bluuebunny/crossref_metadata_2025_split huggingface dataset:
Redox regulation of angiotensin II siganling in the heart
Authors: Das Dipak K. , Maulik Nilanjana , Engelam Rjichard M. 
Published: May 2007

AbstractA large number of studies have demonstrated the role of angiotensin II in cardiac preconditioning against ischemic reperfusion injury. Generally, angiotensin II is a detrimental factor for the heart, and its inhibition with an ACE inhibitor provides cardioprotection. This review provides an explanation for such paradoxical behavior of angiotensin II. Angiotensin II can potentiate the induction of the expression of a variety of redox‐sensitive factors including p38 MAPK, JNK and Akt, IGF‐IR, EGF‐R, and HO‐1 as well as redox‐regulated genes and transcription factors such as NF??B. It becomes increasingly apparent that during the earlier phase, the heart attempts to adapt itself against the detrimental effects of angiotensin II by upregulating several cardioprotective genes and proteins. These genes and proteins are redox‐regulated and the antioxidants or ROS scavengers block their expressions. Interestingly, an identical pattern of cardioprotective proteins and genes are expressed in the preconditioned heart, which are also inhibited with ROS scavengers. It is tempting to speculate that the induction of the expression of the redox‐sensitive cardioprotective proteins is the results of adaptation of the heart against the oxidative stress resulting from angiotensin II; and preconditioning is the net result of harnessing its own protection during ischemic and/or oxidative stress through its ability to trigger redox signaling.
Ca2+ and mitochondria as substrates for deficits in synaptic plasticity in normal brain ageing
Authors: Toescu E. C. , Verkhratsky A. 
Published: May 2007

AbstractNormal brain ageing is associated with a degree of functional impairment of neuronal activity that results in a reduction in memory and cognitive functions. One mechanism proposed to explain the age‐dependent changes was the “Ca2+ hypothesis of ageing” but data accumulated in the last decade revealed a number of inconsistencies. Two important questions were raised: (a) which are, if any, the most reliable age‐associated change in neuronal Ca2+ homeostasis and (b) are these changes primary, and thus determinant of the ageing phenotype, or are they secondary to other changes in the physiology of the aged neurones. After a brief review of the evidence accumulated for the age‐induced changes in synaptic plasticity, we assess the proposal that these changes are, ultimately, determined by changes in the metabolic state of the aged neurones, that are manifest particularly after neuronal stimulation. In this context, it appears that the changes in mitochondrial status and function are of primary importance.
Inorganic phosphate homeostasis and the role of dietary phosphorus
Authors: Takeda Eiji , Yamamoto Hironori , Nashiki Kunitaka , Sato Tadatoshi , Arai Hidekazu , Taketani Yutaka 
Published: May 2007

AbstractInorganic phosphate (Pi) is required for cellular function and skeletal mineralization. Serum Pi level is maintained within a narrow range through a complex interplay between intestinal absorption, exchange with intracellular and bone storage pools, and renal tubular reabsorption. The crucial regulated step in Pi homeostasis is the transport of Pi across the renal proximal tubule. Type II sodium‐dependent phosphate (Na/Pi) cotransporter (NPT2) is the major molecule in the renal proximal tubule and is regulated by Pi, parathyroid hormone and by 1,25‐dihydroxyvitamin D. Recent studies of inherited and acquired hypophosphatemia [X‐linked hypophosphatemic rickets/osteomalacia (XLH), autosomal dominant hypophosphatemic rickets/osteomalacia (ADHR) and tumor‐induced rickets/osteomalacia (TIO)], which exhibit similar biochemical and clinical features, have led to the identification of novel genes, PHEX and FGF23, that play a role in the regulation of Pi homeostasis. The PHEX gene, which is mutated in XLH, encodes an endopeptidase, predominantly expressed in bone and teeth, but not in kidney. FGF‐23 may be a substrate of this endopeptidase and may therefore accumulate in patients with XLH. In the case of ADHR mutations in the furin cleavage site, which prevent the processing of FGF‐23 into fragments, lead to the accumulation of a “stable” circulating form of the peptide which also inhibits renal Pi reabsorption. In the case of TIO, ectopic overproduction of FGF‐23 overwhelms its processing and degradation by PHEX, leading to the accumulation of FGF‐23 in the circulation and inhibition of renal Pi reabsorption. Mice homozygous for severely hypomorphic alleles of the Klotho gene exhibit a syndrome resembling human aging, including atherosclerosis, osteoporosis, emphysema, and infertility. The KLOTHO locus is associated with human survival, defined as postnatal life expectancy, and longevity, defined as life expectancy after 75. In considering the relationship of klotho expression to the dietary Pi level, the klotho protein seemed to be negatively controlled by dietary Pi.
The comparison of different protocols for expansion of umbilical‐cord blood hematopoietic stem cells
Authors: Chivu Mihaela , Diaconu Carmen C. , Bleotu Coralia , Alexiu Irina , Brasoveanu Lorelei , Cernescu C. 
Published: May 2007

