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Related Concept Videos

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

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In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
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Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

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Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
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Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

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Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
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Prokaryotic Transcriptional Activators and Repressors01:58

Prokaryotic Transcriptional Activators and Repressors

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The organization of prokaryotic genes in their genome is notably different from that of eukaryotes. Prokaryotic genes are organized, such that the genes for proteins involved in the same biochemical process or function are located together in groups. This group of genes, along with their regulatory elements, are collectively known as an operon. The functional genes in an operon are transcribed together to give a single strand of mRNA known as polycistronic mRNA.
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The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
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Groupthink

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When in group settings, we are often influenced by the thoughts, feelings, and behaviors around us. Groupthink is another phenomenon of conformity where modification of the opinions of members in a group aligns with what they believe is the group consensus (Janis, 1972). In such situations, the group often takes action that individuals would not perform outside the group setting because groups make more extreme decisions than individuals do. Moreover, groupthink can hinder opposing trains of...
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In Vitro Cellular Activity Evaluation of the Nanoemulsion Vaccine Adjuvant Ophiopogonin D
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Adjuvant polyarthritis. II. Suppression by tilorone

Y H Chang

    The Journal of Pharmacology and Experimental Therapeutics
    |October 1, 1977
    PubMed
    Summary

    Tilorone suppressed arthritis and immune responses in a dose-dependent manner. Its anti-inflammatory and immunomodulatory effects did not fully explain its antiarthritic action, suggesting a potential role for interferon induction.

    Area of Science:

    • Immunology
    • Pharmacology
    • Rheumatology

    Background:

    • Adjuvant-induced arthritis is a model for rheumatoid arthritis.
    • Tilorone is an immunomodulatory compound with known anti-inflammatory properties.

    Purpose of the Study:

    • To investigate the effects of tilorone on adjuvant-induced arthritis.
    • To elucidate the mechanisms underlying tilorone's antiarthritic activity, including its impact on cell-mediated and humoral immune responses.
    • To explore the potential role of interferon induction in tilorone's therapeutic effects.

    Main Methods:

    • Administration of tilorone at varying doses (5-35 mg/kg/day) to rats with adjuvant-induced arthritis.
    • Assessment of cell-mediated and humoral immune responses to EL4 cells.
    • Evaluation of tilorone's anti-inflammatory effects using carrageenan-induced inflammation model.

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  • Analysis of dose-dependency of tilorone's effects.
  • Main Results:

    • Tilorone suppressed adjuvant-induced arthritis and cell-mediated immunity in a dose-related manner.
    • Tilorone exhibited biphasic effects on humoral immunity: stimulatory at low doses and inhibitory at high doses.
    • Tilorone reduced acute inflammation induced by carrageenan.
    • The anti-inflammatory and immunomodulatory effects of tilorone did not fully account for its antiarthritic efficacy.

    Conclusions:

    • Tilorone demonstrates significant antiarthritic properties.
    • The mechanism of action for tilorone's antiarthritic effect may involve interferon induction, independent of its direct anti-inflammatory or immunomodulatory actions.