Medical history, anthropometric measurements and oral habits of eligible patients.

<p>The eligible subjects were recruited patient from 2008 to 2010. N = 10,457.</p><p>Abbreviations: BMI, body mass index; CKD, chronic kidney disease; CVDs, cerebrovascular diseases; HC, healthy control; HR, high risk.</p>a<p>Underweight: BMI<18.5; Normal weight: BMI = 18.5–24; Overweight: BMI = 24–27; Obesity: BMI>27.</p>b<p>Chi-square test. P<0.05 was considered statistically significant.</p

Cumulative OPD expenditures per person in WM, DENT, and TCM from 2000 to 2008.

<p>The eligible subjects were recruited from 2008 to 2010. N = 10,457. Abbreviations: CKD, chronic kidney disease; DENT, Dentistry; HC, healthy control; HR, high risk; OPD, outpatient; NT$, new Taiwan dollars; TCM, Traditional Chinese Medicine; WM, Western Medicine.</p

The average annual number of OPD visits and expenditures per person in WM and DENT among eligible patients and different CKD stages from 2000 to 2008.

<p>The eligible subjects were recruited patient from 2008 to 2010. N = 10,457.</p><p>Abbreviations: CKD, chronic kidney disease; DENT, Dentistry; HC, healthy control; HR, high risk NT$, new Taiwan dollars; OPD, outpatient; WM, Western Medicine.</p>a<p>Expenditures were rounded to the nearest whole dollar.</p>b<p>ANOVA. P<0.05 was considered statistically significant.</p>c<p>Scheffe's test : CKD>HR>HC.</p>d<p>Scheffe's test : HR>HC.</p>e<p>Scheffe's test :Stage5>Stage4>Stage3b>Stage3a>Stage2>Stage1.</p

The average annual number of OPD visits, and expenditures per person of different dental procedures among eligible patients and different CKD stages from 2000 to 2008.

<p>The eligible subjects were recruited patient from 2008 to 2010. N = 10,457.</p><p>Abbreviations: CKD, chronic kidney disease; DENT, Dentistry; HC, healthy control; HR, high risk NT$, new Taiwan dollars; OPD, outpatient; WM, Western Medicine.</p>a<p>Expenditures were rounded to the nearest whole dollar.</p>b<p>ANOVA. P<0.05 was considered statistically significant.</p>c<p>Scheffe's test : HR>CKD.</p>d<p>Scheffe's test : HC>HR>CKD.</p>e<p>Scheffe's test : HR>CKD>HC.</p>f<p>Scheffe's test : HR>CKD>HC.</p>g<p>Scheffe's test : HR>HC>CKD.</p>h<p>Scheffe's test : Stage1>Stage2>Stage3a>Stage3b>Stage4>Stage5.</p>i<p>Scheffe's test : Stage3b>Stage2>Stage3a>Stage4>Stage5.</p

Demographic characteristics and socioeconomic status of eligible subjects.

<p>Unless otherwise indicated, values are number (percentage). The eligible subjects were recruited patient from 2008 to 2010. N = 10,457.</p><p>Abbreviations: CKD, chronic kidney disease; HC, healthy control; HR, high risk; NT$, new Taiwan dollars.</p>a<p>Chi-square test. P<0.05 was considered statistically significant.</p

Tumor Necrosis Factor-Alpha and the ERK Pathway Drive Chemerin Expression in Response to Hypoxia in Cultured Human Coronary Artery Endothelial Cells

<div><p>Background</p><p>Chemerin, a novel adipokine, plays a role in the inflammation status of vascular endothelial cells. Hypoxia causes endothelial-cell proliferation, migration, and angiogenesis. This study was aimed at evaluating the protein and mRNA expression of chemerin after exposure of human coronary artery endothelial cells (HCAECs) to hypoxia.</p><p>Methods and Results</p><p>Cultured HCAECs underwent hypoxia for different time points. Chemerin protein levels increased after 4 h of hypoxia at 2.5% O₂, with a peak of expression of tumor necrosis factor-alpha (TNF-alpha) at 1 h. Both hypoxia and exogenously added TNF-alpha during normoxia stimulated chemerin expression, whereas an ERK inhibitor (PD98059), ERK small interfering RNA (siRNA), or an anti-TNF-alpha antibody attenuated the chemerin upregulation induced by hypoxia. A gel shift assay indicated that hypoxia induced an increase in DNA-protein binding between the chemerin promoter and transcription factor SP1. A luciferase assay confirmed an increase in transcriptional activity of SP1 on the chemerin promoter during hypoxia. Hypoxia significantly increased the tube formation and migration of HCAECs, whereas PD98059, the anti-TNF-alpha antibody, and chemerin siRNA each attenuated these effects.</p><p>Conclusion</p><p>Hypoxia activates chemerin expression in cultured HCAECs. Hypoxia-induced chemerin expression is mediated by TNF-alpha and at least in part by the ERK pathway. Chemerin increases early processes of angiogenesis by HCAECs after hypoxic treatment.</p></div