AbstractHematopoiesis is maintained by the activity of multipotent stem cells, which have the dual capacity to self‐renew and to differentiate into all of the blood cell lineages. The major challenge of stem cells based regenerative therapy is to expand ex vivo the primitive compartment to increase transplantable stem cells number. The present study was designed to evaluate several culture systems for in vitro maintenance of umbilical cord blood stem cells. The influences of different growth conditions such as stromal feeder layer, cytokines supplement and placental conditioned medium (PCM) have been evaluated over a relatively short period of time on CD34+ cell expansion and maintenance of clonogenic progenitors. When cells were expanded on feeder layer in the presence of added cytokines and PCM on average a 2.96‐fold increase of CD34+CD71‐ and a 3.13‐fold increase of CD34+HLA‐DR‐ was observed. The total number of colony forming cells (35±2.65) indicated also that the yield of clonogenic progenitors obtained with a combination of all factors was two folds higher than each of these factors alone and ten time above control (3.67± 2.52). In conclusion, the results of our study clearly show that the ex vivo expansion of hematopoietic progenitor cells obtained from human umbilical cord blood is dependent on controlled experimental conditions, which might be helpful when designing culture systems for clinical applications.
Scanning of β‐globin gene for identification of β‐thalassemia mutation in Romanian population
Authors: Talmaci R. , Traeger‐Synodinos J. , Kanavakis E. , Coriu D. , Colita D. , Gavrila L. 
Published: May 2007

Abstractβ‐Thalassemia is uncommon (0.5%) in the Romanian population, but it must be considered in the differential diagnosis of hypochromic anemia. The molecular characterization of β‐thalassemia is absolutely necessary for molecular diagnosis, as well as any genetic epidermiological study in this region. Molecular analyses consist of mutation detection by molecular scanning of β‐globin gene. This gene has 3 exons and 2 introns, involved in β‐thalassemic pathogenesis. Clinical application of DNA analysis on β‐thalassemic chromosomes allowed characterization of 29 persons with different β‐thalassemia mutations among 58 patients with anemia. The experimental strategy was based on sequential PCR amplification of most of the β‐globin gene and running on denaturing gradient gel electrophoresis of amplification products. Definitive characterization of mutations in samples identified with shifted DGGE patterns was performed ARMS‐PCR and/or PCR‐restriction enzyme analysis methods. Eight different β‐thalassemia alleles were identified, the most common being IVS I‐110 (G‐A) and cd 39 (C‐T). Comparison of overall frequency of mutations in the neighboring countries, shows that these results are in the frame of overall distribution of these mutations in Mediterranean area, especially in Greece and in Bulgaria. Molecular diagnosis is useful for differentiating mild from severe alleles, for genetic counseling, as well as for mutation definition in carriers, identified by hematological analysis necessary for prenatal testing and genetic counseling.
Type 1 diabetes genetic susceptibility encoded by HLA DQB1 genes in Romania
Authors: Guja C. , Guja L. , Nutland S. , Rance H. , Sebastien M. , Todd J. A. , Ionescu‐Tirgoviste C. 
Published: May 2007

