bluuebunny/crossref_metadata_2025_split huggingface dataset:
Real cells ‐ virtual computers
Authors: Popescu George Alex 
Published: May 2007

AbstractNow it is quite usual to use real computers to simulte virtual cells. I suggest that real cells (e.g. cells cultured in vitro) might be considered and used as molecular automata. As an imaginary experience, a molecular automata can be built, using real cells and a chemical inert molecule. I suggest that one could be able to test statistical properties of a 2D gas trapped in a box using this sort of automata. Moreover, I would conjecture that any possible algorithm can be implemented in such molecular automata.
Co‐stimulatory and adhesion molecules of dendritic cells in rheumatoid arthritis
Authors: Balanescu Andra , Radu E. , Nat Roxana , Regalia T. , Bojinca Violeta , Predescu V. , Predeteanu Denisa 
Published: May 2007

AbstractDendritic cells (DCs) in the rheumatoid arthritis (RA) joint mediate the immunopathological process and act as a potent antigen presenting cell. We compared the expression of co‐stimulatory and adhesion molecules on DCs in RA patients versus controls with traumatic joint lesions and evalulated the correlation between the immunophenotypical presentation of DCs and the clinical status of the disease. Samples of peripheral venous blood, synovial fluid (SF) and synovial tissue (ST) were obtained from 10 patients with RA at the time of hip or knee replacement and from 9 control patients with knee arthroscopy for traumatic lesions. Clinical status was appreciated using the DAS28 score. Blood, SF and dissociated ST cell populations were separated by centrifugation and analyzed by flow cytometry. Cells phenotypes were identified using three‐color flow cytometry analysis for the following receptors HLA‐DR, CD80, CD83, CD86, CD11c, CD18, CD54, CD58, CD3, CD4, CD8, CD19, CD20, CD14, CD16, CD56. HLA‐DR molecules, co‐stimulatory receptors CD80, CD86, CD83 and adhesion molecules CD18, CD11c, CD54, CD58, were analyzed by two‐color immunofluorescence microscopy on ST serial sections. In patients with active RA (DAS28>5.1) we found a highly differentiated subpopulation of DCs in the ST and SF that expressed an activated phenotype (HLA‐DR, CD86+, CD80+, CD83+, CD11c+, CD54+, CD58+). No differences were found between circulating DCs from RA patients and control patients. Our data suggest an interrelationship between clinical outcome and the immunophenotypical presentation of DCs. Clinical active RA (DAS28>5.1) is associated with high incidence of activated DCs population in the ST and SF as demonstrated by expression of adhesion and co‐stimulatory molecules.
Synergistic effects of neurons and astrocytes on the differentiation of brain capillary endothelial cells in culture
Authors: Schiera Gabriella , Bono Epifania , Raffa Maria Pia , Gallo Alessia , Pitarresi Giovanna Laura , Di Liegro Italia , Savettieri G. 
Published: May 2007

AbstractBrain capillary endothelial cells form a functional barrier between blood and brain, based on the existence of tight junctions that limit paracellular permeability. Occludin is one of the major transmembrane proteins of tight junctions and its peripheral localization gives indication of tight junction formation. We previously reported that RBE4.B cells (brain capillary endothelial cells), cultured on collagen IV, synthesize occludin and correctly localize it at the cell periphery only when cocultured with neurons. In the present study, we describe a three‐cell type‐culture system that allowed us to analyze the combined effects of neurons and astrocytes on differentiation of brain capillary endothelial cells in culture. In particular, we found that, in the presence of astrocytes, the neuron‐induced synthesis and localization of occludin is precocious as compared to cells cocultured with neurons only.
Adhesion inhibition “in vitro” by heparin derivatives correlates with their activity on angiogenesis in mice
Authors: Savu Simona Rizea , Silvestro L. 
Published: May 2007

AbstractHeparin (HEP) play an important role in angiogenesis. Inhibition of matrix degrading enzymes and binding to adhesion molecules are some of the interaction mechanism. The bleeding risk and the need of parenteral administration, restrict the therapeutic use of HEP as angiogenesis modulator, presently derivatives, with different pharmacokinetic and anticoagulant properties, are available. In this study the “in vitro” anti‐adhesion activity, tested with PMNs and endothelial cells, was compared with the effect on angiogenesis, evaluated in Matrigel implanted mice. Some HEP derivatives, with low anticoagulant activity, showed a significant angiogenesis inhibition. A positive correlation between adhesion inhibition in vitro and anti‐angiogenesis effect in vivo was found suggesting that the interaction with adhesion molecules by HEP derivatives play a relevant role in the angiogenesis control.
Surface wound healing: a new, general function of eukaryotic cells
Authors: Meldolesi J. 
Published: May 2007

