bluuebunny/crossref_metadata_2025_split huggingface dataset:
Taurine release associated to volume regulation in rabbit lymphocytes
Authors: García J. Jesús , Olea R. Sánchez , Pasantes‐Morales H. 
Published: May 2005

AbstractRabbit lymphocytes exposed to hyposmotic media first swell and then recover their initial volume within 6 min. During volume recovery, free amino acids (FAA) decrease from 451.1 to 208 nmoles/mg protein. Taurine was the dominating FAA, accounting for 70% of the FAA pool. The time course of 3H‐taurine release induced by hyposmolarity followed that of volume recovery. Efflux of 3H‐taurine in an 8 min period was 17.8% (of total labeled taurine accumulated during loading) in an isosmotic medium. Reducing osmolarity to 0.87, 0.75, 0.62, and 0.5 increased this release to 24.8%, 38.1%, 56.4% and 70.9%, respectively. The volume‐sensitive release of 3H‐taurine was unaffected by omission of external Na+ or Ca++ and was reduced by 23% in the absence of Cl−. It was unaffected by agents disrupting the cytoskeleton or by tetraethylammonium, barium, quinidine, and gadolinium, but was 26% reduced by DIDS. Taurine release was inhibited at 4°C, but was unchanged at 15°C or 25°C. An involvement of FAA, particularly taurine, in lymphocyte volume regulation is suggested.
Hepatoma‐associated nuclear matrix nonhistone antigens
Authors: Kilianska Zofia , Krajewska Wanda M. , Xie Ronglin , Klyszejko‐Stefanowicz Leokadia , Chiu Jen‐Fu 
Published: May 2005

AbstractPolyclonal antibodies generated against a group of high molecular weight nonhistone proteins from Morris hepatoma 7777 were used in immunological studies of hepatoma‐associated nonhistone proteins in rat and hamster. We revealed the presence of cross‐reactive antigens in rat Morris hepatomas 7777 and 8994, and in hamster Kirkman‐Robbins hepatoma, but not in normal rat or hamster livers. These specific nonhistone proteins were found to be preferentially localized in the nuclear matrix of rat Morris hepatoma 7777 as well as hamster Kirkman‐Robbins hepatoma.
Role of platelet‐derived growth factor in wound healing
Authors: Pierce Glenn F. , Mustoe Thomas A. , Altrock Bruce W. , Deuel Thomas F. , Thomason Arlen 
Published: May 2005

AbstractPlatelet‐derived growth factor (PDGF) is a potent activator for cells of mesenchymal origin. PDGF stimulates chemotaxis, proliferation, and new gene expression in monocytes‐macrophages and fibroblasts in vitro, cell types considered essential for tissue repair. Therefore, we analyzed the influence of exogenously administered recombinant B chain homodimers of PDGF (PDGF‐BB) on two experimental tissue repair paradigms, incisional and excisional wounds. In both types of wounds, as little as 20‐200 picomoles applied a single time to wounds significantly augmented the time dependent influx of inflammatory cells and fibroblasts and accelerated provisional extracellular matrix deposition and subsequent collagen formation. In incisional wounds, PDGF‐BB augmented wound breaking strength 50–70% over the first 3 weeks; in excisional wounds, PDGF‐BB accelerated time to closure by 30%. PDGF‐BB exaggerated, but did not alter, the normal course of soft tissue repair, resulting in a significant acceleration of healing. Long term observations established no apparent differences between PDGF‐BB treated and non‐treated wounds. Thus, the vulnerary effects of PDGF‐BB were transient and fully reversible in both wound healing models. Furthermore, analysis of PDGF‐treated and non‐treated wounds has provided important insights into mechanisms of normal and deficient tissue repair processes. PDGF appears to transduce its signal through wound macrophages and may trigger the induction of positive autocrine feedback loops and synthesis of endogenous wound PDGF and other growth factors, thereby enhancing the cascade of tissue repair processes required for a fully‐healed wound. Thus, PDGF and other wound produced polypeptide growth factors may be the critical regulators of extracellular matrix deposition within healing wounds.
Biocompatible controlled release polymers for delivery of polypeptides and growth factors
Authors: Langer Robert , Moses Marsha 
Published: May 2005

