CT and MR imaging in primary cerebral non-Hodgkin's lymphoma.

Purpose: To determine the morphological appearance and topographical distribution of primary cerebral non-Hodgkin's lymphoma (NHL).

Material And Methods: CT and MR examinations of 68 patients with primary cerebral NHL were analyzed. The NHLs were classified by the Kiel classification and immunohistological data, as centroblastic (25), immunoblastic (24), lymphoblastic (5), Burkitt (1), non-subclassifiable type B (11), and T-cell lymphoma (2).

Upregulation of cell adhesion molecules and the presence of low grade inflammation in human chronic heart failure.

Background: In the present study, the hypothesis was tested that cell adhesion molecules are expressed in failing human hearts and that a chronic inflammatory process contributes to chronic degeneration known to occur in cardiac incompetence. The cell adhesion molecules: ICAM-1, VCAM-1, PECAM-1, and E-selectin were studied, in addition to cellular markers of inflammation.

Methods And Results: Tissue was obtained at transplantation from patients with either myocarditis, chronic ischaemic heart disease, or dilated cardiomyopathy.

Time course of mitosis and collateral growth following coronary microembolization in the porcine heart.

In ischaemic porcine myocardium, the growth of collateral vessels by angiogenesis is observed in clusters in the vicinity of focal necroses. Because mitosis of endothelial cells is a prerequisite for angiogenesis, the purpose of this study has been to evaluate the time course of mitosis as an indicator of vascular growth in a porcine model of coronary microembolization. Ischaemia was induced by injection of 25-microm microspheres in the left circumflex artery, followed by tissue collection from non-ischaemic and ischaemic areas of the same heart after 24, 72 or 168 h microembolization.

Effects of positive inotropic stimulation on postischemic myocardium with graded dysfunction.

Objective: To investigate the effects of moderate prolonged and of maximum short-term positive inotropic stimulation of postischemic myocardium as a function of the severity of stunning.

Methods: Stunned isolated rat hearts (n = 116) after 30 min and 45 min of ischemia were stimulated with dopamine to raise systolic function (double product) back to control levels. In the isovolumetrically beating hearts, left ventricular developed pressure, double product, dp/dtmax, coronary flow, and myocardial oxygen consumption were determined during steady-state conditions.

Coordinate expression of the insulin-like growth factor system after microembolisation in porcine heart.

Objectives: Coronary microembolisation in the pig heart induces angiogenesis in a model of sterile inflammation due to focal necrosis. We have recently shown in this model that insulin-like growth factor I (IGF-I) is involved in inflammation-linked angiogenic processes due to its enhanced transcription after 72 h of ischaemia by infiltrating monocytes in areas of microsphere-induced focal necrosis where capillary sprouting could be detected. To obtain further insights into this process we studied by means of Northern blot analysis and in situ hybridisation the gene expression of other members of the IGF family, i.

Tumor necrosis factor-alpha in macrophages of heart, liver, kidney, and in the pituitary gland.

Tumor necrosis factor-alpha (TNFalpha) is an important mediator in bacterial lipopolysaccharide (LPS)-induced fever and shock. New data on TNFalpha-producing macrophages in heart, pituitary gland, kidneys and liver in correlation with TNFalpha plasma levels are reported here. In adult rabbits, core temperature and TNFalpha plasma levels are significantly increased at 3 and 24 h after treatment with LPS.

Expression of adhesion molecules is specific and time-dependent in cytokine-stimulated endothelial cells in culture.

The time course of expression of the adhesion molecules E-selectin, VCAM-1, ICAM-1 and PECAM-1 was studied in interleukin-1 beta-stimulated human umbilical vein cells (HUVEC) and the subcellular sites of synthesis were determined by means of fluorescence immunohistochemistry. The maximal number of cells labelled for E-selectin was observed at 2-4 h, for VCAM-1 at 4-8 h and ICAM-1 at 6-72 h. At 8 h, E-selectin and VCAM-1 started to disappear, but ICAM-1-positive cells persisted.

