tuberculoma/hypoxia

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[A case of tuberculous meningitis with pleural effusion as a manifestation of a paradoxical reaction during anti-tuberculosis therapy].

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We present a case of tuberculous meningitis (TBM), wherein pleural effusion developed as a manifestation of paradoxical reaction during anti-tuberculosis therapy. An 87-year-old diabetic man was referred to our clinic for fever and impaired consciousness. He did not obey vocal commands. No ocular

Pulmonary arteriovenous malformation: An uncommon disease with common presentation.

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A 45-year-old male presented with massive hemoptysis, clubbing in all limbs, disproportionate hypoxia and persistent ill-defined shadow in left lower zone in chest radiograph since his childhood. The patient received empirical anti-tuberculosis treatment and the chest X-ray finding was

Paroxysmal Autonomic Instability with Dystonia after Severe Traumatic Brain Injury

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Background: Paroxysmal autonomic instability with dystonia (PAID) syndrome, a subset of dysautonomia, is characterized by paroxysms of marked agitation, diaphoresis, hyperthermia, hypertension, tachycardia and tachypnea accompanied by

Local ischemia and increased expression of vascular endothelial growth factor following ocular dissemination of Mycobacterium tuberculosis.

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The pathogenesis of intraocular tuberculosis remains poorly understood partly due to the lack of adequate animal models that accurately simulate human disease. Using a recently developed model of ocular tuberculosis following aerosol infection of guinea pigs with Mycobacterium tuberculosis, we

tRNA-mediated codon-biased translation in mycobacterial hypoxic persistence.

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Microbial pathogens adapt to the stress of infection by regulating transcription, translation and protein modification. We report that changes in gene expression in hypoxia-induced non-replicating persistence in mycobacteria-which models tuberculous granulomas-are partly determined by a mechanism of

Interception of host angiogenic signalling limits mycobacterial growth.

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Pathogenic mycobacteria induce the formation of complex cellular aggregates called granulomas that are the hallmark of tuberculosis. Here we examine the development and consequences of vascularization of the tuberculous granuloma in the zebrafish-Mycobacterium marinum infection model, which is

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