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Biomedical subjects

Z Ge

Publications and source records attributed to Z Ge.

At least 19 recordsLinked to original sources
PubMed2006

Rapid onset of ulcerative typhlocolitis in B6.129P2-IL10tm1Cgn (IL-10-/-) mice infected with Helicobacter trogontum is associated with decreased colonization by altered Schaedler's flora.

Infection with Helicobacter trogontum, a urease-positive helicobacter isolated from subclinically infected rats, was evaluated in B6.129P2-IL10(tm1Cgn) (interleukin-10(-/-) [IL-10(-/-)]) and C57BL/6 (B6) mice. In a first experiment, IL-10(-/-) mice naturally infected with Helicobacter rodentium had subclinical typhlocolitis but developed severe diarrhea and loss of body condition with erosive to ulcerative typhlocolitis within 1 to 3 weeks of experimental infection with H. trogontum. A second experiment demonstrated that helicobacter-free IL-10(-/-) mice dosed with H. trogontum also developed severe clinical signs and typhlocolitis within 2 to 4 weeks, whereas B6 mice colonized with H. trogontum were resistant to disease. In a third experiment, using helicobacter-free IL-10(-/-) mice, dosing with H. trogontum resulted in acute morbidity and typhlocolitis within 8 days. Acute typhlocolitis was accompanied by signs of sepsis supported by degenerative hemograms and recovery of Escherichia coli and Proteus spp. from the livers of infected mice. Quantitative PCR data revealed that H. rodentium and H. trogontum may compete for colonization of the lower bowel, as H. trogontum established higher colonization levels in the absence of H. rodentium (P < 0.003). H. trogontum-induced typhlocolitis was also associated with a significant decrease in the levels of colonization by five of eight anaerobes that comprise altered Schaedler's flora (P < 0.002). These results demonstrate for the first time that H. rodentium infection in IL-10(-/-) mice causes subclinical typhlocolitis and that infection with H. trogontum (with or without H. rodentium) induces a rapid-onset, erosive to ulcerative typhlocolitis which impacts the normal anaerobic flora of the colon and increases the risk of sepsis.

Animals↗
PubMed2006

Clostridium piliforme infection in two farm-raised white-tailed deer fawns (Odocoileus virginianus) and association with copper toxicosis.

Necropsy of 2 white-tailed deer fawns who died acutely revealed diarrhea and melena in case No. 1 and no gross changes in case No. 2. Histologically, the livers of both deer displayed multifocal coagulative necrosis, with infiltrations of neutrophils, macrophages, and lymphocytes. By Warthin-Starry staining, bundles of filamentous bacteria were identified within hepatocytes at the periphery of the necrotic foci in case No. 1. There was multifocal myocardiocyte necrosis in case No. 1 and multifocal lymphoid necrosis of the Peyer's patches in case No. 2. Clostridium piliforme 16S ribosomal ribonucleic acid gene was detected in both livers by polymerase chain reaction (PCR) with C. piliforme-specific primers. The liver copper levels in both cases were normal to slightly elevated. The kidney copper level in case No. 2 was elevated. This represents the first published cases of Tyzzer's disease in deer, a novel use of PCR for the diagnosis of C. piliforme infection, and a possible association between copper toxicosis and Tyzzer's disease.

Animal Diseases↗
PubMed2006

The role of intra-luteal factors in the control of the porcine corpus luteum.

In this paper we review three intra-luteal factors and their roles in the corpus luteum (CL). Insulin-like growth factor (IGF)-I, together with its receptor and IGF-binding proteins (IGFBPs), represent an important control system in the CL. IGF-I is a product of small luteal cells and has steroidogenic (i.e. luteotrophic) actions on large luteal cells via the type I receptor, while IGFBPs (e.g. BP-2 and 3; small cells) generally inhibit IGF-Is actions. IGF-I is particularly important in early CL development (up to day 7 of the oestrous cycle) in the pig. Tumour necrosis factor (TNF)-alpha is a product of luteal macrophages that infiltrate CLs in increasing numbers as the cycle progresses. TNF-alpha has been shown to play an important role in luteolysis, but we hypothesise that in the pig, this factor plays an additional role during the mid-luteal phase (days 7-13) in promoting the acquisition of luteal sensitivity to the luteolytic actions of prostaglandin (PG)F2alpha (= luteolytic sensitivity; LS). Endothelin (ET)-1 is a product of (luteal) endothelial cells, and along with its receptors (ETA and ETB) and endothelin-converting enzyme (ECE)-1, represent an intra-luteal system that also plays a role in luteolysis, in association with PGF2alpha. Since TNF-alpha induces endothelial cells to secrete ET-1, we hypothesise that ET-1 mediates the sensitising effects of TNF-alpha on the porcine CL during the mid-luteal phase (days 7-13). Finally, we hypothesise that TNF-alpha and/or ET-1 act to up-regulate luteal protein kinase C (e.g. isoforms betaII and epsilon) activity and thereby sensitises luteal cells to PGF2alpha.

