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Related Concept Videos

Genome-wide Association Studies-GWAS01:11

Genome-wide Association Studies-GWAS

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Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
GWAS does not require the identification of the target gene involved in...
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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Rheumatic Heart Disease I: Introduction01:23

Rheumatic Heart Disease I: Introduction

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Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies01:22

Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies

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The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
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Connective Tissue Cell Types01:22

Connective Tissue Cell Types

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Connective tissue develops from the mesoderm of a developing embryo and consists of cells, fibers, and ground substance: a gel-like material containing large complexes of carbohydrates and proteins. Connective tissue was first identified as a separate tissue family in the 18th century, and Johannes Peter Muller coined the term connective tissue.
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Related Experiment Video

Updated: Mar 19, 2026

Preliminary Study on Acupuncture Combined with Grain-sized Moxibustion for Treating Rheumatoid Arthritis with Finger Joint Pain
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[Basic research overview in rheumatoid arthritis].

Yukiko Iwasaki, Kazuhiko Yamamoto

    Nihon Rinsho. Japanese Journal of Clinical Medicine
    |June 18, 2016
    PubMed
    Summary

    Rheumatoid arthritis (RA) is an autoimmune disease causing joint inflammation. This review explores the unknown causes of RA, focusing on genetic and environmental factors contributing to its pathogenesis.

    Area of Science:

    • Immunology
    • Pathogenesis of autoimmune diseases

    Context:

    • Rheumatoid arthritis (RA) affects 0.5-1.0% of the global population.
    • RA involves synovial inflammation, cartilage/bone erosion, and autoantibody production (RF, ACPA).
    • Despite therapeutic advances, RA's etiology remains unclear.

    Purpose:

    • To review recent advances in understanding RA pathogenesis.
    • To address key questions regarding genetic-environmental interactions, joint-specific inflammation, and chronic synovial inflammation.
    • To highlight insights from basic research into RA mechanisms.

    Summary:

    • RA pathogenesis involves complex interactions between genetic predisposition and environmental triggers.
    • The review examines the mechanisms underlying joint-localized inflammation in RA.

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  • Key cellular and molecular players perpetuating synovial inflammation are discussed.
  • Impact:

    • Provides a comprehensive overview of current RA pathogenetic research.
    • Identifies critical knowledge gaps in understanding RA onset and progression.
    • Informs future research directions for novel RA therapeutics.