Cellular

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Cellular

  • inflammatory cellular

  • Terms modified by Cellular

  • cellular accumulation
  • cellular action
  • cellular activation
  • cellular activity
  • cellular adaptation
  • cellular adhesion
  • cellular adhesion molecule
  • cellular ageing
  • cellular aging
  • cellular alteration
  • cellular analysis
  • cellular apoptosi
  • cellular architecture
  • cellular area
  • cellular arrangement
  • cellular aspect
  • cellular atp
  • cellular atp level
  • cellular attachment
  • cellular atypia
  • cellular barrier
  • cellular base
  • cellular basis
  • cellular behavior
  • cellular behaviour
  • cellular biochemistry
  • cellular biology
  • cellular body
  • cellular change
  • cellular characteristic
  • cellular communication
  • cellular compartment
  • cellular component
  • cellular composition
  • cellular concentration
  • cellular condensation
  • cellular condition
  • cellular constituent
  • cellular content
  • cellular context
  • cellular control
  • cellular cytotoxicity
  • cellular damage
  • cellular debris
  • cellular defect
  • cellular defence
  • cellular defence mechanism
  • cellular defense
  • cellular defense mechanism
  • cellular degeneration
  • cellular delivery
  • cellular density
  • cellular development
  • cellular differentiation
  • cellular distribution
  • cellular dna
  • cellular dynamics
  • cellular dysfunction
  • cellular effect
  • cellular effects
  • cellular element
  • cellular energy
  • cellular energy status
  • cellular engineering
  • cellular environment
  • cellular event
  • cellular excitability
  • cellular expression
  • cellular extract
  • cellular factor
  • cellular feature
  • cellular form
  • cellular fraction
  • cellular fractionation
  • cellular function
  • cellular gene
  • cellular gene expression
  • cellular genome
  • cellular glutathione
  • cellular growth
  • cellular gsh
  • cellular gsh level
  • cellular heterogeneity
  • cellular homeostasi
  • cellular hypertrophy
  • cellular identity
  • cellular imaging
  • cellular immune response
  • cellular immune system
  • cellular immunity
  • cellular immunotherapy
  • cellular infiltration
  • cellular inflammatory response
  • cellular inhibitor
  • cellular injury
  • cellular insult
  • cellular integrity
  • cellular interaction
  • cellular internalization
  • cellular layer
  • cellular level
  • cellular life
  • cellular lineage
  • cellular lipid
  • cellular localization
  • cellular location
  • cellular locations
  • cellular lysate
  • cellular machinery
  • cellular marker
  • cellular material
  • cellular matrix
  • cellular mechanism
  • cellular mechanism underlying
  • cellular membrane
  • cellular metabolism
  • cellular microenvironment
  • cellular migration
  • cellular model
  • cellular models
  • cellular morphology
  • cellular motility
  • cellular movement
  • cellular network
  • cellular neural network
  • cellular organelle
  • cellular organization
  • cellular origin
  • cellular origins
  • cellular outcome
  • cellular oxidative stress
  • cellular pathology
  • cellular pathway
  • cellular pattern
  • cellular phenotype
  • cellular phone
  • cellular physiology
  • cellular pleomorphism
  • cellular polarity
  • cellular population
  • cellular prion protein
  • cellular probe
  • cellular process
  • cellular production
  • cellular profile
  • cellular proliferation
  • cellular property
  • cellular protection
  • cellular protein
  • cellular receptor
  • cellular redox state
  • cellular redox status
  • cellular regulation
  • cellular rejection
  • cellular repair
  • cellular reprogramming
  • cellular resistance
  • cellular resolution
  • cellular respiration
  • cellular response
  • cellular responsiveness
  • cellular retention
  • cellular rna
  • cellular ro level
  • cellular role
  • cellular senescence
  • cellular sensitivity
  • cellular signal
  • cellular signaling
  • cellular signaling pathway
  • cellular signalling
  • cellular site
  • cellular solid
  • cellular source
  • cellular states
  • cellular stress
  • cellular stress response
  • cellular structure
  • cellular studies
  • cellular substrate
  • cellular survival
  • cellular system
  • cellular target
  • cellular therapy
  • cellular toxicity
  • cellular transformation
  • cellular type
  • cellular uptake
  • cellular viability
  • cellular volume

  • Selected Abstracts


    ETHICAL ISSUES IN CELLULAR AND MOLECULAR MEDICINE AND TISSUE ENGINEERING

    JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 5b 2008
    Raymund E. Horch
    First page of article [source]


    Cellular and molecular dissection of pluripotent adult somatic stem cells in planarians

    DEVELOPMENT GROWTH & DIFFERENTIATION, Issue 1 2010
    Norito Shibata
    Freshwater planarians, Plathelminthes, have been an intriguing model animal of regeneration studies for more than 100 years. Their robust regenerative ability is one of asexual reproductive capacity, in which complete animals develop from tiny body fragments within a week. Pluripotent adult somatic stem cells, called neoblasts, assure this regenerative ability. Neoblasts give rise to not only all types of somatic cells, but also germline cells. During the last decade, several experimental techniques for the analysis of planarian neoblasts at the molecular level, such as in situ hybridization, RNAi and fluorescence activated cell sorting, have been established. Moreover, information about genes involved in maintenance and differentiation of neoblasts has been accumulated. One of the molecular features of neoblasts is the expression of many RNA regulators, which are involved in germline development in other animals, such as vasa and piwi family genes. In this review, we introduce physiological and molecular features of the neoblast, and discuss how germline genes regulate planarian neoblasts and what differences exist between neoblasts and germline cells. [source]


