Gotowe bibliografie tematyczne / H. pylori

Gotowa bibliografia na temat „H. pylori”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 6 września 2023

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Artykuły w czasopismach na temat "H. pylori"

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Sakaguchi, Takuki, Takaaki Sugihara, Ken Ohnita, Daisuke Fukuda, Tetsuro Honda, Ryohei Ogihara, Hiroki Kurumi, Kazuo Yashima i Hajime Isomoto. "Pyloric Incompetence Associated with Helicobactor pylori Infection and Correlated to the Severity of Atrophic Gastritis". Diagnostics 12, nr 3 (23.02.2022): 572. http://dx.doi.org/10.3390/diagnostics12030572.

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Duodenogastric reflux (DGR) causes bile reflux gastritis (BRG) and may develop into gastric cancer. DGR is classified as primary in non-operated stomachs or secondary to surgical intervention. Primary DGR and Helicobacter pylori (H. pylori) infection are reportedly related. However, the mechanism is not fully understood. This study aimed to elucidate the relationship between H. pylori infection and pyloric incompetence in a non-operated stomach. A total of 502 non-operated participants who underwent an upper intestinal endoscopy were prospectively enrolled. Endoscopic findings (EAC, endoscopic atrophy classification; nodular gastritis; xanthoma; fundic gland polyp; and incompetence of pylorus), sex, age, gastrin, pepsinogen (PG) I and PG II levels were evaluated. PG I/PG II ratio, anti-H. pylori-Ab positivity, and atrophic gastritis status were significantly different between the normal and incompetent pylori (p = 0.043, <0.001, and 0.001, respectively). Open-type atrophic gastritis was significantly higher in the incompetent pylori. Incompetence of the pylorus and EAC were moderately correlated (Cramer’s V = 0.25). Multivariate analysis revealed that the presence of anti-H. pylori-Ab was the only independent factor associated with the incompetence of the pylorus, with an adjusted odds ratio of 2.70 (95% CI: 1.47–4.94, p = 0.001). In conclusion, pyloric incompetence was associated with H. pylori infection and moderately correlated to the severity of atrophic gastritis in non-operated stomachs.
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 . "NSAID, gebruikNSAID-gebruik en H. pylori, tetracycline H. pylori, naproxen H. pylori, metronidazol H. pylori, bismutoxideH. Pylori-eradicatie". Medisch-Farmaceutische Mededelingen 38, nr 4 (kwiecień 2000): 72. http://dx.doi.org/10.1007/bf03057514.

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Garcés-Duran, R., S. Kindt, K. Kotilea, S. François, G. Rasschaert, A. Smet, B. Hauser i in. "Belgian consensus for Helicobacter pylori management 2023". Acta Gastro Enterologica Belgica 86, nr 1 (marzec 2023): 74–91. http://dx.doi.org/10.51821/86.1.11327.

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Helicobacter pylori (H. pylori) infection causes chronic gastritis, peptic ulcers and gastric cancer. Although H. pylori prevalence is decreasing worldwide, regional variations exist in Europe, with the lowest infection prevalence in Northern Europe, and the highest in Eastern and Southern Europe (1). Changes in the treatment recommendations and the increasing available evidence have justified the implementation of new recommendations since last Belgian consensus in 1998 (2). Several non-H. pylori Helicobacter species (NH.PYLORI-H), colonizing the stomach of domestic animals, also have the ability to cause gastric disease in humans, although to a lesser extent. These zoonotic NH. PYLORIH are not the subject of the current recommendations.
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Hayashi, Shunji, Toshiro Sugiyama, Ken-Ichi Amano, Hiroshi Isogai, Emiko Isogai, Miki Aihara, Mikio Kikuchi i in. "Effect of Rebamipide, a Novel Antiulcer Agent, onHelicobacter pylori Adhesion to Gastric Epithelial Cells". Antimicrobial Agents and Chemotherapy 42, nr 8 (1.08.1998): 1895–99. http://dx.doi.org/10.1128/aac.42.8.1895.

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ABSTRACT Helicobacter pylori is a major etiological agent in gastroduodenal disorders. The adhesion of H. pylori to human gastric epithelial cells is the initial step of H. pylori infection. Inhibition of H. pylori adhesion is thus a therapeutic target in the prevention of H. pyloriinfection. Experiments were performed to evaluate the effect of rebamipide, a novel antiulcer agent, on H. pylori adhesion to gastric epithelial cells. MKN-28 and MKN-45 cells, derived from human gastric carcinomas, were used as target cells. Ten H. pylori strains isolated from patients with chronic gastritis and gastric ulcer were used in the study. We evaluated the effect of rebamipide on H. pylori adhesion to MKN-28 and MKN-45 cells quantitatively using our previously established enzyme-linked immunosorbent assay. The adhesion of H. pylori to MKN-28 and MKN-45 cells was significantly inhibited by pretreatment of these cells with 100 μg of rebamipide per ml. However, the adhesion was not affected by the pretreatment of H. pylori with rebamipide. On the other hand, the viabilities of H. pylori, MKN-28 cells, and MKN-45 cells were not affected by rebamipide. Our studies suggest that rebamipide inhibits the adhesion of H. pylorito gastric epithelial cells.
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Öztekin, Merve, Birsen Yılmaz, Duygu Ağagündüz i Raffaele Capasso. "Overview of Helicobacter pylori Infection: Clinical Features, Treatment, and Nutritional Aspects". Diseases 9, nr 4 (23.09.2021): 66. http://dx.doi.org/10.3390/diseases9040066.

