The effect of (A) non-liganded PPARγ1 on PPARδ signalling and of (B) non-liganded PPARδ on PPARγ1 signalling.

<p>COS-1 cells were transiently transfected with (per well in six-well plates) 50 ng (A) pCLDN-hPPARδ or (B) pCDLN-hPPARγ1 and 250 ng (A) pCLDN or pCLDN-hPPARγ1 and (B) pCLDN or pCLDN-hPPARδ, respectively.</p

PPARδΔAF2 represses (A) PPARδ and (B) PPARγ1 signalling. (C) PPARδΔAF2 represses TK-promoter activity in a ligand-enhanced fashion.

<p>COS-1 cells were transiently transfected with (per well in six-well plates) (A) 50 ng pCLDN-hPPARδ or (B) pCDLN-hPPARγ1 and 250 ng pCLDN or pCLDN-hPPARδΔAF2. (C) and (D) T47D cells were transfected with (per well in a six-well plate) 500 ng pCLDN, pCLDN-hPPARδΔAF2 or pCLDN-hPPARδ. (D) is identical to (C) except for the two additional bars representing over-expression of PPARδ with and without CF.</p

(A) The PPARδ LBD is functional with respect to transcriptional transactivation and RXR heterodimerisation and (B), (C) and (D) possess ligand-dependent dominant negative behaviour.

<p>(A) COS-1 cells were transfected with 500 ng pCMVgRXR and 500 ng pCLDN or pCLDN-δLBD. (B), (C) and (D) COS-1 cells were transiently transfected with: (B) 500 ng pJ3Nuc (hPPARδ expression plasmid) and 0 to 500 ng pCLDN or pCLDN-δLBD; (C) 50 ng pCLDN-hPPARγ1 and 0 to 500 ng pCLDN or pCLDN-δLBD; (D) 50 ng pCLDN-hPPARγ1 and 500 ng pCLDN-δLBD.</p

Effect of <i>FLG</i> R501X and 2282del4 on bilateral middle ear effusion.

<p>Type A indicates normal middle ear function. Type B indicates middle ear effusion. Type C1 indicates slight negative middle ear pressure. Type C2 indicates negative middle ear pressure. Other indicates grommet, perforation, or type C2 tympanogram in at least one ear. Expected correspond to the expected contingency values were the null hypothesis is that the probabilities for each phenotype are independent of the mutation.</p

Effect of carrier (1) (<i>FLG</i> R501X or <i>FLG</i> 2282del4) versus non-carrier (0) status on 30 hearing variables as tested by one-way ANOVA tests.

<p>Effect of carrier (1) (<i>FLG</i> R501X or <i>FLG</i> 2282del4) versus non-carrier (0) status on 30 hearing variables as tested by one-way ANOVA tests.</p

Effect of <i>FLG</i> R501X on 30 hearing variables as tested by one-way ANOVA tests.

<p>Effect of <i>FLG</i> R501X on 30 hearing variables as tested by one-way ANOVA tests.</p

Multivariate regression analysis of Risk of Type 2 Diabetes Mellitus in the Go-DARTS study.

*<p>P-values were calculated under an additive model using a binary logistic regression model including gender as a categorical variable (Males  =  referent) and age and BMI as continuous variables.</p><p>P value for interaction between severe obesity and I148M for type 2 diabetes risk  = 0.002.</p><p>Abbreviations: Go-DARTS, Genetics of Diabetes Audit and Research Tayside Scotland; OR, odds ratio; F, female; BMI, body mass index; PNPLA3, patatin-like phospholipase domain-containing 3.</p

Clinical Characteristics of Go-DARTS Study Participants Stratified by PNPLA3 I148M Genotype.

<p>Abbreviations: Go-DARTS, Genetics of Diabetes Audit and Research Tayside Scotland; PNPLA3, patatin-like phospholipase domain-containing 3; II, individuals with two 148I alleles; MM, individuals with two 148M alleles; IM, heterozygotes; n, number; HOMA-IR, homeostasis model assessment for insulin resistance HDL, high-density lipoprotein; ALT, alanine transferase; HbA1c, glycated hemoglobin; ns, P value≥0.05.</p><p>Plus-minus values are means ± SD.</p>*<p>P values were calculated using linear regression model including age, body-mass index and gender for all variables. HOMA-IR, triglycerides and ALT were log-transformed before entering the model. See methods for more details on the statistical analyses.</p

Serum triglycerides and homeostasis model assessment for insulin resistance (HOMA-IR) at 2- and 10-year follow-up.

<p>Serum triglycerides (panel A and B) levels and HOMA-IR (panel C and D) at 2- and 10- year follow up (FU) in the control (A, C) and the surgery (B, D) group across the <i>PNPLA3</i> genotypes. Values are means and standard deviations. * HOMA-IR values are shown only in non-diabetic individuals.</p

Baseline Clinical Characteristics of SOS Study Participants Stratified by <i>PNPLA3</i> I148M Genotype.

<p>Abbreviations: SOS, Swedish obese subjects; PNPLA3, patatin-like phospholipase domain-containing 3; II, individuals with two 148I alleles; MM, individuals with two 148M alleles; IM, heterozygotes; n, number; HOMA-IR, homeostasis model assessment for insulin resistance; HDL, high-density lipoprotein; AST, aspartate transferase; ALT, alanine transferase.</p><p>Plus-minus values are means ± SD.</p>*<p>P values were calculated using linear regression model including age, gender and body-mass index for all variables. HOMA-IR, triglycerides, ALT and AST were log-transformed before entering the model. Male gender, lipid-lowering medications and type 2 diabetes distribution were compared by χ2 test. See methods for more details on the statistical analyses.</p>†<p>Fasting insulin and HOMA-IR are shown only in non-diabetic individuals.</p