AbstractMost cases of type 1 diabetes (T1DM) are due to an immune‐mediated destruction of the pancreatic beta cells, a process that is conditioned by multiple genes and environmental factors. The main susceptibility genes are represented by the class II HLA‐DRB1 and DQB1 alleles. The aim of our study was to reconfirm the contribution of HLA‐DQB1 polymorphisms to T1DM genetic susceptibility for the Romanian population. For this, 219 Romanian T1DM families were genotyped at high resolution for HLA DQB1 using the PCR‐SSOP method (Polymerase Chain Reaction ‐ Sequence Specific Oligonucleotide Probes). Allele transmission to diabetics and unaffected siblings was studied using the Transmission Disequilibrium Test (TDT). We found an increased transmission of DQB1 *02 (77.94% transmission, PTDT= 7.18 × 10−11) and DQB1*0302 (80.95% transmission, PTDT= 2.25 × 10−10) alleles to diabetics, indicating the diabetogenic effect of these alleles. Conversely, DQB1*0301, DQB1*0603, DQB1*0602, DQB1*0601 and DQB1*05 alleles are protective, being significantly less transmitted to diabetics. In conclusion, our results confirmed the strong effect of HLA‐DQB1 alleles on diabetes risk In Romania, with some characteristics which can contribute to the low incidence of T1DM in this country.
Kinetic logic: a tool for describing the dynamics of infectious disease behavior
Authors: Martinet‐Edelist Claire 
Published: May 2007

AbstractMost of the infectious diseases imply biological regulations controlled by several feedback loops or circuits. Kinetic logic, which is a method easily accessible to biologists or physicians, and which takes time and thresholds of activity into account, seems a convenient method for building simplified models related to this field. This implies usually qualitative predictions concerning the dynamics of such biological systems, leading to a movement back and forth between experimentation or observation and logical description. Here, we illustrate this simple modelling method in building elementary models concerning prion infection to demonstrate how to proceed. We also discuss and summarize how this method has been used for studying several viral diseases. As an example, we show how predictions related to the rhabdovirus cycle, were experimentally verified.
The involvement of endothelial progenitor cells in tumor angiogenesis
Authors: Ribatti Domenico 
Published: May 2007

AbstractEndothelial progenitor cells (EPCs) have been isolated from peripheral blood CD34, VEGFR‐2, or AC 133 (CD133) antigen‐positive cells, which may home to site of neovascularization and differentiate into endothelial cells in situ. Endothelial cells contribute to tumor angiogenesis, and can originate from sprouting or co‐option of neighbouring pre‐existing vessels. Emerging evidence indicate that bone marrow‐derived circulating EPCs can contribute to tumor angiogenesis and growth of certain tumors. This review article will summarize the literature data concerning this new role played by EPCs in tumor angiogenesis.
Double transgenic mice with Type 1 diabetes mellitus develop somatic, metabolic and vascular disorders
Authors: Radu D. L. , Georgescu Adriana , Stavaru Crina , Carale Alina , Popov Doina 
Published: May 2007

AbstractThe double transgenic mice (dTg) were obtained by mating: (i) transgenic mice expressing the hemagglutinin of influenza virus under the insulin promoter with (ii) transgenic mice expressing specific T lymphocytes with receptor for the immunodominant epitope of the same virus. In this study we show that dTg mice developed type 1 diabetes mellitus associated with hyperglycemia, low level of plasma insulin, glucosuria, weight loss and ∼ 90% mortality (at 3 months biological age). The membrane of red blood cells was more sensitive to osmotic shock in diabetic mice, compared to non‐diabetic mice, assessing systemic oxidative stress. Both vasoconstriction and vasorelaxation of the renal arteries decreased significantly in diabetic mice (compared to the control group of non‐diabetic mice) related to the phenotypic change of endothelium and smooth muscle cells within the artery wall. This animal model, may be used in developing various strategies to study pancreatic β‐cell function, as well as for a better metabolic control conducting to a reduced risk of vascular complications.
Vesicle traffic through intercellular bridges in DU 145 human prostate cancer cells
Authors: Vidulescu Cristina , Clejan Sanda , O'Connor Kim C. 
Published: May 2007

AbstractWe detected cell‐to‐cell communication via intercellular bridges in DU 145 human prostate cancer cells by fluorescence microscopy. Since DU 145 cells have deficient gap junctions, intercellular bridges may have a prominent role in the transfer of chemical signals between these cells. In culture, DU 145 cells are contiguous over several cell diameters through filopodial extensions, and directly communicate with adjacent cells across intercellular bridges. These structures range from 100 nm to 5 μm in diameter, and from a few microns to at least 50–100 μm in length. Time‐lapse imagery revealed that (1) filopodia rapidly move at a rate of microns per minute to contact neighboring cells and (2) intercellular bridges are conduits for transport of membrane vesicles (1–3 μm in diameter) between adjacent cells. Immunofluorescence detected alpha‐tubulin in intercellular bridges and filopodia, indicative of microtubule bundles, greater than a micron in diameter. The functional meaning, interrelationship of these membrane extensions are discussed, along with the significance of these findings for other culture systems such as stem cells. Potential applications of this work include the development of anticancer therapies that target intercellular communication and controlling formation of cancer spheroids for drug testing.
Apoptosis of pancreatic acinar cells in acute pancreatitis: is it good or bad?
Authors: Bhatia M. 
Published: May 2007

