Human immunodeficiency virus-1 (HIV-1) is a life- threatening virus which disrupts host immune system, and about half of the HIV-1 infected individuals develop neurocognitive impairment in brain. Neuronal autoimmunity is also observed in patients with HIV-1 infection, resulting in inflammation and damage in neurons and axons. Mannose binding lectin, MBL, plays important role in HIV by its direct binding of gp120, envelope protein present on the surface of HIV-1through lectin mediated complement activation pathway. MBL is also associated with initiation of autoimmunity due to its involvement in clearance of apoptotic cells. This study focuses on determining the role of MBL mediated complement pathway in the induction of neuronal autoimmunity during HIV-1 infection of the brain. Overall, higher MBL/gp120 immune complex deposition, and MBL/gp120 interaction with axonal damage marker amyloid precursor protein (APP) in HIV encephalitis (HIVE) brain suggest MBL mediated neuroinflammation and neuronal damage in HIVE. Increased immunoreactivitv of MBL/gp120 immune complex with myelin oligodendrocyte glycoprotein (MOG), and myelin basic protein (MBP) suggest that these interactions potentially damage oligodendrocytes and interfere with myelination in HIVE. Increased deposition of MBL mediated immune complexes (C3d,C5b9,IgG) in HIVE suggests that deposition of these aggregates may play a key role in axonal damage, demyelination and neuroinflammation in HIV encephalitis. Presence of C4, C5, and MBL autoantibodies and higher inflammatory cytokine response (IL-1[beta], IL-6, IL-2, and IL-8, Rantes,MIP- 1[beta]2, and MCP-1)in the cerebrospinal fluid (CSF) of HIV-1 infected individuals with neurocognitive impairment suggests that presence of MBL autoantibodies is associated with proinflammatory cytokine immune response in HIV-1 related CNS impairment

High-throughput synthesis of Samarium-Cobalt sub-micron fibers with controlled composition and dimension was demonstrated by combining electrospinning and reduction-diffusion processes. The composition of fibers was readily varied (8 < Sm < 20 at.%) by adjusting precursor composition whereas the diameter of fibers was precisely controlled by varying electrospinning parameters (e.g., applied voltage, solution feed rate, temperature, and humidity) to reach single-domain size. X-ray diffraction patterns confirmed that single phase Sm2Co17 fibers were synthesized when the metal precursor ratio (Sm3+/(Sm3++Co2+)) was precisely controlled at 10.6%, whereas mixed phases (i.e., Co-Sm2Co17 or Sm2Co17-Sm2Co7) were observed when the ratio is deviated from the stoichiometric. Magnetic saturation (Ms ) of the synthesized fibers monotonically decreased with an increased in Sm content. In contrast, coercivity (Hci) monotonically increased with an increase in Sm content.

Aggregated and hyperphosphorylated Tau is one of the pathological hallmarks of Alzheimer's disease. Tau is a polyampholytic and intrinsically disordered protein (IDP). In this paper, we present for the first time experimental results on the ionic strength dependence of the radius of gyration (R_g) of human Tau 4RS and 4RL isoforms. Synchrotron X-ray scattering revealed that 4RS R_g is regulated from 65.4 to 58.5 Å and 4RL R_g is regulated from 70.9 to 57.9 Å by varying ionic strength from 0.01 to 0.592 M. The R_g of 4RL Tau is larger than 4RS at lower ionic strength. This result provides an insight into the ion-responsive nature of intrinsically disordered and polyampholytic Tau, and can be implicated to the further study of Tau-Tau and Tau-tubulin intermolecular structure in ionic environments.