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R Bang

Publications and source records attributed to R Bang.

At least 19 recordsLinked to original sources
PubMed2001

Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice.

Liver resident NK1.1+ T cells are supposed to play a pivotal role in the onset of inflammatory liver injury in experimental mouse models such as concanavalin A (Con A)-induced hepatitis. These cells, expressing the adhesion receptor, CD44, are largely depleted from the liver by a single intravenous injection of low-molecular-weight fragments of hyaluronic acid (LMW-HA). Here, we report that LMW-HA pretreatment protected mice from liver injury in several models of T-cell- and macrophage-dependent, tumor necrosis factor alpha (TNF-alpha)-mediated inflammatory liver injury, i.e., from liver injury induced by either Con A or Pseudomonas exotoxin A (PEA) or PEA/lipopolysaccharide (LPS). Interestingly, apart from inhibition of cellular adhesion, pretreatment of mice with LMW-HA was also capable of preventing hepatocellular apoptosis and activation of caspase-3 induced by direct administration of recombinant murine (rmu) TNF-alpha to D-galactosamine (GalN)-sensitized mice. LMW-HA-induced hepatoprotection could be neutralized by pretreatment with the nuclear factor-kappaB (NF-kappaB) inhibitor, pyrrolidine dithiocarbamate (PDTC), demonstrating the involvement of NF-kappaB in the observed protective mechanism. Indeed, injection of LMW-HA rapidly induced the production of TNF-alpha by Kupffer cells and the translocation of NF-kappaB into hepatocellular nuclei. Both LMW-HA-induced TNF-alpha production and NF-kappaB translocation were blocked by pretreatment with PDTC. Our findings provide evidence for an unknown mechanism of LMW-HA-dependent protection from inflammatory liver disease, i.e., induction of TNF-alpha- and NF-kappaB-dependent cytoprotective proteins within the target parenchymal liver cells.

ADP Ribose Transferases↗
PubMed2001

Inducible nitric oxide synthase is critical for immune-mediated liver injury in mice.

Concanavalin A (Con A) causes severe TNF-alpha-mediated and IFN-gamma-mediated liver injury in mice. In addition to their other functions, TNF-alpha and IFN-gamma both induce the inducible nitric oxide (NO) synthase (iNOS). Using different models of liver injury, NO was found to either mediate or prevent liver damage. To further elucidate the relevance of NO for liver damage we investigated the role of iNOS-derived NO in the Con A model. We report that iNOS mRNA was induced in livers of Con A-treated mice within 2 hours, with iNOS protein becoming detectable in hepatocytes as well as in Kupffer cells within 4 hours. iNOS-/- mice were protected from liver damage after Con A treatment, as well as in another TNF-alpha-mediated model that is inducible by LPS in D-galactosamine-sensitized (GalN-sensitized) mice. iNOS-deficient mice were not protected after direct administration of recombinant TNF-alpha to GalN-treated mice. Accordingly, pretreatment of wild-type mice with a potent and specific inhibitor of iNOS significantly reduced transaminase release after Con A or GalN/LPS, but not after GalN/TNF-alpha treatment. Furthermore, the amount of plasma TNF-alpha and of intrahepatic TNF-alpha mRNA and protein was significantly reduced in iNOS-/- mice. Our results demonstrate that iNOS-derived NO regulates proinflammatory genes in vivo, thereby contributing to inflammatory liver injury in mice by stimulation of TNF-alpha production.

Animals↗
PubMed2000

Localization and regulation of cyclo-oxygenase-1 and -2 and neuronal nitric oxide synthase in mouse spinal cord.

Prostaglandins are important mediators in spinal nociceptive processing. They are produced by cyclo-oxygenase isoforms, cyclo-oxygenase-1 and -2, which are both constitutively expressed in the central nervous system. The present immunohistochemical study details localization and regulation of cyclo-oxygenase-1 and -2 and neuronal nitric oxide synthase in lumbar spinal cord before and after induction of a painful paw inflammation in mice. Cyclo-oxygenase-1 immunoreactivity was found in glial cells of the dorsal and ventral horns, but not in neurons. In unstimulated mice, cyclo-oxygenase-2 immunoreactivity was found in motoneurons of the ventral horns and in lamina X, but not in dorsal horn neurons. After induction of a paw inflammation with zymosan, cyclo-oxygenase-2 immunoreactivity increased dramatically in dorsal horn neurons of laminae I-VI and X, paralleled by a significant increase in prostaglandin E(2) release from lumbar spinal cord. Cyclo-oxygenase-2 was co-localized with neuronal nitric oxide synthase immunoreactivity in several neurons in superficial laminae of the dorsal horns and in the area surrounding the central canal. Nitric oxide synthase was distributed in the cytoplasm and extended to processes of some neurons. In contrast, electron microscopy revealed that cyclo-oxygenase-2 immunoreactivity was restricted to the nuclear membrane and rough endoplasmic reticulum. It is shown in the present study that both cyclo-oxygenase isoforms are constitutively expressed in the spinal cord, cyclo-oxygenase-1 in glial cells of the dorsal and ventral horns and cyclo-oxygenase-2 in motoneurons. After induction of a hindpaw inflammation, several dorsal horn neurons express cyclo-oxygenase-2. Some of them are also positive for neuronal nitric oxide synthase, which is also induced following peripheral inflammation. Intracellularly, cyclo-oxygenase-2 is bound to the membranes of the nucleus and endoplasmic reticulum, whereas neuronal nitric oxide synthase is found in the cytoplasm.

