当社グループは 3,000 以上の世界的なカンファレンスシリーズ 米国、ヨーロッパ、世界中で毎年イベントが開催されます。 1,000 のより科学的な学会からの支援を受けたアジア および 700 以上の オープン アクセスを発行ジャーナルには 50,000 人以上の著名人が掲載されており、科学者が編集委員として名高い
。オープンアクセスジャーナルはより多くの読者と引用を獲得
700 ジャーナル と 15,000,000 人の読者 各ジャーナルは 25,000 人以上の読者を獲得
Neelapu NRR, Nammi D, Pasupuleti ACM and Surekha C
Helicobacter pylori infection induces gastric inflammation, ulcer, and cancer. H. pylori infection is coordinated in a cascade manner that helps it to colonize in the host. Colonization of bacterium starts by adapting itself to the harsh acidic environment in the stomach. H. pylori has the necessary machinery to neutralise the pH of its surroundings. It also has the ability to sense the pH of its surroundings and move towards the less acidic region. H. pylori’s next hurdle is gastric mucosal barrier in the stomach and it has the capability to overcome this gastric mucosal barrier. Once the gastric mucosal barrier is weakened, pathogen uses different adhesion molecules to adhere to the epithelial lining of the stomach. Pathogen then establishes interaction with the host using several toxins that indirectly leads to development of inflammation or gastritis. Prolonged inflammation damages epithelial cells leading to ulcers in the stomach. Genetic changes in the host cell due to H. pylori infection leads to development of gastric cancer. The present paper reviews in detail H. pylori induced gastritis, gastric ulcers and gastric cancer.