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  • Book
    Nayoung Kim, editor.
    Contents:
    Part 1. Epidemiology-Prevalence and Transmission routes of H. pylori
    Part 2. Pathophysiology
    1) Colonization of H. pylori in the stomach
    2) Brief description of Pathophysiology
    3) Immune mechanism
    4) Change of acid secretion, ghrelin and leptin by H. pylori
    5) H. pylori virulence factors
    A: toxin (CagA, VacA, DupA, OipA, IceA)
    B: genetic polymorphism of toxin and disease
    6) Host factors: genetic polymorphism, etc
    Part 3. Diagnosis
    1) Serology
    2) Histology
    3) Culture
    4) UBT
    5) Stool antigen
    6) Specific conditions
    A: Children
    B: Bleeding
    Part 4. Symptom
    1)Symptom of acute and chronic H. pylori infection
    Part 5. Disease
    1) Atrophic gastritis and Intestinal metaplasia
    2) Functional dyspepsia
    3) Peptic ulcer
    4) MALToma
    5) Gastric cancer
    A: Synopsis and Epidemiology of gastric cancer
    B1: Pathogenesis: i.Genetic alternation (mutations in tumor-related genes) induced by Activation-induced cytidine deaminase (AID)
    B2: Pathogenesis: ii. Epigenetic mechanisms: aberrant DNA methylation, microRNA
    B3: Pathogenesis:iii. Macrophage inhibitory factor (MIF)
    B4: Pathogenesis: iv. Epidermal mesenchyme transition (EMT)
    B5: Pathogenesis: v. ABO blood type
    B6: Pathogenesis: vi. First relatives of gastric cancer
    C: H. pylori-negative gastric cancer
    6) Gastroesophageal reflux disease (GERD)
    7) NSAID-induced gastropathy and H. pylori infection
    8) Extraintestinal manifestations of H. pylori infection
    A: Iron deficiency anemia
    B: Idiopathic thrombocytopenic purpura
    C: Heart disease
    D: Atopy and allergy
    Part 6. Antibiotic resistance
    1) Synopsis of antibiotic resistance
    2) Clarithromycin
    3) Amoxicillin
    4) Quinolone
    5) Metronidazole
    Part 7. Treatment
    1) Synopsis of antibiotic treatment
    2) Triple therapy
    3) Quadruple therapy
    4) Sequential therapy
    5) Concomitant therapy
    6) Tailored therapy based on antibiotic resistance
    7) Levofloxacin or rifabutin based triple therapy
    8) Probiotics
    9) Treatment guidelines
    10) Screening method of early gastric cancer
    11) Recrudescence and reinfection
    Part 8. Consequences of H. pylori eradication
    1) Peptic ulcer disease
    2) atrophic gastritis and Intestinal metaplasia
    3) Gastric cancer
    Part 9. The effect of H. pylori on the other microbiota of stomach
    The effect of H. pylori on the other microbiota of stomach
    Part 10. Animal model- H. pylori, H. felis.
    Digital Access Springer 2016
  • Article
    Bianchetti R, Lucchini G, Crosti P, Tortora P.
    J Biol Chem. 1977 Apr 25;252(8):2519-23.
    The effect of N10-formyl-H4folate on mitochondrial peptide chain initiation has been studied in isolated mitochondria of Saccharomyces cerevisiae. The addition of N10-formyl-H4-folate strongly stimulates the incorporation of amino acids into mitochondrial protein at both 6 and 15 mm Mg2+. Still higher stimulation (up to 10-fold) has been obtained in the production of de novo synthesized initial peptides, measured as peptidyl puromycin derivatives. The maximum effect is observed at 0.1 mM N10-formyl-H4folate. At 5 mM puromycin, the ratio formylated/unformylated peptides is 3, as shown by electrophoretic analysis. At 10 mM puromycin, the ratio is increased to more than 6. This is due to the presence of deformylase and amidohydrolase activities, which are more effective the longer the initial peptide is synthesized; at increasing puromycin concentrations, progressively shorter peptide chains are formed. Chemically synthesized fMet-puromycin and Met-puromycin are virtually stable when incubated with intact or frozen and thawed mitochondria. More careful kinetic analysis shows an early cessation of the initial peptide formation in the samples without N10-formyl-H4-folate. This indicates that the formylation of methionyl-tRNA formylatable species is an absolute requirement for mitochondrial peptide chain initiation.
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