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Related Concept Videos

Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

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Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
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In a three-phase circuit, line loss is an indicator of energy dissipated as heat due to the resistance of transmission lines. To address this, incorporating transformers into the system—a step-up transformer at the source and a step-down transformer at the load—is a strategic solution. Two three-phase transformers are introduced to improve this.
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The signs and symptoms of fever include hot and dry skin, flushed face, thirst, muscle aches, anorexia, headache, tachycardia, tachypnea, and fatigue. Elevated body temperature is reduced using two methods: pharmacological and nonpharmacological. Proper identification and treatment of the root cause of a fever is of utmost importance.
Pharmacological Methods of Reducing Fever:
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The microscopic anatomy of the liver is a complex and intricate system that comprises numerous structural units known as liver lobules, each of which is comparable in size to a sesame seed. These hexagonal structures consist of plates of liver cells or hepatocytes, which are characterized by their versatility and abundance of cellular apparatus like rough and smooth ER, Golgi apparatus, peroxisomes, and mitochondria.
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The liver, an essential organ in the human body, performs over 200 vital functions that can be broadly categorized into metabolic, hematological, endocrine regulation, and bile production.
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Related Experiment Video

Updated: Feb 4, 2026

The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
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Dabigatran Reduces Liver Fibrosis in Thioacetamide-Injured Rats.

Kuei-Chuan Lee1,2, Wei-Fan Hsu3,4, Yun-Cheng Hsieh1,2

  • 1Division of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, #201, Section 2, Shih-Pai Road, Taipei 112, Taiwan.

Digestive Diseases and Sciences
|October 6, 2018
PubMed
Summary

Dabigatran, a direct thrombin inhibitor, effectively reduced liver fibrosis and angiogenesis in rats by inhibiting thrombin activity. This suggests dabigatran as a potential therapeutic for liver fibrosis.

Keywords:
DabigatranIntrahepatic angiogenesisLiver fibrosisPortal pressureThrombin

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A Mouse Model of Chronic Liver Fibrosis for the Study of Biliary Atresia
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Area of Science:

  • Hepatology
  • Pharmacology
  • Biochemistry

Background:

  • Liver fibrosis is a progressive condition with limited treatment options.
  • Thrombin plays a key role in activating hepatic stellate cells (HSCs), driving fibrosis.
  • Investigating direct thrombin inhibitors like dabigatran offers a novel therapeutic strategy.

Purpose of the Study:

  • To evaluate the efficacy of dabigatran, a direct thrombin inhibitor, in ameliorating liver fibrosis.
  • To explore dabigatran's effects on hepatic stellate cell activation and intrahepatic angiogenesis.
  • To assess dabigatran's impact on portal hypertension in a rat model of liver fibrosis.

Main Methods:

  • Liver fibrosis was induced in Sprague-Dawley rats using thioacetamide (TAA) for 8 or 12 weeks.
  • Dabigatran etexilate was administered orally during the final 4 weeks of TAA treatment.
  • Control groups received saline or vehicle, with subsequent analysis of liver tissue and hemodynamic parameters.

Main Results:

  • Dabigatran significantly reduced liver fibrosis, fibrin deposition, and phosphorylated ERK1/2 in TAA-induced rats.
  • In vitro studies confirmed dabigatran's inhibition of thrombin-induced HSC activation.
  • Treatment with dabigatran decreased intrahepatic angiogenesis and portal hypertension in fibrotic rats.

Conclusions:

  • Dabigatran effectively mitigates liver fibrosis and intrahepatic angiogenesis by inhibiting thrombin.
  • The findings support dabigatran's potential as a therapeutic agent for liver fibrosis.
  • Further research is warranted to explore dabigatran's clinical application in liver disease.