AbstractAcute pancreatitis is a disease of variable severity in which some patients experience mild, self‐limited attacks while others manifest a severe, highly morbid, and frequently lethal attack. The events that regulate the severity of acute pancreatitis are, for the most part, unknown. Several recent studies have suggested that the acinar cell response to injury may be an important determinant of disease severity. In these studies, mild acute pancreatitis was found to be associated with extensive apoptotic acinar cell death while severe acute pancreatitis was found to involve extensive acinar cell necrosis but very little acinar cell apoptosis. These observations have led to the hypothesis that apoptosis might be a favorable response to acinar cell and that interventions which favor induction of apoptotic, as opposed to necrotic, acinar cell death might reduce the severity of an attack of acute pancreatitis. This review aims to discuss our current understanding of the contribution of acinar cell apoptosis to the severity of acute pancreatitis.
Endothelial progenitor cells: past, state of the art, and future
Authors: Iwami Yo , Masuda Haruchika , Asahara Takayuki 
Published: May 2007

AbstractRecent evidences suggest that endothelial progenitor cells (EPCs) derived from bone marrow (BM) contribute to de novo vessel formation in adults occurring as physiological and pathological responses. Emerging preclinical trials have shown that EPCs home to sites of neovascularization after ischemic events in limb and myocardium. On the basis of these aspects, EPCs are expected to develop as a key strategy of therapeutic applications for the ischemic organs. Such clinical requirements of EPCs will tentatively accelerate the translational research aiming at the devices to acquire the optimized quality and quantity of EPCs. In this review, we attempt to discuss about biological features of EPCs and speculate on the clinical potential of EPCs for therapeutic neovascularization.
Endothelial progenitor cells: characterization, pathophysiology, and possible clinical relevance
Authors: Hristov Mihail , Weber Christian 
Published: May 2007

AbstractBone marrow and peripheral blood of adults contain a special sub‐type of progenitor cells which are able to differentiate into mature endothelial cells, thus contributing to re‐endothelialization and neo‐vascularization. These angiogenic cells have properties of embryonal angioblasts and were termed endothelial progenitor cells (EPCs). In general, three surface markers (CD133, CD34 and the vascular endothelial growth factor receptor‐2) characterize the early functional angioblast, located predominantly in the bone marrow. Later, when migrating to the systemic circulation EPCs gradually lose their progenitor properties and start to express endothelial marker like VE‐cadherin, endothelial nitric oxide synthase and von Willebrand factor. The number of circulating EPCs in healthy subjects is rather low and a variety of conditions or factors may further influence this number. In the context of possible therapeutic application of EPCs recent clinical studies employing these cells for neo‐vascularization of ischemic organs have just been published. However, the specificity of the observed positive clinical effects, the mechanisms regulating the differentiation of EPCs and their homing to sites of injured tissue remain partially unknown at present.
Endothelial progenitor cells: A source for therapeutic vasculogenesis?
Authors: Rumpold Holger , Wolf Dominik , Koeck Ruth , Gunsilius Eberhard 
Published: May 2007

AbstractAngiogenesis has been defined as sprouting of blood vessels from pre‐existing vascular structures. Risau and coworkers defined the term vasculogenesis while studying the formation of new blood vessels in embryoid bodies. This process is characterized by the recruitment of endothelial progenitor cells (EPC) to sites of new vessel formation with subsequent differentiation of EPC into mature endothelial cells, extensively proliferating in situ. Data from recent years provided evidence that EPC also exist in the adult and contribute to new vessel formation, a process called postnatal vasculogenesis. The existence of EPC has been convincingly shown in both, animals and humans. They represent a perfect cellular progenitor cell population for the ex vivo generation of EC, which in turn serve as cellular source for therapeutic vasculogenesis or tumor targeting. This review provides an overview on this hot topic of cellular‐based therapeutic concepts and the therapeutic potential of ex vivo generated EPC.
Role of STAT‐1 and STAT‐3 in ischaemia/reperfusion injury
Authors: Stephanou A. 
Published: May 2007