AbstractThe development of biocompatible, controlled release systems for macromolecules has provided the opportunity for researchers and clinicians to target and deliver, on site, biologically active factors. This advance has also facilitated the purification and characterization of a number of important biomolecules. These systems include controlled release delivery systems which release proteins through porous polymer matrices, degradable polymeric delivery systems, and modulated polymer release systems. These areas of research will be reviewed with regards to their design, release kinetics, and biocompatibilities. The utilization of these systems to release such biologically important polypeptides as growth factors (e.g., fibroblast growth factor, epidermal growth factor, transforming growth factor‐B) as well as a number of important inhibitory factors (e.g., nitrosoureas, angiogenesis inhibitors) in both in vivo and in vitro studies will be discussed.
EGF and TGF‐α in wound healing and repair
Authors: Schultz Gregory , Clark Warren , Rotatori D. Scott 
Published: May 2005

AbstractWound healing is a localized process which involves inflammation, wound cell migration and mitosis, neovascularization, and regeneration of the extracellular matrix. Recent data suggest the actions of wound cells may be regulated by local production of peptide growth factors which influence wound cells through autocrine and paracrine mechanisms. Two peptide growth factors which may play important roles in normal wound healing in tissues such as skin, cornea, and gastrointestinal tract are the structurally related peptides epidermal growth factor (EGF) and transforming growth factor alpha (TGF‐α). EGF/TGF‐α receptors are expressed by many types of cells including skin keratinocytes, fibroblasts, vascular endothelial cells, and epithelial cells of the GI tract. In addition, EGF or TGF‐α are synthesized by several cells involved in wound healing including platelets, keratinocytes, and activated macrophages. Healing of a variety of wounds in animals and patients was enhanced by treatment with EGF or TGF‐α. Epidermal regeneration of partial thickness burns on pigs or dermatome wounds on patients was accelerated with topical application of EGF or TGF‐α, and EGF treatment accelerated healing of gastroduodenal ulcers. EGF also increased tensile strength of skin incisions in rats and corneal incisions in rabbits, cats, and primates. Additional research is needed to better define the roles of EGF, TGF‐α, and their receptor in normal wound healing, to determine if alterations have occurred in the EGF/TGF‐α system in chronic wounds, and to optimize vehicles for effective delivery of peptide growth factors to wounds.
Mammalian hepatocytes as a foundation for treatment in human liver failure
Authors: Jauregui Hugo O. , Gann Kathryn L. 
Published: May 2005

AbstractTechnological advances in the separation and culture of mammalian hepatocytes have facilitated the use of these cells as the foundation for either hepatocyte transplantation or hepatocyte‐seeded hollow fiber liver assist devices (LAD). To fully appreciate the practical applications of these tissue engineering solutions, it is necessary to understand the types of human liver failure as well as the corresponding animal models. The most immediate application of this type of technology is the treatment of hepatic encephalopathy (HE), an acute and highly fatal complication of fulminant hepatic failure. Although the pathogenesis of HE is unknown, failure of the detoxification function of the liver is accepted as playing an important role in this disorder. Consequently, the assaying and preservation of P450 activity in the grafted cells or in the LAD must be among the main targets of this research. This review explores the problems in hepatocyte transplantation and culture that deserve special consideration and emphasizes the conditions contributing to the vitro maintenance of phenotypic expression of these cells.
Cellular response to double‐stranded RNA
Authors: Haines Dale S. , Strauss Kenneth I. , Gillespie David H. 
Published: May 2005

AbstractThe study of double‐stranded RNA (dsRNA) encompasses a variety of fields. Basic research in this area has contributed to a greater mechanistic understanding of gene induction, tumor cell growth arrest, the establishment of antiviral states, and immunomodulation. Because of the possible clinical value of these molecules, physicians are now exploring the use of synthetic dsRNA to treat patients with cancer, HIV‐1 disease, and immune dysfunction. Continued studies of the mechanisms of action of dsRNA are likely to suggest an even wider scope of clinical applications.
Leukemia inhibitory factor: A biological perspective
Authors: Hilton Douglas J. , Gough Nicholas M. 
Published: May 2005

