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Lubrication of microelectromechanical systems (MEMS) became very critical as the devices became complex and its reliability began to deteriorate. In this paper, ionic liquids (ILs) with low volatility and high environmental stability were investigated as lubricants for sliding MEMS devices. A method that is based on atomic force microscopy (AFM) with a liquid cell was developed to study friction and wear properties of surfaces lubricated with ILs, having a systematic variation in molecular geometry and chemistry. Six-member pyridinium and five-member imidazolium rings are compared as cations in ethyl methyl pyridinium and ethyl methyl imidazolium ethyl sulfate; influence of short and long alkyl chain lengths on lubrication is studied with butyl methyl pyrrolidinium and hexyl methyl pyrrolidinium bis(trifluro methyl sulfonyl) imide. Formation of a surface-screening cation layer was discovered and linked to low friction and wear of IL-lubricated hydrogenated-silicon (H-Si) substrates. Several promising IL lubricants were identified from the AFM study and were tested in real MEMS motor devices. The friction and wear data obtained for these tests showed good correlation with the failure life span of lubricated MEMS motors. This supports a conclusion that the AFM-liquid-cell technique can be used in screening IL lubricants for MEMS devices. [2007-0023] Index Terms--Atomic force microscopy (AFM), boundary lubrication, ionic liquid (IL), microelectromechanical system (MEMS).

Thin films are grown by a beam of ionized, accelerated atom clusters in the ionized cluster beam deposition. Since earlier attempts that used one millimeter by one millimeter nozzles at a crucible pressure of two Torr were unsuccessful, a converging-diverging nozzle 18 millimeters long, with a diameter of 0.4 millimeters, and a crucible pressure in the 1000 Torr range were used. This yielded considerable numbers of large zinc clusters.

Background: The use of microsomal triglyceride transfer protein (MTP) inhibitors is limited to severe hyperlipidemias because of associated hepatosteatosis and gastrointestinal adverse effects. Comprehensive knowledge about the structure-function of MTP might help design new molecules that avoid steatosis. Characterization of mutations in MTP causing abetalipoproteinemia has revealed that the central α-helical and C-terminal β-sheet domains are important for protein disulfide isomerase binding and lipid transfer activity. Our aim was to identify and characterize mutations in the N-terminal domain to understand its function., Methods and Results: We identified a novel missense mutation (D169V) in a 4-month-old Turkish male child with severe signs of abetalipoproteinemia. To study the effect of this mutation on MTP function, we created mutants via site-directed mutagenesis. Although D169V was expressed in the endoplasmic reticulum and interacted with apolipoprotein B (apoB) 17, it was unable to bind protein disulfide isomerase, transfer lipids, and support apoB secretion. Computational modeling suggested that D169 could form an internal salt bridge with K187 and K189. Mutagenesis of these lysines to leucines abolished protein disulfide isomerase heterodimerization, lipid transfer, and apoB secretion, without affecting apoB17 binding. Furthermore, mutants with preserved charges (D169E, K187R, and K189R) rescued these activities., Conclusions: D169V is detrimental because it disrupts an internal salt bridge leading to loss of protein disulfide isomerase binding and lipid transfer activities; however, it does not affect apoB binding. Thus, the N-terminal domain of MTP is also important for its lipid transfer activity., (© 2015 American Heart Association, Inc.)

Objectives: ω-3 Fatty acids (FAs), natural ligands for the peroxisome proliferator-activated receptor-α (PPAR-α), attenuate parenteral nutrition-associated liver disease (PNALD). However, the mechanisms underlying the protective role of ω-3 FAs are still unknown. The aim of this study was to determine the effects of ω-3 FAs on hepatic triglyceride (TG) accumulation in a murine model of PNALD and to investigate the role of PPAR-α and microsomal triglyceride transfer protein (MTP) in this experimental setting., Methods: 129S1/SvImJ wild-type or 129S4/SvJaePparatm/Gonz/J PPAR-α knockout mice were fed chow and water (controls); oral, fat-free PN solution only (PN-O); PN-O plus intraperitoneal (IP) ω-6 FA-predominant supplements (PN-ω-6); or PN-O plus IP ω-3 FA (PN-ω-3). Control and PN-O groups received sham IP injections of 0.9% NaCl. Hepatic histology, TG and cholesterol, MTP activity, and PPAR-α messenger RNA were assessed after 19 days., Results: In all experimental groups, PN feeding increased hepatic TG and MTP activity compared with controls. Both PN-O and PN-ω-6 groups accumulated significantly greater amounts of TG when compared with PN-ω-3 mice. Studies in PPAR-α null animals showed that PN feeding increases hepatic TG as in wild-type mice. PPAR-α null mice in the PN-O and PN-ω-6 groups demonstrated variable degrees of hepatic steatosis, whereas no evidence of hepatic fat accumulation was found after 19 days of oral PN plus IP ω-3 FAs., Conclusions: PN induces TG accumulation (steatosis) in wild-type and PPAR-α null mice. In PN-fed wild-type and PPAR-α null mice given IP ω-3 FAs, reduced hepatic TG accumulation and absent steatosis are found. Prevention of steatosis by ω-3 FAs results from PPAR-α-independent pathways., (© 2013 American Society for Parenteral and Enteral Nutrition.)

