Middletonwestermann1496

This study investigated emotion regulation (i.e., emotional integration, suppression and dysregulation) as a transdiagnostic process underlying adolescents' internalizing and externalizing symptoms. Basic psychological need experiences were investigated as a possible underlying mechanism explaining this association. A heterogeneous sample of non-clinical and clinically-referred adolescents reported upon emotion regulation, basic psychological needs (i.e., need satisfaction and frustration), and both internalizing and externalizing problems. Results indicated that dysfunctional emotion regulation was positively linked to internalizing as well as externalizing problems. Need frustration was a partial mediator in this relation between emotion regulation and psychopathology. The findings suggest that both emotion regulation and basic psychological needs may play a transdiagnostic role in adolescents' internalizing and externalizing symptoms.Cerebral ischemia-reperfusion (I/R) injury is an inflammation-related disease. CHRFAM7A can regulate inflammatory responses. Therefore, the present study investigated the mechanism of CHRFAM7A in cerebral I/R injury. CHRFAM7A expression and inflammatory cytokine levels in patients with cerebral I/R injury and oxygen-glucose deprivation/reperfusion (OGD/R)-treated microglia were detected. The proliferation, inflammatory cytokine expressions, nod-like receptor protein 3 (NLRP3) level, cell pyroptosis, and viability and lactate dehydrogenase (LDH) activity in OGD/R-treated microglia were detected after CHRFAM7A overexpression. The NLRP3/Caspase-1 pathway was activated to assess the effect of CHRFAM7A on microglia. Expressions of microglial M1 phenotype marker iNOS and M2 marker Arg1 were detected. Downregulated CHRFAM7A and elevated inflammatory cytokine levels were observed in patients with cerebral I/R injury and OGD/R-treated microglia. In OGD/R-treated microglia, CHRFAM7A overexpression promoted cell proliferation and viability, reduced inflammation and LDH activity, and inhibited NLRP3 inflammasome activation and cell pyroptosis. Mechanically, CHRFAM7A inhibited microglia pyroptosis via inhibiting the NLRP3/Caspase-1 pathway and reduced cell inflammatory injury via promoting microglia polarization from M1 to M2. Overall, CHRFAM7A overexpression attenuated cerebral I/R injury by inhibiting microglia pyroptosis in a NLRP3/Caspase-1 pathway-dependent manner and promoting microglia polarization to M2 phenotype.Progesterone has been shown to regulate immunity during pregnancy, and progesterone administration may reduce inflammation-induced preterm labor. We sought to determine the maternal brain immune response to LPS-induced inflammation in pregnant and non-pregnant mice and whether additional progesterone supplementation attenuates this response. Pregnant (P n = 9) and non-pregnant mice (NP n = 9) were randomized to pretreatment with vaginal progesterone/carrier (Replens), daily from days 13 to 16. On days 15 and 16, LPS/saline was administered by intraperitoneal injection (Replens + saline n = 3; Replens + LPS n = 3; progesterone + LPS n = 3). Mice were sacrificed on day 16 and maternal serum analyzed for IL-6 levels and brains analyzed for nNOS, NF-kB, IL-6 protein levels and for immature myeloid cells (IMCs) and microglial activity. LPS significantly increased brain nNOS, NF-kB, and IL-6 in both NP and P mice, with significantly greater responses in P mice. In both NP and P groups, progesterone significantly attenuated LPS-induced increase of nNOS and NF-kB, however with no effect on serum IL-6. In the NP brains, LPS significantly increased IMC population and progesterone reduced the IMC phenotype to levels similar to controls. In P mice, neither LPS nor LPS + progesterone altered the brain IMC population. LPS significantly increased the microglial activity in both NP and P groups, which was attenuated by progesterone. Progesterone attenuates brain inflammatory response to LPS in both NP and P mice although it has no effect on systemic inflammation. In NP mice, progesterone attenuated the increase in brain IMC following LPS administration. Our results suggest that endogenous progesterone during pregnancy may protect the brain from LPS-induced inflammation.Alpha 7 nicotinic acetylcholine receptor (α7nAChR) is widely distributed in the nervous and non-cholinergic immune systems. It is necessary for the cholinergic transmitter to participate in the regulation of inflammatory response and is the key element of cholinergic anti-inflammatory pathway (CAP). Because of the profound impact of CAP on the immune system, α7nAChR is considered as a potential therapeutic target for the treatment of inflammatory diseases. Available evidences confirmed that manipulation of CAP by activating α7nAChR with either endogenous acetylcholine (ACh) or cholinergic agonists can substantially alleviate inflammatory responses both in vivo and in vitro. However, the mechanism through which CAP curbs the excessive pro-inflammatory responses and maintains immune homeostasis is not fully understood. Obtained clues suggest that the crosstalk between CAP and classical inflammatory pathways is the key to elucidate the anti-inflammatory mechanism, and the impacts of CAP activation in α7nAChR-expressing immune cells are the foundation of the immunoregulatory property. In this article, we review and update the knowledge concerning the progresses of α7nAChR-based CAP, including α7nAChR properties, signal transductions, interactions with classic immune pathways, and immunoregulatory functions in different immune cells. Certain critical issues to be addressed are also highlighted. By providing a panoramic view of α7nAChR, the summarized evidences will pave the way for the development of novel anti-inflammatory reagents and strategy and inspire further researches.Rheumatoid arthritis (RA) is an autoimmune and inflammatory disease with strong genetic influence, especially upon immune response components. Several cytokines from the toll-like receptors activation pathway display recognized role for RA establishment. However, few studies have verified the role of key mediators such as MYD88 gene and its genetic variants. In the present study, we aim to evaluate the rs6853 functional single-nucleotide variation (SNV) role in RA etiopathogenesis, clinical severity status, and its impact in MYD88 mRNA levels and IL-lβ protein levels. Necrosulfonamide For the association study, a total of 423 RA patients and 346 health individuals, enrolled as control, from Northeast and Southeast Brazil were genotyped using specific Taqman probe. For the gene expression assays, we performed a MYD88 rs6853 genotype-guided monocyte cell culture divided into non-stimulated and lypopolysaccharides (LPS)-stimulated cells from healthy individuals. MYD88 gene expression was measured using primer specifics while IL-1β levels were evaluated by ELISA.