Understanding the expression and trafficking of Plasmodium falciparum Maurer’s clefts proteins

Malaria is a potentially fatal disease caused by parasites in the genus Plasmodium. Of the five species that cause human malaria, P. falciparum causes an estimated 1 million deaths annually, particularly in young children in sub-Saharan Africa. Plasmodium falciparum is most commonly found in tropical and subtropical regions of the world. After invasion into human red blood cells, parasite induced transport structures known as Maurer\u27s clefts, are formed within red cells. In previous studies, two Maurer\u27s clefts proteins were identified; an approximately 130 kDa peripheral membrane protein and a 20-kDa integral membrane protein. Immunofluorescence and confocal microscopy identified both proteins within large cytoplasmic vesicles in the red cell cytoplasm. The 20 kDa protein, known as P. falciparum Maurer\u27s cleft two transmembrane protein (PfMC2TM), is encoded by a family of genes identified using proteomic analysis of immune complexes (IC). The gene encoding the 130 kDa protein is unknown. Furthermore, the mechanism of protein trafficking after protein expression is also unknown. Our goal in this study was to prepare IC using schizont extracts for use in proteomic analysis to identify the gene encoding the 130 kDa protein, identify the pathway of protein traffic using Brefeldin A (BFA) in P. falciparum cultures and perform bioinformatics analysis of the PfMC2TM gene family using the database, PlasmoDB (plasmodb.org). The 110 kDa Rhop-3 rhoptry protein and PfMC2TM were identified using immunoprecipitation and western blotting analysis of parasite extracts prepared with Triton X-100 in stage specific and BFA treated parasites. PfMC2TM proteins encoded by family members in P. falciparum strains 3D7 and IT were compared to one another and across species in P. reichenowi. Among the proteins encoded by paralogs in P. falciparum, there were some differences found. However, there was no reported expression data annotated for P. reichenowi within PlasmoDB. Increasing knowledge of the Maurer\u27s clefts proteins is crucial in understanding P. falciparum biology and the role of the clefts in malaria vaccine development.https://engagedscholarship.csuohio.edu/u_poster_2016/1010/thumbnail.jp

New England Medical Center Posterior Circulation Stroke Registry II. Vascular Lesions

Among 407 New England Medical Center Posterior Circulation Registry (NEMC-PCR) patients, the extracranial (ECVA) and intracranial vertebral arteries (ICVA) were the commonest sites of severe occlusive disease followed by the basilar artery (BA). Severe occlusive lesions were found in >1 large artery in 148 patients; 134 had unilateral or bilateral severe disease at one arterial location. Single arterial site occlusive disease occurred most often in the ECVA (52 patients, 15 bilateral) followed by the ICVA (40 patients, 12 bilateral) and the BA (46 patients). Involvement of the ICVAs and the BA was very common and some patients also had ECVA lesions. Hypertension, smoking, and coronary and peripheral vascular disease were most prevalent in patients with extracranial disease while diabetes and hyperlipidemia were more common when occlusive lesions were only intracranial. Intra-arterial embolism was the most common mechanism of brain infarction in patients with ECVA and ICVA occlusive disease. ICVA occlusive lesions infrequently caused infarction limited to the proximal territory (medulla and posterior inferior cerebellum). BA lesions most often caused infarcts limited to the middle posterior circulation territory (pons and anterior inferior cerebellum). Posterior cerebral artery occlusive lesions were predominantly embolic. Penetrating artery disease caused mostly pontine and thalamic infarcts. Prognosis was poorest in patients with BA disease. The best prognosis surprisingly was in patients who had multiple arterial occlusive lesions; they often had position-sensitive transient ischemic attacks during months or years

Craniectomy for acute ischemic stroke: how to apply the data to the bedside

Malignant hemispheric infarction is associated with a high mortality rate, approximately 80%, as a result of the development of intracranial pressure gradients, brain tissue shift, and herniation. By allowing the brain to swell outwards and equalizing pressure gradients, decompressive craniectomy appears to significantly reduce the mortality to approximately 20%. This review takes a comprehensive look at the evidence highlighting the benefits and limits of decompressive craniectomy in malignant cerebral infarction. Three recent European randomized trials have provided compelling evidence that decompressive hemicraniectomy for large hemispheric infarction is not only lifesaving, but also leads to improved functional outcome in patients 60 years of age or less when treated within 48 h of stroke onset. Early decompressive hemicraniectomy (60 years old) and perhaps, when delayed beyond 48 h

A Case of Neuro-Behcet's Disease Presenting with Central Neurogenic Hyperventilation

Behcet's disease is a chronic inflammatory disorder usually characterized by the triad of oral ulcers, genital ulcers, and uveitis. Central to the pathogenesis of Behcet's disease is an autoimmune vasculitis. Neurological involvement, so called "Neuro-Behcet's disease", occurs in 10-20% of patients, usually from a meningoencephalitis or venous thrombosis. We report the case of a 46-year-old patient with Neuro-Behcet's disease who presented with central neurogenic hyperventilation as a result of brainstem involvement from venulitis. To the best of our knowledge, central neurogenic hyperventilation has not previously been described in a patient with Neuro-Behcet's disease

Acute Bilateral Ophthalmoplegia Due to Vertebrobasilar Dolichoectasia: A Report of Two Cases

Case series Patient: Male, 52 • Female, 68 Final Diagnosis: VBD Symptoms: Ophthalmoplegia Medication: — Clinical Procedure: — Specialty: Neurolog

Functional in vivo characterization of sox10 enhancers in neural crest and melanoma development

By performing ATAC-Seq on zebrafish melanoma tumours, Cunningham et al identify putative sox10 enhancers with embryonic activity in zebrafish. They identify a region upstream of sox10, termed peak5, that is needed for full expression of embryonic sox10 and for adult stripe patterning demonstrating an enhancer function for peak5 and provide insights into neural crest development and melanoma initiation