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Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder affecting both the upper and lower motor neurons. Although ALS typically leads to death within 3 to 5 years after initial symptom onset, approximately 10% of patients with ALS live more than 10 years after symptom onset. We set out to determine similarities and differences in clinical presentation and neuropathology in persons with ALS with long vs. those with standard duration. Participants were United States military Veterans with a pathologically confirmed diagnosis of ALS (n = 179), dichotomized into standard duration (<10 years) and long‐duration (≥10 years). The ALS Functional Rating Scale‐Revised (ALSFRS‐R) was administered at study entry and semi‐annually thereafter until death. Microglial density was determined in a subset of participants. long‐duration ALS occurred in 76 participants (42%) with a mean disease duration of 16.3 years (min/max = 10.1/42.2). Participants with long‐duration ALS were younger at disease onset (P = 0.002), had a slower initial ALS symptom progression on the ALSFRS‐R (P < 0.001) and took longer to diagnose (P < 0.002) than standard duration ALS. Pathologically, long‐duration ALS was associated with less frequent TDP‐43 pathology (P < 0.001). Upper motor neuron degeneration was similar; however, long‐duration ALS participants had less severe lower motor neuron degeneration at death (P < 0.001). In addition, the density of microglia was decreased in the corticospinal tract (P = 0.017) and spinal cord anterior horn (P = 0.009) in long‐duration ALS. Notably, many neuropathological markers of ALS were similar between the standard and long‐duration groups and there was no difference in the frequency of known ALS genetic mutations. These findings suggest that the lower motor neuron system is relatively spared in long‐duration ALS and that pathological progression is likely slowed by as yet unknown genetic and environmental modifiers. [ABSTRACT FROM AUTHOR]

People over the age of 50 are the fastest growing segment of the HIV-infected population in the USA. Although antiretroviral therapy has remarkable success controlling the systemic HIV infection, HIV-associated neurocognitive disorder (HAND) prevalence has increased or remained the same among this group, and cognitive deficits appear more severe in aged patients with HIV. The mechanisms of HAND in the aged population are not completely understood; a leading hypothesis is that aged individuals with HIV might be at higher risk of developing Alzheimer's disease (AD) or one of the AD-related dementias (ADRD). There are a number of mechanisms through which chronic HIV disease alone or in combination with antiretroviral therapy and other comorbidities (e.g., drug use, hepatitis C virus (HCV)) might be contributing to HAND in individuals over the age of 50 years, including (1) overlapping pathogenic mechanisms between HIV and aging (e.g., decreased proteostasis, DNA damage, chronic inflammation, epigenetics, vascular), which could lead to accelerated cellular aging and neurodegeneration and/or (2) by promoting pathways involved in AD/ADRD neuropathogenesis (e.g., triggering amyloid β, Tau, or α-synuclein accumulation). In this manuscript, we will review some of the potential common mechanisms involved and evidence in favor and against a role of AD/ADRD in HAND. [ABSTRACT FROM AUTHOR]

Virtual three-dimensional (3D) surface models of autopsied human brain hemispheres were constructed by integrating multiple two-dimensional (2D) photographs. To avoid gravity-dependent deformity, formalin-fixed hemispheres were placed on non-refractile, transparent acrylic plates, which allowed us to take 2D photographs from various different angles. Photogrammetric calculations using software (ReCap Pro cloud service, Autodesk, San Rafael, CA, USA) allowed us calculate the 3D surface of each brain hemisphere. Virtual brain models could be moved and rotated freely to allow smooth, seamless views from different angles and different magnifications. When viewing rotating 3D models on 2D screens, 3D aspects of the models were enhanced using motion parallax. Comparison of different brains using this method allowed us to identify disease-specific patterns of macroscopic atrophy, that were not apparent in conventional 2D photographs. For example, we observed frontal lobe atrophy in a progressive supranuclear palsy brain, and even more subtle atrophy in the superior temporal gyrus in amyotrophic lateral sclerosis-frontotemporal lobar degeneration. Thus, our method facilities recognition of gyral atrophy. In addition, it provides a much more powerful and suitable way of visualizing the overall appearance of the brain as a three-dimensional structure. Comparison of normal and diseased brains will allow us to associate different macroscopic changes in the brain to clinical manifestations of various diseases. [ABSTRACT FROM AUTHOR]

A longitudinal file was developed containing statistics on almost all colleges and universities in the country and was used to compute 61 indicators of institutional viability. Particular colleges were identified as being in distress based on a combination of objective measures: closure, default on a federal loan, extreme enrollment declines, extreme reduction in faculty salaries, and extreme declines in current fund revenues and balances. These colleges were used to validate the indicators as being related to distress. separately by type of college. The validated indicators for each type of college were then used to construct a summary index of viability which was found to classify accurately colleges that are viable or in distress. Distributions of the summary measure are displayed for various kinds of colleges (e.g., traditionally black colleges, women's colleges, 2-year vocational colleges). Twelve kinds of colleges were found to frequently receive low scores on the summary measure. [ABSTRACT FROM AUTHOR]

Background: The aim of the study is to assess the clinical effect of an antibacterial monomer-containing primer on preventing white spot lesions (WSLs) during fixed orthodontic treatment. Subject and methods: The study included 35 patients. A split-mouth design was used during bonding of the brackets. In Clearfil (CF) group, adhesive-coated brackets (APC Plus Victory series, 3M Unitek, Monrovia, CA, USA) were bonded with an antibacterial monomer-containing primer (Clearfil Protect Bond, Kuraray Medical, Okayama, Japan). In Transbond (TB) group, the same adhesive-coated brackets were bonded using a conventional primer (Transbond XT Primer; 3M Unitek, Monrovia, CA, USA). The mean duration of orthodontic treatment was 16 months. Digital images of each tooth were used to assess the WSLs. The areas of the WSLs were measured with a software. The bond failures during orthodontic treatment were also recorded. Results: After fixed orthodontic treatment, 23 of the 35 patients showed one or more WSLs. Of the total of 666 teeth, 114 WSLs occurred over the orthodontic treatment time. Rates of WSL in the CF and TB groups were 8.03% and 9.24%, respectively. The difference in WSL rates between the two groups was not statistically significant. No significant difference was observed in the lesion areas between the groups. Moreover, the difference in bracket failure rates between the two groups was also not statistically significant. Conclusion: The results of this long-term clinical study indicated no significant difference between the antibacterial monomer-containing primer group and the control group in the efficacy of reducing demineralization throughout the orthodontic treatment. [ABSTRACT FROM AUTHOR]