AbstractThe ability to repair surface wounds is a property, necessary for long‐term survival, expressed to various extents by all eukaryotic cell types except erythrocytes. The process is based on the rapid Ca2+‐induced exocytosis of various types of specific organelles, such as lysosomes and enlargeosomes, that decreases surface tension and makes possible the spontaneous fusion of lipid monolayers at the lesion edges. The recognized importance of the process in physiology and in several cases of pathology is discussed.
Involvement of protein kinase C‐δ in DNA damage‐induced apoptosis
Authors: Basu Alakananda 
Published: May 2007

AbstractApoptosis is a highly orchestrated cell suicidal program required to maintain a balance between cell proliferation and cell death. A defect in apoptotic machinery can cause cancer. Many anticancer drugs are known to kill tumor cells by inducing apoptosis, and a defect in apoptosis can lead to anticancer drug resistance. Apoptosis is regulated by a complex cellular signaling network. Several members of the protein kinase C (PKC) family serve as substrates for caspases and PKCδ isozyme has been intimately associated with DNA damage‐induced apoptosis. It can act both upstream and downstream of caspases. In response to apoptotic stimuli, the full‐length and the catalytic fragment of PKCδ may translocate to distinct cellular compartments, including mitochondria and the nucleus, to reach their targets. Both activation and intracellular distribution of PKCδ may have significant impact on apoptosis. This review intends to assimilate recent views regarding the involvement of PKCδ in DNA damage‐induced apoptosis.
Genetic clock of biologic rhythms
Authors: Badiu C. 
Published: May 2007

AbstractBiologic rhythms are tighly regulated in all species, in order to addapt to circadian variations of light, temperature and other biological related living conditions. The intrinsic mechanisms of rhythm regulation from every cell to a whole organism is embedded into the genetic clockwork. The mammalian clock genes are reviewed with their interrelation. The per gene promoter is stimulated by clock/bmall heterodimer and trigger the per protoeins synthesis. Innitialy considered as a simple negative feed‐back, from to the phosphorylated per/cry heterodimer towards clock/bmall transcription stimulus, the clockweb of the cell became complex. General characteristics of cell clock genes are integrated in a model. In addition, the involvement of clock genes in peripheral tissues is discussed.
Differential gene expression in infarct scar and viable myocardium from rat heart following coronary ligation
Authors: Xu Y.‐J. , Chapman D. , Dixon I. M.C. , Sethi R. , Guo X. , Dhalla N. S. 
Published: May 2007

AbstractPost‐myocardial infarction (MI) remodeling of cardiac myocytes and the myocardial interstitium results in alteration of gross ventricular geometry and ventricular dysfunction. To investigate the mechanisms of the remodeling process of the heart after large MI, the expression of various genes in viable left ventricle and infarct scar tissue were examined at 16 weeks post‐MI. Steady‐state expression of Na+‐K+ATPase α‐1 and −2, phospholamban (PLB), α‐myosin heavy chain (α‐MHC), ryanodine receptor (Rya) and Ca2+ ATPase (Serca2) mRNAs were decreased in the infarct scar vs noninfarcted sham‐operated controls (P < 0.05). On the other hand, Giα2 and β‐MHC mRNAs were upregulated (P < 0.05, respectively) in the infarct scar whereas Na+‐K+ ATPase‐β, Na+‐Ca2+ exchanger and Gs mRNAs were not altered vs control values. In viable left ventricle, the a‐1 subunit of Na+‐K+ATPase, α‐3, β‐isoforms, Rya, β‐MHC, Giα2, Gs and Na+‐Ca2+ exchanger were significantly elevated while expression of the a‐2 subunit of Na+‐K+ ATPase, PLB and Serca2 were significantly decreased compared to controls. Expression of CK2α mRNA was elevated in noninfarcted heart (145 ± 15%) and diminished in the infarct scar (66 ± 13%) vs controls. Expression of β‐MHC mRNA was elevated in both viable and infarct scar tissues of experimental hearts (140 ± 31% and 183 ± 30% vs. controls, respectively). These results suggest that cardiac genes in the infarcted tissue and viable left ventricle following MI are differentially regulated.
Electro‐cortical signs of early neuronal damage following transient global cerebral ischemia in rat
Authors: Moldovan M. , Zagrean Ana‐Maria , Avramescu S. , Savaran V. , Zagrean L. 
Published: May 2007

