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Biomedical subjects

Z Nagy

Publications and source records attributed to Z Nagy.

At least 91 records · Page 5Linked to original sources
PubMed1999

[Risk factors in various groups of stroke patients (Analysis of 500 cases of the Budapest Stroke Database)].

Risk factor profile of 500 consecutive acute++ stroke cases in the protocol of the Budapest Stroke Data Bank has been analysed. High frequency of risk factors and additive occurrence have been documented when compared with other stroke registries; hypertension 75%, hypercholesterolemia 68%, ischemic heart disease 61%, hypertriglycerolemia 39%, smoking 38%, serious hypercholesterolemia 36%, diabetes mellitus 30%, peripheral artery disease 10%, elevated hematocrit 7% and elevated number of platelets 7%. More than one risk factors have been registered in 85% of the patients. Three risk factors at the same patient have been found in 28%. The highest number of risk factors is seven at the same patient. The stroke subtypes have been characterized with "cluster-like" association of risk factors. In the hemorrhagic group (9.4% of all cases) hypertension and alcoholism are the main factors; in the atherosclerotic group (49.4%) more male, smoking peripheral artery disease and hypercholesterolemia have been registered; in the lacunar stroke group (27%) high frequency of hypertension, smoking, diabetes mellitus, hypercholesterolemia and hypertriglycerolemia have been found and in the cardiogenic embolia group (10.6%) more female, higher age, ischemic heart disease and atrial fibrillation are the recurrent risk factors. There is no difference between the risk factor profile++ registered in the left versus right hemispheral strokes, in the anterior versus posterior strokes and in the first ever or recurrent strokes.

Aged↗
PubMed1999

[Surgical treatment of mitral insufficiency using annuloplasty suture technic].

In 1991 a simple and cheap technique was introduced for mitral valve repair at our department. After repairing the mitral leaflets, where indicated a posterior leaflet annuloplasty was performed with a semicircular suture and the annulus fixed for the appropriate size by tying the stitch. Between July 1991 and December 1995 86 patients underwent the above procedure (average age 56.8 +/- 10.4 years). 45 patients had primary mitral valve disease (myxomatous degeneration, rheumatoid disease, endocarditis), the other 41 had functional mitral regurgitation secondary to severe aortic valve or coronary artery disease. Echocardiography showed severe mitral regurgitation in 77% of the patients. In 45 cases the mitral valve itself was also repaired (valvotomy, quadrangular resection, wedge resection, etc.) in 29 cases the aortic valve was replaced as well, while 24 patients required additional revascularisation of the myocardium. The 30 day mortality was 3.5%. One week after surgery echocardiography was performed at all patients and showed acceptable mitral valve area (2.28 +/- 0.39 cm2). In 28 cases mild mitral regurgitation was found, the other valves were competent. All but 3 patients were followed up (96.4%). There were 6 late deaths (3 cardiac, 2 non cardiac, 1 embolic, 7.2% late mortality). During the follow up period (31.7 +/- 11.2 months) 5 patients required mitral valve replacement for severe recurrent mitral regurgitation (6.0%). In two cases new chorda rupture caused the recurrence, in an other case the suture had torn out of the annulus due to inadequate surgical technique. In the last two cases the annulus had dilated with intact Prolene annuloplasty stitch present, 86.8% of the survivors were in NYHA class I. or II. Our results suggest that mitral valve repair in selected cases can be performed without using expensive annuloplasty rings. The suture used for annuloplasty should be strong, non absorbable and non stretchable. Since 1994, when we started using GoreTex suture instead of Prolene no more patients required reoperation for annuloplasty failure.

Adult↗
PubMed1999

Expression of membrane-bound and soluble cell adhesion molecules by human brain microvessel endothelial cells.

