Biomedical subjects

L Braun

Publications and source records attributed to L Braun.

At least 37 records · Page 2Linked to original sources

PubMed2001

Herb-drug interaction guide.

Herbal medicines now fall into the category of complementary medicines. With their increasing popularity, a new set of circumstances has arisen--the herb-drug interaction. In an effort to streamline the interaction information available, the author has designed two charts. The first lists the 21 most popular herbal medicines sold in Australia, sourced from the largest natural supplement manufacturer in Australia, Bullivant Natural Health Products. The second lists the 12 commonly prescribed prescription drug classes. This list was sourced from F H Faulding & Co Ltd, together with Australian Prescriber. Specific interaction information was collated from a variety of sources--medical and complementary medicine journals, pharmacy practice journals and respected phytotherapy texts. These tables are excerpts from these charts.

Drug Interactions↗

PubMed2001

Transcutaneous bilirubinometry in preterm infants.

UNLABELLED: The aim of this study was to evaluate the accuracy and safety of transcutaneous bilirubinometry in preterm infants using the new bilirubin analyser BiliCheck. The study included 145 preterm children (23-36 wk gestation). Capillary blood sampling for determination of serum bilirubin (BS) was combined with transcutaneous bilirubin measurement (BTc) every morning until the sixth postnatal day and related to several clinical data (phototherapy (PT), infection signs, breathing disturbances, skin bleeding, etc.). Overall bilirubin concentration ranged from 17 to 371 micromol/l, and from 21 to 325 micromol/l for BS and BTc, respectively. Mean values obtained by BTc were significantly higher than BS values. The correlation coefficient between BS and BTc was r= 0.64 for the whole group, and r = 0.73 in infants without PT. As demonstrated by multiple regression analysis, BS-BTc correlations were related only to gestational age (beta -0.32) and breathing disturbances (beta 0.29), indicating that the lower the gestational age and the more seriously ill the baby, the higher the incoherence between BS and BTc. CONCLUSION: BiliCheck provides a convenient, non-invasive possibility for bilirubin estimation in preterm infants. However, there are limitations: the method gives reliable results only in newborns older than 30 wk gestation, without PT and artificial ventilation.

Bilirubin↗

PubMed2001

Herb-drug interaction guide.

Explore the source record for details and available documents.

Drug Interactions↗

PubMed2000

A framework for interpreting the leucine-rich repeats of the Listeria internalins.

The surface protein InlB of the bacterial pathogen Listeria monocytogenes is required for inducing phagocytosis in various nonphagocytic mammalian cell types in vitro. InlB causes tyrosine phosphorylation of host cell adaptor proteins, activation of phosphoinositide 3-kinase, and rearrangements of the actin cytoskeleton. These events lead to phagocytic uptake of the bacterium by the host cell. InlB belongs to the internalin family of Listeria proteins, which also includes InlA, another surface protein involved in host cell invasion. The internalins are the largest class of bacterial proteins containing leucine-rich repeats (LRR), a motif associated with protein-protein interactions. The LRR motif is found in a functionally diverse array of proteins, including those involved in the plant immune system and in the mammalian innate immune response. Structural and functional interpretations of the sequences of internalin family members are presented in light of the recently determined x-ray crystal structure of the InlB LRR domain.

Amino Acid Sequence↗

PubMed2000

gC1q-R/p32, a C1q-binding protein, is a receptor for the InlB invasion protein of Listeria monocytogenes.

InlB is a Listeria monocytogenes protein that promotes entry of the bacterium into mammalian cells by stimulating tyrosine phosphorylation of the adaptor proteins Gab1, Cbl and Shc, and activation of phosphatidyl- inositol (PI) 3-kinase. Using affinity chromatography and enzyme-linked immunosorbent assay, we demonstrate a direct interaction between InlB and the mammalian protein gC1q-R, the receptor of the globular part of the complement component C1q. Soluble C1q or anti-gC1q-R antibodies impair InlB-mediated entry. Transient transfection of GPC16 cells, which are non-permissive to InlB-mediated entry, with a plasmid-expressing human gC1q-R promotes entry of InlB-coated beads. Furthermore, several experiments indicate that membrane recruitment and activation of PI 3-kinase involve an InlB-gC1q-R interaction and that gC1q-R associates with Gab1 upon stimulation of Vero cells with InlB. Thus, gC1q-R constitutes a cellular receptor involved in InlB-mediated activation of PI 3-kinase and tyrosine phosphorylation of the adaptor protein Gab1. After E-cadherin, the receptor for internalin, gC1q-R is the second identified mammalian receptor promoting entry of L. monocytogenes into mammalian cells.