    Cellular and molecular basis of cadmium-induced deformities in zebrafish embryos

    ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 12 2000
    Shuk Han Cheng
    Abstract Cadmium is known to cause developmental defects in a varietyof vertebrate species, but relatively little is known about the underlying molecular mechanisms. In this study, we used zebrafish (Danio rerio) embryos as a model system to investigate cadmium-induced toxicities. Fertilized embryos collected at 5-h after fertilization were incubated for 18 h in culture media containing 1 to 1, 000 ,M CdCl2. The median embryolethal concentration (LC50) was 168 ,M, whereas the median effect concentration (EC50) for total adverse effect (mortality and developmental defects) was 138 ,M. Six major types of deformities were observed: head and eye hypoplasia, hypopigmentation, cardiac edema, yolk sac abnormalities, altered axial curvature, and tail malformations. The frequency of malformations increased with cadmium concentration. Somites of embryos with altered axial curvature were investigated using the antimyosin antibody MF-20. This study demonstrated, to our knowledge for the first time, reduced myotome formation in cadmium-induced spinal deformity. Embryos with head and eye hypoplasia were studied using the anti-neural tissue antibody zns-2, and a poorly developed central nervous system was revealed. Head and eye hypoplasia were associated with lack of expression of the sonic hedgehog gene, which controls the patterning of the neural tube and somites. Genes involved in tail formations, such as evenskipped 1 and no tail, were ectopically expressed in embryos with tail malformations. Our data support the hypothesis that fish embryonic malformations induced by cadmium might be mediated through ectopic expression of developmental regulatory genes. [source]


    FMRFamide gene and peptide expression during central nervous system development of the cephalopod mollusk, Idiosepius notoides

    EVOLUTION AND DEVELOPMENT, Issue 2 2010
    Tim Wollesen
    SUMMARY Mollusks are a showcase of brain evolution represented by several classes with a varying degree of nervous system centralization. Cellular and molecular processes involved in the evolution of the highly complex cephalopod brain from a simple, monoplacophoran-like ancestor are still obscure and homologies on the cellular level are poorly established. FMRFamide (Phe-Ile-Arg-Phe-NH2)-related peptides (FaRPs) constitute an evolutionarily conserved and diverse group of neuropeptides in the central nervous system (CNS) of many metazoans. Herein, we provide a detailed description of the developing FMRFamide-like immunoreactive (Fa-lir) CNS of the pygmy squid Idiosepius notoides using gene expression analyses and immunocytochemistry. The open reading frame of the I. notoides FMRFamide gene InFMRF predicts one copy each of FIRFamide, FLRFamide (Phe-Leu-Arg-Phe-NH2), ALSGDAFLRFamide (Ala-Leu-Ser-Gly-Asp-Ala-Phe-Leu-Arg-Phe-NH2), and 11 copies of FMRFamide. Applying matrix-assisted laser desorption/ionization time-of-flight (ToF) mass spectrometry-based peptide profiling, we characterized all predicted FaRPs except ALSGDAFLRFamide. Two cell clusters express InFMRF and show FMRFamide-like-immunoreactivity within the palliovisceral ganglia, that is, the future posterior subesophageal mass, during the lobe differentiation phase. They project neurites via ventral axonal tracts, which form the scaffold of the future subesophageal mass. In the supraesophageal mass, InFMRF is first expressed during mid-embryogenesis in the superior and inferior buccal lobes. A neurite of the peduncle commissure represents the first Fa-lir element. Later, the sub- and supraesophageal mass interconnect via Fa-lir neurites and more brain lobes express InFMRF and FMRFamide-like peptides. InFMRF expression was observed in fewer brain lobes than Fa-lir elements. The early expression of InFMRF and FMRFamide-lir peptides in the visceral system and not the remaining CNS of the cephalopod I. notoides resembles the condition found in the majority of investigated gastropods. [source]


    Cellular and molecular mechanisms of bleomycin-induced murine scleroderma: current update and future perspective

    EXPERIMENTAL DERMATOLOGY, Issue 2 2005
    Toshiyuki Yamamoto
    Abstract:, Scleroderma is a fibrotic condition characterized by immunologic abnormalities, vascular injury and increased accumulation of matrix proteins in the skin. Although the aetiology of scleroderma is not fully elucidated, a growing body of evidence suggests that extracellular matrix overproduction by activated fibroblasts results from complex interactions among endothelial cells, lymphocytes, macrophages and fibroblasts, via a number of mediators. Cytokines, chemokines and growth factors secreted by inflammatory cells and mesenchymal cells (fibroblasts and myofibroblasts) play an important role in the fibrotic process of scleroderma. Recently, we established a murine model of scleroderma by repeated local injections of bleomycin. Dermal sclerosis was induced in various mouse strains, although the intensity of dermal sclerosis varied among various strains. Histopathological and biochemical analysis demonstrated that this experimental murine scleroderma reflected a number of aspects of human scleroderma. Further investigation of the cellular and molecular mechanisms of inflammatory reaction, fibroblast activation and extracellular matrix deposition following dermal injury by bleomycin treatment will lead to the better understanding of the pathophysiology and the exploration of effective treatment against scleroderma. This review summarizes recent progress of the cellular and molecular events in the pathogenesis of bleomycin-induced scleroderma; moreover, further perspective by using this mouse model has been discussed. [source]


    Cellular and molecular studies of B cells exhibiting reverse somatic mutation throughout life