AbstractThe notion that a single hormone may exert a broad range of effects has become well established. As such, leukemia inhibitory factor (LIF) is a prime example. LIF was initially described, purified, and genetically cloned on the basis of its ability to induce the differentiation and suppress the clonogenicity of the monocytic leukemia cell line, M1. Subsequently, it has become apparent that in vitro LIF inhibits the differentiation of pluripotential ES cells, stimulates the synthesis of hepatic acute‐phase proteins, induces a switch in neurotransmitter phenotype from adrenergic to cholinergic, suppresses adipocyte lipoprotein lipase activity, and results in an increase in bone resorption. Moreover, elevation of LIF levels in vivo has a number of patho‐physiological consequences, many of which parallel those effects observed in vitro. The challenge that lies ahead is to determine whether other sites of LIF action exist and to define more clearly the physiological role LIF plays in vivo.A major mechanism of cell‐cell communication is by the production and secretion of polypeptide hormones by one cell type, which act either systemically or locally, via interaction with specific receptors on the surface of responsive cells. Recently, it has become apparent that hormones initially described and named, on the basis of a specific action, in many cases exert a spectrum of effects on a broad range of cell types. Moreover, the effects exerted are often mimicked closely by other hormones. Hormones that act in a pleiotropic manner are, for example, transforming growth factor‐β (TGF‐β), the various fibroblast growth factors (FGFs), interleukin‐6 (IL‐6), and leukemia inhibitory factor (LIF). This review will focus on the various biological effects ascribed to LIF.
Novel immunomodulators with pronounced in vivo effects caused by stimulation of cytokine release
Authors: Rasmussen L.‐T. , Seljelid R. 
Published: May 2005

AbstractBeta‐1,3‐D‐polyglucose derivatives protect mice against otherwise lethal bacterial infections. This protective effect has been considered to be mediated through mononuclear phagocytes. By using radioactive labelling, we localized the β‐1,3‐D‐polyglucose derivatized microbeads (GDM) during the period following injection. The GDM was recovered mainly in the milky spots of the omentum. In animals treated with GDM, the total white cell number was significantly increased in peritoneal fluid of mice before and after challenge with E. coli. Bacterial counts in peritoneal fluid of GDM treated animals declined to zero after 24 h. In untreated animals there was a slight increase in bacterial counts until the animals died after about 12 h. Mouse peritoneal macrophages stimulated with GDM released significant amounts of IL‐1 and PGE2. There was no significant release of TNF. Levels of IL‐1 and PGE2 in peritoneal fluid increased significantly during the first 48 h after treatment with GDM. There was no increase of levels of TNF. After challenge with E. coli, the levels of IL‐1, TNF, and PGE2 were significantly lower compared with control animals. In untreated animals the levels of IL‐1 and TNF remained elevated until the animals died after about 12 h. These studies demonstrate that the raised levels of arachidonic acid metabolites after pretreatment with GDM or AG seems to inhibit the otherwise lethal elevation of IL‐1 and TNF in body fluids which is seen in untreated animals.
Annexin VI is associated with calcium‐sequestering organelles
Authors: Hazarika Parul , Kaetzel Marcia A. , Sheldon Adrian , Karin Norman J. , Fleischer Sidney , Nelson T. E. , Dedman John R. 
Published: May 2005

AbstractAnnexin VI is a member of a Ca2+‐dependent, phospholipid‐binding protein family. Although functions for this annexin have been proposed from in vitro studies, most remain controversial. Díaz‐Muñoz et al. (J Biol Chem 265:15894, 1990) demonstrated that annexin VI modified, in a Ca2+‐dependent manner, the gating behavior of the sarcoplasmic reticulum Ca2+‐release channel, reconstituted into artificial bilayers, by increasing both the open probability and the mean open time. This effect was specific to the trans chamber, which represents the luminal side of the sarcoplasmic reticulum. In agreement with those findings, we show herein that annexin VI produced no effect on Ca2+‐uptake or ‐release by intact heavy sarcoplasmic reticulum vesicles (analogous to the cis chamber). We also used monospecific antibodies to evaluate the subcellular localization of annexin VI by immunofluorescent microscopy. Studies in rat skeletal muscle suggest that annexin VI is present surrounding individual myofibrils. Double immunolocalization studies with cultured muscle cells (chick myotubes) using anti‐annexin VI and anti‐SR Ca2+‐ATPase antibodies demonstrated superimposable staining patterns. In non‐muscle tissue (normal rat kidney (NRK) cells), a punctate, perinuclear anti‐annexin VI staining pattern was observed. Collectively, these data suggest that annexin VI may play a regulatory role in the Ca2+‐release/uptake cycle in the sarcoplasmic reticulum as well as in non‐muscle organelles, a key process in stimulus‐response systems.
Bacterial resistances to mercury and copper
Authors: Morby Andrew P. , Parkhill Julian , Lee Barry T. O. , Brown Nigel L. , Rouch Duncan A. , Camakaris James , Williams Tracey 
Published: May 2005