Animals↗
PubMed2005

Characterization of knitted polymeric scaffolds for potential use in ligament tissue engineering.

Different scaffolds have been designed for ligament tissue engineering. Knitted scaffolds of poly-L-lactic acid (PLLA) yarns and co-polymeric yarns of PLLA and poly(glycolic acid) (PLGA) were characterized in the current study. The knitted scaffolds were immersed in medium for 20 weeks, before mass loss, molecular weight, pH value change in medium were tested; changes in mechanical properties were evaluated at different time points. Results showed that the knitted scaffolds had 44% porosity. There was no significant pH value change during degradation, while there was obvious mass loss at initial 4 week, as well as smooth molecular weight drop of PLLA. PLGA degraded more quickly, while PLLA kept its integrity for at least 20 weeks. Young's modulus increased while tensile strength and strain at break decreased with degradation time; however, all of them could maintain the basic requirements for ACL reconstruction. It showed that the knitted polymeric structures could serve as potential scaffolds for tissue-engineered ligaments.

Biodegradation, Environmental↗
PubMed2004

High performance liquid chromatographic method for the determination of sumatriptan with fluorescence detection in human plasma.

A rapid and sensitive high performance liquid chromatography (HPLC) method with fluorescence detection has been developed for the determination of sumatriptan in human plasma. The procedure involved a liquid-liquid extraction of sumatriptan and terazosin (internal standard) from human plasma with ethyl acetate. Chromatography was performed by isocratic reverse phase separation on a C18 column. Fluorescence detection was achieved with an excitation wavelength of 225 nm and an emission wavelength of 350 nm. The standard curve was linear over a working range of 1-100 ng/ml and gave an average correlation coefficient of 0.9997 during validation. The limit of quantitation (LOQ) of this method was 1 ng/ml. The absolute recovery was 92.6% for sumatriptan and 95.6% for the internal standard. The inter-day and intra-day precision and accuracy were between 0.8-3.3 and 1.1-6.3%, respectively. This method is simple, sensitive and suitable for pharmacokinetics or bioequivalence studies.

Chromatography, High Pressure Liquid↗
PubMed2003

Multiple-dose safety and pharmacokinetics of oral garenoxacin in healthy subjects.

Garenoxacin (T-3811ME, BMS-284756) is a novel des-F(6) quinolone that has been shown to be effective in vitro against a wide range of clinically important pathogens, including gram-positive and gram-negative aerobes and anaerobes. This study was conducted to evaluate the safety and tolerability of multiple oral doses (100 to 1200 mg/day) of garenoxacin in healthy subjects and to determine its multiple-dose pharmacokinetics. Forty healthy male and female subjects (18 to 45 years of age) were enrolled in this randomized, double-blind, placebo-controlled, sequential, multiple- and ascending-dose study. Each subject received a once-daily oral dose of garenoxacin (100, 200, 400, 800, or 1200 mg) or a placebo for 14 days. Blood and urine samples were collected for measurements of garenoxacin by validated liquid chromatography with dual mass spectrometry, and plasma garenoxacin concentration-time data were analyzed by noncompartmental methods. The effects of garenoxacin on Helicobacter pylori, psychometric test performance, and electrocardiograms were assessed, as was drug safety. Over the 14 days of dosing, geometric mean peak concentrations of garenoxacin in plasma (C(max)) at the 100- and 1200-mg doses were within the ranges of 1.2 to 1.6 and 16.3 to 24 microg/ml, respectively. The corresponding values for the geometric mean area under the concentration-time curve over the dosing interval (AUC(tau)) for garenoxacin in plasma at the 100- and 1200-mg doses were within the ranges of 11.5 to 15.7 and 180 to 307 microg. h/ml, respectively. Increases in systemic exposure to garenoxacin in terms of AUC and C(max) were approximately dose proportional over the 100- to 400-mg dose range but demonstrated increases that were somewhat greater than the dose increments at the 800- and 1200-mg doses. Median values for the time to achieve C(max) were in the range of 1.13 to 2.50 h for all doses. The mean elimination half-life for garenoxacin in plasma appeared to be independent of dose and ranged from 13.3 to 17.8 h (day 14). Approximately 30 to 50% of an administered garenoxacin dose was excreted unchanged in the urine. At doses of 100 to 400 mg, steady-state concentrations of garenoxacin in plasma appeared to be attained by the fourth dose. Multiple oral doses of garenoxacin were well tolerated and did not demonstrate clinically significant effects on QT(c) or psychometric test results. Garenoxacin administered alone for 14 days at doses of >or=400 mg demonstrated activity against H. pylori. These results suggest that multiple once-daily oral doses of garenoxacin of up to 1200 mg are safe and well tolerated and that the pharmacokinetics of garenoxacin support once-daily administration.