    GENES TO CELLS, Issue 11 2004
    Takao Kodera
    Somatic mutation of immunoglobulin (Ig) genes plays an important role in generating antibody diversity. The frequency of somatic mutation appears to vary throughout life. However, this process has been difficult to study in vivo because the DNA in and around rearranged V genes undergoes random mutation, causing silent or replacement mutations. Therefore, we have developed a transgenic mouse model for studying the frequency of B cells exhibiting mutation in young and old mice. The system is based on a reporter transgene (HuG-X) that encodes a chimeric Ig heavy chain composed of a murine VDJ segment and a human IgG1 constant region. The VDJ has been mutated to contain a TAG stop codon in the D segment. Therefore, the transgene is transcribed but not translated. Point mutation of the stop codon results in expression of the chimeric H chain, which is readily detected as human IgG1 expression. In vivo, we found that the transgene undergoes spontaneous reverse somatic mutation at a low frequency. Treatment of HuG-X mice with anti-IgD greatly increases the frequency of somatic mutation. The observed mutation frequency in anti-IgD-treated mice increases with age until adulthood, then plateaux and finally declines in aged mice. The mutations in the stop codon were associated with increased double-stranded DNA breaks (DSB) within and around the TAG site. Our results demonstrate that the rate of frequency of spontaneous reverse mutation is very low in vivo, yet it is significantly increased after stimulation with anti-IgD antibodies. The frequency of point mutation is age dependent and correlates with increased DSB. [source]


    "A Murmur of Amazement"

    GERMAN RESEARCH, Issue 1 2009
    Marco Finetti
    How well known is the Excellence Initiative abroad, and what is its image? Following an information and advertising tour through the USA, Marco Finetti talked to Annette Schmidtmann from the DFG and Hans-Georg Kräusslich from the cluster of excellence "Cellular Networks" [source]


    Natural Killer Cell Protocols: Cellular and Molecular Methods.

    HEMATOLOGICAL ONCOLOGY, Issue 1 2001
    2000., Kerry S. Campbell, Marco Colonna (Eds.). Humana Press Inc
    No abstract is available for this article. [source]


    Cellular and humoral autoimmunity directed at bile duct epithelia in murine biliary atresia,,

    HEPATOLOGY, Issue 5 2006
    Cara L. Mack
    Biliary atresia is an inflammatory fibrosclerosing lesion of the bile ducts that leads to biliary cirrhosis and is the most frequent indication for liver transplantation in children. The pathogenesis of biliary atresia is not known; one theory is that of a virus-induced, subsequent autoimmune-mediated injury of bile ducts. The aim of this study was to determine whether autoreactive T cells and autoantibodies specific to bile duct epithelia are present in the rotavirus (RRV)- induced murine model of biliary atresia and whether the T cells are sufficient to result in bile duct inflammation. In vitro analyses showed significant increases in IFN-,,producing T cells from RRV-diseased mice in response to bile duct epithelial autoantigen. Adoptive transfer of the T cells from RRV-diseased mice into naïve syngeneic SCID recipients resulted in bile duct,specific inflammation. This induction of bile duct pathology occurred in the absence of detectable virus, indicating a definite response to bile duct autoantigens. Furthermore, periductal immunoglobulin deposits and serum antibodies reactive to bile duct epithelial protein were detected in RRV-diseased mice. In conclusion, both cellular and humoral components of autoimmunity exist in murine biliary atresia, and the progressive bile duct injury is due in part to a bile duct epithelia,specific T cell,mediated immune response. The role of cellular and humoral autoimmunity in human biliary atresia and possible interventional strategies therefore should be the focus of future research. (HEPATOLOGY 2006;44:1231,1239.) [source]


    Epidermal growth factor receptor and cancer: control of oncogenic signalling by endocytosis

    JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 5a 2008
    Michael Vibo Grandal
    ,,Introduction ,,Endocytosis of EGFR -,Kinase activity -,Clathrin-coated pits -,Ubiquitination -,Effects of EGFR-ErbB2 heterodimerization on EGFR internalization ,,Cellular and molecular requirements for lysosomal degradation of EGFR -,Intracellular EGFR degradation depends on luminal sorting at multivesicular bodies -,Molecular requirements for EGFR sorting in multivesicular endosomes Abstract The epidermal growth factor receptor (EGFR) and other members of the EGFR/ErbB receptor family of receptor tyrosine kinases (RTKs) are important regulators of proliferation, angiogenesis, migration, tumorigenesis and metastasis. Overexpression, mutations, deletions and production of autocrine ligands contribute to aberrant activation of the ErbB proteins. The signalling output from EGFR is complicated given that other ErbB proteins are often additionally expressed and activated in the same cell, resulting in formation of homo-and/or heterodimers. In particular, association of EGFR with ErbB2 prevents its down-regulation, underscoring the importance of the cellular background for EGFR effects. Signalling from ErbB proteins can either be terminated by dissociation of ligand resulting in dephosphorylation, or blunted by degradation of the receptors. Although proteasomal targeting of ErbB proteins has been described, lysosomal degradation upon ligand-induced endocytosis seems to play the major role in EGFR down-regulation. Preclinical and clinical data have demonstrated that EGFR is a central player in cancer, especially in carcinomas, some brain tumours and in non-small cell lung cancer. Such studies have further validated EGFR as an important molecular target in cancer treatment. This review focuses on mechanisms involved in ligand-induced EGFR activation and endocytic down-regulation. A better understanding of EGFR biology should allow development of more tumour-selective therapeutic approaches targeting EGFR-induced signalling. [source]