Expression of membrane-bound (mb) and soluble (s) forms of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) induced by tumor necrosis factor-alpha (TNF-alpha) has been measured by enzyme-linked immunosorbent assay in cultured human brain microvessel endothelial cells. Both the mb and the s forms of VCAM-1 and ICAM-1 were upregulated by TNF-alpha; however, the stimulation of the s forms was delayed in time. When piracetam, a neuroprotective drug, was added to the tissue culture medium simultaneously with TNF-alpha, the expression of mbVCAM-1 and ICAM-1 was lowered. Differential upregulation of mb and s forms of adhesion molecules and a novel effect of piracetam have been demonstrated in human brain microvessel endothelial cell cultures.

Brain↗
PubMed1999

Mechanisms of neuronal death in Down's syndrome.

There is growing evidence that neuronal death in Down's syndrome is due to apoptotic mechanisms. The phenomena, however, that trigger and regulate programmed cell death in the Down's syndrome-related neurodegeneration are still much debated. In vitro evidence has suggested that the main factor responsible for neuronal death in this condition is the accumulation of beta-amyloid, due to the overexpression of its precursor protein. Another hypothesis argues for the importance of reactive oxygen species in neuronal death. However, the in vivo findings do not entirely support either theories. We propose that neuronal apoptosis, as well as the formation of Alzheimer-type pathology, in Down's syndrome is due to an aberrant re-entry of neurones into the cell division cycle. Due to the simultaneous overexpression of conflicting cell cycle regulatory signals the mitogenic amyloid precursor and the differentiation factor S100, the cell cycle is abandoned. Subsequently the cell cycle arrest may lead to either the formation of Alzheimer-related pathology or to apoptotic cell death.

Alzheimer Disease↗
PubMed1999

Suppressive effect of pentoxifylline on natural killer cell activity; experimental and clinical studies.

The methylxanthine derivative pentoxifylline, widely used in the treatment of vascular diseases, also has numerous immunological effects. In in vitro experiments, the human natural killer cell cytotoxicity was investigated in the presence of pentoxifylline. A clinical trial involved an investigation of the natural killer cell activity in patients to whom pentoxifylline had been administered for different periods. The natural cytotoxicity in macroangiopathic patients treated with pentoxifylline was compared with that in healthy controls and that in patients with vascular diseases who did not receive pentoxifylline therapy. A total of 62 macroangiopathic patients and 20 healthy controls were investigated. The natural killer cell activity in patients receiving pentoxifylline therapy for more than a year proved to be significantly lower (P<0.005). The presence of vascular disease did not influence the natural killer activity. In the in vitro cytotoxicity reaction, pentoxifylline at a concentration of 100 microg/ml was found to suppress the natural killer cell cytotoxicity at any stage of the reaction. The influence of pentoxifylline on the natural killer cell activity was not due to inhibition of the expression of intercellular adhesion molecule-1. However, this drug significantly decreases (P<0.05) the apoptosis of target cells. It is presumed that the suppressor effect of pentoxifylline on natural killer cell activity should be taken into consideration in the treatment of clinical diseases where this drug is administered chronically.

Adult↗
PubMed1999

Mitochondrial enzyme expression in the hippocampus in relation to Alzheimer-type pathology.

Recent reports have suggested that mitochondrial dysfunction may contribute to the progression of the pathology of Alzheimer's disease (AD). However, both increases and decreases in the activity of cytochrome oxidase have been described in the hippocampi of AD patients. In this study we used immunohistochemistry and quantitative autoradiographic methods to study the expression pattern of two cytochrome oxidase subunit proteins (nuclear-encoded COX IV and mitochondrial-encoded COX I) in the hippocampus in relation to the development of AD-type pathology. We found heterogeneous expression of both COX subunits in AD with an increased expression of both subunit proteins in healthy, non-tangle-bearing, neurones but absence of both subunit proteins in tangle-bearing neurones. Levels of COX IV but not of COX I were related to the amount of hyperphosphorylated tau accumulated in the same hippocampal region but not to the amount of amyloid deposited in sporadic AD. In Down's syndrome COX I and COX IV were similarly increased in the presence of AD pathology in non-tangle-bearing neurones. However, in these cases levels of enzyme expression were correlated to the amount of amyloid accumulation but not the amount of hyperphosphorylated tau in the hippocampus. We believe that heterogeneity of expression of mitochondrial enzyme proteins between neurones may contribute to the conflicting conclusions in previous reports regarding relative levels of cytochrome oxidase activity in the hippocampus in AD. We hypothesise that the increased mitochondrial enzyme expression in healthy-appearing neurones of AD brains may represent a physiological response to increased functional demand on surviving neurones as a consequence of AD-related neuronal pathology.