AbstractDuring recovery after a transient global cerebral ischemia (TGCI), rat electrocorticogram (ECoG) shows epochs of synchronized activity (SA) alternating with epochs of low amplitude background activity (BA). The aim of this study was to compare the changes in these electrical activities during a 30‐min recovery period that followed either a noninjuring (3 minutes, N=10) or an injuring (10 minutes, N=10) TGCI. During TGCI there was a 3 fold reduction in amplitudes of both SA and BA but no changes in frequency. During reperfusion following a 3 minutes TGCI, the amplitudes of both SA and BA recovered to about 70%. During the reperfusion that followed a 10 minutes TGCI, BA showed no recovery, whereas SA recovered to about 40%. During the 30 min reperfusion, there was a timedependent decrease in the frequency of SA, but independent on the duration of TGCI. In contrast, the frequency of the BA did not change during reperfusion. Our data indicate that following cerebral ischemia the recovery of SA can take place independently of BA. The lack of recovery in BA may indicate early subcortical neuronal damage.
Intracellular calcium signals and control of cell proliferation: how many mechanisms?
Authors: Munaron L. , Antoniotti S. , Lovisolo D. 
Published: May 2007

AbstractThe progression through the cell cycle in non‐transformed cells is under the strict control of extracellular signals called mitogens, that act by eliciting complex cascades of intracellular messengers. Among them, increases in cytosolic free calcium concentration have been long realized to play a crucial role; however, the mechanisms coupling membrane receptor activation to calcium signals are still only partially understood, as are the pathways of calcium entry in the cytosol. This article centers on the role of calcium influx from the extracellular medium in the control of proliferative processes, and reviews the current understanding of the pathways responsible for this influx and of the second messengers involved in their activation.
Soluble, insoluble and geometric signals sculpt the architecture of mineralized tissues
Authors: Ripamonti U. 
Published: May 2007

AbstractBone morphogenetic and osteogenic proteins (BMPs/OPs), members of the transforming growth factor‐β (TGF‐β) superfamily, are soluble mediators of tissue morphogenesis and induce de novo endochondral bone formation in heterotopic extraskeletal sites as a recapitulation of embryonic development. In the primate Papio ursinus, the induction of bone formation has been extended to the TGF‐β isoforms per se. In the primate and in the primate only, the TGF‐β isoforms are initiators of endochondral bone formation by induction and act in a species‐, site‐ and tissue‐specific mode with robust endochondral bone induction in heterotopic sites but with limited new bone formation in orthotopic bone defects. The limited inductive capacity orthotopically of TGF‐β isoforms is associated with expression of the inhibitory Smads, Smad6 and Smad7. In primates, bone formation can also be induced using biomimetic crystalline hydroxyapatite matrices with a specific surface geometry and without the exogenous application of osteogenic proteins of the TGF‐β superfamily, even when the biomimetic matrices are implanted heterotopically in the rectus abdominis muscle. The sequence of events that directs new bone formation upon the implantation of highly crystalline biomimetic matrices initiates with vascular invasion, mesenchymal cell migration, attachment and differentiation of osteoblast‐like cells attached to the substratum, expression and synthesis of osteogenic proteins of the TGF‐β superfamily resulting in the induction of bone as a secondary response. The above findings in the primate indicate enormous potential for the bioengineering industry. Of particular interest is that biomimetic matrices with intrinsic osteoinductivity would be an affordable option in the local context.
Morphological and functional changes in rat hippocampal slice cultures after short‐term oxygen‐glucose deprivation
Authors: Lushnikova I. V. , Voronin K. Y. , Malyarevskyy P. Y. , Skibo G. G. 
Published: May 2007

AbstractTo study effects of short‐term cerebral ischemia, hippocampal slice cultures were subjected to oxygen and glucose deprivation (OGD) followed by a period of normoxic reoxygenation. Propidium iodide staining, and MTT/formazanassay were used to evaluate cell viability and metabolic activity. CA1 pyramidal cells were analyzed at the light‐and electron microscopic levels. Cell damage was found to be insignificant during the first hour after 10 min OGD but profound following 4 h, showing delayed neuronal cell damage caused by short‐term OGD. Our model can be used to characterize the mechanisms of cell damage caused by mild cerebral ischemia. These data might apply to further development of neuroprotective tools for the treatment of brain diseases.
The central role of Fas‐ligand cell signaling in inflammatory lung diseases
Authors: DosReis G. A. , Borges Valeria M. , Zin W. A. 
Published: May 2007

