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Related Concept Videos

Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...

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Updated: Jun 16, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

P-selectin-dependent platelet aggregation and apoptosis may explain the decrease in platelet count during

Jeng-Jung Yeh1, Sharon Tsai, Deng-Chyang Wu

  • 1Institute of Biomedical Sciences, Sun Yat-Sen University, Kaohsiung, Taiwan.

Blood
|January 26, 2010
PubMed
Summary
This summary is machine-generated.

Helicobacter pylori infection triggers P-selectin-dependent platelet aggregation and phosphatidylserine expression, leading to decreased platelet counts. This study clarifies P-selectin

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Last Updated: Jun 16, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

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Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
05:49

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Published on: November 29, 2024

Area of Science:

  • Immunology
  • Microbiology
  • Hematology

Background:

  • P-selectin expression is observed in Helicobacter pylori-infected individuals.
  • H. pylori infection is linked to platelet disorders like idiopathic thrombocytopenic purpura.
  • The precise role of P-selectin in H. pylori infection is not fully understood.

Purpose of the Study:

  • To investigate the association between P-selectin expression and platelet aggregation during H. pylori infection.
  • To elucidate the mechanisms by which H. pylori influences platelet function and count.

Main Methods:

  • Flow cytometry was used to analyze H. pylori-platelet adhesion.
  • P-selectin and phosphatidylserine (PS) expression levels were measured.
  • Bacterial strains, including pro-aggregatory and non-aggregatory H. pylori, were utilized.

Main Results:

  • High levels of adhesion were observed between pro-aggregatory H. pylori and platelets.
  • H. pylori IgG is necessary for inducing P-selectin expression.
  • P-selectin release is crucial for H. pylori-induced platelet aggregation.
  • Platelet aggregates showed signs of apoptosis, including membrane blebbing.
  • PS expression was detected on platelets during infection with both aggregatory and non-aggregatory H. pylori strains.

Conclusions:

  • H. pylori infection induces platelet aggregation and phosphatidylserine expression.
  • P-selectin-dependent aggregation and PS expression contribute to the reduction in platelet counts during H. pylori infection.
  • H. pylori IgG plays a key role in initiating these platelet-altering mechanisms.