bluuebunny/crossref_metadata_2025_split huggingface dataset:
Beneficial effect of enalapril in spontaneously hypertensive rats cardiac remodeling with nitric oxide synthesis blockade
Authors: de Andrade Zorzi R. L. , Meirelles Pereira Leila M. , Mandarim‐de‐Lacerda C. A. 
Published: May 2007

AbstractAims. To study the efficiency of an angiotensin converting enzyme inhibitor on the blood pressure (BP) and the myocardium remodeling when spontaneously hypertensive rats (SHRs) are submitted to nitric oxide synthesis (NOs) blockade (with L‐NAME) and simultaneously treated.Methods. Young adult male SHRs were separated in four groups (n = 5) and treated for 20 days: Control, L‐NAME, L‐NAME+Enalapril, and Enalapril. The alterations of the BP, heart mass/body mass ratio and stereological parameters for myocytes, connective tissue and intramyocardial vessels were studied among the groups.Results. The SHRs with NOs blockade showed a great modification of the myocardium with extensive areas of reparative and interstitial fibrosis and accentuated hypertrophy of the cardiac myocytes (cross sectional area 60% higher in animals taking L‐NAME than in Control SHRs). Comparing the SHRs with NO deficiency (L‐NAME group), the Control SHRs and the Enalapril treated SHRs significant differences were found in the BP and in all stereological parameters. The NO deficiency caused an important BP increment in SHRs that was partially attenuated by Enalapril. This Enalapril effect was more pronounced in Control SHRs. A significant increment of the intramyocardial vessels was observed in NO deficient SHRs and Control SHRs treated with Enalapril demonstrated by the stereology (greater microvascular densities in treated SHRs).Conclusion. Enalapril administration showed a beneficial effect on vascular remodeling and myocardial hypertrophy in SHRs. In SHRs with NO blockade, however, the beneficial effect of Enalapril occurred only in vascular remodeling.
Effect of ischemia‐reperfusion on the post‐rest inotropy of isolated perfused rat heart
Authors: Juggi J.S. 
Published: May 2007

AbstractThis paper aims to study of the effects of ischemia‐reperfusion on the post‐rest inotropy and to characterize post‐rest B1:B2 ratio as an index of intracellular Ca2+ overload. When the rest interval between the cardiac beats is increased, the magnitude of the post‐rest beats is increased. First beat (B1) is maximally potentiated with exponental decline of the second (B2) and subsequent beats, thereby establishing a normal B1:B2 ratio of post‐ rest inotropy of the cardiac muscle. The rest potentiation of B1 and subsequent decay in the magnitude B2 is thought to develop from the time‐dependent changes in the Ca2+‐uptake and release from the sarcoplasmic reticulum (SR). Ca2+‐kinetics of SR can be modulated by a variety of interventions which produce Ca2+ loading of the SR. Methods: Isolated perfused (K‐H buffer, 34°C) rat hearts were paced at 1 Hz (steady state frequency). Interbeat intervals between 1s and 10s were introduced and the recovery in the left ventricular contractile force (Pmax) of post‐rest B1 and B2 for each interval was recorded. Their relative relationship was computed and compared under control and experimental conditions. Results: High extracellular Ca2+ (2.50 to 7.0 mM) or low extracellular Na+ (50% of control), and ischemia (60 min, 34°C) ‐ reperfusion (30 min, 34°C) caused the reversal of the control relationship of the B1 to B2, with B2 being more potentiated than B1, accompanied by the appearance of after‐contractions during the rest intervals of 4s or more. The mean (± SE) control B1:B2 ratio (at 4s interval) of 1.12 ± 0.05 was significantly (P<0.001) reduced to 0.93 ± 0.07; 0.89 ± 0.01; and 0.96 ± 0.02 after high Ca2+ (6 mM) perfusion, low Na+(50%) perfusion and ischemia‐reperfusion respectively. Simultaneous perfusion with ryanodine (1 μM) abolished the after‐contractions and significantly increased the reduced ratios. The time course of changes in B1:B2 ratio after graded ischemia‐reperfusion showed a significant fall in the ratio between 30 and 60 min of ischemia. A parallel change in Pmax and a significant rise in the left ventricular end‐diastolic pressure, indicating an irreversible phase of the injury was recorded. No significant changes in B1:B2 ratio were detected during the reversible phase (<30 min) of the ischemia‐reperfusion injury. Conclusions: Ischemia‐reperfusion induces significant alterations in the relative ratio of the post‐rest contractions of the left ventricle in isolated perfused rat heart. The altered ratios were characterized to predict the irreversibility of the reperfusion injury and to index the extent of Ca2+‐loading of the sarcoplasmic reticulum.
Highly effective techniques in computerized dental tissue morphometry
Authors: Caruntu Irina‐Draga 
Published: May 2007