Microsomal triglyceride transfer protein (MTP) is a target to reduce plasma lipids because of its indispensable role in triglyceride-rich lipoprotein biosynthesis. MTP inhibition in Western diet fed mice decreased plasma triglycerides/cholesterol, whereas increasing plasma alanine/aspartate aminotransferases (ALT/AST) and hepatic triglycerides/free cholesterol. Free cholesterol accumulated in the endoplasmic reticulum (ER) and mitochondria resulting in ER and oxidative stresses. Mechanistic studies revealed that MTP inhibition increased transcription of the GPT/GOT1 genes through up-regulation of the IRE1α/cJun pathway leading to increased synthesis and release of ALT1/AST1. Thus, transcriptional up-regulation of GPT/GOT1 genes is a major mechanism, in response to ER stress, elevating plasma transaminases. Increases in plasma and tissue transaminases might represent a normal response to stress for survival.

Central nervous system manifestations of West Nile virus (WNV) infection include meningitis, encephalitis, and poliomyelitis-like syndrome. We describe a 44-year-old man with no past medical history who presented with a meningoencephalitic syndrome and spastic paralysis bilaterally in the upper and lower extremities, hyperreflexia, and myoclonus and was ultimately diagnosed as being infected with HIV and WNV.

Endothelial lipase (EL) is a major negative regulator of plasma HDL levels in mice, rabbits, and most probably, humans. Although this regulatory function is critically dependent on EL's hydrolysis of HDL phospholipids, as yet there is no phospholipase assay specific for EL in plasma. We developed such an assay for the mouse enzyme using a commercially available phospholipid-like fluorescent substrate in combination with an EL neutralizing antibody. The specificity of the assay was established using EL knockout mice and its utility demonstrated by detection of an increase in plasma EL phospholipase activity following exposure of wild-type mice to lipopolysaccharide. The assay revealed that murine pre-heparin plasma does not contain measurable EL activity, indicating that the hydrolysis of HDL phospholipids by EL in vivo likely occurs on the cell surface.

The production of IgE specific to different viruses (HIV-1, Parvovirus B19, RSV), and the ability for IgE anti-HIV-1 to suppress HIV-1 production in vitro, strongly suggest an important role for IgE and/or anti viral specific IgE in viral pathogenesis. Previous studies in our laboratory were the first to report the presence of IgE anti-varicella zoster virus (VZV) in an adolescent patient with shingles. However, the presence and long term persistence of IgE anti VZV antibodies has not been studied in adults. The presence of serum IgE in addition to IgE and IgG anti-VZV antibody in sera were studied in children (N=12) (0-16 y/o) and adults (N=9) (32-76 y/o) with either a past history of (wild type) chicken pox (N=7 children, 9 adults) or 5 years after vaccination with varicella zoster (N=2 children) (Varicella virus vaccine live, Oka/Merck), as well as in non-infected subjects (N=3 children). Of the patients who had a positive history of chicken pox 13 of 16 (81%) contained IgE anti-VZV antibodies; they were both serum IgEHi (>100 IU/ml) and IgELo (<100 IU/ml). Of the patients who were vaccinated, IgE anti-VZV antibodies were undetected. In contrast, serum from the patients without a history of chicken pox or vaccination did not make either IgE or IgG anti-VZV antibodies. This is the first demonstration of the existence of IgE anti-VZV antibodies, and its long-term persistence in serum of previously infected subjects. Future studies regarding the functional role of anti-viral IgE and its relationship to VZV are warranted.

Blood lymphocyte distributions, serum immunoglobulin and cytokine levels, and serum IgE and IgG anti-varicella zoster virus (VZV) levels were measured in an atopic girl (age 15 yr) who developed shingles 10 yr after infection with chicken pox. Before, during, and 5 months after the shingles episode, the child's distributions of blood lymphocytes (excluding CD23+) and serum immunoglobulin levels (excluding IgE) were within the normal ranges. Her blood level of CD23+ lymphocytes decreased >50% during the shingles episode and remained low thereafter. Her serum level of IgE was elevated before and during shingles (154 and 168 IU/ml, respectively), but was reduced after recovery from shingles (<100 IU/ml). Before, during, and after shingles, her serum contained IgE and IgG anti-VZV antibodies. Before, during, and after shingles, low levels of IFN-gamma were detected in serum, but neither IL-1beta nor IL-4 were detected. Before shingles, low levels of IL-10 were detected in serum; during shingles, the serum level of IL-10 was increased 30-fold; it subsequently diminished at 5 mo after shingles. The role of IgE in immunity against varicella zoster virus (VZV) has not previously been studied. Our observations in this patient suggest that immunomodulation of IgE and accessory proteins may play a role in VZV pathogenesis.