Through whole-genome sequencing of 2,630 Icelanders and imputation into 11,114 Icelandic cases and 267,140 controls followed by testing in Danish and Iranian samples, we discovered 4 previously unreported variants affecting risk of type 2 diabetes (T2D). A low-frequency (1.47%) variant in intron 1 of CCND2, rs76895963[G], reduces risk of T2D by half (odds ratio (OR) = 0.53, P = 5.0 × 10(-21)) and is correlated with increased CCND2 expression. Notably, this variant is also associated with both greater height and higher body mass index (1.17 cm per allele, P = 5.5 × 10(-12) and 0.56 kg/m(2) per allele, P = 6.5 × 10(-7), respectively). In addition, two missense variants in PAM, encoding p.Asp563Gly (frequency of 4.98%) and p.Ser539Trp (frequency of 0.65%), confer moderately higher risk of T2D (OR = 1.23, P = 3.9 × 10(-10) and OR = 1.47, P = 1.7 × 10(-5), respectively), and a rare (0.20%) frameshift variant in PDX1, encoding p.Gly218Alafs*12, associates with high risk of T2D (OR = 2.27, P = 7.3 × 10(-7)).

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Growing evidence suggests that metabolic syndrome (MetS) has both genetic and environmental bases. We estimated the heritability of the MetS and its components in the families from the Tehran Lipid and Glucose Study (TLGS). We investigated 904 nuclear families in TLGS with two biological parents and at least one offspring (1565 parents and 2448 children), aged 3-90 years, for whom MetS information was available and had at least two members of family with MetS. Variance component methods were used to estimate age and sex adjusted heritability of metabolic syndrome score (MSS) and MetS components using SOLAR software. The heritability of waist circumference (WC), HDL-cholesterol (HDL-C), triglycerides (TGs), fasting blood sugar (FBS), systolic blood pressure (SBP) and diastolic blood pressure (DBP) as continuous traits after adjusting for age and gender were 27, 46, 36, 29, 25, 26 and 15%, respectively, and MSS had a heritability of 15%. When MetS components were analysed as discrete traits, the estimates of age and gender adjusted heritability for MetS, abdominal obesity, low HDL-C, high TG, high FBS and high blood pressure (BP) were 22, 40, 34, 38 and 23%, respectively (P < 0·05). Three factors were extracted from the six continuous traits of the MetS including factor I (BP), factor II (lipids) and factor III (obesity and FBS). Heritability estimation for these three factors were 7, 13 (P < 0·05) and 2%, respectively. The highest heritability was for HDL-C and TG. The results strongly encourage efforts to identify the underlying susceptibility genes.

Thrust-related anticlines in the Zagros Simply Folded Belt provide excellent exposed analogue structures for fractured reservoirs located in the more external sectors of the belt. In these structures it is possible to study the fracture network attributes and understand their relationships to the folding process, thus gathering fundamental information for fracture modelling in reservoirs. In this work we analyse the mesoscopic deformation pattern of the NW–SE-trending Bangestan anticline (SW Zagros, Iran) and discuss its relationship to the kinematic evolution of the hosting structure. The deformation pattern mostly includes extensional structures and pressure solution cleavages striking parallel to the fold axial trend (i.e. longitudinal), transversal extensional structures, and N–S- and E–W-striking extensional structures (oriented oblique to the fold axis). With the aid of deep wells and a transversal reflection seismic profile, we constructed a balanced cross-section of the anticline and propose a kinematic evolution pathway constrained by the mesoscopic deformation pattern. Longitudinal and transversal deformation structures developed before and/or in the very early stages of fold growth. During this stage, the Bangestan anticline grew as a set of unconnected décollement anticlines involving the Cambrian to Pliocenic sedimentary cover. In a later stage, inherited basement faults were reactivated with a right-lateral strike-slip component and the previously developed anticlines propagated laterally up to their complete linkage and thrust breakthrough. This produced the right-lateral strike-slip reactivation of longitudinal joints and the development of N–S- and E–W-striking extensional structures, which were also frequently reworked as strike-slip faults.