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Helicobacter pylori (H. pylori) is a 0.5–1 µm wide, 2–4 µm long, short helical, S-shaped Gram-negative microorganism. It is mostly found in the pyloric region of the stomach and causes chronic gastric infection. It is estimated that these bacteria infect more than half of the world’s population. The mode of transmission and infection of H. pylori is still not known exactly, but the faecal–oral and oral–oral routes via water or food consumption are thought to be a very common cause. In the last three decades, research interest has increased regarding the pathogenicity, microbial activity, genetic predisposition, and clinical treatments to understand the severity of gastric atrophy and gastric cancer caused by H. pylori. Studies have suggested a relationship between H. pylori infection and malabsorption of essential micronutrients, and noted that H. pylori infection may affect the prevalence of malnutrition in some risk groups. On the other hand, dietary factors may play a considerably important role in H. pylori infection, and it has been reported that an adequate and balanced diet, especially high fruit and vegetable consumption and low processed salty food consumption, has a protective effect against the outcomes of H. pylori infection. The present review provides an overview of all aspects of H. pylori infection, such as clinical features, treatment, and nutrition.
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Blasiak, Janusz, Jan Chojnacki i Cezary Chojnacki. "Inflammation, oxidative stress, DNA damage response and epigenetic modifications interact behind the beneficial actions of melatonin on H. pylori-mediated gastric disorders". Melatonin Research 6, nr 2 (30.06.2023): 135–47. http://dx.doi.org/10.32794/mr112500145.

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Helicobacter pylori (H. pylori) infection is associated with several disorders of the gastrointestinal tract, including gastric cancer. Studies of ours and others suggest that H. pylori infection may affect melatonin synthesis in the gastric epithelial cells. On the other hand, melatonin ameliorates gastric disorders as shown in clinical trials and experimental studies. Moreover, melatonin not only suppresses the DNA-damaging reaction of diet-related mutagens that can initiate carcinogenesis in gastric mucosa, but also the oxidative DNA damage evoked by reactive oxygen and nitrogen species produced during H. pylori-related gastric inflammation. H. pylori infection is associated with several functional and organic gastric disorders, including gastritis, peptic ulcer disease and gastric cancer, but the precise mechanism behind this association is not known and many pathways can be involved. Some of beneficial effects of melatonin in the gastrointestinal tract are underlined by mechanisms that likely play a role in detrimental effects of H. pylori in the stomach. Therefore, melatonin may modulate these mechanisms resulting in ameliorating H. pylori-related symptoms. In this narrative review the role of inflammation, oxidative stress, DNA damage response and epigenetic modifications in H. pylori­-associated gastric disorders will be discussed with an emphasis on gastric cancer. We also suggest that melatonin may have potential to inhibit H. pylori-mediated pathologies through its interaction with essential pathways as described herein. Overlapping mechanisms of H. pylori-associated pathogenesis and beneficial effects of melatonin justify further studies on the action of melatonin on gastric disorders associated with H. pylori infection, including clinical trials.
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Asonuma, Sho, Akira Imatani, Naoki Asano, Tomoyuki Oikawa, Hidetomo Konishi, Katsunori Iijima, Tomoyuki Koike, Shuichi Ohara i Tooru Shimosegawa. "Helicobacter pylori induces gastric mucosal intestinal metaplasia through the inhibition of interleukin-4-mediated HMG box protein Sox2 expression". American Journal of Physiology-Gastrointestinal and Liver Physiology 297, nr 2 (sierpień 2009): G312—G322. http://dx.doi.org/10.1152/ajpgi.00518.2007.

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Helicobacter pylori is a major cause of the transdifferentiation into intestinal metaplasia that may develop gastric cancer. However, the molecular pathogenesis of this transdifferentiation is poorly understood. A SRY-related HMG box protein Sox2 is an essential transcription factor of organ development in brain, lung, and stomach. Our aim of this study was to investigate the mechanism responsible for regulation of Sox2 in host Th1-dominant response to H. pylori. Sox2 protein was immunohistochemically expressed in both human oxyntic and pyloric glands with H. pylori infection, but not in intestinal metaplasia. Western immunoblotting of gastric epithelial cell lines showed that IL-4, a Th2-related cytokine, dose dependently enhanced Sox2 expression among H. pylori infection-mediated cytokines. Small changes of Sox2 expression were observed after each treatment with IFN-γ, IL-1β, or TNF-α. IL-4-mediated Sox2 induction was suppressed by the inhibition of STAT6 activation with STAT6 RNA interference, and electrophoretic mobility shift assay indicated that activation of the Sox2 promoter by IL-4 occurred through the action of STAT6. Furthermore, H. pylori and IFN-γ inhibited the phosphorylation of STAT6, resulting in the suppression of IL-4-mediated Sox2 expression. Immunohistochemical analyses showed significantly the suppressed STAT6 activity in H. pylori-infected human gastric mucosa. Additionally, downregulation of Sox2 by knockdown experiments led to intestinal phenotype with expressions of Cdx2 and MUC2. These results suggest that H. pylori and IFN-γ interfere with the differentiation into oxyntic and pyloric glands by the downregulation of Sox2 on IL-4/STAT6 signaling, which may contribute to the transdifferentiation into intestinal metaplasia.
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Rao, Prashant, Sarika Mayekar, Vishwajit Pawar i Mohan Achyut Joshi. "Endoscopic assessment and Helicobacter pylori status evaluation in operated cases of peptic ulcer perforation". International Surgery Journal 7, nr 2 (27.01.2020): 535. http://dx.doi.org/10.18203/2349-2902.isj20200310.