AbstractHeavy metals are toxic to living organisms. Some have no known beneficial biological function, while others have essential roles in physiological reactions. Mechanisms which deal with heavy metal stress must protect against the deleterious effects of heavy metals, yet avoid depleting the cell of a heavy metal which is also an essential nutrient. We describe the mechanims of resistance in Escherichia coli to two different heavy metals, mercury and copper. Resistance of E. coli to mercury is reasonably well understood and is known to occur by transport of mercuric ions into the cytoplasmic compartment of the bacterial cell and subsequent reductive detoxification of mercuric ions. Recent mutational analysis has started to uncover the mechanistic detail of the mercuric ion transport processes, and has shown the essential nature of cysteine residues in transport of Hg(II). Resistance to copper is much less well understood, but is known to involve the increased export of copper from the bacterial cell and modification of the copper; the details of the process are still being elucidated.Expression of both metal resistance determinants is regulated by the corresponding cation. In each case the response enables the maintenance of cellular homeostasis for the metal. The conclusions drawn allow us to make testable predictions about the regulation of expression of resistance to other heavy metals.
Constitutive production of lymphocyte activating factors by normal tissues in the adult rat
Authors: Granholm Tina , Söder Olof 
Published: May 2005

AbstractLymphocyte activating factors (LAFs), e.g., interleukin‐1 (IL‐1) and IL‐1‐like factors, have previously been demonstrated outside the immune system in the skin, thymus epithelium, and the human and rat testis. We have studied the presence of LAFs in normal tissues of the adult rat, utilizing a highly IL‐1 sensitive murine thymocyte proliferation assay. We have demonstrated high amounts of LAF activity in the tongue, esophagus, proventricular part of the stomach, and the liver. Some activity was also demonstrated in the duodenum, placenta, spleen, Peyer's patches, glandular stomach, and jejunum, but no bioactivity was present in other gastrointestinal, endocrine, lymphoid, or haematopoietic tissues. We were also unable to detect any LAF activity in the reproductive organs (except for the testis), urinary tract, skeletal and muscular tissues, brain, eyes, salivary glands, or lung. In the esophagus the activity was mainly localized to the mucosa. The LAF activity in the skin was partly inhibited by treatment with a mixture of antibodies against human IL‐1α and IL‐1β Dose response curves and gel filtration on a Sephacryl S‐200 column suggested the presence of a high molecular weight (90,000–100,000 Da) LAF inhibitory factor in the liver. In all positive tissues, the demonstrated LAFs had a molecular weight of 15,000–25,000 Da, as determined by Sephacryl S‐200 gel filtration. Of the positive tissues, the skin, tongue, esophagus, and the proventricular part of the stomach all contain stratified squamous epithelium. It is tempting to suggest that the detected LAFs have a similar function in these barrier tissues, e.g., to serve as host defence factors, or, alternatively or additionally, as tissue growth factors.
Poly(ADP‐ribosylation) of atypical CS histone variants is required for the progression of S phase in early embryos of sea urchins
Authors: Imschenetzky M. , Montecino M. , Puchi M. 
Published: May 2005

AbstractThe patterns of poly(ADP‐ribosylation) in vivo of CS (cleavage stage) histone variants were compared in sea urchin zygotes at the entrance and the exit of S1 and S2 in the initial developmental cell cycles. This post‐translational modification was detected by Western immunoblots with rabbit sera anti‐poly(ADP‐ribose) that was principally reactive against ADP‐ribose polymers and slightly against ADP‐ribose oligomers. The effect of 3 aminobenzamide (3‐ABA), an inhibitor of the poly(ADP‐ribose) synthetase, on S phase progression was determined in vivo by measuring the incorporation of 3H thymidine into DNA. The results obtained indicate that the CS histone variants are poly(ADP‐ribosylated) in a cell cycle dependent manner. A significantly positive reaction of several CS variants with sera anti‐poly(ADP‐ribose) was found at the entrance into S phase, which decreases after its completion. The incubation of zygotes in 3‐ABA inhibited the poly(ADP‐ribosylation) of CS variants and prevented both the progression of the first S phase and the first cleavage division. These observations suggest that the poly(ADP‐ribosylation) of atypical CS histone variants is relevant for initiation of sea urchin development and is required for embryonic DNA replication.
Prostatic epithelial cells in culture: Phosphorylation of protein tyrosyl residues and tyrosine protein kinase activity
Authors: Bourassa C. , Nguyen L. T. , Durocher Y. , Roberts K. D. , Chevalier S. 
Published: May 2005