AbstractThe effectiveness of computer‐aided morphometry is greatly dependent of the capabilities of the software platforms, but the literatutre provides only information about the measurement methods and thier medical interpretation. The purpose of our work is to create a link between the technical algorithm and the medical significance, by a detialed description of measurement procedures, accompained by the interpretation of thier results. The developmed techniques operate at a pixel level, by deriving a full benefit from the computational resources avilable in the modern software evnvironments for image processing. The approach is built on three illustrative cases, formulated in a large sense, so as to cover classes of general problems, referring to cellular entities and tubular structures in cross and longitudinal section. Specimens belonging to the dentin‐pulp complex were chosen, because they permit a quantitiative analysis for each morphological element, as well as comparative discussion. With appropriate adaptations of the procedures, the measurements of other types of normal and pathological tissues and be analogously addressd. The design, implementation and exploittion of our procedures are supported by specific references to the use of an image analysis system (Zeiss KS400). The algorithmic background remains valid (except for some possible minor changes) when similar software is used. Consequently, the results and thier interpretations, prove the importance of the numerical analysis in automating the quantitative evaluation of the structural features.
Angiogenesis and chemokines in rheumatoid arthritis and other systemic inflammatory rheumatic diseases
Authors: Bodolay Edit , Koch Alisa E. , Kim Joon , Szegedi Gyula , Szekanecz Zoltan 
Published: May 2007

AbstractAngiogenesis, the formation of new vessels, is important in the pathogenesis of rheumatoid arthritis (RA) and other inflammatory diseases. Chemotactic cytokines termed chemokines mediate the ingress of leukocytes, including neutrophils and monocytes into the inflamed synovium. In this review, authors discuss the role of the most important angiogenic factors and angiogenesis inhibitors, as well as relevant chemokines and chemokine receptors involved in chronic inflammatory rheumatic diseases. RA was chosen as a prototype to discuss these issues, as the majority of studies on the role of angiogenesis and chemokines in inflammatory diseases were carried out in arthritis. However, other systemic inflammatory (autoimmune) diseases including systemic lupus erythematosus (SLE), systemic sclerosis (SSc), Sjögren's syndrome (SS), mixed connective tissue disease (MCTD), polymyositis/dermatomyositis (PM/DM) and systemic vasculites are also discussed in this context. As a number of chemokines may also play a role in neovascularizaton, this issue is also described here. Apart from discussing the pathogenic role of angiogenesis and chemokines, authors also review the regulation of angiogenesis and chemokine production by other inflammatory meditors, as well as the important relevance of neovascularization and chemokines for antirheumatic intervention.
Angiotensinogen gene M235T variant and pre‐eclampsia in Romanian pregnant women
Authors: Procopciuc Lucia , Jebeleanu Gh. , Surcel I. , Puscas M. 
Published: May 2007

Abstract Background. Association between the human angiotensinogen gene and essential hypertension has been confirmed in recent studies. Pre‐eclampsia is a complication of pregnancy characterised by increased vascular resistance, high blood pressure, proteinuria and oedema, that appears in the second and third trimester of pregnancy. The aim of our study was the analysis of M235T mutation in the gene encoding angiotensinogen in Romanian women with different forms of hypertension during pregnancy. Methods. Fourteen women with obstetric complications were tested for M235T angiotensinogen gene mutation. Indications for testing were: severe or mild pre‐eclampsia and pre‐eclampsia associated with chronic hypertension. We also tested for control 6 healthy women. The M235T angiotensinogen gene mutation was analysed by polymerase chain reaction followed by enzymatic digestion with Tth 111I restriction endonuclease enzyme and agarose gel electrophoresis of the products. Results. Eleven (78.57%) of the 14 women with complications of pregnancy had M235T mutation: 9 (64.28%) were found to be heterozygous carriers of the M235T variant of the angiotensinogen gene and 2(14.28%) were found to be homozygous carriers. In the group of women with normal pregnancy, 3 (50%) of the 6 women had M235T mutation: 2 (33.33%) were found to be heterozygous carriers of the M235T variant of the angiotensinogen gene and 1 (16.66%) was found to be homozygous carrier. Conclusions. Our study shows that the M235T variant in the gene encoding angiotensinogen could be a risk factor in mild and severe pre‐eclampsia.
Oxidative stress in the pathogenesis of nonalcoholic fatty liver disease, in rats fed with a choline‐deficient diet
Authors: Oliveira Claudia P.M.S. , Da Costa Gayotto L. Carlos , Tatai Caroline , Della Bina Bianca Ishimoto , Janiszewski M. , Lima E.S. , Abdalla Dulcinéia S.P. , Lopasso F.P. , Laurindo F.R.M. , Laudanna A.A. 
Published: May 2007

