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Abstract: Objectives: To compare the half-life of STD and Polidocanol air-based foams and the damage they inflict upon human great saphenous vein in an in-vitro model. Methods: The time for the volume of 3% STD and polidocanol foams to reduce by 10% (T 90) and 50% (T 50) was recorded in an incubator at 37 °C. Segments of proximal GSV harvested during varicose vein surgery were filled with foam for 5 or 15 min. Histological analysis determined percentage endothelial cell loss and depth of media injury. Results: Median (±IQR) T 90 and T 50 for polidocanol were 123.3 s (111.7–165.6) and 266.3 s (245.6–383.1) versus 102.03 s (91.1–112) and 213.13 s (201–231.6) for STD (T 90 p = 0.008, T 50 p = 0.004). Median endothelial loss with polidocanol was; 63.5% (62.2–82.8) and 85.9% (83.8–92.5) versus 86.3% (84.8–93.7) and 97.64% (97.3–97.8) for STD after 5 and 15 min (p = 0.076 and p = 0.009). The median depth and % media thickness injured were 0 μm (0–0 μm) and 0% for both assessments with polidocanol versus 37.4 μm (35.3–45.8 and 43.4 μm (42.1–46.7) and 3.5% (3.1–3.6) and 5.3% (3.7–6.0) after 5 and 15 min for STD (p < 0.01 for all comparisons). Conclusion: Although polidocanol foam shows greater stability than STD foam perhaps remaining in the vein for longer, endothelial cell loss and damage to the media were significantly greater with STD. [Copyright &y& Elsevier]

The “Gigabit access passive optical network using wavelength division multiplexing” project aims to implement 64-Gb/s data transmission over 20-km single-mode fiber. Per-user symmetric data rates of 1-Gb/s will be achieved using wavelength division multiplexing passive optical network (WDM-PON) architecture with a 1:64 user split per PON segment. Enabling technologies being developed within the scope of the project include tunable transceivers and athermal 50-GHz array waveguide grating multiplexer devices. The future-proof WDM architecture will enable convergence triple-play (telephony, TV, and broadband internet) service over existing optical infrastructure, and also facilitate cost-effective dense wavelength division multiplexing for metro aggregation and mobile backhaul networks. [ABSTRACT FROM PUBLISHER]

Abstract: Background: The effect of antipsychotics on the blood oxygen level dependent signal in schizophrenia is poorly understood. The purpose of the present investigation is to examine the effect of antipsychotic medication on independent neural networks during a motor task in a large, multi-site functional magnetic resonance imaging investigation. Methods: Seventy-nine medicated patients with schizophrenia and 114 comparison subjects from the Mind Clinical Imaging Consortium database completed a paced, auditory motor task during functional magnetic resonance imaging (fMRI). Independent component analysis identified temporally cohesive but spatially distributed neural networks. The independent component analysis time course was regressed with a model time course of the experimental design. The resulting beta weights were evaluated for group comparisons and correlations with chlorpromazine equivalents. Results: Group differences between patients and comparison subjects were evident in the cortical and subcortical motor networks, default mode networks, and attentional networks. The chlorpromazine equivalents correlated with the unimotor/bitemporal (rho=−0.32, P =0.0039), motor/caudate (rho=−0.22, P =0.046), posterior default mode (rho=0.26, P =0.020), and anterior default mode networks (rho=0.24, P =0.03). Patients on typical antipsychotics also had less positive modulation of the motor/caudate network relative to patients on atypical antipsychotics (t 77 =2.01, P =0.048). Conclusion: The results suggest that antipsychotic dose diminishes neural activation in motor (cortical and subcortical) and default mode networks in patients with schizophrenia. The higher potency, typical antipsychotics also diminish positive modulation in subcortical motor networks. Antipsychotics may be a potential confound limiting interpretation of fMRI studies on the disease process in medicated patients with schizophrenia. [Copyright &y& Elsevier]

Human CD26 has dipeptidyl peptidase-4 (DPP IV) enzyme activity and binds to adenosine deaminase (ADA). CD26 is costimulatory for lymphocytes and has a circulating soluble form (sCD26). DPP IV enzyme inhibition is a new successful type 2 diabetes therapy. We examined whether the ADA binding and catalytic functions of sCD26 contribute to its effects on T-cell proliferation. Wildtype soluble recombinant human CD26 (srhCD26), an enzyme inactive mutant (srhCD26E-) and an ADA non-binding mutant (srhCD26A-) were co-incubated in in vitro T-cell proliferation assays with peripheral blood mononuclear cells (PBMC) stimulated with phytohaemagglutinin (PHA), muromonab-CD3 or Herpes simplex virus antigen (HSV Ag). Both srhCD26 and srhCD26E- enhanced PHA-induced T-cell proliferation dose-dependently in all six subjects tested. srhCD26 and srhCD26A- had no overall effect on anti-CD3-stimulated PBMC proliferation in four of five subjects. srhCD26, srhCD26E- and srhCD26A- enhanced HSV Ag induced PBMC proliferation in low responders to HSV Ag, but had no effect or inhibited proliferation in HSV-high responders. Thus, effects of soluble human CD26 on human T-cell proliferation are mechanistically independent of both the enzyme activity and the ADA-binding capability of sCD26. [ABSTRACT FROM AUTHOR]