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Infection01:20

Infection

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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...
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The pathophysiology of urinary tract infections (UTIs) encompasses several progressive stages, beginning with bacterial colonization and culminating in potential systemic complications if untreated. UTIs are primarily initiated by bacteria, such as Escherichia coli, which often originate from the gastrointestinal tract and migrate to the urinary system through the periurethral area. This migration can occur via several routes, including improper hygiene practices, sexual activity, or...
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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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The pathophysiology of pneumonia involves the following steps:
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Stages of Infection

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Stages of infection describe what happens to a susceptible host once a pathogen invades the human body. The stages of infection are incubation, prodromal, illness, stage of decline, and convalescence. The incubation stage is the period from exposure to a pathogen until symptoms start. The infected person is unaware of impending illness as the pathogens grow and multiply within the body. The duration may vary depending on the type of infection. The incubation period of measles averages ten to...
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Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
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Video Experimental Relacionado

Updated: Jan 7, 2026

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
09:07

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses

Published on: June 14, 2020

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Ciencia básica y patogénesis

Michelle Gk Tan1,2, Frances Tw Lim2, Clara Yb Low1

  • 1Singapore General Hospital, Singapore, Singapore.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 24, 2025
PubMed
Resumen

La tirosina quinasa FynT promueve la neuroinflamación y la neurodegeneración en la enfermedad de Alzheimer (EA) y la demencia con cuerpos de Lewy (ECL). La reducción de FynT puede ofrecer una estrategia terapéutica para estas afecciones.

Palabras clave:
tirosina quinasa FynTneuroinflamaciónenfermedad de Alzheimerdemencia con cuerpos de Lewyneurodegeneración

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Área de la Ciencia:

  • Neurociencia
  • Biología Molecular
  • Inmunología

Sus antecedentes:

  • La tirosina quinasa FynT se regula al alza en los cerebros de pacientes con enfermedad de Alzheimer (EA) y demencia con cuerpos de Lewy (ECL).
  • La expresión de FynT se correlaciona con la patología tau y la neuroinflamación.
  • Se implica a FynT en la activación del inflamasoma NLRP3 por microglía, lo que exacerba la neuroinflamación.

Objetivo del estudio:

  • Investigar el papel de FynT en la activación de la microglía y la señalización de inflamasomas en la EA y la ELC.
  • Determinar si FynT modula la neuroinflamación y la neurodegeneración.

Principales métodos:

  • Se analizaron los marcadores de FynT, microglía e inflamasomas en tejidos cerebrales post mortem de casos de EA, ELC y controles mediante RT-PCR.
  • Se examinaron ratones P301S con tauopatía de edad avanzada con y sin depleción de FynT para detectar cambios en la expresión génica.

Principales resultados:

  • Los marcadores de microglía e inflamasomas se regularon al alza en los cerebros de EA y ELC, lo que se correlacionó con la expresión de FynT.
  • La depleción de FynT en ratones P301S redujo significativamente la activación de la microglía y los marcadores de inflamasomas.
  • Estos hallazgos sugieren un papel directo de FynT en los procesos neuroinflamatorios.

Conclusiones:

  • La tirosina quinasa FynT contribuye a la activación de la microglía y los inflamasomas, impulsando la neuroinflamación y la neurodegeneración.
  • La depleción dirigida de FynT presenta una estrategia terapéutica potencial para la EA y enfermedades neurodegenerativas relacionadas.