AbstractBackground/Aim: The pathogenesis of Nonalcoholic Fatty Liver Disease remains largely unknown, but oxidative stress seems to be involved. The aim of this study was to evaluate the role of oxidative stress in experimental hepatic steatosis induced by a choline‐deficient diet.Methods: Fatty liver disease was induced in Wistar rats by a choline‐deficient diet. The animals were randomized into three groups: I (G1) and II (G2), n=6 each ‐ fed with a choline‐deficient diet for four and twelve weeks respectively; Group III (control‐G3; n=6) ‐ fed with a standard diet for twelve weeks. Samples of plasma and liver were submitted to biochemical, histological and oxidative stress analysis. Variables measured included serum levels of aminotransferases (AST, ALT), cholesterol and triglycerides. Oxidative stress was measured by lucigenin‐enhanced luminescence and the concentration of hydroperoxides (CE‐OOH‐cholesteryl ester) in the liver tissue. Results: We observed moderate macro‐ and microvesicular fatty change in periportal zones G1 and G2 as compared to controls (G3). In G2, fatty change was more severe. The inflammatory infiltrate was scanty and no fibrosis was seen in any group. There was a significant increase of AST and triglycerides in G1 and G2 as compared to control group G3. The lucigenin‐amplified luminescence (cpm/mg/min × 103) was significantly increased in G1 (1393±790) and G2 (7191±500) as compared to controls (513±170),p<0.05. The concentrations of CE‐OOH were higher in G1 (5.7±0.9 nmol/mg protein) as compared to control (2.6±0.7 nmol/mg protein),p<0.05. Conclusion: 1) Oxidative stress was found to be increased in experimental liver steatosis; 2) The production of reactive oxygen species was accentuated when liver steatosis was more severe; 3) The alterations produced by oxidative stress could be an important step in the pathogenesis of nonalcoholic fatty liver disease.
Tissue cultures from adult human postmortem subcortical brain areas
Authors: Verwer R.W.H. , Dubelaar E.J.G. , Hermens W.T.J.M.C. , Swaab D.F. 
Published: May 2007

AbstractAnimal models used to study human aging and neurodegeneration do not display all symptoms of these processes as they are found in humans. Recently, we have shown that many cells in neocortical slices from adult human postmortem brain may survive for extensive periods in vitro. Such cultures may enable us to study age and disease related processes directly in human brain tissue. Here, we present observations on subcortical brain tissue.
The role of fibroblast growth factor‐2 in the vascularization of the chick embryo chorioallantoic membrane
Authors: Ribatti D. , Presta M. 
Published: May 2007

AbstractThe CAM is an extraembryonic membrane which serves as a gas exchange surface and its respiratory function is provided by an extensive capillary network. The development of the vascular system of the CAM is a complex, highly regulated process that depends on genetic and epigenetic factors expressed by endothelial and non‐endothelial cells. In spite of the evidence that several growth factors are angiogenic in the CAM assay, poorly investigated is their role in the development of the CAM's vascular system. This article reviews our studies concerning the role of exogenous and endogenous fibroblast growth factor‐2 (FGF‐2) in the CAM vascularization. The findings in all these studies support the importance of FGF‐2 as an autocrine paracrine stimulator of angiogenesis and its key role in the development of the vascular system in the avian embryo.
Tetrathiomolybdate anticopper therapy for Wilson's disease inhibits angiogenesis, fibrosis and inflammation
Authors: Brewer G. J. 
Published: May 2007

AbstractThe need for agents to lower body copper in Wilson's disease, a disease which results from copper toxicity has been the driving force for the development of the effective anticopper drugs penicillamine, trientine, zinc, and now tetrathiomolybdate (TM). Because of its rapid action, potency, and safety, TM is proving to be a very effective drug for initial treatment of acutely ill Wilson's disease patients. Beyond this, TM has antiangiogenic effects, because many proangiogenic cytokines require normal levels of copper. This has led to use of TM in cancer, where it is generally effective in animal tumor models, and has shown efficacy in preliminary clinical studies. Most recently, it has been found that TM has antifibrotic and antiinflammatory effects through inhibition of profibrotic and proinflammatory cytokines.
Physiological and pathological roles of Apaf1 and the apoptosome
Authors: Ferraro E. , Corvaro M. , Cecconi F. 
Published: May 2007