    Regulatory issues in cellular therapies

    JOURNAL OF CELLULAR BIOCHEMISTRY, Issue S38 2002
    Adrian P. Gee, Article first published online: 23 APR 200
    Cellular and gene therapies offer considerable promise as new treatment modalities. The Food and Drug Administration has been developing strategies to regulate these rapidly evolving fields in a manner that sustains progress and also ensures minimization of potential risks. The death of a patient on a gene therapy study highlighted a number of potential problems that have galvanized the agency to examine their strategy and to review current regulations for gene therapy. Meanwhile, a unified regulatory approach is emerging for cell-based therapies. This stratifies the level of regulation based upon the potential risk to the donor of the cells and the recipient. In this article the history and status of regulation of cellular therapy is briefly reviewed. J. Cell. Biochem. Suppl. 38: 104,112, 2002. © 2002 Wiley-Liss, Inc. [source]


    Carotenoid and protein supplementation have differential effects on pheasant ornamentation and immunity

    JOURNAL OF EVOLUTIONARY BIOLOGY, Issue 1 2007
    H. G. SMITH
    Abstract A currently popular hypothesis states that the expression of carotenoid-dependent sexual ornaments and immune function may be correlated because both traits are positively affected by carotenoids. However, such a correlation may arise for another reason: it is well known that immune function is dependent on nutritional condition. A recent study has suggested that the expression of ornaments may too depend on nutritional condition, as males in good nutritional condition are better at assimilating and/or modulating carotenoids. Thus, carotenoid-dependent ornaments and immune function may be correlated because both are dependent on nutritional condition. To elucidate if, and how, ornamentation and immune function are linked, pheasant diets were supplemented with carotenoid and/or protein in a fully factorial experiment. Carotenoid treatment affected wattle coloration and tail growth, but not cellular or humoral immunity. Immunity was unrelated to males' initial ornamentation including wattle colour. Males in better body condition, measured as residual mass, increased their wattle coloration more when carotenoid supplemented. Protein positively affected humoral but not cellular immunity, but had no effect on ornaments. Cellular, but not humoral, immunity increased with male body condition. Thus, there was no evidence that an immune-stimulatory effect of carotenoids resulted in wattle coloration honestly signalling immune function, but wattle coloration may still signal male body condition. [source]


    Cellular and humoral immune responses to measles in immune adults re-immunized with measles vaccine

    JOURNAL OF MEDICAL VIROLOGY, Issue 2 2003
    Rosa Maria Wong-Chew
    Abstract The objective of this study was to characterize the kinetics of the cellular and humoral immune responses elicited by measles vaccine given to previously immune adults. The cellular and humoral immune responses to measles were measured in seven healthy adults, before vaccination and at 1, 2, 3, and 4 weeks and 3 months after vaccination, using measles-specific T-cell proliferation and plaque reduction neutralization assays. All study subjects had detectable measles antibodies, but only six (85%) showed protective titers, defined as >1:120, before immunization. However measles-specific T-cell proliferation was not detectable before vaccination in any of the subjects. The six subjects with protective titers showed a positive stimulation index (SI) of >3.0 within the first 4 weeks after vaccination, an SI of 5 at the 4th week, and an SI of 3 at 3 months after vaccination. The subject with a low antibody titer (1:99) before vaccination developed a high SI at 3 months after vaccination. This subject was the only participant whose neutralizing antibody titers increased more than 4-fold by 3 months after vaccination. No significant increases in geometric mean titers were detected in the other six subjects during the follow-up period. These data suggest that high measles antibody titers interfere with the humoral response in subjects who receive a booster immunization, whereas the cellular response is boosted at least transiently, after revaccination. J. Med. Virol. 70: 276,280, 2003. © 2003 Wiley-Liss, Inc. [source]


    Cellular and behavioural effects of the adenosine A2a receptor antagonist KW-6002 in a rat model of l -DOPA-induced dyskinesia

    JOURNAL OF NEUROCHEMISTRY, Issue 6 2003
    M. Lundblad
    Abstract We have examined the ability of KW-6002, an adenosine A2a antagonist, to modulate the dyskinetic effects of l -DOPA in 6-hydroxydopamine-lesioned rats. In animals rendered dyskinetic by a previous course of l -DOPA treatment, KW-6002 did not elicit any abnormal involuntary movements on its own, but failed to reduce the severity of dyskinesia when coadministered with l -DOPA. A second experiment was undertaken in order to study the effects of KW-6002 in l -DOPA-naive rats. Thirty-five animals were allotted to four groups to receive a 21-day treatment with: (i) KW-6002 (10 mg/kg/day); (ii) l -DOPA (6 mg/kg/day) i.p.; (iii) KW-6002 plus l -DOPA (same doses as above) or (iv) vehicle. Chronic treatment with KW-6002-only produced a significant relief of motor disability in the rotarod test in the absence of any abnormal involuntary movements. Combined treatment with l -DOPA and KW-6002 improved rotarod performance to a significantly higher degree than did each of the two drugs alone. However, this combined treatment induced dyskinesia to about the same degree as did l -DOPA alone. In situ hybridization histochemistry showed that KW-6002 treatment alone caused an approximately 20% reduction in the striatal levels of preproenkephalin mRNA, whereas neither the coadministration of KW-6002 and l -DOPA nor l -DOPA alone significantly altered the expression of this transcript in the dopamine-denervated striatum. Either alone or in combination with l -DOPA, KW-6002 did not have any modulatory effect on prodynorphin mRNA expression or FosB/,FosB-like immunoreactivity in the dopamine-denervated striatum. These results show that monotreatment with an adenosine A2a receptor antagonist can relieve motor disability without inducing behavioural and cellular signs of dyskinesia in rats with 6-hydroxydopamine lesions. Cotreatment with KW-6002 and l -DOPA potentiates the therapeutic effect but not the dyskinesiogenic potential of the latter drug. [source]