Adolescent↗
PubMed1999

Scalp distribution of the dimensional complexity of the EEG and the P3 ERP component in stroke patients.

The use of recently developed techniques allows the quantitative investigation of the non-linear properties of the electrical activity of the brain not only in basic but also in applied research. The point correlation dimension (PD2) was used in this study for the analysis of the electroencephalogram (EEG) recorded in patients with unilateral stroke caused by middle cerebral artery occlusion. The scalp distribution of the PD2 and that of the P3 event-related potential component was mapped and frequency spectra were calculated. Compared to normal controls, asymmetrical PD2 distribution was observed with low values on the side of the stroke, the extension of which depended on recording conditions (level of vigilance) and only partially corresponded to the region characterized by slow frequencies. In one case, ipsilateral reduction of the P3 wave was caused by a small subcortical stroke. The efficacy of the linear and non-linear methods in localizing brain pathology are evaluated and compared.

Electroencephalography↗
PubMed1999

Elevated serum TNF-alpha level as a link between endothelial dysfunction and insulin resistance in normotensive obese patients.

AIMS: The aim of the study was to analyse the role of tumour necrosis factor-alpha (TNF-alpha) in insulin resistance and endothelial dysfunction in patients with different types of obesity. PATIENTS AND METHODS: Fasting serum TNF-alpha immunoreactive concentration (enzyme-linked immunosorbent assay, ELISA) and bioactivity (L929 cell cytotoxicity assay), endothelin-1 and C-peptide levels (radioimmunoassay, RIA) were measured in 15 patients with android- and 13 patients with gynoid-type obesity and 15 lean healthy controls with normal glucose tolerance and blood pressure. RESULTS: Significantly (P<0.01) higher TNF-alpha concentration (8.92 +/- 0.44 pg/ml) and bioactivity (3.12 +/- 0.48 U/ml) were found in patients with android obesity as compared to patients with gynoid obesity (7.01 +/- 0.30 pg/ml, 0.97 +/- 0.11 U/ml) and to the lean controls (6.88 +/- 0.26 pg/ml, 0.88 +/- 0.08 U/ml). Serum endothelin-1 (5.38 +/- 0.30 pg/ml) and C-peptide levels (4.82 +/- 0.71 ng/ml) were also significantly higher (P < 0.01) in patients with android-type obesity than in controls (3.89 +/- 0.43 pg/ml, 1.46 +/- 0.25 ng/ml, respectively). In patients with gynoid-type obesity, only the C-peptide levels proved to be significantly higher (2.84 +/- 0.29 ng/ ml). Endothelin-1 levels, although were found to be slightly higher, did not differ statistically from in controls (4.56 +/- 0.31 pg/ml). There were significant positive linear correlations only in patients with android-type obesity between TNF-alpha, body mass index (BMI), serum endothelin-1 and C-peptide levels. CONCLUSIONS: TNF-alpha may be one of the factors contributing to insulin resistance and vascular dysfunction in patients with android obesity.

Adult↗
PubMed1999

The enhanced peroxidase one step method increases sensitivity for detection of Ki-67 in pituitary tumours.

