Correlation between sTWEAK and AS but only in men, although this association disappeared after adjusting for potential confounders. Moreno et al. observed that intima-media thickness was positively associated with sCD163 concentrations with independence of traditional CVRF and inflammatory markers. However, we failed to find any association between AS and sCD163 in our cohort. Thereafter, we could not confirm the association between these two markers and AS; a Gefitinib EGFR/HER2 inhibitor marker of subclinical atherosclerosis, in T1DM patients. There are no previous data on the role of sTWEAK or sCD163 in the pathogenesis of AS. It is likely that carotid intima-media thickness reflects more advanced structural atherosclerotic changes in the arterial wall than AS. Our population was younger than those included in previous studies reporting associations between intima-media thickness and sTWEAK or sCD163 concentrations. Perhaps these differences may explain the lack of association between AS and these markers in our study. In prospective studies sTWEAK serum levels independently predicted an adverse prognosis in patients with chronic heart failure. In addition, decreased sTWEAK level is an independent predictor of CV outcomes in patients with nondialysis chronic kidney disease and with peripheral arterial disease. In contrast, elevated sTWEAK levels predicted an adverse short-term outcome in patients with ST-elevation myocardial infarction and CV and all-cause mortality in hemodialysis patients. Therefore, future prospective studies are needed to better understand the potential role of these markers in atherosclerosis and their prognosis value. We are aware that one of the limitations of our study is the cross-sectional design; therefore any inference regarding causality cannot be made. In addition, its observational design does not allow us to ensure complete control of all the potential confounding factors. The concentrations of sTWEAK and sCD163 were measured only once, which might underestimate the association between them and AS. In conclusion, our study demonstrates sTWEAK is decreased in T1DM patients compared with age and sex-matched healthy subjects, even after controlling for classic CVRF. However, neither marker is associated with AS after adjusting for potential confounders. The core features of schizophrenia include disturbances in diverse cognitive functions that depend on the neural circuitry of the cerebral cortex. In the cortex of subjects with schizophrenia, inhibitory neurotransmission mediated by c-aminobutyric acid appears to be altered, as indicated by lower levels of the mRNAs encoding the 67 kilodalton isoform of glutamic acid decarboxylase, the enzyme principally responsible for GABA synthesis, and the GABA membrane transporter 1, which mediates the reuptake of synaptically released GABA. These alterations appear to involve specific subsets of GABA neurons. For example, the mRNAs encoding parvalbumin and somatostatin, each of which is expressed in a separate subset of cortical GABA neurons, are decreased in schizophrenia. Moreover, the reductions in GAD67 and GAT1 appear to be prominent in PV- as well as SSTexpressing GABA neuron subsets. On the other hand, measures of the mRNA and protein for calretinin, which is expressed by a third subset of GABA neurons, were unaltered in the cortex of subjects with schizophrenia. Together, these findings indicate that cortical dysfunction in schizophrenia selectively involves two separate subsets of GABA neurons: PV and SST neurons. Understanding the molecular processes in these neurons and that contribute to their distinctive functions.