    Establishment of OC3 oral carcinoma cell line and identification of NF-,B activation responses to areca nut extract

    JOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 2 2004
    Shu-Chun Lin
    Background:, Cell lines derived from oral squamous cell carcinoma (OSCC) exposed to variable etiological factors can bestow advantages in understanding the molecular and cellular alterations pertaining to environmental impacts. Most OSCC cell lines have been established from smoker patients or areca chewing/smoker patients, carrying the genomic alterations in p53. Methods:, A new cell line, oral carcinoma 3 (OC3), was established from an OSCC in a long-term areca (betel) chewer who does not smoke. Cellular and molecular features of OC3 were determined by variable assays. Results:, The cultured monolayer cells were mainly polygonal and had the expression of cytokeratin 14. The chromosomal analysis using comparative genomic hybridization has revealed the gain in chromosomes 1q, 5q, and 8q, the loss in 4q, 6p, and 8p as well as the gain of entire chromosome 20. Loss of heterozygosity and instability in multiple microsatellite markers in chromosome 4q were also noted. OC3 cells bear wild-type p53 coding sequence and have a high level of p53 expression. Its p21 expression was similar to that in normal human oral keratinocyte (NHOK). Interestingly, activation of nuclear factor ,B (NF-,B) in OC3 cells following the treatment of areca nut extract was observed. Conclusion:, OC3 cell line could be valuable in understanding the genetic impairments and phenotypic changes associated with areca in oral keratinocyte. [source]


    Cellular and molecular characterization of a murine non-union model

    JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 5 2004
    P. Choi
    Abstract Purpose. We have developed a method to study the molecular and cellular events underlying delayed skeletal repair in a model that utilizes distraction osteogenesis. Methods. The clinical states of delayed union and non-union were reproduced in this murine model by altering distraction parameters such as the inclusion and exclusion of a latency phase and variations in the rate and rhythm of distraction. Radiographic, cellular, and molecular analyses were performed on the distraction tissues. Results. Eliminating the latency period delayed bony union, but did not appreciably alter the extent of platelet endothelial cell adhesion marker (PECAM) immunostaining. Following elimination of a latency phase and a threefold increase in the rate of distraction, there was a further delay in bone regeneration and a higher rate of non-union (60%). Instead of bone, the distraction gap was comprised of adipose or fibrous tissue. Once again, despite the rigorous distraction protocol, we detected equivalent PECAM staining within the distraction gap. In a minority of cases, cartilage and osseous tissues occupied the distraction gap likely by a prolonged process of endochondral ossification. Conclusions. Here, we have altered the mechanical environment in such a way to reproducibly create delays in skeletal regeneration. These delays in skeletal tissue regeneration appear to develop even in the presence of endothelial cells, which suggests that mechanisms other than a disruption to the vascular network can account for some cases of non-union. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved. [source]


    Leptin and Cellular and Innate Immunity in Abstinent Alcoholics and Controls

    ALCOHOLISM, Issue 11 2003
    Sarosh J. Motivala
    Background: Basic studies indicate that in vitro and in vivo doses of leptin modulate cellular immune responses. Given evidence that concentrations of leptin are altered in alcoholics who also show immune abnormalities, this study examined the relationships between circulating levels of leptin and markers of cellular and innate immunity. Methods: Circulating levels of leptin, natural killer cell (NK) activity, interleukin-2 (IL-2),stimulated NK activity, and concanavalin A,stimulated production of IL-2, IL-6, IL-10, and IL-12 were compared between abstinent DSM-IV alcohol-dependent men (n= 27) and age- and gender-matched controls (n= 34). Results: As compared with controls, alcoholics showed lower NK activity (p < 0.01) and a trend for lower levels of leptin (p= 0.055). In the total sample, leptin predicted NK activity (,= 0.33; p < 0.05) after controlling for the confounding influence of body mass index, alcohol intake, and smoking. Leptin was not correlated with any of the cytokine measures. To examine whether the effects of leptin were mediated by its direct action on NK, additional studies examined in vitro effects of leptin on NK activity in healthy volunteers (n= 10); leptin doses (0.1, 1, and 10 nM) yielded levels of NK activity comparable to those with media alone. Conclusions: These data show that circulating levels of leptin are associated with NK activity in humans and suggest that abnormal in vivo concentrations of leptin may contribute to the declines of NK activity in alcoholics who are at risk for infectious diseases. [source]


    Review article: RNA interference , potential therapeutic applications for the gastroenterologist

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2008
    R. S. PELLISH
    Summary Background, A new technique of gene regulation, termed RNA interference, has emerged recently. RNA interference utilizes short double-stranded RNA to inhibit selectively gene expression of complementary RNA nucleotide sequences after transcription, but prior to translation. Gastrointestinal and hepatic disorders may be particularly amenable to therapeutic RNA interference intervention because of the relative ease of delivery of drugs to the gastrointestinal tract and liver. Aim, To examine the published literature for potential clinical uses of RNA interference in gastroenterology and speculate on future therapies for luminal disease. Methods, Reports were identified using PubMed and the search term ,RNA interference', focusing on therapeutic uses related to gastrointestinal and liver disease. Results, Cellular and animal models demonstrate the potential application of short-interfering RNA-based therapies for viral hepatitis and inflammatory bowel disease. With validation of specific targets and better in vivo delivery of short-interfering RNA, RNA interference may represent a new frontier for molecular-targeted therapy in gastroenterology and hepatology. Conclusions, Short-interfering RNA provides a novel and specific means to inhibit gene expression. Translation to the clinical arena will require further definition of side-effects, off-target effects and delivery systems. Ultimately, mucosally applied or endoscopically delivered short-interfering RNA could be one of the earliest clinical uses of short-interfering RNA therapy. [source]