AbstractFollowing inflammation and injury in the lung, loss of epithelial cell precursors could determine the balance between tissue regeneration and fibrosis. This review discusses evidence that proapoptotic Fas‐Fas ligand (FasL) signaling plays a central role in pulmonary inflammation, injury and fibrosis. FasL signaling induces inflammatory apoptosis in epithelial cells and alveolar macrophages, with concomitant IL‐1β and chemokine release, leading to neutrophil infiltration. FasL signaling plays a critical role in models of acute lung injury, idiopathic pulmonary fibrosis and silicosis; blockade of Fas‐FasL interactions either prevents or attenuates pulmonary inflammation and fibrosis. Serologic and immunohistochemical studies in patients support a major pathogenic role of Fas and FasL molecules in inflammatory lung diseases. Identification of the pathogenic role of FasL could facilitate the discovery of more effective treatments for currently untreatable inflammatory lung diseases.
Adult mesenchymal stem cells: characterization, differentiation, and application in cell and gene therapy
Authors: Baksh D. , Song L. , Tuan R. S. 
Published: May 2007

AbstractA considerable amount of retrospective data is available that describes putative mesenchymal stem cells (MSCs). However, there is still very little knowledge available that documents the properties of a MSC in its native environment. Although the precise identity of MSCs remains a challenge, further understanding of their biological properties will be greatly advanced by analyzing the mechanisms that govern their self‐renewal and differentiation potential. This review begins with the current state of knowledge on the biology of MSCs, specifically with respect to their existence in the adult organism and postulation of their biological niche. While MSCs are considered suitable candidates for cell‐based strategies owing to their intrinsic capacity to self‐renew and differentiate, there is currently little information available regarding the molecular mechanisms that govern their stem cell potential. We propose here a model for the regulation of MSC differentiation, and recent findings regarding the regulation of MSC differentiation are discussed. Current research efforts focused on elucidating the mechanisms regulating MSC differentiation should facilitate the design of optimal in vitro culture conditions to enhance their clinical utility cell and gene therapy.
Immunomodulatory benefits of cyclosporine A in inflammatory bowel disease
Authors: Kountouras Jannis , Zavos Christos , Chatzopoulos Dimitrios 
Published: May 2007

AbstractEtiopathogenesis of mucosal inflammation in inflammatory bowel disease remains a complex and enigmatic field; various factors (genetic, environmental and microbial) trigger an event that activates intestinal immune and nonimmune systems cluminating in inflammation and tissue injury. Specifically, both innate and adaptive immune systems seem to play important roles in the pathophysiology of this disease. Cyclosporine A represents a macrolide immune modulator with primary inhibitory effects on T helper lymphocyte production of interleukin‐2, and other cytokines leading to altered T‐lymphocyte and B‐lymphocyte function. The diversity of its therapeutic outcome reported in inflammatory bowel disease may be due to the intricate immuno‐pathogenic profile of the disease and the variety of the applied dose‐dependent courses of therapy. Cyclosporine A exerts additional actions on other components of the inflammatory infiltrate, including neutrophils and mast cells, thereby appearing to be a multi‐dynamic therapeutic approach, although with potential drawbacks, that may be applied alone or combined with other immunomodulatory agents in inflammatory bowel disease patients. Because cyclosporine A induces apoptosis of T‐lymphocytes responsible for perpetuation of the chronic inflammatory process in the disease with potential tumorigenic effect, it may exert a further inhibitory effects on cancer development in inflammatory bowel disease patients, and can be combined with other relative agents, such as rapamycin, which also promotes T‐lymphocyte apoptosis. Therefore, recently established multifactorial action of cyclosporine A in relation to the pathogenesis of the disease can open new horizons for prospective, controlled trials in large cohorts, aiming to emphasize cyclosporine A's potential.
Glutathione depletion‐induced chromosomal DNA fragmentation associated with apoptosis and necrosis
Authors: Higuchi Yoshihiro 
Published: May 2007