Adaptor Proteins, Signal Transducing↗

PubMed2000

Beta-glucuronidase latency in isolated murine hepatocytes.

The physiological function of microsomal beta-glucuronidase is unclear. Substrates may be either glucuronides produced in the lumen of endoplasmic reticulum (ER) or those taken up by hepatocytes. In the latter case, efficient inward transport of glucuronides at the plasma membrane and the ER membrane would be required. Therefore, the potential role of beta-glucuronidase in ER was investigated. Isolated mouse hepatocytes and mouse and rat liver microsomal vesicles were used in the experiments. Selective permeabilization of the plasma membrane of isolated hepatocytes with saponin or digitonin resulted in an almost 4-fold elevation in the rate of beta-nitrophenol glucuronide hydrolysis, while the permeabilization of plasma membrane plus ER membrane by Triton X-100 caused a further 2-fold elevation. In microsomal vesicles, the p-nitrophenol glucuronide or phenolphthalein glucuronide beta-glucuronidase activity showed about 50% latency as revealed by alamethicin or Triton X-100 treatment. A light-scattering study indicated that the microsomes are relatively impermeable to both glucuronides and to glucuronate. On the basis of our results, the role of liver microsomal beta-glucuronidase in the deconjugation of glucuronides taken up by the liver seems unlikely. Hydrolysis of the glucuronides produced in the ER lumen may play a role in substrate supply for ascorbate synthesis or in "proofreading" of glucuronidation.

Animals↗

PubMed2000

A role for bovine herpesvirus 1 (BHV-1) glycoprotein E (gE) tyrosine phosphorylation in replication of BHV-1 wild-type virus but not BHV-1 gE deletion mutant virus.

Bovine herpesvirus 1 (BHV-1), an alphaherpesvirus, is a major pathogen that causes respiratory and reproductive infections. We observed tyrosine phosphorylation of a 95-kDa viral protein and dephosphorylation of 55- and 103-kDa cellular proteins during the course of BHV-1 infection. We demonstrated BHV-1 glycoprotein E (gE) to be the tyrosine phosphorylated viral protein by immunoprecipitation. Inhibition of phosphorylation of BHV-1 gE by tyrosine kinase inhibitors genistein and tyrphostin AG1478 substantially lowered the viral titer in Madin-Darby bovine kidney cells. The decrease in viral titer was directly proportional to the decrease in phosphorylation of the BHV-1 gE. Interestingly, these kinase inhibitors did not inhibit the replication of the BHV-1 gE deletion mutant virion (BHV-1gEDelta3.1). Our findings suggest that the wild-type BHV-1, with a functional gE protein, uses a different pathway of signaling events than the BHV-1 gE deletion mutant in replication. Our results indicate that the tyrosine phosphorylation of the cytoplasmic tail of BHV-1 gE is an important post-translational modification of the functional protein. An application of this study may be the use of tyrosine kinase inhibitors in controlling the BHV-1 infection.

Animals↗

PubMed2000

Transcriptional induction of bilirubin UDP-glucuronosyltransrase by ethanol in rat liver.

Several drug-metabolizing enzymes including bilirubin UDP-glucuronosyltransferase (UGT1A1) are influenced by long-term ethanol consumption. In the present study, the activity and expression of UGT1A1 were investigated in livers of ethanol-treated rats. Animals were treated daily for 15 days with ethanol or isocaloric amount of glucose solution by gastric intubation. Microsomes and total RNA were prepared from the liver of rats and analyzed by Western blot and Northern hybridization using UGT1A1 specific antibody and cDNA probe. Microsomal bilirubin UGT activity was also measured. The elevation of UGT1A1 mRNA was observed in the liver of ethanol consumer animals with the simultaneous increase in microsomal UGT1A1 protein leading to stimulated bilirubin glucuronidation both in vivo and in microsomal vesicles. These results arise the possibility of the transcriptional induction and/or the mRNA stabilization by ethanol consumption, which can be caused by ethanol itself or the metabolic changes due to the treatment.

Animals↗

PubMed2000

Interactions between Listeria monocytogenes and host mammalian cells.

Bacterial pathogens have developed a variety of strategies to induce their own internalization into mammalian cells which are normally nonphagocytic. The Gram-positive bacterium Listeria monocytogenes enters into many cultured cell types using two bacterial surface proteins, InlA (internalin) and InlB. In both cases, entry takes place after engagement of a receptor and induction of a series of signaling events.

Animals↗

PubMed2000

Knowledge of human papillomavirus infection among young adult men and women: implications for health education and research.