AbstractDifferent cellular pathways can lead to apoptosis. Apaf1 is the molecular core of the apoptosome, a multiproteic complex mediating the so‐called mitochondrial pathway of cell death. The importance of this pathway during development has been clearly demonstrated by knocking out key genes. Also, the relevance of Apaf1 dosage during development has been recently underlined. Moreover, a growing body of evidences seems to point out a possible role of the mitochondria‐dependent apoptosis in different pathologies. In particular, we discuss here some recent evidences regarding the putative role of the apoptosome in neurodegeneration and cancer.
RNA‐binding ability of PIPP in requires the entire protein
Authors: Raimondi Lavinia , D'Asaro Matilde , Proia Patrizia , Nastasi Tommaso , Di Liegro Italia 
Published: May 2007

AbstractPost‐transcriptional fate of eukaryotic mRNAs depends on association with different classes of RNA‐binding proteins (RBPs). Among these proteins, the cold‐shock domain (CSD)‐containing proteins, also called Y‐box proteins, play a key role in controlling the recruitment of mRNA to the translational machinery, in response to environmental cues, both in development and in differentiated cells. We recently cloned a rat cDNA encoding a new CSD‐protein that we called PIPPin. This protein also contains two putative double‐stranded RNA‐binding motifs (PIP1 and PIP2) flanking the central CSD, and is able to bind mRNAs encoding H1° and H3.3 histone variants. In order to clarify the role of each domain in the RNA‐binding activity of PIPPin, we constructed a number of different recombinant vectors, encoding different regions of the protein. Here we report that only recombinant proteins that contain all the putative PIPPin domains show RNA‐binding ability.
Scrreening for microdeletions in human Y chromosome‐AZF candidate genes and male infertility
Authors: Raicu Florina , Popa L. , Apostol Pompilia , Cimpomeriu D. , Dan Letitia , Ilinca Elena , Dracea Laura Luana , Marinescu B. , Gavrila L. 
Published: May 2007

AbstractAbout 30% of couple infertilities are of male origin, some of them caused by genetic abnormalities of the Y chromosome. Deletions in AZF region can cause severe spermatogenic defects ranging from non‐obstructive azoospermia to oligospermia. The intracytoplasmatic sperm injection technique (ICSI) is rapidly becoming a versatile procedure for human assisted reproduction in case of male infertility. The use of ICSI allows Y chromosome defects to be passed from father. The goal of our study is to evaluate the frequency of microdeletions in the long arm of Y chromosome, within the AZF regions, in these cases of infertilities, using molecular genetics techniques. Thirty infertile men with azoospermia or oligozoospermia, determined by spermogram, were studied after exclusion of patients with endocrine or obstructive causes of infertility. Peripheral blood DNA was extracted from each patient, then amplified by multiplex PCR with STS genomic markers from the Y chromosome AZF zones. Each case was checked by multiplex PCR through coamplification with the SRY marker. Three men with microdeletions of the long arm of the Y chromosome were diagnosed among the 30 patients, corresponding to a proportion of 10%. The relatively high proportion of microdeletions found in our population suggest the need for strict patient selection to avoid unnecessary screening for long arm Y chromosome microdeletions. The molecular diagnostics was performed according to the current European Academy of Andrology laboratory guidelines for molecular diagnosis of Y chromosomal microdeletions.
Glucose deprivation induces mitochondrial dysfunction and oxidative stress in PC12 cell line
Authors: Liu Yan , Song Xiao‐Dong , Liu Wen , Zhang Tian‐Yi , Zuo Ji 
Published: May 2007

AbstractGlucose metabolism plays a pivotal role in many physiological and pathological conditions. To investigate the effect of hypoglycemia (obtained by glucose deprivation) on PC12 cell line, we analyzed the cell viability, mitochondrial function (assessed by MTT reduction, cellular ATP level, mitochondrial transmembrane potential), and the level of reactive oxygen species (ROS) after glucose deprivation (GD). Upon exposure to GD, ROS level increased and MTT reduction decreased immediately, intracellular ATP level increased in the first 3 hours, followed by progressive decrease till the end of GD treatment, and the mitochondrial transmembrane potential (ΔΨm) dropped after 6 hours. Both necrosis and apoptosis occurred apparently after 24 hours which was determined by nuclei staining with propidium iodide(PI) and Hoechst 33342. These data suggested that cytotoxity of GD is mainly due to ROS accumulation and ATP depletion in PC12 cells.
Imbalance of peripheral B lymphocytes and NK cells in rheumatoid arthritis
Authors: Manda Gina , Neagu Monica , Livescu Alexandra , Constantin Carolina , Codreanu C. , Radulescu Alina 
Published: May 2007