AIM: To compare the Ki-67 labelling index determined using the enhanced peroxidase one step (EPOS) method with that using the standard ABC technique in pituitary tumours. METHODS: Adjacent sections were immunostained using the EPOS and ABC techniques with the same Ki-67 antibody and same antigen retrieval method. RESULTS: The labelling index measurements with the EPOS Ki-67 antibody were significantly higher than when using the traditional ABC method, and there was a positive correlation between the two techniques when performed on the same cases. This suggests that a higher proportion of cells are within the cell cycle than previously thought, although it gives no direct information on the rate of proliferation of the tumour. CONCLUSIONS: It appears that the EPOS system is not only more convenient but may be more sensitive than traditional techniques for detecting Ki-67 in the nuclei of cells, thus demonstrating more accurately which cells have entered the cell cycle.

Cell Division↗
PubMed1999

Ultrastructural localization of Hsp-72 examined with a new polyclonal antibody raised against the truncated variable domain of the heat shock protein.

In spite of the intensive search for the determination of the continuously widening physiological and pathological roles of different stress proteins, their ultrastructural localization at the electron microscopic (EM) level has hardly been examined. As it becomes increasingly evident that the function and physiological effectiveness of stress proteins are highly dependent on their spatial location and their associations with diverse regulator proteins, the demand for morphological studies which can identify their detailed distribution within the cells is evident. The reason for the practical lack of studies carried out at the EM level, lies in the shortage of reagents with suitable specificity and avidity necessary for this type of examination. To create such a reagent, a polyclonal antibody was raised using a recombinant truncated form of the inducible Hsp-72 protein. The antibody was extensively characterized, using different immunochemical methods to determine and verify its specificity, and then it was tried in ultrastructural examinations. Using the new antibody, it was possible to analyze the intracellular distribution of Hsp-72 with the immunogold technique. The localization of Hsp-72 was demonstrated directly at the ultrastructural level in the cytoplasm (especially at the cisterns of the RER), in the nucleus (mainly around the heterochromatic regions) and at both sides of the nuclear envelope close to the membrane pores. Apart from these localizations, Hsp-72 was found in several membrane bordered intracellular structures, which mainly belong to the endosomal-lysosomal system. We provide the first morphological verification of the appearance of Hsp-72 on the surface of the cells. Also novel is the indication, that the stress protein may recycle from the cell surface using a common route which includes coated pits and the endosomal system.

3T3 Cells↗
PubMed1999

Quantitative trait loci for blood pressure exist near the IGF-1, the Liddle syndrome, the angiotensin II-receptor gene and the renin loci in man.

Blood pressure (BP) is heritable and finding quantitative trait loci that influence BP is an important step in identifying genes responsible for BP regulation. Sixty-six pairs of dizygotic (DZ) twin subjects and their parents were used in a sib-pair analysis to look for linkage of selected candidate genes to the quantitative trait BP. Microsatellite markers were tested in the vicinity of the gene loci for insulin-like growth factor-1 (IGF-1), Liddle syndrome, autosomal-dominant hypertension with brachydactyly, angiotensinogen, angiotensin II type 1 receptor, angiotensin-converting enzyme, renin, and lipoprotein lipase. BP was measured in a standardized manner. Heart size was determined echocardiographically. Significant linkage was found at the IGF-1, Liddle syndrome, and AT1 receptor gene for systolic BP. Linkage for diastolic BP was found at the autosomal-dominant hypertension with brachydactyly locus. Both systolic and diastolic BP were linked to the renin gene locus. The linkage was most consistent for the IGF-1 gene locus and systolic BP. Linkage was also found between the IGF-1 gene locus and posterior cardiac wall thickness, septal thickness, and left ventricular mass index. It is suggested that these quantitative trait loci may be important for the subsequent detection of allelic variants for elevated BP. Furthermore, these results linking the IGF-1 gene locus to both BP and cardiac dimensions underscore the importance of the IGF-1 gene as a candidate gene for cardiovascular disease.

Adult↗
PubMed1998

[In vitro and clinical effect of pentoxifylline on natural killer cell activity].