Administration, Oral↗
PubMed2003

Steroidogenic responses of pig corpora lutea to insulin-like growth factor I (IGF-I) throughout the oestrous cycle.

This study was designed to investigate the roles of insulin-like growth factor I (IGF-I), IGF-type I receptor (IGF-IR) and IGF-binding proteins (IGFBPs) in regulating progesterone secretion by pig corpora lutea during the oestrous cycle, and the signal transduction pathways involved in mediating the steroidogenic actions of IGF-I. Corpora lutea were collected on days 4, 7, 10, 13 and 15 or 16 of the oestrous cycle, enzyme dissociated and the luteal cells were cultured for 24 h in Medium 199 with IGF-I (0-100 ng ml(-1)), long R(3)-IGF-I (0-100 ng ml(-1)), anti-IGF-I (Sm 1.2B; 0-10 microg ml(-1)), anti-IGF-IR (alphaIR3; 0-2 microg ml(-1)), or IGF-I signal transduction pathway inhibitors (phosphatidylinositol (PI)-3-kinase: 100 nmol Wortmannin l(-1) and 10 micromol LY 294002 l(-1); MAP kinase: 50 micromol PD 98059 l(-1)) to investigate their effects on IGF-I (100 ng ml(-1)) stimulated progesterone secretion. Pig luteal cells displayed dose-dependent responses to IGF-I and long R(3)-IGF-I on days 4 and 7 of the oestrous cycle, but not on days 10-16. There was no difference in the ED(50) or V(max) (maximal response) values between IGF-I and long R(3)-IGF-I. Neither anti-IGF-I nor anti-IGF-IR had significant effects on progesterone secretion, at any dose or day. Wortmannin and LY 294002 blocked IGF-I stimulated progesterone secretion, but PD 98059 was without effect. Finally, IGF-I (6 microg) infused into the ovary on day 7 in vivo significantly increased progesterone secretion within 45 min of infusion. The conclusions of this study are: (1) IGF-I has steroidogenic actions only on 'young' (days 4-7) pig corpora lutea; (2) endogenous IGF-I and IGFBP are insufficient to modulate progesterone secretion in vitro; and (3) the steroidogenic actions of IGF-I are mediated via PI-3-kinase.

Androstadienes↗
PubMed2001

Genomic characterization of Helicobacter hepaticus: ordered cosmid library and comparative sequence analysis.

Helicobacter hepaticus is an important pathogen in laboratory mice and induces the development of liver tumors and gastrointestinal disease in susceptible strains of mice. In this study, a miniset of 36 cosmid clones from a genomic library of H. hepaticus was ordered and grouped into four large contigs representing approximately 1 Mb of the H. hepaticus genome using PCR, DNA sequencing, Southern and dot-blot hybridization and pulsed-field gel electrophoresis. From the 200-300 terminal nucleotide sequences of 38 cosmid clones, 56 coding regions were predicted, of which 51 were found to have orthologs in the public databases and five appeared to be unique to H. hepaticus. Of these 51 genes, 36 have orthologs in Helicobacter pylori and 25 display the highest sequence similarity to H. pylori. However, chromosomal positions of these genes are not conserved between these two helicobacters. In addition, 10 H. hepaticus genes had the highest sequence similarity to orthologs in Campylobacter jejuni. The GC content in a randomly selected 21-kb H. hepaticus genomic sequence was 35.8%, which approximates the average between H. pylori (39%) and C. jejuni (30.6%). These results demonstrate that: (1) H. hepaticus is more closely related to H. pylori than C. jejuni; (2) significant genomic alterations exist between H. hepaticus and H. pylori, including gene organization, protein sequences and GC content, probably in part due to specific adaptation to distinct ecological niches.