AbstractChromosomal DNA and mitochondrial dysfunctions play a role on mammalian cell death induced by oxidative stress. The major biochemical dysfunction of chromosome is the presence of an ordered cleavage of the DNA backborn, which is separated and visualized as an electrophoretic pattern of fragments. Oxidative stress provides chromatin giant DNA, 200‐800 kb or 50‐300 kb high molecular weight (HMW) DNA and internucleosomal DNA fragments are produced during apoptosis or necrosis induced by oxidative stress such as gluthione (GSH) depletion in several types of mammalian cells. Reactive oxygen species (ROS)‐mediated DNA fragmentation is Mitochondrial dysfunction on decrease of trans membrane potential, accumulation of ROS, membrane permeability transition transition and release of apoptotic factors during apoptosis or necrosis has been implicated. This review refers to the correlation of chromo‐somal DNA fragmentation and apoptosis or necrosis induced by GSH depletion, and the possible mechanisms of oxidative stress‐induced cell death.
Binding affinities for sulfonamide inhibitors with matrix metalloproteinase‐2 using a linear response method
Authors: Svab I. , Alexandru D. , Vitos Gabriella , Flonta Maria‐Luiza 
Published: May 2007

AbstractDue to their involvement in many pathological conditions, matrix metalloproteinases (MMPs), are very attractive therapeutic targets. Our study focuses on one of them, MMP‐2, which is involved in tumor progression and metastasis. Recently, the solution structure of the catalytic domain of MMP‐2 complexed with a hydroxamic acid inhibitor (SC‐74020) was published by Feng et al. Using the Hanessian group published binding affinity data and the structure published by Feng as a basis, we have built a binding affinity model by targeting the S2’pocket of the enzyme with set of nine α‐N‐sulfonulamino hydroxamic acid derivatives. Two binding geometries of each ligand have been generated corresponding to two binding modes denoted A and B, respectively, of which the first one is targeting the S2’pocket and the second one the S1 pocket. For the binding affinity model developed for mode A the computed activities show a rmsd of 0.583 kcal/mol as compared with experimental data, and a correlation coefficient r2 of 0.779, while in the case of the binding mode B a rmsd of 0.834 kcal/mol and correlation coefficient r2 of 0.500, respectivley, were obtained. In conclusion, our data suggest a higher probability for the Phe76 gated S2’open form pocket to accommodate the substituent α versus the wide solvent exposed S1 subsite, probability which some research groups could have overlooked due to extensive use in their calculations of non revealing S2’pocket open state crystallographic structures instead of NMR ones.
Molecular diversity of HLA‐A, ‐B and ‐C alleles in a North Indian population as determined by PCR‐SSOP
Authors: Rani R. , Marcos C. , Lazaro A. M. , Zhang Y. , Stastny P. 
Published: May 2007

SummaryWe have used molecular methods to determine the frequencies of human leukocyte antigen (HLA)‐A, ‐B and ‐C alleles in normal, healthy, unrelated individuals from North India using polymerase chain reaction and hybridization with sequence‐specific oligonucleotide probes as there is no comprehensive report showing molecular diversity of all the class‐I alleles present in North Indians. A*0101, A*0206, A*0301, A*1101, A*6801, A*2401 and A*3101 were the most prevalent alleles of the A locus with 91.11% of the samples showing heterozygosity. At the HLA‐B locus a total of 47 B locus alleles were observed and the only allele found with an allele frequency of 15% was B*5801. Other frequent B‐locus alleles observed were B*5101, B*3503 and B*4006 with relatively less frequent alleles like B*5201, B*3501, B*0702, B*4403, B*5701, B*1801 and B*5501. Of the samples studied 92.31% were heterozygous for B‐locus alleles. Cw*0602 and Cw*0401 were the most frequent C‐locus alleles. Other frequent C‐locus alleles were Cw*0102, Cw*0302, Cw*0701, Cw*0702, Cw*1202, Cw*1203, Cw*1502 and Cw*1503. HLA alleles common in Africans like B*5801, A*68012, B*5301, B*44032, B*4006 and Cw*1701 were observed in the North Indians besides oriental alleles like B*1301, B*1502 and B*4001 confirming that the genetic make‐up of North Indians is Caucasoid with elements of Mongoloid and Negrito races. Some new/rare alleles like B*1802, described as a new allele from Thailand and B*8101, described earlier in a Bubi population were also observed although with low frequencies, showing the diversity of HLA class‐I alleles present in the North Indians.