    Mechanobiology and the Microcirculation: Cellular, Nuclear and Fluid Mechanics

    MICROCIRCULATION, Issue 3 2010
    KRIS NOEL DAHL
    Microcirculation (2010) 17, 179,191. doi: 10.1111/j.1549-8719.2009.00016.x Abstract Endothelial cells are stimulated by shear stress throughout the vasculature and respond with changes in gene expression and by morphological reorganization. Mechanical sensors of the cell are varied and include cell surface sensors that activate intracellular chemical signaling pathways. Here, possible mechanical sensors of the cell including reorganization of the cytoskeleton and the nucleus are discussed in relation to shear flow. A mutation in the nuclear structural protein lamin A, related to Hutchinson-Gilford progeria syndrome, is reviewed specifically as the mutation results in altered nuclear structure and stiffer nuclei; animal models also suggest significantly altered vascular structure. Nuclear and cellular deformation of endothelial cells in response to shear stress provides partial understanding of possible mechanical regulation in the microcirculation. Increasing sophistication of fluid flow simulations inside the vessel is also an emerging area relevant to the microcirculation as visualization in situ is difficult. This integrated approach to study,including medicine, molecular and cell biology, biophysics and engineering,provides a unique understanding of multi-scale interactions in the microcirculation. [source]


    Cellular and molecular mechanisms leading to cortical reaction and polyspermy block in mammalian eggs

    MICROSCOPY RESEARCH AND TECHNIQUE, Issue 4 2003
    Qing-Yuan Sun
    Abstract Following fusion of sperm and egg, the contents of cortical granules (CG), a kind of special organelle in the egg, release into the perivitelline space (cortical reaction), causing the zona pellucida to become refractory to sperm binding and penetration (zona reaction). Accumulating evidence demonstrates that mammalian cortical reaction is probably mediated by activation of the inositol phosphate (PIP2) cascade. The sperm-egg fusion, mediated by GTP-binding protein (G-protein), may elicit the generation of two second messengers, inositol 1,4,5 triphosphate (IP3) and diacylglycerol (DAG). The former induces Ca2+ release from intracellular stores and the latter activates protein kinase C (PKC), leading to CG exocytosis. Calmodulin-dependent kinase II (CaMKII) may act as a switch in the transduction of the calcium signal. The CG exudates cause zona sperm receptor modification and zona hardening, and thus block polyspermic penetration. Oolemma modification after sperm-egg fusion and formation of CG envelope following cortical reaction also contribute to polyspermy block. Microsc. Res. Tech. 61:342,348, 2003. © 2003 Wiley-Liss, Inc. [source]


    Pulmonary fibrosis: Cellular and molecular events

    PATHOLOGY INTERNATIONAL, Issue 3 2003
    Mohammed S. Razzaque
    Connective tissue remodeling of the interstitium is an important feature of chronic lung diseases encompassing interstitial inflammatory changes and subsequent pulmonary fibrosis. The early inflammatory phase is usually associated with the release of several cytokines and chemokines by activated resident cells and infiltrating cells which, in turn, help further recruit inflammatory mononuclear cells. Cytokines and growth factors secreted by inflammatory cells and by interstitial cells (fibroblasts and myofibroblasts) play an important role in the fibrogenic phase of pulmonary fibrosis by inducing matrix synthesis. In addition, matrix-degrading enzymes and their inhibitors also contribute to extracellular matrix (ECM) remodeling in pulmonary fibrosis. This review addresses the pathophysiology of wound healing and different phases of pulmonary fibrosis. [source]


    Cellular and molecular susceptibility determinants for periodontitis

    PERIODONTOLOGY 2000, Issue 1 2007
    Thomas E Van Dyke
    First page of article [source]


    Cellular and Hormonal Regulation of Pigmentation in Human Ocular Melanocytes

    PIGMENT CELL & MELANOMA RESEARCH, Issue 4 2001
    Linda C. Smith-Thomas
    The purpose of this study was to examine some of the factors that may be relevant to regulating pigmentation in the human eye, specifically whether choroidal and iridial melanocytes are sensitive to regulation by epithelial and stromal cells and ,-melanocyte stimulating hormone (,-MSH). Human choroidal and iridial melanocytes were established in culture and co-cultured with epithelial cells and stromal cells derived both from skin and from eye in order to determine their influence on choroidal and iridial melanocyte dopa oxidase activity. In all cases, co-culture of melanocytes with either epithelial cells or fibroblasts led to an increase in dopa oxidase activity during 5 days of co-culture. The extent of the increase ranged from 60% (non-significant) to as much as 185% when both fibroblasts and keratinocytes were present. The optimal ratio of fibroblasts to melanocytes was 1:10 (for dermal fibroblasts) or 1:2 (for iridial fibroblasts) and 1:1 for all epithelial cells to melanocytes. Both choroidal (three out of three cultures) and iridial (two out of three cultures) melanocytes showed increases in dopa oxidase activity to ,-MSH when cultured in Green's media but the same cells cultured in MCDB153 were unresponsive to ,-MSH. These in vitro studies suggest that ocular melanocytes have the capacity to be influenced by adjacent epithelial and stromal cells with respect to pigmentation. [source]