Animals↗
PubMed2000

Transformationalism, taxism, and developmental biology in systematics.

Issues concerning transformational and taxic comparisons are central to understanding the impact of the recent proliferation of molecular developmental data on evolutionary biology. More importantly, an understanding of taxism and transformationalism in comparative biology is critical to assessing the impact of the recent developmental data on systematic theory and practice. We examine the philosophical and practical aspects of the transformational approach and the relevance of this approach to recent molecular-based developmental data. We also examine the theoretical basis of the taxic approach to molecular developmental data and suggest that developmental data are perfectly amenable to the taxic approach. Two recent examples from the molecular developmental biology literature--the evolution of insect wings and the evolution of dorsal ventral inversion in vertebrates and invertebrates--are used to compare the taxic and transformational approaches. We conclude that the transformational approach is entirely appropriate for ontogenetic studies and furthermore can serve as an excellent source of hypotheses about the evolution of characters. However, the taxic approach is the ultimate arbiter of these hypotheses.

Animals↗
PubMed1999

Requirement of peptidergic sensory innervation for disease activity in murine models of immune hepatitis and protection by beta-adrenergic stimulation.

To investigate the interaction between the peripheral nervous and the immune system in vivo, we used two mouse models of T cell and TNF-alpha dependent liver injury inducible by either concanavalin A or a combination of D-galactosamine and staphylococcal enterotoxin B. Mice depleted of peptidergic sensory nerve fibres by capsaicin were protected from liver injury. Moreover, TNF-alpha production was significantly reduced. Examination of the effect of catecholamines on liver injury showed that the beta2-adrenergic agonist salbutamol prevented, whereas chemical sympathectomy by 6-hydroxydopamine, deteriorated the disease. Hence, strategies reducing the activity of peptidergic sensory nerve fibres or stimulating beta2-adrenoreceptors, may be of benefit in immune-mediated liver disease.

Adrenergic beta-Agonists↗
PubMed1998

Acute hepatotoxicity of Pseudomonas aeruginosa exotoxin A in mice depends on T cells and TNF.

The most potent virulence factor of Pseudomonas aeruginosa, its exotoxin A (PEA), inhibits protein synthesis, especially in the liver, and is a weak T cell mitogen. This study was performed to correlate hepatotoxic and possible immunostimulatory features of PEA in vivo. Injection of PEA to mice caused hepatocyte apoptosis, an increase in plasma transaminase activities, and the release of TNF, IFN-gamma, IL-2, and IL-6 into the circulation. Most strikingly, liver damage depended on T cells. Athymic nude mice or mice depleted of T cells by anti-Thy1.2 mAb pretreatment failed to develop acute hepatic failure, and survival was significantly prolonged following T cell depletion. Neutralization of TNF or lack of TNF receptors prevented liver injury. In the liver, TNF was produced by Kupffer cells before hepatocellular death occurred. After T cell depletion, Kupffer cells failed to produce TNF. Transaminase release was significantly reduced in perforin knockout mice, and it was even elevated in lpr/lpr mice. These results demonstrate that PEA induces liver damage not only by protein synthesis inhibition but also by TNF- and perforin-dependent, Fas-independent, apoptotic signals.

ADP Ribose Transferases↗
PubMed1998

Signet-ring squamous cell carcinoma: a case report.

A-50-year-old Hispanic man presented to the dermatology clinic with a 0.6-cm eroded, erythematous, scaly plaque on the left side of his neck. On shave biopsy, the lesion was composed of intra-epidermal and invasive dermal cells characterized by a signet-ring appearance. One area suggestive of typical squamous cell carcinoma prompted the inclusion of that entity in the differential diagnosis. Mucicarmine stains were negative, while the extra-vacuolar cytoplasm focally reacted with periodic acid-Schiff staining, the positive reaction for which was abolished by diastase, consistent with glycogen. Malignant cells expressed keratins by reacting to antibodies, Mak6, AE1/AE3, Ker 903, and CAM5.2. Additionally, weak reactivity occurred with antibodies to CEA and EMA. Tumor cells did not express S-100, HM-B45, Leu M1, or actin. By ultrastructural examination, the large vacuoles corresponded to markedly dilated endoplasmic reticulum. A diagnosis of signet-ring squamous cell carcinoma, a rare form of cutaneous squamous cell carcinoma which has been described in only one case report in the last 10 years, was made. Immunohistochemical staining provided information useful in differentiating this lesion from other clear cell and signet-ring cell tumors which involve the skin.

