Related Experiment Video

Updated: Jul 6, 2026

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
07:30

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

[Pathogenesis of the lethal postoperative cerebral inflammatory-purulent complications in neurooncological patients]

O Ia Hlavats'kyĭ, S M Lysenko, O L Koliada

    Klinichna Khirurhiia
    |April 12, 2008
    PubMed

    More Related Videos

    Modelling Brain Metastasis: Standardized Analysis of Metastatic Colonization and Histological Growth Patterns by Stereotactic Intracortical Injection07:42

    Modelling Brain Metastasis: Standardized Analysis of Metastatic Colonization and Histological Growth Patterns by Stereotactic Intracortical Injection

    Published on: January 16, 2026

    Related Concept Videos

    Bacterial Meningitis II: Pathophysiology01:26

    Bacterial Meningitis II: Pathophysiology

    Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
    Brain Abscess l: Introduction01:26

    Brain Abscess l: Introduction

    A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...
    Bacterial Meningitis I: Introduction01:22

    Bacterial Meningitis I: Introduction

    Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
    Cryptococcal Meningitis01:27

    Cryptococcal Meningitis

    Cryptococcal meningitis is a life-threatening opportunistic infection predominantly associated with HIV/AIDS, accounting for over 100,000 deaths annually worldwide. However, it also affects individuals with other forms of immunosuppression, including those undergoing immunosuppressive therapy, organ transplant recipients, patients with innate immunodeficiencies, and individuals with hematological disorders. The infection is caused mainly by Cryptococcus neoformans and Cryptococcus gattii,...
    Cytotoxic Edema: Pathophysiology01:21

    Cytotoxic Edema: Pathophysiology

    Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
    Ischemic Stroke ll: Pathophysiology01:15

    Ischemic Stroke ll: Pathophysiology

    An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...