully treated by intravenous administration of anti-CD20 antibody. Testing of possible clinical and laboratory predictors of EBV reactivation did not reveal any clinically useful association. CONCLUSIONS: The cornerstone of predicting EBV-LPD in AHSCT is a regular monitoring of EBV viral load using quantitative methods. Using this strategy with a threshold of 10,000 EBV copies per 100,000 human genome equivalents was proved to be effective, as shown by no death of EBV for the study period, compared to four cases in the year before the quantitative monitoring.

Child↗
PubMed2000

Model of convergent extension in animal morphogenesis.

We argue that energy minimization can explain the pattern of cell movements in the morphogenetic process known as convergent extension provided that the cell-cell adhesive energy has a certain type of anisotropy, which we describe. This single simple property suffices to cause the cell elongation, cell alignment, and lengthening of a cellular array that characterize convergent extension. We show that the final aspect ratio of the array of cells depends on the anisotropy and is independent of the initial configuration and of the degree of cell elongation.

Animals↗
PubMed2000

Stability of cefotaxime sodium in solid state.

The influence of temperature and relative humidity on the stability of cefotaxime sodium in the solid state was investigated. Changes in the concentration of cefotaxime sodium were followed by a HPLC method with UV detection. The kinetic and thermodynamic parameters of the decomposition reaction were calculated.

Cefotaxime↗
PubMed1996

[Reliability and interobserver concordance in detection of prostatic carcinoma with magnetic resonance tomography].

PURPOSE: To determine the reliability and the measuring agreement between two radiologists in the identification of relevant structures of prostate anatomy in patients with prostate carcinoma. PATIENTS AND METHOD: 15 patients with prostate carcinoma proved by histology underwent MR Imaging on 1.5 Tesla MR-system (Siemens Erlangen). T1- and T2-weighted sequences were used in the depiction of important anatomic structures for diagnosing prostate cancer. 5 sequences of every patient were evaluated for 5 times by each reader. Reliability was proved by the intraclass correlation coefficient and the measuring agreement was proved by Cohen's cappa test. RESULTS: Only the T2-weighted sequence was of sufficient sensitivity to reach a moderate reliability (r1 = 0.74) and a moderate measurement agreement between the two readers (kappa = 0.5). CONCLUSION: For the evaluation of MR images in staging prostate carcinoma, besides the validity and the measuring agreement, the reliability of the radiologist is the important factor.

Analysis of Variance↗
PubMed1993

Hypertrophy or hyperplasia in cardiac muscle. Post-mortem human morphometric study.

In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, and density of myocyte nuclei. The values of all histometric parameters correlated well with left ventricular (LV) weight up to 350 g. In heavier hearts these parameters remained approximately of the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g. The influence on LV weight of age, coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue was also evaluated. On the basis of a linear discriminant function, hearts were divided into three classes: (1) LV weight < or = 250 g (absence of hyperplasia, hypertrophy only); (2) LV weight 251-350 g (hypertrophy+signs of hyperplasia); (3) LV weight > 350 g (marked signs of hyperplasia). The percent of fibrosis increased proportionally to LV weight. Where LV weight was above 250 g there was a subsequent increase in the mean percent of fibrosis (approx. 26%). This phenomenon (plateau of percent fibrosis) is the result of an increased number of myocytes (myocyte hyperplasia). We suggest that, independent of aetiology, in all hearts above 350 g (patients with congestive heart failure) hyperplasia phenomenon exists.

Adult↗
PubMed1992

[Hypertrophy or hyperplasia of myocytes in heart hypertrophy?].

One of the most controversial problem in cardiac muscle pathology is the existence of myocyte hyperplasia. The term hypertrophy indicates an increase in size of the individual muscle cells without changing their total number, whereas in hyperplasia there occurs proliferation of the myocyte. This fundamental question of the character of cardiac growth remains unresolved in spite of the wide attention it has received. Contemporary views concerning the cardiac muscle hyperplasia are presented. From clinical point of view the problem is significant for two reasons. The loss of the ability of muscle cells to proliferate is responsible for the irreversible myocardial destruction after injury. From another point of view, if the increase of the heart muscle is maintained, although a complete remission of cardiac hypertrophy becomes impossible. In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, as well as the density of nuclei of myocytes. The values of all histometric parameters correlated well with the LV weight up to 350 g. In heavier hearts these parameters were approximately at the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g than in hearts below 250 g: 5.53 x 10(9) vs 4.31 x 10(9), p < 0.001. The influence of coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue and age on LV weight were evaluated as well. From these parameters only coronary artery diameters significantly influenced on LV weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗
PubMed1991

Cyclosporine monitoring by fluorescence polarization immunoassay.