Pentoxifylline used in the treatment of vascular diseases has also some immunological effects. Among of these effects the influence of pentoxifylline on the natural killer cell activity was studied. In in vitro experiments the human natural killer cell cytotoxicity was examined in the presence of pentoxifylline. In our clinical trial we investigated the topic whether this drug has an immunomodulatory effect while administering it for different periods. The natural cytotoxicity of macroangiopathic patients treated with pentoxifylline was compared with the values of healthy controls and patients suffering from vascular disease and obtaining no pentoxifylline therapy. Sixty two macroangiopathic patients and twenty healthy controls were investigated altogether. In the in vitro natural killer cell reaction we found that the pentoxifylline was able to suppress the cytotoxicity at any time of the reaction. The influence of pentoxifylline on natural killer cell activity was neither due to the expression of intercellular adhesion molecule-1, nor to the alteration of membrane fluidity. However, this drug significantly (p < 0.05) decreases the apoptosis of target cells. The natural killer cell activity of patients with chronic pentoxifylline therapy lasting for more than a year was proved to be significantly (p < 0.005) lower. The presence of vascular disease does not influence the natural killer activity by itself. Concluding our results we can state that the suppressing effect of pentoxifylline on natural killer cell activity needs to be taken into consideration in case of clinical diseases where this drug is administered chronically.

Adult↗
PubMed1998

Neurotrophin-mediated neuroprotection by solid fetal telencephalic graft in middle cerebral artery occlusion: a preventive approach.

In the present study, embryonic rat neocortex was implanted into the parietal subcortical area of adult naive animals. On the 7th day, the middle cerebral artery was permanently occluded ipsilateral to the graft. Twenty-four hours after middle cerebral artery occlusion, the extent of infarct was visualized by means of 2,3,5-triphenyltetrazolium chloride histochemistry and quantified in four different standardized coronal plains. Subsequently, the effects of fetal tissue grafting and those of transplantation were identified by using glial fibrillary acidic protein and nerve growth factor immunocytochemistry. The grafts integrated well into their new environment and significantly reduced the size of infarct in middle cerebral artery-occluded animals compared with both sham-operated and control rats 24 h postoperation. The underlying mechanism of this phenomenon might be an increased neurotrophic, particularly nerve growth factor, release by the grafted fetal tissue. Moreover, reactive astroglial cells may also trigger the neuroprotection by additional ischemia-induced nerve growth factor release. The present data demonstrate the potential neurotrophin-mediated protective effects of fetal brain tissue implanted into the adult rat brain before unilateral middle cerebral artery occlusion and the beneficial effects of astrocyte activation.

Animals↗
PubMed1998

Experimental acute pancreatitis results in increased blood-brain barrier permeability in the rat: a potential role for tumor necrosis factor and interleukin 6.

Pancreatic encephalopathy is a severe complication of acute pancreatitis. Proinflammatory cytokines may play a role in the development of multi-organ failure during pancreatitis. In the present study, we measured the changes in the blood-brain barrier (BBB) permeability concomitantly with the determination of serum tumor necrosis factor (TNF) and interleukin-6 (IL-6) levels in rats before, as well as 6, 24 and 48 h after the beginning of intraductal taurocholic acid-induced acute pancreatitis. Cytokine concentrations were measured in bioassays with specific cell lines (WEHI-164 for TNF and B-9 for IL-6), while the BBB permeability was determined for a small (sodium fluorescein, molecular weight (MW) 376 Da), and a large (Evans' blue-albumin, MW 67000 Da) tracer by spectrophotometry in the parietal cortex, hippocampus, striatum, cerebellum and medulla of rats. The serum TNF level was significantly (P < 0.05) increased 6 and 24 h after the induction of pancreatitis, while the IL-6 level increased after 24 and 48 h. A significant (P < 0.05) increase in BBB permeability for both tracers developed at 6 and 24 h in different brain regions of animals with acute pancreatitis. We conclude that cytokines, such as TNF and IL-6, may contribute to the vasogenic brain edema formation during acute pancreatitis.