AbstractIschaemia/reperfusion (I/R) injury results in the death of irreplaceable cardiac myocytes by a programme cell death or apoptosis. The signal transducers and activators of transcription (STAT) factors function as modulators of cytokine signaling and sensors responding to cellular stress. Interestingly, many studies have demonstrated that although they have a similar structural organization, STAT‐1 and STAT‐3 have apposing effects on processes such as differentiation or apoptosis. For example, STAT‐1 has been shown to induced apoptosis, whilst STAT3 is able protect cardiac myocytes following ischaemia/reperfusion (I/R) injury. Many of the effects of STAT‐1 and STAT‐3 involve the direct binding to DNA and transcriptional activation of target genes. However, recent studies have shown that for STAT‐1 some of its effects appear not to require DNA binding. For example, induction of apoptosis by STAT‐1 can be produced by the C‐terminal activation domain in the absence of the DNA binding domain. This therefore, appears to involve a co‐activator effect in which STAT‐1 is recruited to DNA via a DNA‐bound transcription factor. In this regard, it is of interest that STAT‐1 but not STAT‐3 has been shown to interact with p53 and enhance its growth arrest and apoptosis‐ inducing properties. Hence, the finding that STAT‐1 and STAT‐3 can modulate the apoptotic programme both by direct DNA binding or via a co‐activator mechanism and despite their very similar structures, suggests that these related factors may be therapeutic targets against the damage myocardium following I/R injury. Recently, we reported that the polyphenolic agent epigallocatechin‐3‐gallate (EGCG), a major constituent of green tea and a potent inhibitor of STAT‐1 activation, protects the myocardium against I/R injury.
Effects of estrogen and progesterone treatment on rat hippocampal NMDA receptors: Relationship to Morris water maze performance
Authors: El‐Bakri Nahid K. , Islam Atiqul , Zhu Shunwei , Elhassan Adlan , Mohammed Abdul , Winblad Bengt , Adem Abdu 
Published: May 2007

AbstractEstrogen modulates NMDA receptors function in the brain. It increases both dendritic spine density and synapse number in the hippocampus, an effect that can be blocked by NMDA antagonist. In this study, we investigated the effect of 17β‐estradiol and progesterone treatment on NMDA receptors in ovariectomized rats. Two different doses were used for 10 weeks. Receptor autoradiography was done on brain sections using [3H] MK‐801 as a ligand. Our results showed a significant increase in [3H] MK‐801 binding in the dentate gyrus, CA3 and CA4 areas of the hippocampus of ovariectomized compared to sham operated rats. In addition, we observed similar changes in CA1. 17β‐estradiol treatment in both doses reduced the binding back to the normal level while progesterone treatment did not show any effect. Spatial reference memory was tested on Morris water maze task. Ovariectomy severely impaired spatial reference memory. Estradiol but not progesterone treatment significantly improved the memory performance of the ovariectomized rats. Low dose treatment showed better learning than high dose estrogen treatment. The decrease in the antagonist sites by estradiol treatment could result in an increase in the sensitivity of the hippocampus to the excitatory stimulation by glutamate system and hence the effect of estradiol on learning and memory. The changes of NMDA receptors in the hippocampus support the concept that estrogen‐enhancing effect on spatial reference memory could be through the enhancing of NMDA function.
Molecular and morphologic analyses of expression of ESX1L in different stages of human placental development
Authors: Figueiredo A. L. S. , Salles M. G. F. , Albano R. M. , Porto L. C. 
Published: May 2007

AbstractThe mRNA expression of the ESX1L gene was analyzed by RT‐PCR and in situ hybridization in human normal cytogenetically placentas, of different gestational ages. Our RT‐PCR analysis showed that ESX1L mRNA is expressed from 5 weeks of gestation until term, suggesting a role not only in trophoblast differentiation but also in the maintenance of the villi and microvasculature. We also observed, by in situ hybridization, that ESX1L mRNA is expressed by cytotrophoblast from chorinic plate, syncytiotrophoblast and stromal cells of all terminal, intermediate and stem villi of term placentas. ESX1L mRNA expression was more pronounced in trophoblast cells of terminal villi than in intermediate and sterm villi. In conclusion, ESX1L is expressed during all stages of placental development and is localized to sparse areas of trophoblast in terminal villi in association with cytotrophoblastic cells.