Human papillomavirus (HPV) infection of the genital tract is one of the most common sexually transmitted diseases (STDs), and a subset of genital tract HPVs are etiologically associated with cervical cancer. The prevalence of HPV infection is highest among adolescents and young adults. This study was undertaken to explore first year college students' knowledge about HPVs and to determine whether there were gender differences in this knowledge. An anonymous survey was distributed to all first year students at a private university. The results were analyzed by gender. We found that 96.2% of males and 95.4% of females had heard of genital warts, although only 4.2% of males and 11.6% of females knew that HPV caused genital warts. Although there was a greater awareness of genital warts than HPV in this population, students were uncertain about modes of transmission of both genital warts and HPVs, and unclear about the importance of HPV infection relative to other STDs. For both men and women (87% and 87.4%, respectively), health education classes were the major source of information about STDs. We conclude that health education should be reconceptualized to incorporate a better understanding of STDs, including HPV infection, by engaging adolescents and young adults in exploring the biological and social context of STDs, their public health importance, strategies for prevention, and the uncertainty of our scientific knowledge.

Adult↗

PubMed2000

A novel function of InIB from Listeria monocytogenes: activation of NF-kappaB in J774 macrophages.

Listeria monocytogenes causes a pro-inflammatory response on adhesion to macrophages. Upregulation of inflammation genes involves the transcription factor NF-kappaB. Several components of L. monocytogenes, including lipoteichoic acid (LTA), phospholipases and listeriolysin O (LLO), have since been shown to mediate NF-kappaB activation. Here, we report that purified recombinant InlB, but not internalin (InlA), is a potent activator of NF-kappaB in the mouse macrophage-like cell line J774. Expression of InlB in Listeria innocua enhances its ability to activate NF-kappaB, while deletion of InlB from L. monocytogenes marginally decreases its effect on NF-kappaB, possibly because of the presence of NF-kappaB activators such as LTA and LLO. The effect correlates with the rapid degradation of IkappaBalpha, a sustained degradation of IkappaBbeta and increases in tumour necrosis factor alpha (TNF-alpha) and interleukin (IL) 6 production, two cytokines controlled by NF-kappaB. Using a series of anti-InlB monoclonal antibodies and domains of InlB, NF-kappaB activation was shown to be dependent upon the N-terminal 213-amino-acid leucine-rich repeat (LRR) domain of InlB, recently demonstrated to be responsible for InlB-mediated L. monocytogenes invasion and phosphoinositide-3 (PI-3) kinase activation. The effect of InlB was blocked by PI-3 kinase inhibitors, indicating the involvement of PI-3 kinase in this response. This report thus illustrates that InlB not only promotes invasion, but also contributes to the macrophage pro-inflammatory response.

Animals↗

PubMed2000

Herb-drug interaction guide.

Drug Interactions↗

PubMed1999

Different induction of gulonolactone oxidase in aromatic hydrocarbon-responsive or -unresponsive mouse strains.

The role of aromatic hydrocarbon receptor (AhR)-mediated signal transduction pathways was investigated in the regulation of ascorbate synthesis by using Ah-responsive and Ah-unresponsive mouse strains. In vivo 3-methylcholanthrene treatment increased hepatic and plasma ascorbate concentrations only in the Ah-responsive strain. The mRNA level of gulonolactone oxidase and the microsomal ascorbate production from p-nitrophenyl glucuronide, D-glucuronic acid or gulonolactone in the liver of Ah-responsive and Ah-unresponsive mice were compared. In Ah-responsive mice, these parameters were higher originally, and they further increased upon in vivo addition of 3-methylcholanthrene, while in Ah-unresponsive mice the treatment was not effective. These results suggest that the transcription of gulonolactone oxidase gene is regulated by an Ah receptor-dependent signal transduction pathway.

Animals↗

PubMed1999

Ascorbate-mediated electron transfer in protein thiol oxidation in the endoplasmic reticulum.

Addition of, or gulonolactone oxidase-dependent in situ generation of, ascorbate provoked the oxidation of protein thiols, which was accompanied by ascorbate consumption in liver microsomal vesicles. The maximal rate of protein thiol oxidation was similar upon gulonolactone, ascorbate or dehydroascorbate addition. Cytochrome P450 inhibitors (econazole, proadifen, quercetin) decreased ascorbate consumption and the gulonolactone or ascorbate-stimulated thiol oxidation. The results demonstrate that the ascorbate/dehydroascorbate redox couple plays an important role in electron transfer from protein thiols to oxygen in the hepatic endoplasmic reticulum, even in gulonolactone oxidase deficient species.