AbstractThe study was focused on several cellular immune disorders correlated with the imbalance between peripheral blood B lymphocytes and NK cells in severe rheumatoid arthritis. By flow cytometry we calculated the proportions of T, T helper, T cytotoxic/suppressor, B lymphocytes and natural killer cells in peripheral blood. The mitogen‐induced proliferation of peripheral lymphocytes was measured by tritium‐labeld uridine incorporation. Experimental data highlight a connection between annomal values of the B to natural killer cells ratio and disorders of the peripheral mononuclear cells concentration. We also showed that the polyclonal proliferation capacity of peripheral lymphocytes in rheumatoid arthritis is solely related to the B to natural killer cells ratio or to the natural killer cells proportion. The study reveals a potential role of the imbalance between proportions of peripheral B lymphocytes and natural killer cells in the immune pathogenesis of rheumatoid arthritis, thus pointing out an interrelation between the adaptive and innate immune systems.
Plasma 249Ser p53 mutation in patients with hepatocellular carcinoma residing in a high risk area
Authors: Dong‐Dong Lu , Xi‐Ran Zhang 
Published: May 2007

Abstract Objective: To investigate plasma p53 mutation in hepatocellular carcinoma (HCC) patients from Qidong and to define its significance. Methods: Blood samples from 25 hepatocellular carcinoma patients, 20 cirrhotic patients and 30 healthy controls in Qidong area. DNA was extracted and purified from 200μl of plasma from each sample. The 249Ser p53 mutation was detected by restriction digestion analysis and by direct sequencing of exon‐7 PCR products. Results: G→T transversion at the third base of 249 codon resulting in 249Arg→249Ser mutation in exon 7 of p53 gene were found in 11/25(44%) hepatocellular carcinoma cases, 4/20 (20%) cirrhotics, and 2/30 (7%) healthy controls (p<0.01). Conclusions: These data show that the 249Ser p53 mutation in plasma is strongly associated with hepatocellular carcinoma patients in Qidong area and the mutation should be screened as a new early diagnostic marker for HCC.
Stemness, fusion and renewal of hematopoietic and embryonic stem cells
Authors: Constantinescu S. 
Published: May 2007

AbstractDevelopment of replacement cell therapies awaits the identification of factors that regulate nuclear reprogramming and the mechanisms that control stem cell renewal and differentiation. Once such factors and signals will begin to be elucidated, new technologies will have to be envisaged where uniform differentiation of adult or embryonic stem cells along one differentiation pathway can be induced. Controlled differentiation of stem cells will require the engineering of niches and extracellular signal combinations that would amplify a particular signaling network and allow uniform and selective differentiation. Three recent advances in stem cell research open the possibility to approach engineering studies for cell replacement therapies. Fusion events between stem cells and adult cells or between adult and embryonic stem cells have been shown to result in altered fates and nuclear reprogramming of cell hybrids. Hematopoietic stem cells were shown to require Wnt signaling in order to renew. The purification of Wnt proteins would allow their use as exogenous purified cytokines in attempts to amplify stem cells before bone marrow transplantation. The homeodomain protein Nanog has been shown to be crucial for the embryonic stem cell renewal and pluripotency. However, the cardinal question of how stemness is preserved in the early embryo and adult stem cells remains opened.
Polyamine metabolism and cancer
Authors: Thomas Thresia , Thomas T. J. 
Published: May 2007

AbstractPolyamines are aliphatic cations present in all cells. In normal cells, polyamine levels are intricately controlled by biosynthetic and catabolic enzymes. The biosynthetic enzymes are ornithine decarboxylase, S‐adenosylmethionine decarboxylase, spermidine synthase, and spermine synthase. The catabolic enzymes include spermidine/spermine acetyltransferase, flavin containing polyamine oxidase, copper containing diamine oxidase, and possibly other amine oxidases. Multiple abnormalities in the control of polyamine metabolism and uptake might be responsible for increased levels of polyamines in cancer cells as compared to that of normal cells. This review is designed to look at the current research in polyamine biosynthesis, catabolism, and transport pathways, enumerate the functions of polyamines, and assess the potential for using polyamine metabolism or function as targets for cancer therapy.