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Results of time-of-day upon neuromuscular function within inexperienced males: Distinct replies of high morning hours performers and also nighttime entertainers.
BACKGROUND HIV-associated neurocognitive disorders (HAND) persist despite the widespread implementation of combined antiretroviral therapy (ART). As people with HIV (PWH) age on ART regimens, the risk of age-related comorbidities such as Alzheimer's disease (AD) may increase. However, questions remain as to whether HIV or ART will alter such risks. Beta amyloid (Aβ) and phosphorylated-tau (p-tau) proteins are associated with AD and their levels are altered in the CSF of AD cases. METHODS To better understand how these AD-related markers are affected by HIV-infection and ART, postmortem CSF collected from 70 well-characterized HIV+ decedents was analyzed for Aβ1-42, Aβ1-40, and p-tau levels. RESULTS Aβ1-42 and Aβ1-40 CSF levels were higher in cases that were exposed to ART. Aβ1-42 and Aβ1-40 CSF levels were also higher in cases on protease inhibitors (PI) compared to those with no exposure to PIs. Aβ1-42 and Aβ1-40 levels in CSF were lowest in HIV+ cases with HIV-associated dementia (HAD) and levels were highest in those diagnosed with asymptomatic neurocognitive impairment (ANI) and minor neurocognitive disorder (MND). read more Aβ1-42 and Aβ1-40 were inversely related with p-tau levels in all cases, as previously reported. CONCLUSIONS These data suggest that ART exposure is associated with increased levels of Aβ1-42 and Aβ1-40 in the CSF. Also, HAD, but not ANI/MND diagnosis is associated with decreased levels of Aβ1-42 and Aβ1-40 in CSF, potentially suggesting impaired clearance. These data suggest that HIV infection and ART may impact pathogenic mechanisms involving Aβ1-42 and Aβ1-40, but not p-tau.OBJECTIVE Nonoccupational postexposure prophylaxis (nPEP) programs offer antiretroviral therapy to prevent HIV following at-risk exposures like sexual assault. We investigated the levels of elective nPEP uptake among sexual assault cases presenting for emergency medical care. DESIGN Retrospective analysis. METHODS The analysis included over 3 years (1Jan2015 to 30Sep2018) of clinic information from the Sexual Assault and Partner Abuse Care Program (SAPACP) at The Ottawa Hospital, the regional emergency department care point following sexual assault. Descriptive analyses assessed the number of cases eligible for nPEP and those who started nPEP. Bivariable/multivariable logistic regression modelling assessed factors most strongly associated with starting nPEP using odds ratios (OR), adjusted OR (AOR), and 95% confidence intervals (CI). RESULTS The SAPACP saw 1712 patients; 1032 were sexual assault cases, 494 were eligible for nPEP, and 307/494 (62%) eligible patients started nPEP. The median age was 23 years (IQR20-31), with 446 (90%) cases being women. There were 86 (17%) cases who arrived by ambulance, and 279 (56%) assaults involving a known assailant. Reduced odds of starting nPEP were observed among female cases (AOR0.44, 95% CI0.21-0.93), those who arrived by ambulance (AOR0.56, 95% CI0.35-0.91), and those with a known assailant (AOR0.56, 95% CI0.36-0.78). CONCLUSIONS We found that 62% of eligible sexual assault cases started nPEP. Key groups most likely to decline nPEP included female cases, those who arrived by ambulance, and with known assailants. Providers can use these findings to provide recommendations to sexual assault survivors most likely to decline nPEP, yet still in need of care.OBJETIVE To examine the clinical burden and disease spectrum, as well as time trends for HTLV-1 and HTLV-2 hospital admissions. DESIGN Retrospective, observational study using the Spanish National Hospital Discharge Database. METHODS Information for the diagnostic codes HTLV, -1 and -2 using the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) was retrieved from the national public registry since 1997 to 2015. RESULTS From a total of 66,462,136 nationwide hospital admissions recorded during the study period, 135 included HTLV diagnosis, being HTLV-1 in 115 (85.2%) and HTLV-2 in 20 (14.8%). The overall hospital admission rate due to HTLV was 2.03 per million, without significant yearly changes. First admissions represented 104 (77%) whereas 31 (23%) were re-admissions. The median in-hospital stay for HTLV patients was 9 days. In-hospital death occurred in 11 (8.1%). The median age of individuals with HTLV admission was 48 years-old and 60 (44.4%) were female. HTLV was recorded as the main diagnosis in 20%. The most frequent clinical conditions recorded alongside HTLV diagnosis were myelopathy (61; 45.2%), leukemia/lymphoma (30; 22.2%), solid organ transplantation (14; 10.4%) and child delivery (7; 5.2%). CONCLUSION The rate of HTLV diagnosis in hospitalized patients in Spain is low, roughly of 2 per million admissions. Despite continuous large immigrant flows from HTLV-1 endemic areas, no significant rising in hospitalizations due to HTLV-1 associated illnesses were noticed during the last two decades. Classical clinical complications of HTLV-1 infection, such as myelopathy and lymphoma account for more than two third of cases.OBJECTIVE Postmortem brains of subjects diagnosed with human immunodeficiency virus-1 (HIV) associated neurocognitive disorders (HAND) exhibit loss of dendrites. However, the mechanisms by which synapses are damaged are not fully understood. DESIGN Dendrite length and remodeling occurs via microtubules (MTs) the dynamics of which are regulated by microtubule binding proteins, including MT associated protein 2 (MAP2). The HIV protein gp120 is neurotoxic and interferes with neuronal MTs. We measured MAP2 concentrations in human cerebrospinal fluid (CSF) and MAP2 immunoreactivity in rat cortical neurons exposed to HIV and gp120. METHODS First, we examined whether HIV affects MAP2 levels by analyzing the CSF of 27 persons living with HIV (PLH) whose neurocognitive performance had been characterized. We then used rat cortical neurons to study the mechanisms of HIV-mediated dendritic loss. RESULTS PLH who had HAND had greater MAP2 concentrations within the CSF than cognitive normal PLH. In cortical neurons, the deleterious effect of HIV on MAP2 positive dendrites occurred through a gp120-mediated mechanism. The neurotoxic effect of HIV was blocked by a CCR5 antagonist and prevented by Helix-A, a peptide that displaces gp120 from binding to MTs, conjugated to a nanolipoprotein particle delivery platform. CONCLUSIONS Our findings support that HIV at least partially effects its neurotoxicity via neuronal cytoskeleton modifications and provide evidence of a new therapeutic compound that could be used to prevent the HIV-associated neuropathology.
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