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Background: Helicobacter pylori’s role in delaying ulcer healing after surgical repair for peptic ulcer perforation causing ulcer persistence hasn’t been definitively established as it has been for uncomplicated ulcers.Methods: Authors performed an endoscopy and H. pylori status evaluation in 30 patients at an average of 6.2 weeks after simple omental patch closure for perforated peptic ulcer.Results: A positive H. pylori status was found in 12 patients (40%) of which 9 had active ulcers. None in the negative group had an active ulcer. H. pylori infection was the only factor found to be responsible for ulcer persistence after surgery.Conclusions: A reasonable approach would thus be to perform an endoscopy 6 weeks after surgery to assess ulcer healing and H. pylori status. H. pylori eradication therapy should then be selectively initialled for patients with an active ulcer or positive H. pylori status.
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Elshenawi, Yasmine, Shuai Hu i Skander Hathroubi. "Biofilm of Helicobacter pylori: Life Cycle, Features, and Treatment Options". Antibiotics 12, nr 8 (31.07.2023): 1260. http://dx.doi.org/10.3390/antibiotics12081260.

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Helicobacter pylori is a gastric pathogen that infects nearly half of the global population and is recognized as a group 1 carcinogen by the Word Health Organization. The global rise in antibiotic resistance has increased clinical challenges in treating H. pylori infections. Biofilm growth has been proposed to contribute to H. pylori’s chronic colonization of the host stomach, treatment failures, and the eventual development of gastric diseases. Several components of H. pylori have been identified to promote biofilm growth, and several of these may also facilitate antibiotic tolerance, including the extracellular matrix, outer membrane proteins, shifted morphology, modulated metabolism, efflux pumps, and virulence factors. Recent developments in therapeutic approaches targeting H. pylori biofilm have shown that synthetic compounds, such as small molecule drugs and plant-derived compounds, are effective at eradicating H. pylori biofilms. These combined topics highlight the necessity for biofilm-based research in H. pylori, to improve current H. pylori-targeted therapeutic approaches and alleviate relative public health burden. In this review we discuss recent discoveries that have decoded the life cycle of H. pylori biofilms and current biofilm-targeted treatment strategies.
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Samra, Zahoor Qadir, Umber Javaid, Sadia Ghafoor, Aleeza Batool, Nadia Dar i Muhammad Amin Athar. "PCR assay targeting virulence genes of Helicobacter pylori isolated from drinking water and clinical samples in Lahore metropolitan, Pakistan". Journal of Water and Health 9, nr 1 (3.02.2011): 208–16. http://dx.doi.org/10.2166/wh.2010.169.

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Helicobacter pylorus is considered for chronic gastritis, gastric ulcers and adenocarcinoma and its high infection rate is observed in overcrowded and lower socioeconomic groups in developing countries. This study was designed to identify the role of drinking water in the transmission and prevalence of H. pylori (HP). Selective HP medium was developed for enrichment and presumptive identification of H. pylori by urease, catalase and species specific 16S rRNA tests. The virulence genes (vacA ‘s’ and ‘m’ regions and cagA) of H. pylori in 90 out of 225 H. pylori positive drinking water samples were present (40%). Ten out of 18 biopsies (55.55%) and 15 out of 50 vomiting fluids of gastric disease patients (30%) were also positive for virulence genes. Anti-H. pylori antibodies were also detected in 31 out of 50 patients’ sera. The presence of virulence genes was also directly confirmed by hybridization studies using non-radioactive DNA probes of 16S rRNA, vacA and cagA genes. The presence of H. pylori in water is due to poor sanitary conditions, improper waste disposal and lack of public health education. PCR-based analysis and colony hybridization can be used for detection of H. pylori in clinical and environmental samples.
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Rozprawy doktorskie na temat "H. pylori"

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Warren, John Robin. "The discovery and pathology of H pylori /". Title page and contents only, 1999. http://web4.library.adelaide.edu.au/theses/09MD/09mdw289.pdf.

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Сорокман, Т. В. "Кіотський глобальний консенсус щодо H. pylori-асоційованого гастриту". Thesis, БДМУ, 2017. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/17155.

