Association of <i>CRYAB</i> C-802G genotype with oral cancer recurrence and metastasis.

a<p><i>P</i> based on two-sided Chi-square test without Yate's correction.</p>b<p>The ORs were estimated with multivariate logistic regression analysis.</p>c<p>Statistically identified as significant.</p

PCR-based restriction analysis of the <i>CRYAB</i> C-802G rs14133 polymorphism shown on 2.5% agarose electrophoresis.

<p>M: 100 bp DNA size marker, G/G: enzyme indigestible homozygote, C/G: heterozygote, and C/C: enzyme digestible homozygote.</p

Disease-free survival of oral cancer patients after diagnosis stratified by genotypes of <i>CRYAB</i> C-802G.

<p>Statistical analysis was performed by the log-rank test.</p

Carnosic Acid Prevents 6‑Hydroxydopamine-Induced Cell Death in SH-SY5Y Cells via Mediation of Glutathione Synthesis

Understanding the neuroprotective effects of the rosemary phenolic diterpene carnosic acid (CA) has attracted increasing attention. We explored the mechanism by which CA modulates the neurotoxic effects of 6-hydroxydopamine (6-OHDA) in SH-SY5Y cells. Cells were pretreated with CA for 12 h followed by treatment with 100 μM 6-OHDA for 12 or 24 h. Cell viability determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolim bromide (MTT) assay indicated that 0.1 to 1 μM CA dose-dependently attenuated the cell death induced by 6-OHDA, whereas the effect of 3–5 μM CA was weaker. CA at 1 μM suppressed the 6-OHDA-induced nuclear condensation, reactive oxygen species generation, and cleavage of caspase 3 and PARP. Immunoblots showed that the phosphorylation of c-Jun NH₂-terminal kinase (JNK) and p38 by 6-OHDA was reduced in the presence of CA. Incubation of cells with CA resulted in significant increases in the total glutathione (GSH) level and the protein expression of the γ-glutamylcysteine ligase catalytic subunit and modifier subunit. l-Buthionine-sulfoximine, an inhibitor of GSH synthesis, attenuated the effect of CA on cell death and apoptosis. Treatment with CA also led to an increase in nuclear factor erythroid-2 related factor 2 (Nrf2) activation, antioxidant response element (ARE)-luciferase reporter activity, and DNA binding to the ARE. Silencing of Nrf2 expression alleviated the reversal of p38 and JNK1/2 activation by CA. These results suggest that the attenuation of 6-OHDA-induced apoptosis by CA is associated with the Nrf2-driven synthesis of GSH, which in turn down-regulates the JNK and p38 signaling pathways. The CA compound may be a promising candidate for neuroprotection in Parkinson’s disease

Distribution of the <i>MTHFR</i> genotypes among 266 childhood ALL patients and 266 controls.

<p>^a Based on Pearson’s chi-square test</p><p>^b OR: odds ratio; CI: confidence interval</p><p>* Statistically significant</p><p>Distribution of the <i>MTHFR</i> genotypes among 266 childhood ALL patients and 266 controls.</p

Distribution of the <i>MTHFR</i> C677T and A1298C genotypes stratified by age and gender

<p>^a<i>P</i> for trend based on chi-square test.</p><p>^b<i>P</i> for interaction based on likelihood ratio test; NS, non-significant.</p><p>^c OR, odds ratio; CI, confidence interval.</p><p>* Statistically significant.</p><p>Distribution of the <i>MTHFR</i> C677T and A1298C genotypes stratified by age and gender</p

Demographic data of 266 childhood ALL patients and 266 controls.

<p>^a Based on a chi-square test.</p><p>Demographic data of 266 childhood ALL patients and 266 controls.</p

Summary of the original international literature investigating the association of the <i>MTHFR</i> C677T genotypes with childhood leukemia.

<p>Note: Some studies that had less than 70 cases and 70 controls of a redundant population were not included.</p><p>The survey of literature was updated 2014/09/18.</p><p>Summary of the original international literature investigating the association of the <i>MTHFR</i> C677T genotypes with childhood leukemia.</p

Inhibition of TNF-α-Induced Inflammation by Andrographolide via Down-Regulation of the PI3K/Akt Signaling Pathway

Andrographolide (<b>1</b>), an active constituent of <i>Andrographis paniculata,</i> decreased tumor necrosis factor-α (TNF-α)-induced intercellular adhesion molecule-1 (ICAM-1) expression and adhesion of HL-60 cells onto human umbilical vein endothelial cells (HUVEC), which are associated with inflammatory diseases. Moreover, <b>1</b> abolished TNF-α-induced Akt phosphorylation. Transfection of an activated Akt1 cDNA vector increased Akt phosphorylation and ICAM-1 expression like TNF-α. In addition, <b>1</b> and LY294002 blocked TNF-α-induced IκB-α degradation and nuclear p65 protein accumulation, as well as the DNA-binding activity of NF-κB. Compound <b>1</b> exhibits anti-inflammatory properties through the inhibition of TNF-α-induced ICAM-1 expression. The anti-inflammatory activity of <b>1</b> may be associated with the inhibition of the PI3K/Akt pathway and downstream target NF-κB activation in HUVEC cells

The relationships among the diameter of microfibers, width of observation channel and flow rate of continuous phase.

<p>The relationships among the diameter of microfibers, width of observation channel and flow rate of continuous phase.</p