Myocyte degeneration and cell death in hibernating human myocardium.

Objectives: The aim of this study was to analyze the morphologic characteristics of myocyte degeneration leading to replacement fibrosis in hibernating myocardium by use of electron microscopy and immunohistochemical techniques.

Background: Data on the ultrastructure and the cytoskeleton of cardiomyocytes in myocardial hibernation are scarce. Incomplete or delayed functional recovery might be due to variable degree of cardiomyocyte degeneration in hibernating myocardium.

Pathogenesis of dilated cardiomyopathy and heart failure: insights from cell morphology and biology.

The cause of dilated cardiomyopathy is not yet clear but the recent discovery of a chromosomal aberration as well as the presence of autoantibodies indicate a multicausal origin. Knowledge of pathogenetic mechanisms continues to evolve and includes decreased sarcoplasmic reticulum Ca2+ uptake, reduced beta-receptor density and decreased contractility, the presence of enlarged myocytes showing numerous degenerative alterations, and fibrosis. Defects in titin, a large sarcomeric protein, may be responsible for disturbances of sarcomerogenesis in dilated cardiomyopathy.

[Critique of compulsory responsibilities of insured persons in endangerment according to the therapeutic drug law].

The authors discuss the 5th amendment of the law which regulates the application of therapeutical drugs in Germany (Arzneimittelgesetz), regarding the probands' insurance according to section 40 (3), from the viewpoint of the ethics committee of the Medical Chamber of Rheinland-Pfalz introduced under State (Land) law to protect patients and probands. The authors criticize a number of regulations which might have disadvantages for patients and probands in the case of damage (injury), after they have participated in therapeutical drug trials for the benefit of the general public and by taking a certain personal risk. To overcome these problems, specific proposals for the improvement of the law are being made.

Ultrastructural Evaluation of Postischemic Cell Death (Lethal Reperfusion Injury) in Porcine Hearts.

This study investigated whether reperfusion results in an increase of ultrastructurally determined myocardial injury in pig hearts. The left anterior descending coronary artery (LAD) was distally occluded in 12 pigs for 35-45 minutes and then reperfused for 3 hours. At the end of ischemia, as well as after 3 hours of reperfusion, one transmural biopsy was removed from the center of the risk region and subdivided into four-specimens, representing the subendocardial (I), subendo-midmyocardial (II), subepi-midmyocardial (III), and subepicardial layers (IV).

Ischemia affects cardiac proteins in healthy animals less severely than in human patients.

Background: Recently, our group showed that in human hearts proteins are extremely sensitive to ischemic injury. The purpose of this investigation was to evaluate the effects of ischemia on contractile and cytoskeletal proteins in rabbit and pig hearts and to compare these findings with those obtained in humans.

Methods: Rabbit hearts were arrested by perfusion with Euro-Collins solution at different temperatures.

Ischemia induces early changes to cytoskeletal and contractile proteins in diseased human myocardium.

Ischemia is known to produce damage to subcellular organelles, such as nuclei and mitochondria, in myocardial tissue. We tested the hypothesis that during myocardial ischemia various cytoskeletal and contractile proteins also undergo changes. We induced total global ischemia by incubation in buffer of tissue samples from six human left ventricles that were obtained from heart transplant recipients.

Angiotensin converting enzyme inhibitors, left ventricular hypertrophy and fibrosis.

From pharmacological investigations and clinical studies, it is known that angiotensin converting enzyme (ACE) inhibitors exhibit additional local actions, which are not related to hemodynamic changes and which cannot be explained only by interference with the renin angiotensin system (RAS) by means of an inhibition of angiotensin II (ANG II) formation. Since ACE is identical to kininase II, which inactivates the nonapeptide bradykinin (BK) and related kinins, potentiation of kinins might be responsible for these additional effects of ACE inhibitors. a) In rats made hypertensive by aortic banding, the effect of ramipril in left ventricular hypertrophy (LVH) was investigated.