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Leslie, Kevin Alexander. "Investigation of Prophage in Clinical Isolates of H pylori". W&M ScholarWorks, 2013. https://scholarworks.wm.edu/etd/1539626941.

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Arebi, Naila. "Identification of novel factors regulating mucosal somatostatin in H. pylori gastritis". Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289867.

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Zhou, Yong. "An antimicrobial agent from celery seed active against H. pylori". Thesis, Sheffield Hallam University, 2008. http://shura.shu.ac.uk/20709/.

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As well as peptic ulcers, Helicobacter pylori is associated with the development of gastritis, gastric adenocarcinoma and lymphoma, and has been classified as a class I carcinogen in humans (International Agency for Research on Cancer Working Group, 1994). Although the bacteria can be eradicated in up to 90% of patients, side effects, poor compliance and the resistance of the bacteria to antibiotics are common causes of frequent treatment failure. Celery seed extracts (CSE) from a unique source in India has been used as herbal medicine since antiquity and found to have anti-inflammatory and gastroprotective properties (Butters et al., 2004; Whitehouse et al., 2001). This study followed on observations that crude extracts exhibited anti-helicobacter activity (Rainsford & Liu, 2006).CSE was selectively fractionated followed by HPLC. Fractions were collected and bio-assayed against different strains of H. pylori using conventional culture methods. The most potent component that was obtained from HPLC and purified was designated celery seed with anti-Helicobacter activity (CAH). This component has strong bactericidal effects against H. pylori; the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) were 3.15 mug ml[-1] and 6.25 - 12.5 mug ml[-1], respectively. This compares favourably with the MIC and MBC of tetracycline, which are in the region of 3.15 mug ml[-1]. The isolated compound has highly specific inhibitory effect on H. pylori, since no inhibitory activity was detected against Campylobacter jejuni or Escherichia coli at these levels. The molecular ion of CAH was measured as 384.23 by mass spectrometry, giving the empirical formula as C[24]H[32]O[4]. The MS and NMR data strongly suggest this compound is a phthalide dimer. From radioactive bioassay, CAH inhibits RNA synthesis by 50% of that seen in a negative control in 3 days, while DNA and protein synthesis were unchanged. These suggested that the new compound may be suitable for further investigation as an agent for treating H. pylori infections.
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Iwano, Masahiro. "Characteristics of gastric MALT lymphoma resistant to eradication of H. pylori". Kyoto University, 2008. http://hdl.handle.net/2433/124330.

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Jimenez-Guerra, Francisco. "Prevalence of, and risk factors for, Helicobacter pylori infection and its effect on growth of children in Mexico". Thesis, London School of Hygiene and Tropical Medicine (University of London), 1999. http://researchonline.lshtm.ac.uk/4649359/.

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Helicobacter pylori (H. pylori) infection causes achlorydria, depressed gastric acid barrier, impaired immune response and is suspected in bacterial overgrowth and diarrhoea. These features of the infection are known to cause significant malabsorption of nutrients and impairment of linear growth in children. The prevalence of H. pylori infection in children is known to be much higher in developing countries, especially among the lower socio-economic groups. The true prevalence of infection in urban children in Mexico and its impact on their growth are largely unknown. This study examined the prevalence of H. pylori infection in school children from an urban area in Northwest Mexico and attempted to identify the risk factors that predispose individuals to infection in childhood; as well as to relate the presence of this infection to growth of children. The cross-sectional study was conducted in 1997/98 in the poorest socio-economic sectors of the city of Hermosillo, Sonora, among 178 children aged 9 and 10 years. H. pylori status was determined in children by the 13C-urea breath test. Anthropometric (weight and height) and haemoglobin measurements along with analysis of faecal samples and a 24-hour dietary recall were carried out in each child. Family sociodemographic/socio-economic status and living conditions data were elicited from parents by interview via structured questionnaires. The overall prevalence rate of H. pylori infection for the children in Hermosillo as determined by this study was 47.1%. The findings indicate that rural-born father, number of siblings, the type of main water supply (one tap in the yard) and the sharing of bed by the study child are important risk factors for acquiring the H. pylori infection. A borderline significant but small effect of H. pylori infection on height for-age was observed in this study. H. pylori infection was found to be positively highly associated with Hymenolepis nana. No differences in mean energy, protein and iron intakes between H. pylori positive and negative children were observed. However, significant differences in the mean energy, protein and iron intakes were observed between boys and girls. H. pylori infection and enteric parasites were not significantly correlated with the presence of anaemia.
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Vallström, Anna. "Helicobacter pylori : molecular mechanisms for variable adherence properties". Doctoral thesis, Umeå universitet, Institutionen för medicinsk kemi och biofysik, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-25931.