    Cellular and subcellular localization of the neuron-specific plasma membrane calcium ATPase PMCA1a in the rat brain

    THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 16 2010
    Katharine A. Kenyon
    Abstract Regulation of intracellular calcium is crucial both for proper neuronal function and survival. By coupling ATP hydrolysis with Ca2+ extrusion from the cell, the plasma membrane calcium-dependent ATPases (PMCAs) play an essential role in controlling intracellular calcium levels in neurons. In contrast to PMCA2 and PMCA3, which are expressed in significant levels only in the brain and a few other tissues, PMCA1 is ubiquitously distributed, and is thus widely believed to play a "housekeeping" function in mammalian cells. Whereas the PMCA1b splice variant is predominant in most tissues, an alternative variant, PMCA1a, is the major form of PMCA1 in the adult brain. Here, we use immunohistochemistry to analyze the cellular and subcellular distribution of PMCA1a in the brain. We show that PMCA1a is not ubiquitously expressed, but rather is confined to neurons, where it concentrates in the plasma membrane of somata, dendrites, and spines. Thus, rather than serving a general housekeeping function, our data suggest that PMCA1a is a calcium pump specialized for neurons, where it may contribute to the modulation of somatic and dendritic Ca2+ transients. J. Comp. Neurol. 518:3169,3183, 2010. © 2010 Wiley-Liss, Inc. [source]


    Cellular and subcellular localization of the neuron-specific plasma membrane calcium ATPase PMCA1a in the rat brain

    THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 16 2010
    Katharine A. Kenyon
    Abstract Regulation of intracellular calcium is crucial both for proper neuronal function and survival. By coupling ATP hydrolysis with Ca2+ extrusion from the cell, the plasma membrane calcium-dependent ATPases (PMCAs) play an essential role in controlling intracellular calcium levels in neurons. In contrast to PMCA2 and PMCA3, which are expressed in significant levels only in the brain and a few other tissues, PMCA1 is ubiquitously distributed, and is thus widely believed to play a "housekeeping" function in mammalian cells. Whereas the PMCA1b splice variant is predominant in most tissues, an alternative variant, PMCA1a, is the major form of PMCA1 in the adult brain. Here, we use immunohistochemistry to analyze the cellular and subcellular distribution of PMCA1a in the brain. We show that PMCA1a is not ubiquitously expressed, but rather is confined to neurons, where it concentrates in the plasma membrane of somata, dendrites, and spines. Thus, rather than serving a general housekeeping function, our data suggest that PMCA1a is a calcium pump specialized for neurons, where it may contribute to the modulation of somatic and dendritic Ca2+ transients. J. Comp. Neurol. 518:3169,3183, 2010. © 2010 Wiley-Liss, Inc. [source]


    Cellular and subcellular localization of the GABAB receptor 1a/b subunit in the rat periaqueductal gray matter

    THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 5 2007
    Paolo Barbaresi
    Abstract The inhibitory effects of ,-aminobutyric acid (GABA)ergic neurotransmission in the periaqueductal gray matter (PAG) are mediated, at least partly, by metabotropic GABAB receptor subtypes whose cellular and subcellular localization is still unknown. We performed immunohistochemical experiments with an antibody against GABAB receptor subtype 1a/b (GABABR1a/b) by using light and electron microscopy. On light microscopy, GABABR1a/b immunoreactivity (IR) was in all columns, defined by cytochrome oxidase histochemistry. Neuropil labeling was strongest in the lateral portion of dorsolateral PAG. Labeled neurons, albeit not numerous, were in ventrolateral, dorsal, and medial subdivisions and were sparser in dorsolateral PAG. Labeling was mostly on the soma of PAG neurons. Sometimes GABABR1a/b IR spread along proximal dendrites; in these cases bipolar neurons were the most common type. On electron microscopy, GABABR1a/b IR was mainly on dendrites (54.92% of labeled elements) and axon terminals (21.90%) making synapses with labeled and unlabeled postsynaptic elements. Presynaptic labeling was also on unmyelinated and myelinated axons (overall 8% of all labeled elements). Postsynaptically, GABABR1a/b IR was at extrasynaptic sites on dendritic shafts; spines were always unlabeled. On axon terminals, GABABR1a/b IR was on extrasynaptic membranes and sometimes on presynaptic membrane specializations. Of the labeled elements, 13.03% elements were distal astrocytic processes (dAsPs) surrounding both symmetric and asymmetric synapses whose pre- and postsynaptic elements were often labeled. Immunoreactive dAsPs were around the soma and dendrites of both labeled and unlabeled neurons. These findings provide insights into the intrinsic PAG organization and suggest that presynaptic, postsynaptic, and glial GABAB receptors may play crucial roles in controlling PAG neuronal activity. J. Comp. Neurol. 505:478,492, 2007. © 2007 Wiley-Liss, Inc. [source]


    Cellular and molecular tunnels surrounding the forebrain commissures of human fetuses

    THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2005
    Roberto Lent
    Abstract Glial cells and extracellular matrix (ECM) molecules surround developing fiber tracts and are implicated in axonal pathfinding. These and other molecules are produced by these strategically located glial cells and have been shown to influence axonal growth across the midline in rodents. We searched for similar cellular and molecular structures surrounding the telencephalic commissures of fetal human brains. Paraffin-embedded brain sections were immunostained for glial fibrillary acidic protein (GFAP) and vimentin (VN) to identify glial cells; for microtubule-associated protein-2 (MAP-2) and neuronal nuclear protein (NeuN) to document neurons; for neurofilament (NF) to identify axons; and for chondroitin sulfate (CS), tenascin (TN), and fibronectin (FN) to show the ECM. As in rodents, three cellular clusters surrounding the corpus callosum were identified by their expression of GFAP and VN (but not MAP-2 or NeuN) from 13 to at least 18 weeks postovulation (wpo): the glial wedge, the glia of the indusium griseum, and the midline sling. CS and TN (but not FN) were expressed pericellularly in these cell groups. The anterior commissure was surrounded by a GFAP+/VN+ glial tunnel from 12 wpo, with TN expression seen between the GFAP+ cell bodies. The fimbria showed GFAP+/VN+ cells at its lateral and medial borders from 12 wpo, with pericellular expression of CS. The fornix showed GFAP+ cells somewhat later (16 wpo). Because these structures are similar to those described for rodents, we concluded that the axon guiding mechanisms postulated for commissural formation in nonhuman mammals may also be operant in the developing human brain. J. Comp. Neurol. 483:375,382, 2005. © 2005 Wiley-Liss, Inc. [source]


    Brain Death Activates Donor Organs and Is Associated with a Worse I/R Injury After Liver Transplantation

    AMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2007
    S. Weiss
    The majority of transplants are derived from donors who suffered from brain injury. There is evidence that brain death causes inflammatory changes in the donor. To define the impact of brain death, we evaluated the gene expression of cytokines in human brain dead and ideal living donors and compared these data to organ function following transplantation. Hepatic tissues from brain dead (n = 32) and living donors (n = 26) were collected at the time of donor laparotomy. Additional biopsies were performed before organ preservation, at the time of transplantation and one hour after reperfusion. Cytokines were assessed by real-time reverse transcriptase,polymerase chain reaction (RT,PCR) and cytometric bead array. Additionally, immunohistological analysis of tissue specimens was performed. Inflammatory cytokines including IL-6, IL-10, TNF-,, TGF-, and MIP-1, were significantly higher in brain dead donors immediately after laparotomy compared to living donors. Cellular infiltrates significantly increased in parallel to the soluble cytokines IL-6 and IL-10. Enhanced immune activation in brain dead donors was reflected by a deteriorated I/R injury proven by elevated alanin-amino-transferase (ALT), aspartat-amino-transferase (AST) and bilirubin levels, increased rates of acute rejection and primary nonfunction. Based on our clinical data, we demonstrate that brain death and the events that precede it are associated with a significant upregulation of inflammatory cytokines and lead to a worse ischemia/reperfusion injury after transplantation. [source]


    Rat Cytomegalovirus Infection Interferes with Anti-CD4 mAb-(RIB 5/2) Mediated Tolerance and Induces Chronic Allograft Damage

    AMERICAN JOURNAL OF TRANSPLANTATION, Issue 9 2006
    A. Pascher
    In order to assess the role of heterologous immunity on tolerance induction (TI) by signal 1 modification, the influence of rat cytomegalovirus infection (RCMVI) on TI by a non-depleting monoclonal anti-CD4 mAb (monoclonal antibody) (RIB 5/2) in a rat kidney transplant (KTx) model was investigated. Orthotopic rat KTx (Dark Agouty (DA) , Lewis (LEW)) was performed after TI with RIB 5/2 [10 mg/kg body weight (BW); day ,1, 0, 1, 2, 3; i.p. (intraperitoneal route)]. RCMVI (5 × 10E5 Plaque forming units [PFU] i.p.) was simultaneously conducted to KTx, 50 days after KTx, and 14 days before and after KTx. RIB 5/2 induced robust allograft tolerance even across the high-responder strain barrier. RCMVI broke RIB 5/2-induced tolerance regardless of the time of RCMVI but did not induce acute graft failure during the 120 days follow-up. RCMVI induced a significant chronic deterioration of allograft function (p < 0.01) and enhanced morphological signs of chronic allograft damage (p < 0.05). Cellular infiltrates and major histo-compatibility complex (MHC)-expression were more pronounced (p < 0.05) in the infected groups. RCMVI induced not only RCMV-specific T-cell response but also enhanced the frequency of alloreactive T cells. RCMV interferes with anti-CD4 mAb-induced tolerance and leads to chronic allograft damage. The data we presented suggest a potentially important role of viral infections and their prophylaxis in clinical TI protocols. [source]


    Cellular and biochemical markers in semen indicating male accessory gland inflammation

    ANDROLOGIA, Issue 5 2003
    W. Krause
    Summary. Leucocytospermia is considered to be a sign of male accessory gland inflammation. The leucocytes in semen are mainly polymorphonuclear neutrophilic granulocytes. Leucocytospermia is not associated with the presence of bacteria and antibiotic treatment does not significantly lower the extent of leucocytospermia. A higher frequency of elevated herpes simplex antibodies titres were found in men with leucocytospermia. The concentration of inflammatory cytokines, interleukin-6 and -8, is closely correlated with the number of leucocytes. Their determination does not provide additional information. Reactive oxygen species (ROS) are generated at least in part by seminal leucocytes in response to stimulating factors. Purified leucocytes produce high levels of ROS. The determination of ROS appears to represent a parameter of functional activity of leucocytes. The role of chlamydiae in male accessory gland infection is unclear. Their determination in semen by DNA amplification and by immunological tests does not provide reliable results. [source]