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Supplemental Digital Content is available in the text.

Supplemental Digital Content is available in the text.

The concept of a double rotor motor presented earlier and its equivalent circuit has been developed, showing a non-linear parameter content. The two rotors (which are recommended to be double cage type for development of high starting torque) can run with equal or unequal speed independently, depending on their individual loading. This paper presents the elaborate design procedure, step-by-step, for the double rotor double cage motor and verifies the designed data with that obtained from three separate tests (compared to two for conventional motor) on a prototype, such that optimum performance can be obtained from the motor.

Supplemental Digital Content is available in the text.

Chemokines modulate leukocyte integrin avidity to coordinate adhesion and subsequent transendothelial migration, although the sequential signaling pathways involved remain poorly characterized. Here we show that integrin-linked kinase (ILK), a 59-kDa serine-threonine protein kinase that interacts principally with β1integrins, is highly expressed in human mononuclear cells and is activated by exposure of leukocytes to the chemokine monocyte chemoattractant protein-1. Biochemical inhibitor studies show that chemokine-triggered activation of ILK is downstream of phosphoinositide 3-kinase. In functional assays under physiologically relevant flow conditions, overexpression of wild-type ILK in human monocytic cells diminishes β1integrin/vascular cell adhesion molecule-1-dependent firm adhesion to human endothelial cells. These data implicate ILK in the dynamic signaling events involved in the regulation of leukocyte integrin avidity for endothelial substrates.

The infertility associated with oligospermia had been suspected to be a direct consequence of the impairment in fertilizing ability of the spermatozoa rather than the presence of low sperm number perse.This study defines some of these impairments, which include an over expression of superoxide dismutase, poor superoxide anion radical generation capacity and a lack of sperm-surface thiols in oligospermia. The abnormal biochemical make-up of spermatozoa could explain their low fertilizing ability in case of oligospermia.

In the absence of its substrate hydrogen peroxide, peroxidase exhibits perturbations in its Fe3+-heme center, when incubated with ascorbic acid. The electron paramagnetic pattern sprang towards a higher g-value side, denoting a sharpening of the rhombic axial symmetry around the heme-center. The interpretation is that the ascorbate dependent peroxidase action starts with the formation of an Fe3+-ascorbate charge transfer complex intermediate.

Supplemental Digital Content is available in the text.

Introduction:Anthracyclines are commonly used for the treatment of breast cancer, but they cause cardiotoxicity in 10% of all patients. We hypothesized that changes in circulating plasma proteins shortly after the completion of anthracyclines are associated with the development of cardiotoxicity.Methods:We used an aptamer-based proteomic platform to measure 1317 proteins in plasma samples obtained from 30 breast cancer patients. Proteins were measured at baseline and at 3 months, following completion of anthracyclines. In a subset of patients (n = 12), proteins were measured at 6 months, during treatment with trastuzumab. Protein levels were log-normalized, and the change in protein level at 3 or 6 months was compared to the change in global longitudinal strain (GLS) at 3 months for each patient using Pearson?s correlation coefficient.Results:Across the cohort, GLS decreased by a median of 16.4% (absolute value) at 3 months. Six patients developed clinical congestive heart failure during the course of the study. Change in GLS was inversely associated with the change in hemopexin at 3 months (r = -0.59, p = 0.0005, FDR q = 0.2) and at 6 months (r = -0.52, p = 0.09). Of the five patients with the greatest increase in hemopexin, three developed congestive heart failure. We also observed changes in plasma proteins that have been previously reported in the setting of anthracycline cardiotoxicity, including neuregulin-1 (r = 0.44, p = 0.01 at 3 months), glutathione S-transferase (r = - 0.4, p = 0.02 at 3 months), interleukin receptor 1 antagonist (r = -0.72, p = 0.009 at 6 months), and myosin binding protein C (r = 0.59, p = 0.04).Conclusions:In this initial discovery cohort, increased levels of hemopexin, a circulating heme-binding protein, were associated with decreased myocardial strain in patients treated for breast cancer. Iron-mediated oxidative stress has been proposed to contribute to anthracycline cardiotoxicity, and increased hemopexin levels may serve as an early marker of cardiotoxicity. Studies are ongoing to validate these findings using complementary techniques in other patient populations.

Introduction:PCSK9 (proprotein convertase subtilisin/kexin type 9) is a secreted plasma protein that regulates the hepatocellular expression of low-density lipoprotein receptor (LDL-R) and plays a critical role in atherosclerotic cardiovascular disease (ASCVD) risk. Emerging data indicate that PCSK9 may have additional important extrahepatic effects on non-LDL-R mediated metabolic pathways. In order to identify novel biological pathways regulated by PCSK9, we characterized the associations of the naturally occurring PCSK9 loss-of-function genetic variant 137G>T (encoding R46L) with the human plasma proteome.Methods:We recently performed aptamer-based proteomic profiling of 1304 protein levels in plasma samples from 1578 participants of the Framingham Heart Study (FHS) Offspring Cohort with available exome array-based genotype data. Inverse normalized transformed levels of each protein and clinical characteristics were compared between PCSK9 137G>T carriers and non-carriers using a linear mixed-effects model to accommodate pedigree structure, adjusted for age and sex.Results:Consistent with prior studies, 3.1% (n=49) of the FHS participants were PCSK9 137G>T carriers, and this variant was associated with a significant 23.6% decrease in plasma PCSK9 protein levels (mean 526.9 ? 25.6 vs. 689.6 ? 6.1 RFU, p=3.7E-08), 10.3% decrease in plasma LDL cholesterol levels (112 ? 4.0 vs. 125.6 ? 0.8 mg/dL, p=1.7E-3), and 7.2% decrease in plasma total cholesterol levels (190.5 ? 4.0 vs. 205.3 ? 0.9 mg/dL, p=3.1E-3) compared to non-carriers (n=1529). Plasma levels of 52 measured proteins differed between carriers vs. non-carriers with at least nominal statistical significance (p?0.05). These included proteins with established roles in LDL-R biology such as LDL-R related protein 1B (beta -0.52, p=6.3E-3), as well as proteins with less-established roles in PCSK9-associated pathways such as interleukin-22 (beta -0.55, p=1.9E-4) and bone morphogenetic protein receptor type-1A (beta 0.42, p=4.3E-3).Conclusions:Proteomic profiling of plasma from individuals harboring the PCSK9 R46L loss-of-function genetic variant represents one strategy to integrate proteomic and genomic data for pathway discovery in human PCSK9 biology.

Long-term treatment of obese, insulin-resistant nonhuman primates with a seed-targeting antimiR oligonucleotide against the microRNA-33 family derepresses hepatic expression of miR-33 targets, increases circulating HDL cholesterol, and has a clean safety profile.

Several letters to the editor are presented in response to previous articles and topics including an obituary in the August 2015 issue, the automated home, and an article about healthcare design by Justin de Syllas.

A letter to the editor is presented expessing the reader's opinion on the importance of hospital architecture in the context of the British National Health Service (NHS) Foundation Trust's budget on health facilities, described by the author as "limited."

Presents a letter to the editor in response to the article about Ray O'Rourke, chairman and CEO of Laing O'Rourke, and the right to free speech in the May 19, 2006 issue.