AbstractThe ability of dividing canine prostatic epithelial cells in primary monolayers to phosphorylate protein tyrosyl residues was evaluated by metabolic studies performed through incorporation of [32P]‐phosphate into alkali‐resistant phosphoproteins and by the assay of their tyrosine protein kinase activity. The presence of sodium orthovanadate during cell incubation with [32P]‐phosphate greatly enhanced the relative labelling intensity of a 44 kDa alkali‐resistant phosphoprotein and the total cellular content of phosphotyrosine in proteins; in this respect, growth factors such as epidermal growth factor, insulin, and insulin‐like growth factor I, and the steroids dihydrotestosterone and estradiol were inactive. When the cells were solubilized, sodium orthovanadate stimulated their tyrosine protein kinase activity and inhibited their phosphotyrosine phosphatase activity. To characterize the tyrosine protein kinase of these cultured cells, conditions for optimal activity were established using the substrate poly [Glu80Na, Tyr20]. The subcellular localization of the enzyme was determined upon cell fractionation: 88% of the kinase activity was associated with the particulate fraction and 30% of this activity was partially solubilized with 0.5% Triton X–100; this solubilization was improved to 83% in the presence of 0.25 M KCl. The enzyme directly solubilized from prostatic cells with Triton X–100 (38% of activity) mainly catalyzed the alkali‐resistant phosphorylation of pp63, pp59, and pp44, which contained phosphotyrosine. These proteins were also phosphorylated by the major peak of kinase activity which was eluted at an apparent molecular weight of 300–350 kDa upon gel filtration. On a cell basis, the kinase activity was four‐ to eleven‐fold higher in the dividing epithelial cells in culture compared to quiescent secretory and non‐secretory epithelial cells, freshly isolated from dog prostates. It is proposed that this tyrosine protein kinase is implicated in the regulation of the proliferation of prostatic epithelial cells.
Adenosine deaminase deficiency due to heterozygous abnormality consisting of a deletion of exon 7 and the absence of enzyme mRNA
Authors: Kashii Saburo , Ito Kazuhiko , Monden Sumie , Sasai Yoshiki , Tsuchida Kunihiro , Fujita Masahiro , Kawamoto Hiroshi , Norioka Mihoko , Okuma Minoru 
Published: May 2005

AbstractAn adenosine deaminase (ADA;EC 3.5.4.4)‐deficient B lymphoblastoid cell line BADO5 derived from a Japanese patient with severe combined immunodeficiency disease and two B lymphoblastoid cell lines, BAMO5 from his mother and BAFO5 from his father, were characterized. To identify mutations affecting ADA activity, we prepared cDNAs to ADA mRNAs of the BADO5 cell line for nucleotide sequencing. Sequence analysis of one of the BADO5 ADA cDNA clones revealed deletion of exon 7, and one point mutation of base 629 from G to A that did not affect the amino acid sequence. All clones of the BADO5 cell line so far examined showed the absence of exon 7 by Southern blotting analysis. Ribonuclease protection assay with an RNA probe spanning from exon 5 to exon 11 showed that the BADO5 ADA mRNA had a deletion of exon 7, the BAMO5 mRNA had normal length, and the BAFO5 mRNA had two species with a deletion of exon 7 and with normal length. Consequently, the patient's ADA genes resulted from one allele of the BAMO5 ADA gene that did not produce a detectable mRNA, and the other allele of the BAFO5 ADA gene producing an aberrant mRNA without exon 7.
Studies on the role of protein kinases in the TNF‐mediated enhancement of murine tumor cell‐endothelial cell interactions
Authors: Bereta Joanna , Bereta Michal , Cohen Stanley , Cohen Marion C. 
Published: May 2005

AbstractWe have previously demonstrated that the exposure of mouse microvascular endothelium (MME) to tumor necrosis factor‐α (TNF) led to the increased binding of mouse mastocytoma cells (P815) to endothelial monolayers (Bereta et al., in press). In the current study we examined the possible involvement of protein kinases in TNF signal transduction in the endothelial cells. PKA does not appear to play a role in the potentiation of binding by TNF. We found that the TNF‐generated signal is inhibited by H‐7 and sangivamycin, but not by staurosporine. TNF did not cause translocation of PKC to the cell membrane and its effect could not be completely mimicked by PMA nor by PMA in the presence of calcium‐raising agents. Thus, we concluded that the “classical” PKC pathway is not completely responsible for TNF signalling in this system. We also found that staurosporine itself strongly enhanced adhesion of tumor cells to endothelium, utilizing a mechanism distinct from that of TNF. Although the data provide evidence for the role of kinases in the effect of TNF on binding of tumor cells to MME, this role appears to be a complex one.