Clade 2 SS2 strains presented high genetic similarity to SS3 and SS7 and shared common competence and defensive elements with them but were significantly different from Clade 1 SS2 strains. Notably, although the cps loci shared by Clade 1 and 2 SS2 strains were almost identical, a specific region of the cps locus of strain NSUI002 (Clade 2 SS2) could be found in the SS3 cps locus but not in the Clade 1 SS2 strain. These data indicated that the SS2 strains in CC28 and CC29 might have acquired the cps locus through capsule switching, which could explain the distinct genetic lineages within the SS2 population.Bipolar disorder (BD) is a complex illness with variability at the level of symptom presentation, clinical course, cognitive capacity, and everyday function. Cognition is a key predictor of functional disability in BD, however, much remains unknown about the development and presentation of cognitive dysfunction in BD. Studies have shown that 30-50% of affectively stable people with BD are indistinguishable from healthy individuals in terms of cognitive presentation. In contrast, many people with BD have moderate to severe cognitive deficits, in some cases on par with what is typically observed in schizophrenia (SZ). Recent research efforts have aimed to parse this cognitive heterogeneity using unsupervised statistical techniques, resulting in more homogeneous subgroups. This method has provided new insights into the clinical and biological predictors of a potentially – neuroprogressive – declinin – gcognitive course in BD. Future studies that include detailed longitudinal follow-up in large BD cohorts hold promise for guiding the development of novel treatments that reach beyond the primary affective symptoms and target functionally relevant outcomes to promote full recovery.

Atherosclerosis is the most prominent underlying cause of cardiovascular disease (CVD). It is initiated by cholesterol deposition in the arterial intima, which causes macrophage recruitment and proinflammatory responses that promote plaque growth, necrotic core formation, and plaque rupture. Lipin-1 is a phosphatidic acid phosphohydrolase for glycerolipid synthesis. We have shown that lipin-1 phosphatase activity promotes macrophage pro-inflammatory responses when stimulated with modified low-density lipoprotein (modLDL) and accelerates atherosclerosis. Lipin-1 also independently acts as a transcriptional co-regulator where it enhances the expression of genes involved in β-oxidation. In hepatocytes and adipocytes, lipin-1 augments the activity of transcription factors such as peroxisome proliferator-activated receptor (PPARs). PPARs control the expression of anti-inflammatory genes in macrophages and slow or reduce atherosclerotic progression. Therefore, we hypothesize myeloid-derived lipin-1 transcriptional co-regulatory activity reduces atherosclerosis.

We used myeloid-derived lipin-1 knockout (lipin-1mKO) and littermate control mice and AAV8-PCSK9 along with high-fat diet to elicit atherosclerosis.

Lipin-1mKO mice had larger aortic root plaques than littermate control mice after 8 and 12 weeks of a high-fat diet. Lipin-1mKO mice also had increased serum proinflammatory cytokine concentrations, reduced apoptosis in plaques, and larger necrotic cores in the plaques compared to control mice.

Combined, the data suggest lipin-1 transcriptional co-regulatory activity in myeloid cells is atheroprotective.

Combined, the data suggest lipin-1 transcriptional co-regulatory activity in myeloid cells is atheroprotective.Extracellular vesicles (EV, exosomes and microvesicles -MV-) are 30-1000 nm particles surrounded by a phospholipid bilayer membrane that are released from almost all cell types through several pathways. EV encapsulate bioactive molecules, and the molecular cargo is determined by the trigger stimulating its release, reflecting its cell origin and biological functions. this website This review is primarily focused on the latest evidence of the roles of EV, released from cells involved in the different stages of atherothrombosis. The potential translation of this information to the clinical arena is also discussed. EV can have both pro- and anti-atherothrombotic effects depending on several factors, such as the type of vesicle (MV/exosome), its molecular cargo, its cell of origin, and the context in which are generated, i.e., the stimulus triggering its release. In fact, EV actively participate in every step of atherosclerosis onset and progression, and also in thrombus formation leading to a major adverse cardiovascular event. Moreover, EV have a determinant role in fibrous cap stability, thus determining the propensity of the plaque to rupture. On the other hand, and again, conditioned by the context and stimulus instigating its secretion, some EV may have protective biological functions, perhaps as a compensatory mechanism or even with reparative or regenerative potential. Therefore, the study of the implication of EV in atherothrombosis might be of relevance to unveil new therapeutic targets, vectors and biomarkers of cardiovascular disease (CVD).Internet addiction (IA), which can have different development patterns, is considered a serious problem among adolescents. Due to the increasing number of adolescent internet users in Mainland China, professionals are obligated to investigate the prevalence and predictors of IA persistence and incidence. This study investigated the prevalence of IA persistence and incidence among 1301 students in Mainland China across two years using a two-wave longitudinal design. Of the 187 students with IA in 7th grade, 40.64% had a persisting addiction by grade 9. Of the 1114 students without an IA in 7th grade, 10.32% had developed an IA by grade 9. Multilevel logistic regression analyses indicated that higher levels of depressive symptoms (odds ratio = 1.04; p = .04) and maternal education (odds ratio = 2.23; p = .01) could increase the likelihood of IA persistence. Significant predictors of IA incidence were being male (odds ratio = 0.59; p = .03), being an only child (odds ratio = 1.91; p = .01), having a low family income (odds ratio = 1.21; p less then .001), and experiencing school maladjustment (odds ratio = 1.01; p less then .01).