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More than half of all people worldwide are infected with H. pylori. The infection always cause a gastric inflammation that may develop into peptic ulcer disease or gastric cancer. Attachment proteins, adhesins, mediate specific adherence of H. pylori to receptor structures on the human gastric mucosa. The best-characterized H. pylori adhesin-receptor interactions are the BabA adhesin and the binding to the fucosylated blood group antigens ABO/Lewis b (Leb) and the SabA adhesin and its binding to the inflammation associated sialyl-Lewis x antigen. During H. pylori infection the availability of receptor structures on the human gastric mucosa changes as a consequence of the host inflammatory and immune responses. Consequently the bacterial population need to adjust its adherence properties to stay colonized. This thesis describes mechanisms that generate H. pylori populations with variable adherence properties and mechanisms for adjustment of adhesin expression levels.In H. pylori strains devoid of Leb-binding, we found bacterial cells with Leb-binding. Isolation of such H. pylori clones demonstrated that the change in receptor binding phenotype was obtained via the mechanisms of homologous recombination and slipped strand mispairing (SSM). Disease presentation in relation to BabA expression was studied in H. pylori infected Mongolian gerbils. We showed that BabA was not essential for colonization but caused severe injury to the gastric mucosa and was turned off during long-term infection by nucleotide changes within the babA gene. Gerbils infected with BabA-weak-expressing strains maintained BabA expressing clones for a longer period than gerbils that were infected with BabA-high-expressing strains. Studies of the gerbil gastric mucosal glycosylation showed that gerbils respond in a similar way as humans and Rhesus monkeys which support gerbils to be a model suitable for studying H. pylori infection and disease outcome in relation to adherence.We studied the SSM mechanism of SabA phase variation and the cognate shift in sLex-binding phenotype and we show sLex-binding activity to be growth phase dependent. H. pylori vesicles were characterized for the major phosholipid and protein components. Virulence factors e.g., VacA, and CagA were identified and both the BabA and the SabA adhesins was shown to be located on the vesicle surface and to mediate specific binding to their cognate receptors present on the human gastric mucosa. H. pylori generate bacterial cells with different receptor binding phenotypes via the mechanisms of homologous recombination, SSM and nucleotide changes. These mechanisms will probably contribute to bacterial fitness by the generation of quasi species populations where some of the clones will be better adapted to the environmental chances during persistent infection.
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de, Albuquerque Mello Luciano. "Análise histomorfométrica de lesões gástricas relacionadas à infecção pelo Hlicobacter pylori". Universidade Federal de Pernambuco, 2007. https://repositorio.ufpe.br/handle/123456789/9072.

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O bacilo Helicobacter pylori é atualmente considerado como o agente etiológico mais importante das gastrites em seres humanos e como um fator de risco para o surgimento das doenças ulcerativas do carcinoma gástrico. Estima-se que 50% da população mundial está infectada por esta bactéria. Atualmente, apenas estudos subjetivos e qualitativos têm sido realizados na análise da colonização do H. pylori. O objetivo deste estudo foi avaliar quantitativamente, através de análise morfométrica, a colonização pelo H. pylori em biópsia de pacientes com diferentes lesões gástricas (gastrites e úlcera). Para o estudo utilizou-se biópsias gástricas de 239 pacientes (95 homens e 144 mulheres) com idade média de 45 anos, provenientes de diferentes municípios do estado de Pernambuco. Os cortes histológicos (4μm) foram corados pelo Giemsa e analisado através de microscopia óptica. O estudo morfométrico foi realizado por meio de um sistema digital de análise de imagens onde as áreas de interesse obtidas foram processadas utilizando-se o software OPTIMAS®. Os resultados indicam uma incidência de 39% de lesões inflamatórias gástricas associadas à infecção por Hp com maior ocorrência (60,3%) no gênero feminino e com faixa etária entre 31-45 anos. Quanto às lesões gástricas mais freqüentes observou-se que a gastrite crônica ativa foi a mais evidente em cerca de 90,2% dos casos estudados. Houve uma correlação positiva entre a análise qualitativa (semi-quantitativa) e a análise morfométrica (número médio de bacilos Hp, por área), principalmente quando se comparou os parâmetros numerosos bacilos com os moderados e raros . A partir destes dados pode-se concluir que os estudos referentes aos aspectos da infecção da mucosa gástrica pelo Hp, e mais especificamente os níveis de infecção quanto ao número de bacilos e extensão das áreas afetadas são de sua importância para que se possa conhecer melhor a evolução das lesões gástricas resultantes deste quadro infeccioso e em que situações e grupos humanos podem representar fatores de risco para o desenvolvimento de lesões mais graves como o câncer
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Benigno, Tiago Gomes da Silva. "Análise da resposta humoral contra H. pylori em pacientes portadores e não portadores de câncer gástrico". reponame:Repositório Institucional da UFC, 2013. http://www.repositorio.ufc.br/handle/riufc/10642.