The monitoring of cyclosporine levels in whole blood and serum has become a routine procedure for the post-transplant management of immunosuppression. We have developed fluorescence polarization immunoassays for cyclosporine in whole blood and in serum using a monoclonal antibody. These assays are fast (20 determinations in less than 22 min), sensitive (25 micrograms/L for whole blood samples and 10 micrograms/L for serum samples), and precise (CV less than 7% in both assays). Cross-reactivities with AM1 (Metabolite 17) and AM4N (Metabolite 21) are less than 8.5 and 2.5%, respectively, for both assays.

Antibodies, Monoclonal↗
PubMed1991

[Coronary lumen diameter and cardiac mass in various forms of cardiac hypertrophy].

Morphometric evaluation of the epicardial arteries is described in detail in 103 patients with various forms of cardiac hypertrophy. Coronary lumen diameter increases with aging regardless of the cardiac mass. Such an increase is observed in some particular types of cardiac hypertrophy and presumably is caused by the changes of intramuscular vessels and diminished perfusion. In patients with so called myocardial atherosclerosis correlation between coronary lumen diameter age and cardiac mass is opposite. In some forms of cardiac hypertrophy the increment of coronary lumen diameter is accompanied by the increase of the cross sectional area of the artery. In this pattern the increase of lumen diameter is not due to passive vessel dilatation because significant thickening of its wall can be seen. Age appeared to be the most important factor influencing the coronary lumen diameter within the whole population, although this correlation can hardly be seen in patients with "myocardial arteriosclerosis".

Aging↗
PubMed1991

[Comparative evaluation of coronary arteriosclerosis in arterial hypertension and ischemic heart disease. Morphometric analysis of 4062 coronary artery specimens].

We performed a postmortem study on 61 hearts from patients who died of acute ischemic heart disease (IA). Chronic ischemic heart disease (IB) and from hypertensive patients who died of heart infarction (IIA) and other hypertensive complications (IIB). Control group consisted of 16 pts. who died of non cardiac diseases. 4062 coronary artery specimens were estimated. Irrespective of the clinical course of ischemic heart disease the mean percent of coronary artery stenosis was similar in both ischemic groups and significantly higher than in control group. In hypertensive pts. who died of heart infarction it was also significantly higher and similar to ischemic pts. We found the highest percent of segments with critical stenosis in the left anterior descending coronary artery in group IA, IB, IIA. It was also significantly higher in the left main coronary artery in the group of ischemic pts. (IA, IB).

Adult↗
PubMed1990

[Myocardial structure in various forms of hypertrophy. I. Myocyte hypertrophy or hyperplasia? Pathophysiological aspects and the methods of study].

One of most controversial problems in cardiac muscle pathology is the existence of myocyte hyperplasia. The term hypertrophy indicates an increase in size of the individual muscle cells without changing their total number, whereas in hyperplasia proliferation of the myocyte occurs. This fundamental question of the character of cardiac growth remains unresolved in spite of the wide attention in has received. Contemporary views concerning the cardiac muscle hyperplasia are presented. From clinical point of view the problem is significant for two reasons. The loss of the ability of muscle cells to proliferate is responsible for the irreversible myocardial destruction after injury. From another point of view, if the increase of the heart muscle is maintained, although a complete remission of cardiac hypertrophy becomes impossible. In the light of these controversies we undertook the attempt to solve this complicated problem. Morphometric evaluation of the cardiac myocyte is described in detail.

Anthropometry↗
PubMed1990

[Myocardial structure in various forms of hypertrophy. II. Myocyte hypertrophy or hyperplasia? Results of the study].

In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, as well as the density of nuclei of myocytes. The values of all histometric parameters correlated well with the LV weight up to 350 g. In heavier hearts these parameters were approximately at the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g than in hearts below 250 g: 5.53 x 10(9) vs 4.31 x 10(9), p less than 0.001. The influence of coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue and age on LV weight were evaluated as well. Only coronary artery diameters significantly influenced on LV weight. On the basis of linear discriminant function, three classes of hearts were separated: 1) LV weight 250 g - absence of hyperplasia, only hypertrophy 2) LV weight 251-350 g - hypertrophy + signs of hyperplasia 3) LV weight 350 g - marked signs of hyperplasia Among 18 patients with the LV weight above 350 g (all patients with congestive heart failure), 11 suffered from valvular disease, 3 were postinfarction patients, 2 suffered from primary hypertension and 2 from primary congestive cardiomyopathy. It indicates that, irrespective to the etiologic factor, hyperplasia is a simple result of the cardiac muscle mass increase.

Adult↗