Animals↗

PubMed1999

Induction and peroxisomal appearance of gulonolactone oxidase upon clofibrate treatment in mouse liver.

Various antihyperlipemic peroxisome proliferators are known to be carcinogenic in rodents but not in human, other primates and guinea pig, which species lost their ability to synthesize ascorbate due to mutations in the gulonolactone oxidase gene. Ascorbate synthesis is accompanied by H2O2 production, consequently its induction can be potentially harmful; therefore, the in vivo effect of the peroxisome proliferator clofibrate was investigated on gulonolactone oxidase expression in mouse liver. Liver weights and peroxisomal protein contents were increased upon clofibrate treatment. Elevated plasma ascorbate concentrations were found in clofibrate-treated mice due to the higher microsomal gulonolactone oxidase activities. Remarkable gulonolactone oxidase activity appeared in the peroxisomal fraction upon the treatment. Increased activity of the enzyme was associated with an elevation of its mRNA level. According to the present results the evolutionary loss of gulonolactone oxidase may contribute to the explanation of the missing carcinogenic effect of peroxisome proliferators in humans.

Animals↗

PubMed1999

Preferential transport of glutathione versus glutathione disulfide in rat liver microsomal vesicles.

A bi-directional, saturable transport of glutathione (GSH) was found in rat liver microsomal vesicles. GSH transport could be inhibited by the anion transport blockers flufenamic acid and 4, 4'-diisothiocyanostilbene-2,2'-disulfonic acid. A part of GSH taken up by the vesicles was metabolized to glutathione disulfide (GSSG) in the lumen. Microsomal membrane was virtually nonpermeable toward GSSG; accordingly, GSSG generated in the microsomal lumen could hardly exit. Therefore, GSH transport, contrary to previous assumptions, is preferred in the endoplasmic reticulum, and GSSG entrapped and accumulated in the lumen creates the oxidized state of its redox buffer.

Alamethicin↗

PubMed1999

Structure of the lnlB leucine-rich repeats, a domain that triggers host cell invasion by the bacterial pathogen L. monocytogenes.

The L. monocytogenes protein lnlB activates phosphoinositide 3-kinase and induces phagocytosis in several mammalian cell types. The 1.86 A resolution X-ray crystal structure of the leucine-rich repeat domain of lnlB that is both necessary and sufficient to induce phagocytosis is presented here. The structure supports a crucial role for calcium in host cell invasion by L. monocytogenes and supplies a rationale for its function. Calciums are bound to the protein in an unusually exposed manner that suggests that the metals may act as a bridge between lnlB and mammalian cell surface receptors. The structure also identifies surfaces on the curved and elongated molecule that may constitute additional interaction sites in forming a bacterial-mammalian signaling complex.

Amino Acid Sequence↗

PubMed1999

The 213-amino-acid leucine-rich repeat region of the listeria monocytogenes InlB protein is sufficient for entry into mammalian cells, stimulation of PI 3-kinase and membrane ruffling.

The Listeria monocytogenes InlB protein is a 630-amino-acid surface protein that mediates entry of the bacterium into a wide variety of cell types, including hepatocytes, fibroblasts and epithelial cells such as Vero, HEp-2 and HeLa cells. Invasion stimulates host proteins tyrosine phosphorylation, PI 3-kinase activity and rearrangements in the actin cytoskeleton. We previously showed that InlB is sufficient for entry of InlB-coated latex beads into cells and recent results indicate that purified InlB can stimulate PI 3-kinase activity and is thus the first bacterial agonist of this lipid kinase. In this study, we identified the region of InlB responsible for entry and stimulation of signal transduction events. Eight monoclonal antibodies directed against InlB were raised and, of those, five inhibited bacterial entry. These five antibodies recognized epitopes within the leucine-rich repeat (LRR) region and/or the inter-repeat (IR) region. InlB-staphylococcal protein A (SPA) fusion proteins and recombinant InlB derivatives were generated and tested for their capacity to mediate entry into cultured mammalian cells. All the InlB derivatives that carried the amino-terminal 213-amino-acid LRR region conferred invasiveness to the normally non-invasive bacterium L. innocua or to inert latex beads and the corresponding purified polypeptides inhibited bacterial entry. In addition, the 213-amino-acid LRR region was able to stimulate PI 3-kinase activity and changes in the actin cytoskeleton (membrane ruffling). These properties were not detected with purified internalin, another invasion protein of L. monocytogenes that displays LRRs similar to those of InlB. Taken together, these results show that the first 213 amino acids of InlB are critical for its specific properties.

Animals↗