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BENIGNO, Tiago Gomes da Silva. Análise da resposta humoral contra H. pylori em pacientes portadores e não portadores de câncer gástrico. 2013. 71 f. Dissertação (Mestrado em Cirurgia) - Universidade Federal do Ceará. Faculdade de Medicina, Fortaleza, 2013.
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Helicobacter pylori have accompanied humanity in all its migration routes across the planet. Being the cosmopolitan H.pylori bacteria that evolved and adapted the most adverse conditions through mutation and genetic exchange that resulted in favorable changes morph physiological. Such changes contributed to the development of highly virulent strains of bacteria which cause different pathophysiological conditions in the host. The high genetic variability of H. pylori hinders research to uncover associations with certain gastrointestinal conditions. However, bacterial virulence markers have been identified and associated with different gastrointestinal diseases. H. pylori strains that express proteins Cag A and Vac A has been found in patients with gastric cancer, others expressing Dup A and Oip A are found in patients with gastric ulcer were considered protective genes, since they are not related with development of gastric cancer. The methods used to detect H. pylori infection can be divided into invasive and non-invasive. The endoscopy is an invasive method is where the biopsy urease test to detect the presence of bacteria. The problem is that endoscopy can’t identify discrete points of colonization of H. pylori, or else, is indicated when the patient is already symptomatic, where you have a situation of advanced gastric epithelial cell injury. Among the non-invasive methods have serological methods. Among these serological methods have immunoblotting method that searches the presence of specific antibodies (Ig G). The antibodies against virulence factors and specific proteins (Cag A, Vac, Ure A, Ure B, and flagellar protein) serves both to detect infection and measure the type strain of H. pylori present in the infected individual. This method can be used to investigate the humoral response in patients with and without gastric cancer infected with H. pylori.
O Helicobacter pylori tem acompanhado a humanidade em todas as suas rotas de migração pelo planeta. Sendo o H.pylori uma bactéria cosmopolita que evoluiu e se adaptou as condições mais adversas através de mutações e troca de material genético que resultaram em mudanças morfofisiológicas favoráveis. Tais mudanças contribuíram no desenvolvimento de estirpes da bactéria altamente virulentas e que provocam diferentes condições fisiopatológicas no hospedeiro. A grande variabilidade genética do H.pylori dificulta a investigação para se descobrir associações com determinadas patologias gastrointestinais. No entanto, marcadores de virulência da bactéria já foram identificados e associados a diferentes doenças gastrointestinais. Cepas de H.pylori que expressam as proteínas Cag A e Vac A tem sido encontradas em pacientes com câncer gástrico, já outros que expressam Oip A e Dup A são encontrados em pacientes com úlcera gástrica sendo considerados como genes de proteção, pois não estão relacionados com o desenvolvimento de câncer gástrico. Os métodos utilizados para detectar a infecção pelo H.pylori se dividem em invasivos e não invasivos. A endoscopia é um método invasivo onde se faz a biopsia e teste da uréase para detectar a presença da bactéria. O problema é que endoscopia não consegue identificar discretos pontos de colonização do H. pylori, ou então, é indicada quando o paciente já esta sintomático, onde se tem uma situação avançada de injúria das células epiteliais gástricas. Entre os métodos não invasivos temos os métodos sorológicos. Entre esses métodos sorológicos temos o immunoblotting um método que pesquisa a presença de anticorpos específicos (Ig G). A pesquisa de anticorpos contra fatores de virulência e proteínas específicas (Cag A, Vac A, Ure A, Ure B, proteína flagelar), serve tanto para detectar a infecção como mensurar o tipo de cepa de H.pylori presente no individuo infectado. Podendo esse método ser utilizado para investigar a resposta humoral em pacientes com e sem câncer gástrico infectados com H.pylori.
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Książki na temat "H. pylori"

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B, Ernst Peter, Michetti Pierre i Smith, Phillip D., M.D., red. The immunobiology of H. pylori: From pathogenesis to prevention. Philadelphia, PA: Lippincott-Raven, 1997.

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Satō, Eisuke. H10-tokubetsu-023, H. pylori no kassei sanso taisha tokusei to idenshi ihen kikō no bunshironteki kaiseki: Heisei 10-nendo kenkyū hōkokusho : Kōseishō kōsei kagaku kenkyūhi hojokin kōsei kagaku tokubetsu kenkyū jigyō. [Japan: s.n.], 1999.

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Benjamin, James. H. Pylori: The Pro Guide on How to Treat and Prevent H. Pylori. Independently Published, 2022.

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ALDO, Adler. H. Pylori Cure Guide: Understanding the Disease, Everything on How to Strive, Prevent and Reverse H. Pylori Completely. Independently Published, 2022.

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Maxwell, Steve. Helicobacter Pylori Solution: The Complete Cure Guide on the Effect Treatment of H. Pylori. Independently Published, 2020.

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BESA, Berwin. Helicobacter Pylori Infection : Lost: Understand to Treat, Prevent, Strive and Reverse H. Pylori Infection. Independently Published, 2022.

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(Editor), Peter B. Ernst, Pierre Michetti (Editor) i Phillip D., M.D. Smith (Editor), red. The Immunobiology of H. Pylori: From Pathogenesis to Prevention. Lippincott Williams & Wilkins, 1997.

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Amelia, Benjamin. Healing Helicobacter Pylori: The Simple Cure Guide on the Most Effective Treatment from H. Pylori from Scratch. Independently Published, 2021.

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Graham, David Y., i Kathleen Graham-lomax. Contemporary Diagnosis And Management of H Pylori-associated Gastrointestinal Diseases. Handbooks in Health Care, 2002.

