lymphocytic choriomeningitis/hypoxia

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Hypoxia induces the gene expression and extracellular transmission of persistent lymphocytic choriomeningitis virus.

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The physiological context of virus-infected cells can markedly affect multiplication and spread of the virus progeny. During persistent infection, the virus exploits the host cell without disturbing its vital functions. However, microenvironmental hypoxia can uncouple this intimate relationship and

[Acid-base balance and electrolytes in cerebrospinal fluid of patients with bacterial and lymphocytic meningitis].

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Acid-base balance and electrolytes concentration in cerebrospinal fluid (CSF) of patients with bacterial and lymphocytic meningitis were assessed. Inflammatory process causing the damage of blood-brain barrier and brains hypoxia leads to statistically significant changes of pH, pO2, bicarbonates and

The permeability of the blood-brain barrier in mice suffering from fatal lymphocytic choriomeningitis virus infection.

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The ultrastructure and the blood-brain-barrier (BBB) permeability were studied in mice suffering from lymphocytic choriomeningitis (LCM). Brains and meninges from mice suffering from LCM virus-induced lymphocytic choriomeningitis were studied by investigating the BBB function and by electron and

Quantitative Proteomics Reveal Peroxiredoxin Perturbation Upon Persistent Lymphocytic Choriomeningitis Virus Infection in Human Cells.

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Experimental data indicate that during persistent infection, lymphocytic choriomeningitis virus (LCMV) may both directly or indirectly modulate regulatory cellular processes and alter cellular functions that are not critical for survival, but are essential for cell homeostasis. In order to shed more

Solid organ transplant donors with central nervous system infection.

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BACKGROUND While donor-derived infections (DDI) remain uncommon, multiple reports describe DDI with pathogens that cause central nervous system (CNS) infection resulting in significant recipient disease. The Ad Hoc Disease Transmission Advisory Committee (DTAC) reviewed the records of potential

HIF1A is a critical downstream mediator for hemophagocytic lymphohistiocytosis.

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Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening syndrome characterized by overwhelming immune activation. A steroid and chemotherapy-based regimen remains as the first-line of therapy but it has substantial morbidity. Thus, novel, less toxic therapy for HLH is urgently needed.

The feasibility of altering the immunogenicity of grafts.

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Most attempts to prolong the survival of allografts have involved treatment of the host to impair its capacity to reject them. Early uncritical attempts to treat the graft rather than the host were received with skepticism because of the prevailing belief that the alloantigens on cell surfaces are

5,6-Dimethylxanthenone-4-acetic acid treatment of a non-immunogenic tumour does not synergize with active or passive CD8+ T-cell immunotherapy.

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The chemotherapeutic drug 5,6-dimethylxanthenone-4-acetic acid (DMXAA) inhibits intratumoural blood flow, causing hypoxia, haemorrhagic necrosis, vascular collapse and tumour cell death. Production of TNF-alpha and IFN is also induced, causing local inflammation and activation of immune cells

Alterations in cellular metabolism modulate CD1d-mediated NKT-cell responses.

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Natural killer T (NKT) cells play a critical role in the host's innate immune response. CD1d-mediated presentation of glycolipid antigens to NKT cells has been established; however, the mechanisms by which NKT cells recognize infected or cancerous cells remain unclear. 5(')-AMP activated protein

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