Animals↗
PubMed2001

Synthesis of (5alpha)-17-azaandrostan-3-ols and (5alpha)-17-aza-D-homoandrostan-3-ols and their N-acylated derivatives.

Two groups of N-acylated D-azasteroids (4 and 5) were synthesized to explore structure-activity relationships for steroid modulation of GABA(A) receptor function. The target compounds were prepared conveniently from (5alpha)-3-hydroxyandrostan-17-ones (6 and 7) via the intermediate (5alpha)-17-aza-D-homoandrostan-3-ols (14 and 15) or (5alpha)-17-azaandrostan-3-ols (18 and 19) precursors in high overall yields. A Beckmann rearrangement and a Hofmann rearrangement were employed as two key steps in the synthetic sequences.

Androstanols↗
PubMed2001

Characterization of proteins in the outer membrane preparation of a murine pathogen, Helicobacter bilis.

Helicobacter bilis is a bacterial pathogen associated with multifocal hepatitis and inflammatory bowel disease in certain strains of mice. This bacterium colonizes the liver, bile, and lower intestine in mice and has also been isolated from a wide spectrum of laboratory animals. In this study, proteins present in the outer membrane preparation (OMP) of four H. bilis strains isolated from a mouse, a dog, a rat, and a gerbil were characterized and compared with that of Helicobacter pylori, a human gastric pathogen. All four H. bilis strains had similar OMP protein profiles that were distinct from those of H. pylori. Immunoblotting demonstrated that OMP proteins from H. bilis and H. pylori have little cross-reactivity, except for their flagellins. Nine major immunogenic polypeptides were present in the H. bilis OMPs. By using two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis, five heat-modifiable proteins with molecular masses of 82, 66, 52, 47 and 37 kDa were identified. The N-terminal sequences of the 46- and 47-kDa OMP proteins had no homology with protein sequences available in public databases. These results indicate that H. bilis has a conserved, unique OMP protein profile that is distinct from those of H. pylori.

Animals↗
PubMed2001

Fluorogenic PCR-based quantitative detection of a murine pathogen, Helicobacter hepaticus.

Helicobacter hepaticus infection in mice is being used as an animal model for elucidating the pathogenesis of gastrointestinal and biliary diseases in humans. H. hepaticus, which forms a spreading film on selective agar, is not amenable to routine quantitative counts of organisms in tissues using a CFU method. In this study, a fluorogenic PCR-based assay was developed to quantitatively detect H. hepaticus in mouse ceca and feces using the ABI Prism 7700 sequence detection system. A pair of primers and a probe for this assay were generated from the H. hepaticus cdtB gene (encoding subunit B of the H. hepaticus cytolethal distending toxin). Using this assay, the sensitivity for detection of H. hepaticus chromosomal DNA prepared from pure culture was 20 fg, which is equivalent to approximately 14 copies of the H. hepaticus genome based on an estimated genome size of approximately 1.3 Mb determined by pulsed-field gel electrophoresis. H. hepaticus present in feces and cecal samples from H. hepaticus-infected mice was readily quantified. The selected PCR primers and probe did not generate fluorescent signals from eight other helicobacters (H. canis, H. cineadi, H. felis, H. mustelae, H. nemestrinae, H. pullorum, H. pylori, and H. rodentium). A fluorescent signal was detected from 20 ng of H. bilis DNA but with much lower sensitivity (10(6)-fold) than from H. hepaticus DNA. Therefore, this assay can be used with high sensitivity and specificity to quantify H. hepaticus in experimentally infected mouse models as well as in naturally infected mice.

Animals↗
PubMed2001

Clinical, brain electric earth map, endothelin and transcranial ultrasonic Doppler findings after hyperbaric oxygen treatment for severe brain injury.

