Sulfur-Containing Carbon Nanospheres as Lubricant Additives for Antiwear and Friction Reduction

Herein, organic–inorganic hybrid sulfur-containing carbon nanospheres (SCNs) were successfully prepared by one-pot chemical oxidation polymerization of a thiophene monomer and then rigorous carbonization. On account of the good structural strength and organic phase derived from the precursor polythiophene, the as-prepared SCNs manifested remarkable oil-dispersing and tribological properties as lubricant nanoadditives. Subsequently, the friction mechanism of SCNs was deduced; the as-prepared SCNs had the capacity to take the shape of a strong protective film on the surface of friction pairs by intricate physical deposition and tribochemical reaction. So, the SCNs exhibited excellent tribological performance, including a high extreme pressure (950 N), an ultralow friction coefficient of less than 0.06, and a significant reduction in abrasion by 90%

Survivin −31G>C Polymorphism and Gastrointestinal Tract Cancer Risk: A Meta-Analysis

<div><h3>Background</h3><p>Emerging evidence showed that common functional −31G>C polymorphism (rs9904341 G>C) in the promoter region of the survivin gene is involved in the regulation of survivin expression, thus increasing an individual’s susceptibility to gastrointestinal tract (GIT) cancer; but individually published results are inconclusive. The aim of this systematic review and meta-analysis was to derive a more precise estimation of the association between survivin −31G>C polymorphism and GIT cancer risk.</p> <h3>Methods</h3><p>A literature search of PubMed, Embase, Web of Science and CBM databases was conducted from inception through July 1st, 2012. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association.</p> <h3>Results</h3><p>Nine case-control studies were included with a total of 2,231 GIT cancer cases and 2,287 healthy controls. The results indicated that survivin −31G>C polymorphism was associated with increased risk of GIT cancer. In the stratified analysis by cancer types, significant associations were observed between survivin −31G>C polymorphism and increased risk of colorectal and gastric cancers. However, the lack of association of survivin −31G>C polymorphism with esophageal cancer risk may be due to a lack of a sufficient number of eligible studies and the influence of different genetic and environmental factors.</p> <h3>Conclusion</h3><p>Results from the current meta-analysis suggests that survivin −31G>C polymorphism might increase the risk of GIT cancer, especially among gastric and colorectal cancers.</p> </div

Effects of cholesterol concentration on matrix calcification and osteoblastic differentiation.

<p>Matrix calcium (A), ALP activity (B) and intracellular cholesterol (C) increased in a dose-dependent manner in HUVSMCs treated with CM with the addition of cell-permeable cholesterol for 72 h. *<i>P</i> < 0.05, ^#<i>P</i> < 0.01, compared with cholesterol 0 μmol/L.</p

Decreased expression of UBIAD1 increased matrix calcification, osteoblastic differentiation, and intracellular cholesterol levels and reduced MK-4 level.

<p>(A) Endogenous levels of UBIAD1 and β-actin after transfection with siControl or siUBIAD1. (B–E) Differences in matrix calcium (B), ALP activity (C), intracellular cholesterol (D) and MK-4 levels (E) after transfection with siControl or siUBIAD1 in HUVSMCs treated with CM for 72 h. *<i>P</i> < 0.05, ^#<i>P</i> < 0.01.</p

Elevated expression of UBIAD1 reduced matrix calcification, ALP activity and intracellular cholesterol levels, and increased MK-4 level.

<p>(A) Endogenous levels of UBIAD1 and β-actin after transfection with pControl or pUBIAD1. (B–E) Differences in matrix calcium (B), ALP activity (C), intracellular cholesterol (D) and MK-4 level (E) after transfection with pControl or pUBIAD1 in HUVSMCs treated with CM for 72 h. *<i>P</i> < 0.05, ^#<i>P</i> < 0.01.</p

UBIAD1 localizes to the endoplasmic reticulum (ER) and the Golgi in HUVSMCs.

<p>(A) UBIAD1 expressed in the cytoplasm of HUVSMCs: (a–b) HUVSMCs transfected with UBIAD1-EGFP plasmid; (c–d) HUVSMCs transfected with EGFP plasmid as control; (e–f) HUVSMCs stained with UBIAD1 antibody and the FITC-conjugated secondary antibody; and (g–h) HUVSMCs stained with the absent UBIAD1 antibody as the negative control. (B) UBIAD1 localized to the ER in HUVSMCs: (a) UBIAD1-EGFP expressed in HUVSMCs; (b and f) the ER marker, ER-tracker red; (c) merged image of a and b; (d) image c with nuclear DAPI staining; (e) HUVSMCs stained with UBIAD1 antibody and the FITC-conjugated secondary antibody; (g) merged image of e and f; (h) image g with nuclear DAPI staining. (C) UBIAD1 localized to the Golgi in HUVSMCs: (a) UBIAD1-EGFP expressed in HUVSMCs; (b and f) the Golgi marker, BODIPY-TR ceramide; (c) merged image of a and b; (d) image c with nuclear DAPI staining; (e) HUVSMCs stained with UBIAD1 antibody and the FITC-conjugated secondary antibody; (g) merged image of e and f; (h) image g with nuclear DAPI staining.</p

Flow chart of literature search and study selection.

<p>Flow chart of literature search and study selection.</p

Exogenous MK-4 reduced intracellular cholesterol levels, matrix calcification and osteoblastic differentiation.

<p>Differences in matrix calcium (A), ALP activity (B), intracellular cholesterol (C) and MK-4 level (D) after addition of blank control or exogenous MK-4 (15 μmol /L) in HUVSMCs treated with CM for 72 h. *<i>P</i> < 0.05, ^#<i>P</i> < 0.01.</p

Subgroup analysis by cancer type of ORs with a random-effects model for associations between survivin −31G>C polymorphism and gastrointestinal tract cancer risk under dominant model (CC+GC vs. GG).

<p>Subgroup analysis by cancer type of ORs with a random-effects model for associations between survivin −31G>C polymorphism and gastrointestinal tract cancer risk under dominant model (CC+GC vs. GG).</p

The genotype distribution of survivin −31G>C polymorphism in case and control groups.

<p>Ref = reference; SNP = single nucleotide polymorphism; MAF = minor allele frequency; HWE = Hardy-Weinberg equilibrium.</p