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Graham, David Y., i Kathleen S. Graham. Contemporary Diagnosis and Management of H pylori-Associated Gastrointestinal Diseases. Handbooks in Health Care, 1998.

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Części książek na temat "H. pylori"

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Mobley, H. L. T., i P. A. Foxall. "H. pylori urease". W Helicobacter pylori, 41–58. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1418-9_3.

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Tytgat, G. N. J., i L. A. Noach. "H. pylori eradication". W Helicobacter pylori, 550–69. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1418-9_53.

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Takafuta, Toshiro, i Kingo Fujimura. "Helicobacter pylori (H. pylori) Eradication". W Autoimmune Thrombocytopenia, 135–43. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4142-6_12.

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Lee, A., i H. Mitchell. "Basic bacteriology of H. pylori: H. pylori colonization factors". W Helicobacter pylori, 59–72. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1418-9_4.

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Figura, N., i J. E. Crabtree. "H. pylori vacuolating toxin". W Helicobacter pylori, 222–31. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1418-9_19.

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Mégraud, F. "H. pylori species heterogeneity". W Helicobacter pylori, 28–40. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1418-9_2.

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Salaspuro, M. "H. pylori alcohol dehydrogenase". W Helicobacter pylori, 232–42. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1418-9_20.

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Graham, D. Y., i R. M. Genta. "Reinfection with H. pylori". W Helicobacter pylori, 113–20. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1418-9_8.

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Rübe, Claudia E., Bernadine R. Donahue, Jay S. Cooper, Caspian Oliai, Yan Yu, Laura Doyle, Rene Rubin i in. "Helicobacter (H.) pylori". W Encyclopedia of Radiation Oncology, 306–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_367.

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Theisler, Charles. "H. Pylori Infection". W Adjuvant Medical Care, 149–50. New York: CRC Press, 2022. http://dx.doi.org/10.1201/b22898-164.

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Streszczenia konferencji na temat "H. pylori"

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Kittner, JM, L. Volksdorf, CC Adarkwah i M. Menges. "H. pylori-Eradikation: Versorgungsrealität in Deutschland". W Viszeralmedizin 2021 Gemeinsame Jahrestagung Deutsche Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS), Sektion Endoskopie der DGVS, Deutsche Gesellschaft für Allgemein und Viszeralchirurgie (DGAV). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1733507.

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Koumoutsos, Ioannis, John Klein, Elisabeta Compot, Sungjae Hwang, Alida Finze i Giovanni Tritto. "PTU-062 “The only good H. pylori is a dead H. pylori” – challenges in isolation and eradication". W British Society of Gastroenterology Annual Meeting, 17–20 June 2019, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-bsgabstracts.278.

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Atikov, A. S. "THE ASSOCIATION OF LIVER PATHOLOGIES WITH THE CONTAMINATION OF THE GASTROINTESTINAL TRACT WITH H.PYLORI". W SPbVetScience. FSBEI HE St. Petersburg SUVM, 2023. http://dx.doi.org/10.52419/3006-2023-11-9-16.

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Currently, one of the most promising areas in bacteriology is the study of the bacterium Helicobacter pylori. New studies show a link between H. pylori and some liver diseases, but their exact mechanisms and connections are still not fully understood. Despite this, studies of H. pylori and its association with liver diseases remain relevant to this day. This article presents an analysis of the association of H. Pylori with liver diseases.
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Çavuş, B., T. Çavuş, B. Akyüz Erdoğan i E. Kumcu. "ERYTHROCYTE DISTRIBUTION WIDTH (RDW) AND HELICOBACTER PYLORI (H. PYLORI) INFECTION: IS THERE AN ASSOCIATION?" W ESGE Days 2018 accepted abstracts. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1637463.

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Шишкина, Виктория, Светлана Клочкова, Наталия Алексеева, Наталья Самодурова, Ольга Герасимова, Татьяна Самойленко i Любовь Антакова. "Морфофункциональные особенности тучных клеток при инфицировании Helicobacter pylori". W Международная научная и методическая конференция, посвященная году фундаментальных наук: "Современные аспекты морфологии, патоморфологии и онкопатологии организма человека". ФГБОУ ВО КГМУ Минздрава России, 2022. http://dx.doi.org/10.21626/cb.22.humanmorphology/32.

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Одними из ключевых промоторов в регуляции каскада воспалительных медиаторов являются тучные клетки, обладающие широким арсеналом биологически активных веществ. В патогенезе гастрита, ассоциированного с H. pylori принимают активное участие различные виды иммунокомпетентных клеток - макрофаги, нейтрофилы, эозинофилы, дендритные клетки, Т- и В-лимфоциты, а также тучные клетки. Антигенпредставляющие свойства тучных клеток представляют интерес в аспекте взаимодействия с Helicobacter pylori (H. Pylori)
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Ferreira, Shirley Cristina Reis, Luísa Neiva Araújo, Sérgio Rubens Lacerda Morais, Maria Fernanda Soares Batista i Silvia Fernandes Ribeiro da Silva. "MÉTODOS DIAGNÓSTICOS DE INFECÇÃO POR H. PYLORI: UMA REVISÃO LITERÁRIA". W I Congresso Brasileiro de Doenças Infectocontagiosas On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/2226.

