Prevalence and risk factors to HIV-infection amongst health care workers within public and private health facilities in Cameroon.

Introduction: This study aimed at assessing the prevalence of Human Immunodeficiency Virus (HIV) among health care workers (HCWs) and to evaluate some risks factors for HCWs. Methods: We conducted a cross sectional study amongst HCWs in public and private healthcare facilities within seven regions amongst the 10 found in Cameroon. We collected data from 446 HCWs within 150 healthcare facilities. We used questionnaires for interviews and biological sampling for HIV test. Results: HIV prevalence was 2.61% (95% CI: 1.32% - 4.61%) regardless of gender and age. HCWs in private health facilities were more infected compared to those in public health facilities 5.00% vs 1.40% (p = 0.028); OR = 3.7 (95% CI: 1.01-12.90). HCWs who had never screened for HIV had a high risk of being infected OR = 7.05 (95% CI: 2.05-24.47). 44.62% of HCWs reported to have been victim of an Accidental Exposure to Blood (AEB). Amongst them, 45.80% in public HF versus 32.1% in private HF reported to have received an HIV screening and Post Exposure Prophylaxis following this incident. 4.20% of HCW victim of AEB were HIV positive, and 36.40% of HCWs had appropriate capacity training for HIV patient care. Conclusion: Though the HIV prevalence in HCWs is lower than in the general population 2.61% vs 4.3%, there is a high risk of infection as we observed a relatively high percentage of AEB amongst HCWs with an HIV prevalence of 4.20%. There is thus, a need in strengthening the capacity and provide psychosocial support to HCWs

Возрастные особенности площади лимфоидных узелков стенки глотки человека

ГЛОТКА /АНАТОМГОРЛО /АНАТОМВОЗРАСТНЫЕ ГРУППЫЛИМФОИДНАЯ ТКАНЬ /АНАТОМЛИМФАДЕНОИДНАЯ ТКАНЬ /АНАТОМЛИМФОРЕТИКУЛЯРНАЯ ТКАНЬ /АНАТОМНОВОРОЖДЕННЫЙМЛАДЕНЕЦ НОВОРОЖДЕННЫЙМЛАДЕНЕЦДЕТИ РАННЕГО ВОЗРАСТАДЕТИПОДРОСТКИЛИЦА ЮНОШЕСКОГО ВОЗРАСТАВЗРОСЛЫЕПРЕСТАРЕЛЫЕСЛИЗИСТАЯ ОБОЛОЧКА /АНАТОМПЛОЩАДЬ ЛИМФОИДНЫХ УЗЕЛКОВ СТЕНКИ ГЛОТКИЛИМФОИДНЫЕ УЗЕЛКИ СТЕНКИ ГЛОТКИВОЗРАСТНЫЕ ОСОБЕННОСТ

Targeted SERPIN (TaSER): a dual-action antithrombotic agent that targets platelets for SERPIN delivery

Background: Occlusive thrombi are not homogeneous in composition. The core of a thrombus is rich in activated platelets and fibrin while the outer shell contains resting platelets. This core is inaccessible to plasma proteins. We produced a fusion protein (targeted SERPIN–TaSER), consisting of a function-blocking V HH against glycoprotein Ibα (GPIbα) and a thrombin-inhibiting serine protease inhibitor (SERPIN; α1-antitrypsin 355AIAR 358) to interfere with platelet-driven thrombin formation. Aim: To evaluate the antithrombotic properties of TaSER. Methods: Besides TaSER, we generated three analogous control variants with either a wild-type antitrypsin subunit, a non-targeting control V HH, or their combination. We investigated TaSER and controls in protease activity assays, (platelet-dependent) thrombin generation assays, and by western blotting. The effects of TaSER on platelet activation and von Willebrand factor (VWF) binding were studied by fluorescence-activated cell sorting, in agglutination studies, and in ATP secretion experiments. We studied the influence of TaSER in whole blood (1) on platelet adhesion on VWF, (2) aggregate formation on collagen, and (3) thrombus formation (after recalcification) on collagen and tissue factor. Results: TaSER binds platelets and inhibits thrombin activity on the platelet surface. It blocks VWF binding and disassembles platelet agglutinates. TaSER delays tissue factor-triggered thrombin generation and ATP secretion in platelet-rich plasma in a targeted manner. In flow studies, TaSER interferes with platelet adhesion and aggregate formation due to GPIbα blockade and limits thrombus formation due to targeted inhibition of platelet-dependent thrombin activity. Conclusion: The synergy between the individual properties of TaSER makes it a highly effective antithrombotic agent with possible clinical implications

Disrupted Thalamus White Matter Anatomy and Posterior Default Mode Network Effective Connectivity in Amnestic Mild Cognitive Impairment

Alzheimer’s disease (AD) and its prodromal state amnestic mild cognitive impairment (aMCI) are characterized by widespread abnormalities in inter-areal white matter fiber pathways and parallel disruption of default mode network (DMN) resting state functional and effective connectivity. In healthy subjects, DMN and task positive network interaction are modulated by the thalamus suggesting that abnormal task-based DMN deactivation in aMCI may be a consequence of impaired thalamo-cortical white matter circuitry. Thus, this article uses a multimodal approach to assess white matter integrity between thalamus and DMN components and associated effective connectivity in healthy controls (HCs) relative to aMCI patients. Twenty-six HC and 20 older adults with aMCI underwent structural, functional and diffusion MRI scanning using the high angular resolution diffusion-weighted acquisition protocol. The DMN of each subject was identified using independent component analysis (ICA) and resting state effective connectivity was calculated between thalamus and DMN nodes. White matter integrity changes between thalamus and DMN were investigated with constrained spherical deconvolution (CSD) tractography. Significant structural deficits in thalamic white matter projection fibers to posterior DMN components posterior cingulate cortex (PCC) and lateral inferior parietal lobe (IPL) were identified together with significantly reduced effective connectivity from left thalamus to left IPL. Crucially, impaired thalamo-cortical white matter circuitry correlated with memory performance. Disrupted thalamo-cortical structure was accompanied by significant reductions in IPL and PCC cortico-cortical effective connectivity. No structural deficits were found between DMN nodes. Abnormal posterior DMN activity may be driven by changes in thalamic white matter connectivity; a view supported by the close anatomical and functional association of thalamic nuclei effected by AD pathology and the posterior DMN nodes. We conclude that dysfunctional posterior DMN activity in aMCI is consistent with disrupted cortico-thalamo-cortical processing and thalamic-based dissemination of hippocampal disease agents to cortical hubs