Are you thinking what I’m thinking? Peer group similarities in adolescent hostile attribution tendencies

A bias towards attributing hostile intent to others has been linked to aggression. In an adolescent sample, we investigated whether peer group homophily exists in the tendency towards attributing hostile intent. We assessed hostile attribution tendencies and self-reported aggressive behaviours in a normative sample of 910 adolescents, and computed average peer group scores based on nominated friend scores. Results indicated that adolescents showed significant correlations between their own level of hostile attributions and that of their peer group. Further analyses indicated that this effect occurred specifically in reciprocal friendships, and was retained even once own and peer group level of aggression were controlled.

Pleiotropic effects of TCF7L2 gene variants and its modulation in the metabolic syndrome: from the LIPGENE study

Aims/hypothesis: Variants of the TCF7L2 gene predict the development of type 2 diabetes mellitus (T2DM). We investigated the associations between gene variants of TCF7L2 and clinical features of the metabolic syndrome (MetS) (an entity often preceeding T2DM), and their interaction with non-genetic factors, including plasma saturated fatty acids (SFA) concentration and insulin resistance (IR). Methods: Fasting lipid profiles, insulin sensitivity, insulin secretion, anthropometrics, blood pressure and 10 gene variations of the TCF7L2 gene were determined in 450 subjects with MetS. Results: Several single nucleotide polymorphisms (SNP) showed phenotypic associations independent of SFA or IR. Carriers of the rare T allele of rs7903146, and of three other SNPs in linkage disequilibrium with rs7903146, had lower blood pressure and insulin secretion. High IR and the presence of the T-allele of rs7903146 acted synergistically to define those with reduced insulin secretion. Carriers of the minor allele of rs290481 exhibited an altered lipid profile, with increased plasma levels of apolipoprotein B, non-esterified fatty acids, cholesterol and apolipoprotein B in triglyceride rich lipoproteins, and LDL cholesterol. Carriers of the minor allele of rs11196224 that had higher plasma SFA levels showed elevated procoagulant/proinflammatory biomarkers, impaired insulin secretion and increased IR, whereas carriers of the minor allele of rs17685538 with high plasma SFA levels exhibited higher blood pressure. Conclusions/interpretation: SNP in the TCF7L2 gene are associated with differences in insulin secretion, blood pressure, blood lipids and coagulation in MetS patients, and may be modulated by SFA in plasma or IR.

Obesity and body fat classification in the metabolic syndrome: impact on cardiometabolic risk metabotype

Obesity is a key factor in the development of the metabolic syndrome (MetS), which is associated with increased cardiometabolic risk. We investigated whether obesity classification by body mass index (BMI) and body fat percentage (BF%) influences cardiometabolic profile and dietary responsiveness in 486 MetS subjects (LIPGENE dietary intervention study). Anthropometric measures, markers of inflammation and glucose metabolism, lipid profiles, adhesion molecules and haemostatic factors were determined at baseline and after 12 weeks of 4 dietary interventions (high saturated fat (SFA), high monounsaturated fat (MUFA) and 2 low fat high complex carbohydrate (LFHCC) diets, 1 supplemented with long chain n-3 polyunsaturated fatty acids (LC n-3 PUFAs)). 39% and 87% of subjects classified as normal and overweight by BMI were obese according to their BF%. Individuals classified as obese by BMI (± 30 kg/m2) and BF% (± 25% (men) and ± 35% (women)) (OO, n = 284) had larger waist and hip measurements, higher BMI and were heavier (P < 0.001) than those classified as non-obese by BMI but obese by BF% (NOO, n = 92). OO individuals displayed a more pro-inflammatory (higher C reactive protein (CRP) and leptin), pro-thrombotic (higher plasminogen activator inhibitor-1 (PAI-1)), pro-atherogenic (higher leptin/adiponectin ratio) and more insulin resistant (higher HOMA-IR) metabolic profile relative to the NOO group (P < 0.001). Interestingly, tumour necrosis factor alpha (TNF-α) concentrations were lower post-intervention in NOO individuals compared to OO subjects (P < 0.001). In conclusion, assessing BF% and BMI as part of a metabotype may help identify individuals at greater cardiometabolic risk than BMI alone.

Nonlinear saturation of baroclinic instability: part I: the two-layer model

A rigorous bound is derived which limits the finite-amplitude growth of arbitrary nonzonal disturbances to an unstable baroclinic zonal flow within the context of the two-layer model. The bound is valid for conservative (unforced) flow, as well as for forced-dissipative flow that when the dissipation is proportional to the potential vorticity. The method used to derive the bound relies on the existence of a nonlinear Liapunov (normed) stability theorem for subcritical flows, which is a finite-amplitude generalization of the Charney-Stern theorem. For the special case of the Philips model of baroclinic instability, and in the limit of infinitesimal initial nonzonal disturbance amplitude, an improved form of the bound is possible which states that the potential enstrophy of the nonzonal flow cannot exceed ϵβ2, where ϵ = (U − Ucrit)/Ucrit is the (relative) supereriticality. This upper bound turns out to be extremely similar to the maximum predicted by the weakly nonlinear theory. For unforced flow with ϵ < 1, the bound demonstrates that the nonzonal flow cannot contain all of the potential enstrophy in the system; hence in this range of initial supercriticality the total flow must remain, in a certain sense, “close” to a zonal state.