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Introdução: A infecção pela bactéria Helicobacter pylori (H. pylori) é mundialmente frequente e relaciona-se a doenças, como dispepsia, úlcera péptica e neoplasias gástricas. É um bastonete espiralado, multiflagelado e gram negativo, que provoca a destruição gradativa das camadas gástricas e duodenais. Objetivo: Revisar os principais métodos que identificam a presença da bactéria H. pylori no TGI. Material e métodos: Este resumo foi realizado com base em uma pesquisa bibliográfica qualitativa exploratória feita nas bases de dados PubMed e SciELO utilizando H. pylori, pathogenicity e diagnosis como descritores. Foram incluídos 10 artigos dos últimos 5 anos. Resultados: A histologia e/ou cultura e exame direto da amostra de biópsia gástrica é padrão ouro para o diagnóstico da infecção pelo H. pylori, com sensibilidade e especificidade de até 95% e 98%, respectivamente. Porém, devido a necessidade de endoscopia para obtenção da amostra, são considerados métodos invasivos, mas fundamentais para o diagnóstico e avaliação do(a): a) grau da inflamação; b) presença de úlceras; e c) gravidade da gastrite. Além disso, pode identificar linfoma MALT e câncer. O teste rápido da urease (RUT), que também necessita da endoscopia para a sua realização, a análise da amostra do patógeno em fezes ou teste do antígeno fecal, a detecção de anticorpos anti-H. pylori e os testes baseados em reação em cadeia da polimerase (PCR), que detecta os genes de virulência, também são opções utilizadas. Alguns autores relatam que há uma relação direta dos genes de virulência com as possíveis manifestações clínicas. Conforme consenso internacional, um único teste não invasivo positivo é fundamental para indicação de endoscopia com avaliação histológica. Embora, o teste respiratório de uréia, possa apresentar resultados falso-positivos, é utilizado, bem como o teste de antígeno fecal, para detectar a erradicação da bactéria durante o tratamento. Conclusão: Os principais métodos diagnósticos utilizados para a confirmação da presença da bactéria H. pylori são testes invasivos, com endoscopia associada à biópsia, sendo a amostra obtida analisada por histologia, cultura, RUT e PCR. Os testes não invasivos sinalizam o uso de testes invasivos para confirmar patologias associadas à infecção e avaliam a erradicação da bactéria durante o tratamento.
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M.Hussein, Ali, Nadir Nanakali i Mohammed M.Hussein. "EFFECT OF HYPERICUM PERFORATUM ON GASTRIC ULCER IN RAT". W 4th International Conference on Biological & Health Sciences (CIC-BIOHS’2022). Cihan University, 2022. http://dx.doi.org/10.24086/biohs2022/paper.742.

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Gastric ulcer is a chronic condition that occurs when the mucosa of the stomach is broken. There is a physiological equilibrium between aggressive factors and mucosal defense. This study aimed to determine the prevention level and efficiency of herbal medicinal plants (Hypericum perforatum) and compared with the omeprazole drug.Many groups were prepared from Albino male rats, first control group (inoculate with H. pylori and fed with standard pellet), Second group, rats inoculated by H. pylori and prevented with aqueous extract H. perforatum in two dosages (250mg/kg, 500mg/kg), Third group inoculated by H. pylori and prevented with standard drug omeprazole at the dose (20mg/kg).The result showed that H. perforatum inhibits (50.65%) stomach ulcer formation with a high dose. Omeprazole's' group results showed (24.50%) stomachs ulcer formation. Although the result of the current study improves, a high dosage of aqueous extracts of plants has more effectiveness than the low dosage of aqueous extracts of plants.
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Devyatko, A. O., T. A. Noskova i N. V. Shevchenko. "EXPERIENCE OF USING THE TEST SYSTEM «GASTROPANEL» IN THE PREVENTIVE MEDICAL EXAMINATION OF WORKFORCE IN JSC RZD". W The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-173-176.

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Abstract: Non-invasive diagnosis of the gastric mucosa was carried out in 181 people in the preventive medical examination of workforce in JSC RZD. A set of diagnostics from Vector-Best (Novosibirsk, Russia) was used for enzyme immunoassay of pepsinogen I, pepsinogen II, and immunoglobulins for Helicobacter pylori. The prevalence of H. pylori infection in more than half of the employees, the presence of deviations of biomarkers from the norm in more than one in three employees were revealed. Laboratory signs of atrophy were detected eight times less frequently than signs of inflammation of the gastric mucosa, but when infected with H. pylori and increased with age.
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Kandulski, A., W. Schirrmeister, C. Langner, A. Link i P. Malfertheiner. "H. pylori-induzierte Th17 Immunantwort ex vivo und in vitro". W Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604842.

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Yu, Guoqin. "Abstract 608: Examining H. pylori core genes for epidemiological typing". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-608.

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