OBJECTIVE: To analyze the effect and mechanism of hyperbaric oxygen (HBO) treatment for severe brain injury (SBI). METHODS: Fifty-five patients were divided into a treatment group of 35 patients and a control group of 20 patients. We observed the alterations of clinical, brain electric earth map (BEAM), endothelin (ET) and transcranial ultrasonic Doppler (TCD) findings before and after HBO treatment as well as outcome. RESULTS: In the treatment group, Glasgow coma scale, BEAM and outcome improved after HBO treatment; compared with that of the control group, it showed a significant difference. After one course of treatment, treatment group ET was reduced from 91.24 +/- 12.18 ng/L to 68.88 +/- 14.37 ng/L (P < 0.01); in control group, ET was reduced from 90.78 +/- 15.71 ng/L to 83.12 +/- 12.22 ng/L, with a statistically significant difference (P < 0.05). TCD records of MCA mean velocity (Vm) was reduced from 64.2 +/- 4.8 cm/s to 51.6 +/- 4.2 cm/s (P < 0.01), and a decrease in MCA systolic velocity (Vs) and pulse index (PI) values was statistically significant (P < 0.01). CONCLUSION: HBO treatment can improve the clinical, BEAM and outcome of severely brain injured patients, by decreasing acute stage ET and improving the blood velocity of MCA and decreasing cerebral vascular resistance. HBO treatment can reduce cerebral vascular spasms, cerebral ischemia and hypoxia. One of the important mechanisms of HBO treatment for severe brain injury is the lowering of intracranial pressure.

Adult↗
PubMed2001

Glasgow Coma Scale, brain electric activity mapping and Glasgow Outcome Scale after hyperbaric oxygen treatment of severe brain injury.

OBJECTIVE: To study the effect of hyperbaric oxy gen (HBO) treatment of severe brain injury. METHODS: Fifty-five patients were divided into a treatment group (n=35 receiving HBO therapy) and a control group (n=20 receiving dehydrating, cortical steroid and antibiotic therapy) to observe the alteration of clinic GCS (Glasgow Coma Scale), brain electric activity mapping (BEAM), prognosis and GOS (Glasgow Outcome Scale) before a nd after hyperbaric oxygen treatment. RESULTS: In the treatment group GCS, BEAM and GOS were improved obviously after 3 courses of treatment, GCS increased from 5.1 to 14.6 (P<0.01-0.001),the BEAM abnormal rate reduced from 94.3% to 38% (P<0.01-0.001), the GOS good-mild disability rate was 83.7%, and the middle-severe disability rate was 26.3% compared with the control group. There was a statistic significant difference between the two groups (P<0.01-0.001). CONCLUSIONS: Hyperbaric oxygen treatment could improve obviously GCS, BEAM and GOS of severe brain injury patients, and effectively reduce the mortality and morbidity. It is an effective method to treat severe brain injury.

Adult↗
PubMed2001

Long-term colonization levels of Helicobacter hepaticus in the cecum of hepatitis-prone A/JCr mice are significantly lower than those in hepatitis-resistant C57BL/6 mice.

Helicobacter hepaticus infection causes hepatitis in A/JCr mice but mild or no disease in C57BL/6 mice. Colonization of H. hepaticus in the cecum of experimentally infected A/JCr and C57BL/6 mice was quantified by use of real-time polymerase chain reaction (PCR) analysis with primers for the H. hepaticus cdtB gene and mouse 18srRNA. Eight-week-old mice were experimentally (n = 48) or sham (n = 24) infected with H. hepaticus, then were necropsied 6 months after infection. Liver specimens from experimentally infected mice had negative results of PCR analysis for H. hepaticus; thus, real-time quantification was not attempted. Quantitative PCR analysis of H. hepaticus in cecal specimens indicated that C57BL/6 mice were colonized to a greater extent than were A/JCr mice (P < 0.006). Appreciable typhlitis was not observed, but was consistent with that of previous reports; A/JCr mice developed more severe parenchymal necrosis, portal inflammation, and phlebitis in the liver (P < 0.0001), with mild disease observed in infected C57BL/6 mice. Thus, hepatitis in A/JCr mice caused by H. hepaticus infection is associated with significantly lower colonization levels of H. hepaticus in the cecum, compared with those of hepatitis-resistant C57BL/6 mice. Host responses of A/JCr mice that limit cecal colonization with H. hepaticus may have important roles in the pathogenesis of hepatic lesions.

