Idiopathic Intracranial Hypertension: A Case Report.

Idiopathic Intracranial Hypertension is a rare occurrence in young, physically fit male and a diagnosis of exclusion among most patients presenting with signs and symptoms of raised intracranial pressure. Here we describe a case of a young male in the ideal weight range with no previous exposure to offending chemicals presented with a history of headache, obscuration of vision, and photopsia. On examination, there were no positive neurological findings. Increased opening pressure was found on the lumbar puncture. Ophthalmological examination revealed bilateral papilledema. Humphrey’s Visual field test showed peripheral field loss. Magnetic resonance imaging scan of the brain and orbits were normal. The patient was diagnosed and managed in primary care setting after neurosurgical consultation. Though rare, we should suspect idiopathic intracranial hypertension in ideal body weighted male if the headache is persistent after other causes of headache have been ruled out.

Toll-Like Receptor 2 Targeted Rectification of Impaired CD8⁺ T Cell Functions in Experimental Leishmania donovani Infection Reinstates Host Protection.

Leishmania donovani, a protozoan parasite, causes the disease visceral leishmanisis (VL), characterized by inappropriate CD8+ T-cell activation. Therefore, we examined whether the Toll-like Receptor 2 (TLR2) ligand Ara-LAM, a cell wall glycolipid from non-pathogenic Mycobacterium smegmatis, would restore CD8+ T-cell function during VL. We observed that by efficient upregulation of TLR2 signaling-mediated NF-κB translocation and MAPK signaling in CD8+ T-cells (CD25+CD28+IL-12R+IFN-γR+), Ara-LAM triggered signaling resulted in the activation of T-bet, which in turn, induced transcription favourable histone modification at the IFN-γ, perforin, granzyme-B promoter regions in CD8+ T-cells. Thus, we conclude that Ara-LAM induced efficient activation of effector CD8+ T-cells by upregulating the expression of IFN-γ, perforin and granzyme-B in an NF-κB and MAPK induced T-bet dependent manner in VL.