Social anxiety and associated factors among graduate students under the normalization of epidemic prevention and control / 中国学校卫生

Objective@#To understand social anxiety and relevant factors among graduate students under the normalization stage of COVID-19 epidemic prevention and control.@*Methods@#Using convenience sampling method, an online questionnaire survey on graduate students from 5 universities in Jiangsu Province was conducted. Measurements used in the survey includes General Self Efficacy Scale (GSES), General Alienation Scale (GAS), Interaction Anxiousness Scale (IAS) and self made survey for basic information and household living conditions.@*Results@#The overall score of graduate students self efficacy was (2.58±0.50). Average score was (30.68±6.22) for alienation, and (47.55±8.77) for interaction anxiety, with detection rate of social anxiety being 43.96%. Increased dependence on smartphones and electronic devices ( OR=1.86, 95%CI =1.32-2.61) and high alienation score (medium level: OR=2.06, 95%CI =1.45-2.92; high level: OR=5.19, 95%CI =1.00-27.00) were positively correlated with social anxiety. Increased communication with friends ( OR=0.65, 95%CI =0.47-0.90 and high self efficacy (medium level: OR= 0.37 , 95%CI =0.21-0.66; high level: OR=0.15, 95%CI =0.08-0.30) were negatively correlated with social anxiety.@*Conclusion@#At the normalization stage of COVID-19 epidemic prevention and control, social anxiety of graduate students is one of the mental health issues which need further attention. Participation in peer support helps prevent social anxiety through developing self efficacy, alleviating individual alienation, and reducing dependence on electronic devices among graduate students.

Correlation analysis between short-term insulin-like growth factor-I and glucose intolerance status after transsphenoidal adenomectomy in acromegalic patients: a large retrospective study from a single center in China

ABSTRACT Objectives: Our study aimed to investigate the associations of glucose tolerance status with insulin-like growth factor-I (IGF-I) and other clinical laboratory parameters of acromegalic patients before and after the patients underwent transsphenoidal adenomectomy (TSA) by conducting a single-center, retrospective study. Subjects and methods: A total of 218 patients with acromegaly who had undergone TSA as the first treatment were retrospectively analyzed. Serum IGF-I, growth hormone (GH) and glucose levels were measured before and after surgery. Results: The follow-up levels for random GH, GH nadir, and the percentage of the upper limit of normal IGF-I (%ULN IGF-I) were decreased significantly. The percentages of normal (39.0%), early carbohydrate metabolism disorders (33.0%) and diabetes mellitus (28.0%) changed to 70.2%, 16.5% and 13.3%, respectively, after TSA. %ULN IGF-I at baseline was higher in the diabetes mellitus (DM) group than in the normal glucose tolerance group and impaired glucose tolerance (IGT) /impaired fasting glucose (IFG) groups before TSA, and the DM group exhibited a greater reduction in %ULN IGF-I value after surgery. The follow-up %ULN IGF-I value after surgery was significantly lower in the improved group, and Pearson's correlation analysis revealed that the reductions in %ULN IGF-I corresponded with the reductions in glucose level. Conclusion: This study examined the largest reported sample with complete preoperative and follow-up data. The results suggest that the age- and sex-adjusted IGF-I level, which reflects altered glucose metabolism, and the change of it are associated with improved glucose tolerance in acromegalic patients both before and after TSA.

Functionally diverse ligands modulate different activation states of the formyl peptide receptor 2, a G protein-coupled receptor / 中国药理学与毒理学杂志

OBJECTIVE To identify the mechanisms by which the formyl peptide receptor 2 (FPR2) mediates both inflammatory and anti-inflammatory signaling in an agonist-dependent manner. METHODS Cells expressing FPR2 were incubated with weak agonists, Aβ42 and Ac2-26, before stimulation with a strong agonist, WKYMVm. Calcium mobilization, cAMP inhibition and MAP kinase activation were measured. Intramolecular FRET were determined using FPR2 constructs with an ECFP attached to the C- terminus and a FlAsH binding motif embedded in the first or third intracellular loop (IL1 or IL3, respectively). RESULTS Aβ42 did not induce significant Ca2 + mobilization, but positively modulated WKYMVm-induced Ca2 + mobilization and cAMP reduction in a dose-variable manner within a narrow range of ligand concentrations. Treating FPR2-expressing cells with Ac2-26, a peptide with anti-inflam?matory activity, negatively modulated WKYMVm-induced Ca2 + mobilization and cAMP reduction. Intra?molecular FRET assay showed that stimulation of the receptor constructs with Aβ42 brought the C-terminal domain closer to IL1 but away from IL3. An opposite conformational change was induced by Ac2-26. The FPR2 conformation induced by Aβ42 corresponded to enhanced ERK phosphorylation and attenuated p38 MAPK phosphorylation, whereas Ac2-26 induced FPR2 conformational change corresponding to elevated p38 MAPK phosphorylation and reduced ERK phosphorylation. CONCLUSION Aβ42 and Ac2-26 induce different conformational changes in FPR2. These findings provide a structural basis for FPR2 mediation of inflammatory vs anti-inflammatory functions and identify a type of receptor modulation that differs from the classic positive and negative allosteric modulation.

Biphasic modulation of chemerin peptide-induced calcium flux and ERK phosphorylation by amyloid beta peptide / 中国药理学与毒理学杂志

OBJECTIVE The chemokine-like receptor 1 (CMKLR1, ChemR23) is a functional receptor for chemerin, the chemerin-derived nonapeptide (C9), and the amyloid β peptide 1-42 (Aβ42). Because these peptides share little sequence homology, studies were conducted to investigate their pharmaco?logical properties and regulation at CMKLR1. METHODS Cells expressing CMKLR1 were incubated with Aβ42 before stimulation with a strong agonist, the C9 peptide. Calcium mobilization, cAMP inhibition and MAP kinase activation were measured. Intramolecular FRET were determined using CMKLR1 constructs with an ECFP attached to the C- terminus and a FlAsH binding motif embedded in the first intracellular loop (IL1). RESULTS Binding of both Aβ42 and the C9 peptide induced CMKLR1 internal?ization, but only the Aβ42-induced receptor internalization involved clathrin-coated pits. Likewise, Aβ42 but not C9 stimulated β-arrestin 2 translocation to plasma membranes. A robust Ca2+ flux was observed following C9 stimulation, whereas Aβ42 was ineffective even at micromolar concentrations. Despite its low potency in calcium mobilization assay, Aβ42 was able to alter C9 -induced Ca2+ flux in dose-dependent manner: a potentiation effect at 100 pmol·L-1 of Aβ42 was followed by a suppression at 10 nmol·L-1 and further potentiation at 1 μmol·L-1. This unusual and biphasic modulatory effect was also seen in the C9-induced ERK phosphorylation but the dose curve was opposite to that of Ca2+ flux and cAMP inhibition, suggesting a reciprocal regulatory mechanism. Intramolecular FRET assay confirmed that Aβ42 modulates CMKLR1 rather than its downstream signaling pathways. CONCLUSION These findings suggest Aβ42 as an allosteric modulator that can both positively and negatively regulate the activation state of CMKLR1 in a manner that differs from existing allosteric modulatory mechanisms.