Importance of monocytes/macrophages and fibroblasts for healing of micronecroses in porcine myocardium.

In porcine heart, embolization of small coronary arteries with microspheres in 25 microns in diameter induces collateral capillary vessel growth by angiogenesis in and around focal necrosis. By histological analysis the inflammatory infiltrates in this porcine tissue were characterized by numerous monocytes/macrophages and fibroblasts as well as neutrophils and numerous capillaries, some in mitosis. The aim of the present study, therefore, was to clarify the role of monocytes/macrophages and fibroblasts in angiogenesis and in repair in ischemic porcine myocardium.

Structural organization and chromosomal localization of the mouse collagenase type I gene.

A clone containing genomic sequences of part of the murine collagenase type 1 (MMP-1) gene was isolated. It contains exons 1-6 encoding all the domains required for collagenase function and 9 kb of 5'-flanking sequences. The gene organization and exon/intron borders are highly similar to the already described human and rabbit MMP-1 genes.

Extracellular matrix deposition in hypertensive hearts antifibrotic effects of ramipril.

Hypertension induced in rats by suprarenal banding has a blood pressure elevating effect that is accompanied by the occurrence of cardiac hypertrophy and fibrosis. This phenomenon is already present at 2 weeks after banding and persists up to 1.5 years.

Insulin-like growth factor II is an experimental stress inducible gene in a porcine model of brief coronary occlusions.

Objective: Previous observations have shown that myocardium activates many adaptive processes after brief ischaemia. The aim of this study was to determine whether insulin-like growth factors (IGF) as well as their receptors and binding proteins (IGFBP), which control the activity of the IGF, may play an important role during these processes.

Methods: Ischaemia was induced in anaesthetised open chest pigs by two 10 min occlusions of the left anterior descending coronary artery, separated by 30 min of reperfusion, and followed by reperfusion up to 210 min.

Collagen VI in the extracellular matrix of normal and failing human myocardium.

Our own previous studies of the composition of the extracellular matrix of human failing hearts showed that collagen VI seems to play a major role in the origin of cardiac fibrosis. Therefore, collagen VI was investigated in more detail in tissue samples taken from clinically normal left ventricle and from myocardium failing because of dilated cardiomyopathy. Tissue sections prepared with collagen VI antibodies were examined by fluorescence microscopy using conventional or confocal laser scanning microscopy.

Pathological changes of myocardial cytoskeleton in cardiomyopathic hamster.

Immunocytochemical investigation was performed on the cytoskeletal proteins in cardiac tissue of the cardiomyopathic hamster. Male cardiomyopathic UM-X7.1 hamsters at 180 days of age (n = 8) and age- and sex-matched normal BIO-RB hamsters (n = 8) were used in this study.

Insulin-like growth factor I is involved in inflammation linked angiogenic processes after microembolisation in porcine heart.

Objective: Angiogenesis in the porcine heart can be induced by myocardial ischaemia following vascular occlusions. This process is characterised by increased numbers of monocytes/macrophages, known to be potent producers of various mitogens such as insulin-like growth factors (IGF) and interleukins (IL). The aim of the study was to examine gene expression of these factors by means of northern blot hybridisation, slot blot analysis, and in situ hybridisation in a porcine model of coronary angiogenesis.

[Interactions between cardiomyocytes and extracellular matrix in the failing human heart].

Numerous morphological changes can be observed in human myocardium failing because of dilated cardiomyopathy. These can be observed by electron microscopy and by immunofluorescence microscopy using monoclonal antibodies. These changes include: 1) the occurrence of hypertrophied and atrophied myocytes as well as cells of normal size, 2) degenerative changes in myocytes; these consist of nuclei of varying size and shape, lack of contractile material, disorganization of the cytoskeleton, and sequestration of cellular particles into the extracellular space and 3) an enlarged extracellular space, that is, fibrosis, which contains increased amounts of the different matrix proteins such as fibronectin and laminin, the various collagens, and chondroitin sulfate, in addition to cellular debris and numerous macrophages and fibroblasts.