Analysis of Associations of Human BAFF Gene Polymorphisms with Autoimmune Thyroid Diseases

<div><p>Background</p><p>The B-lymphocyte-activating factor (BAFF) is associated with B-cell functions, and gene polymorphisms of the BAFF have been linked to autoimmune diseases (AIDs). In this study, we explored possible associations of two BAFF single-nucleotide polymorphisms (SNPs), rs1041569 and rs2893321, with autoimmune thyroid diseases (AITDs) in an ethnic Chinese population.</p><p>Material and Methods</p><p>In total, 319 Graves’ disease (GD), 83 Hashimoto’s thyroiditis (HT) patients, and 369 healthy controls were enrolled. Polymerase chain reaction-restriction fragment length polymorphism and direct sequencing were used to genotype rs2893321 and rs1041569.</p><p>Results</p><p>There was a significant difference in frequencies of the G allele and AG+GG genotype of rs2893321 between the GD and control groups (<i>p</i> = 0.013, odds ratio (OR) = 0.76, and <i>p</i> = 0.017, OR = 0.68, respectively) and between the AITD and control groups (<i>p</i> = 0.009, OR = 0.76, and, <i>p</i> = 0.014, OR = 0.69, respectively). The AA genotype of rs2893321 was associated with low titers of the thyroid-stimulating hormone receptor antibody (TSHRAb) (<i>p</i> = 0.015) in males but not in females. The AA genotype of rs2893321 was associated with the presence of two different types of thyroid autoantibody (TAb) (TSHRAb and Hashimoto’s autoantibody (anti-thyroglobulin or anti-microsomal antibody)) in females and with that of one type in males.</p><p>Conclusions</p><p>rs2893321 may be a susceptible genetic variant for the development of GD and AITDs. Associations of rs2893321 with susceptibility to GD and AITDs and the correlation between rs2893321 and TAb exhibit a dimorphic pattern. Additional studies with larger sample sizes are required to confirm our findings.</p></div

Analysis of Associations of Human BAFF Gene Polymorphisms with Autoimmune Thyroid Diseases - Fig 1

<p>Thyroid-stimulating hormone (TSH) receptor antibody titers at the baseline in different genotypes of rs1041569 (Panel A) and rs2893321 (Panel B) in Graves’ disease in females and males. TSHRAb, thyroid-stimulating hormone receptor antibody; the number in the column indicates the number of patients.</p

The ERK pathway mediates the hypoxia-induced increase in chemerin expression in HCAECs.

<p>(A and B) The hypoxia-induced increase in chemerin expression was blocked by an ERK inhibitor (PD98059), ERK siRNA, or an anti-TNF antibody. Addition of exogenous TNF—alpha during normoxia increased chemerin expression (n = 4 per group); *p < 0.01 compared to control.</p

Binding of chemerin promoter with the SP1 transcription factor and transcriptional activity of the SP1-binding site of the chemerin promoter are increased in hypoxic HCAECs.

<p>(A) The electrophoretic mobility shift assay (EMSA) showed an increase in binding of chemerin promoter and SP1 in HCAECs during 2.5% O₂ hypoxia. (B and C) The luciferase reporter assay revealed that hypoxia at 2.5% O₂ increased the transcriptional activity of SP1 on the chemerin promoter as compared to the chemerin mutant. Transcriptional activity was suppressed by PD98059 and an anti-TNF-alpha antibody (Ab; n = 3 per group); *p < 0.01 compared to control, ^§p < 0.01 compared to time point 1 h.</p