Amylases↗
PubMed1998

Neuronal cyclin expression in the hippocampus in temporal lobe epilepsy.

This study used immunocytochemistry to explore the expression of cyclins A, B, D, and E and the apoptosis-associated Bax protein in hippocampal subfields of 35 lobectomy specimens with medial temporal lobe sclerosis removed for the treatment of temporal lobe epilepsy (TLE), 2 age-matched controls, and 2 elderly patients suffering from drug-responsive epilepsy. Cyclins A and D were not detected at all in neuronal nuclei. Cyclin E was only rarely detected in neuronal nuclei in drug-controlled and TLE groups and in controls. Cyclin B was expressed in significantly more neuronal nuclei in the hippocampi in TLE than in the other groups studied. The nuclear expression of these proteins suggested that neurons had reentered the cell division cycle and reached the G2 phase. The nuclear expression of cyclin B in the hippocampus from these patients was accompanied by neuronal cytoplasmic expression of the death-related Bax protein. We interpret these neuronal findings as evidence of cell cycle disturbances and a possible apoptotic mechanism of hippocampal neuronal cell death in TLE.

Adult↗
PubMed1998

Temporal cortex synaptophysin mRNA is reduced in Alzheimer's disease and is negatively correlated with the severity of dementia.

We measured synaptophysin mRNA in neocortical tissue from 7 prospectively assessed, pathologically verified normal individuals, 17 subjects with Alzheimer's disease (AD), and 13 subjects with a non-AD dementia. In temporal cortex (Brodmann area 21), synaptophysin mRNA was decreased in AD and non-AD dementia groups compared to controls. The loss was also present relative to polyadenylated mRNA content. Synaptophysin mRNA signal correlated negatively with the degree of dementia and negatively with the pathological severity of AD. In occipital cortex (Brodmann area 17) there were no differences between groups nor clinicopathological correlations. These data extend the evidence for a regional synaptic pathology in AD which affects synaptic protein gene expression by temporal cortex neurons.

Aged↗
PubMed1998

Beneficial effect of octreotide treatment in acute pancreatitis in rats.

CONCLUSIONS: Octreotide treatment contributes to the regulation of tumor necrosis factor (TNF) production in sodium taurocholate-induced acute necrotizing pancreatitis in rats. Owing to its complex effect, octreotide can partially ameliorate the deleterious consequences of acute necrotizing pancreatitis. Elevated TNF and interleukin-6 (IL-6) levels in the peritoneal fluid may be considered a consequence of the activation of peritoneal macrophages. BACKGROUND: The effects of octreotide on exocrine pancreatic function have been investigated in numerous studies, but little attention has been paid to its influence on cytokine production in acute pancreatitis. METHODS: Acute pancreatitis was induced by the retrograde injection of taurocholic acid into the pancreatic duct in male Wistar rats. Serum amylase activity, wet pancreatic weight/body weight (pw/bw) ratio, and TNF and IL-6 levels were measured. Four micrograms/kg of octreotide was administered subcutaneously at the time of induction of pancreatitis and 24 or 48 h later. Rats were sacrificed 6, 24, 48, or 72 h after the operation. RESULTS: The serum amylase level and pancreatic weight to body weight ratio were decreased significantly in the octreotide-treated group. The serum TNF level was decreased significantly in the octreotide-treated group as compared with the control group at 6, 24, and 48 h (0.6 +/- 1.5, 2.0 +/- 3.3, and 0 vs 50 +/- 15.5, 37.5 +/- 18.4, and 13.1 +/- 12.5 U/mL, respectively). The ascites TNF level was decreased to 0 in the octreotide-treated group and was elevated in the control group at 72 h (28.0 +/- 49.0 U/mL). IL-6 production in ascites was extremely high in both groups at 6 h (80,000 +/- 43,817 pg/mL and 58,500 +/- 33,335 pg/mL), but the difference was not significant.

Amylases↗