Animals↗
PubMed2000

Fumarate reductase is essential for Helicobacter pylori colonization of the mouse stomach.

Fumarate reductase (FRD) is the key enzyme in fumarate respiration induced by anaerobic growth of bacteria. In Helicobacter pylori, this enzyme appears to be constitutively expressed under microaerobic conditions and is not essential for its survival in vitro. In this study, the role of FRD in the colonization of H. pylori was investigated using a mouse model. The frdA gene coding for subunit A of FRD, and two control genes, copA and copP associated with the export of copper out of H. pylori, were inactivated by insertion of the chloramphenicol acetyltransferase cassette into these individual genes. The isogenic mutants of H. pylori strain AH244 were obtained by natural transformation. Seventy-five ICR mice (15 mice/group) were orogastrically dosed with either the wild type H. pylori strain AH244, its isogenic mutants, or Brucella broth (negative control). Five mice from each group were killed at 2, 4 and 8 weeks post-inoculation (WPI), respectively. H. pylori colonization was not detected in mouse gastric mucosa infected with the frdA mutant at any time point in the study by both quantitative culture and PCR. In contrast, the mice inoculated with either wild type AH244, copA or copPH. pylori mutants became readily infected. These data indicate that FRD plays a crucial role in H. pylori survival in the gastric mucosa of mice. Given that FRD, present in all H. pylori strains, is immunogenic in H. pylori -infected patients and H. pylori growth in vitro can be inhibited by three anthelmintics (morantel, oxantel and thiabendazole), this enzyme could potentially be used both as a novel drug target as well as in the development of vaccines for H. pylori prevention and eradication.

Animals↗
PubMed2000

The importance of root gravitropism for inter-root competition and phosphorus acquisition efficiency: results from a geometric simulation model.

We have observed that low soil phosphorus availability alters the gravitropic response of basal roots in common bean (Phaseolus vulgaris L.), resulting in a shallower root system. In this study we use a geometric model to test the hypotheses that a shallower root system is a positive adaptive response to low soil P availability by (1) concentrating root foraging in surface soil horizons, which generally have the highest P availability, and (2) reducing spatial competition for P among roots of the same plant. The growth of nine root systems contrasting in gravitropic response over 320 h was simulated in SimRoot, a dynamic three-dimensional geometric model of root growth and architecture. Phosphorus acquisition and inter-root competition were estimated with Depzone, a program that dynamically models nutrient diffusion to roots. Shallower root systems had greater P acquisition per unit carbon cost than deeper root systems, especially in older root systems. This was due to greater inter-root competition in deeper root systems, as measured by the volume of overlapping P depletion zones. Inter-root competition for P was a significant fraction of total soil P depletion, and increased with increasing values of the P diffusion coefficient (De), with root age, and with increasing root gravitropism. In heterogenous soil having greater P availability in surface horizons, shallower root systems had greater P acquisition than deeper root systems, because of less inter-root competition as well as increased root foraging in the topsoil. Root P acquisition predicted by SimRoot was validated against values for bean P uptake in the field, with an r2 between observed and predicted values of 0.75. Our results support the hypothesis that altered gravitropic sensitivity in P-stressed roots, resulting in a shallower root system, is a positive adaptive response to low P availability by reducing inter-root competition within the same plant and by concentrating root activity in soil domains with the greatest P availability.

Computer Simulation↗
PubMed2000

Lewis antigens in Helicobacter pylori: biosynthesis and phase variation.

The lipopolysaccharides (LPS) of most Helicobacter pylori strains contain complex carbohydrates known as Lewis antigens that are structurally related to the human blood group antigens. Investigations on the genetic determinants involved in the biosynthesis of Lewis antigens have led to the identification of the fucosyltransferases of H. pylori, which have substrate specificities distinct from the mammalian fucosyltransferases. Compared with its human host, H. pylori utilizes a different pathway to synthesize the difucosylated Lewis antigens, Lewis y. and Lewis b. Unique features in the H. pylori fucosyltransferase genes, including homopolymeric tracts mediating slipped-strand mispairing and the elements regulating translational frameshifting, enable H. pylori to produce variable LPS epitopes on its surface. These new findings have provided us with a basis to further examine the roles of molecular mimicry and phase variation of H. pylori Lewis antigen expression in both persistent infection and pathogenesis of this important human gastric pathogen.

Animals↗