Carcinoma, Signet Ring Cell↗
PubMed1997

Host-cell cyclophilin is important for the intracellular replication of Leishmania major.

The antiparasitic effects of cyclosporin A were examined in leishmanial infection by analysing the role of CsA-binding proteins (cyclophilins) in the host-parasite interaction. We hypothesized that the leishmanicidal effects of CsA on Leishmania major infected macrophages might be mediated through a cyclophilin of either the parasite or the host cell. Two cyclophilins (20 and 22 kDa) were purified from L. major parasites and N-terminally sequenced. Although enzyme activity of these cyclophilins was inhibited by CsA, pretreatment of L. major parasites with CsA did not result in reduction of a subsequent macrophage infection, arguing against a role of L. major cyclophilins as infectivity potentiators. However, host-cell cyclophilin A (CypA) was found to be critically involved in the intracellular replication of L. major parasites in murine macrophages. An antisense oligonucleotide to murine CypA was constructed and added to cultures of peritoneal macrophages prior to infection with L. major parasites. This treatment strongly reduced the expression of CypA in macrophages and resulted in the inhibition of the intracellular replication of L. major amastigotes. These data indicate that interaction of amastigotes with host-cell cyclophilin is an important part of the intracellular replication machinery of L. major and define, for the first time, a direct involvement of a cyclophilin in the survival strategies of an intracellular parasite.

Amino Acid Isomerases↗
PubMed1996

Crossroads, milestones and landmarks in insect development and evolution: implications for systematics.

Our understanding of insect development and evolution has increased greatly due to recent advances in the comparative developmental approach. Modern developmental biology techniques such as in situ hybridization and molecular analysis of developmentally important genes and gene families have greatly facilitated these advances. The role of the comparative developmental approach in insect systematics is explored in this paper and we suggest two important applications of the approach to insect systematics--character dissection and morphological landmarking. Existing morphological characters can be dissected into their genetic and molecular components in some cases and this will lead to more and richer character information in systematic studies. Character landmarking will he essential to systematic studies for clarifying structures such as shapes or convergences, which are previously hard to analyze anatomical regions. Both approaches will aid greatly in expanding our understanding of homology in particular, and insect development in general.

Animals↗
PubMed1995

Cyclophilin-A is a zinc-dependent DNA binding protein in macrophages.

The association of cyclosporin A (CsA) immunosuppression with inhibition of transcription factor-dependent lymphokine gene activation formed the basis of our decision to investigate nuclear-associated Cyp isoforms. Immunofluorescence microscopy of mouse macrophages cell line with a monoclonal antibody mAb7F1 raised against CypA shows a co-localisation of CypA in the nucleus and in the cytosol. Nuclear CypA binds to DNA in a zinc ion-dependent manner, in contrast to recombinant CypB. Peptidyl-prolyl cisltrans isomerase (PPIase) activity of nuclear CypA is inhibited by zinc ions. The zinc inhibited CypA does not bind cyclosporin A (CsA). We suggest that nuclear Cyp in complex with zinc ions recognizes DNA sequences and is involved in transcription modulating processes.

Amino Acid Isomerases↗
PubMed1989

Commentary on a community-based approach to reproductive health care. Society for Education, Action and Research in Community Health Team.

Reproductive care needs to be broadened beyond maternity care and family planning to include care for gynecological and sexual problems, safe abortion services, and sex and reproductive health education. Our epidemiologic study of rural women has shown a very high prevalence of gynecological diseases. We tried to develop a community-based approach to comprehensive reproductive care by undertaking participatory research, fostering mass education with the people's involvement, and by making care available through village-based female workers and improved referral services. We end with two appeals: "MCH" needs to be replaced by WCH: not merely Maternal and Child Health but Woman and Child Health. Care should be provided through a community-based participatory approach, not through narrow technocratic vertical programs. Let people shape their own lives!

Abortion, Illegal↗
PubMed1987

Modifiers of position-effect variegation in the region from 86C to 88B of the Drosophila melanogaster third chromosome.

Four dominant suppressor and one enhancer of variegation loci were mapped in the polytene chromosome region extending from section 86C to section 88B of the Drosophila melanogaster third chromosome using a set of deficiencies. The suppressor locus Su-var(3)14 maps in 86CD, Su-var(3)13 in 86F4-7, Su-var(3)6 in 87B4-7 and Su-var(3)7 in 87E4-5. The enhancer locus E-var(3)3 maps in 87E12-F11. Su-var(3)13, Su-var(3)6 and Su-var(3)7 are also defined by point mutant alleles originally identified by other criteria (Reuter et al. 1986). Duplications covering the suppressor loci Su-var(3)14, Su-var(3)13, Su-var(3)6 and Su-var(3)7 were found to reduce considerably the haplo-abnormal effect of heterozygous point mutants of the corresponding loci. One suppressor locus, Su-var(3)7, maps within a region which has previously been cloned. The positions of deficiency breakpoints delimiting the suppressor locus indicate that all the necessary sequences for its function are located within 10 kb of cloned DNA.

Animals↗