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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.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
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Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

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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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Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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Ciencia básica y patogénesis

Fei Liu1, Ruozhen Wu1,2, Dandan Chu1,3

  • 1New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 25, 2025
PubMed
Resumen
Este resumen es generado por máquina.

La eliminación de los extremos N y C de la tau crea agregados de tau que imitan la patología de la enfermedad de Alzheimer. Estos agregados de tau truncada promueven una mayor agregación y hiperfosforilación de tau en células y cerebros de ratón.

Palabras clave:
tau truncadaagregados de tauenfermedad de Alzheimerhiperfosforilaciónpatología de tau

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Área de la Ciencia:

  • Neurociencia
  • Bioquímica
  • Patología

Sus antecedentes:

  • Los ovillos neurofibrilares (NFT) compuestos de tau hiperfosforilada son clave en la enfermedad de Alzheimer (EA).
  • La patología de tau se propaga a través de mecanismos similares a los priones, originándose en regiones cerebrales específicas y progresando con el tiempo.
  • En la EA, la tau pierde sus extremos N y C, lo que podría impulsar la autoagregación y la progresión de la enfermedad.

Objetivo del estudio:

  • Investigar el papel de la deleción de los extremos de tau en la agregación de tau y las propiedades proteopáticas.
  • Determinar si la tau truncada puede inducir patología de tau in vitro e in vivo.

Principales métodos:

  • Se generó una proteína tau truncada (tau151-391) que carece de los extremos N y C.
  • Se indujo la agregación de tau mediante ultracentrifugación y se sobreexpresó en células HEK-293T.
  • Se evaluaron la fosforilación y las propiedades proteopáticas in vitro e in vivo.

Principales resultados:

  • La tau truncada (tau151-391) formó agregados en células y cerebros de ratón, a diferencia de la tau de longitud completa.
  • La tau151-391 agregada estaba hiperfosforilada y parcialmente resistente a la digestión con proteinasa K.
  • Los agregados de tau151-391 indujeron una mayor agregación y hiperfosforilación de tau en células y cerebros de ratón.

Conclusiones:

  • La deleción de los extremos N y C de la tau promueve la agregación y confiere características proteopáticas.
  • Los agregados de tau151-391 son inductores potentes de la agregación de tau y la hiperfosforilación sitio-específica.