IntroductionThis study aimed to evaluate the knowledge, attitudes, and practices (KAP) of Chinese endocrinologists regarding congenital adrenal hyperplasia (CAH), which is essential for enhancing clinical differentiation skills and improving fertility management in non-classic CAH patients.MethodsThis cross-sectional study was conducted between July 27 and August 23, 2023, using a questionnaire distributed to 475 endocrinologists across China. KAP levels were assessed using a 70% maximum score threshold for descriptive purposes, and factors associated with KAP were identified via multivariate logistic regression.ResultsThe median scores were 21/27 (knowledge), 35/40 (attitudes), and 28/35 (practices). Despite positive attitudes, significant gaps in fertility-related knowledge were evident: nearly 30% of respondents failed to recognize that female CAH patients could achieve natural pregnancy through proper individualized treatment, and 24% failed to identify fertility preservation as a key treatment goal. Diagnostic confidence was also limited (53.9%), with over half of participants unclear on the most common enzyme deficiencies crucial for differential diagnosis. Logistic regression analysis revealed that having a doctoral degree, an intermediate or senior professional rank, and experience in diagnosing CAH were associated with more proactive clinical practices, especially in patient education and reproductive health counseling.ConclusionWhile Chinese endocrinologists demonstrate generally positive attitudes toward CAH, significant knowledge and practice gaps persist, particularly in fertility management and diagnostic differentiation. The limited awareness of reproductive outcomes and low diagnostic confidence highlight an urgent need for targeted education to improve individualized fertility treatment options and reduce misdiagnosis in clinical practice.

Background Recurrent Miscarriage (RM) is a chronic and heterogeneous autoimmune disease. Platelet factor 4 (PF4) has been found to be involved in the pathogenesis of RM.Objective We aimed to explore the role and mechanism of PF4 on trophoblasts in RM in vitro.Methods In this study, the expression of PF4 and PF4 receptor CXC chemokine receptor 3 (CXCR3) in the placentas of patients with RM were analyzed by RT-qPCR and western blotting. Serum PF4 level was tested by ELISA. Following PF4 silencing and SOCS3 overexpression in HTR-8/SVneo cells, cell proliferation was detected by CCK-8, colony formation, and EDU assays. Wound healing and transwell assays separately evaluated cell migration and invasion. Immunofluorescence assay determined E-cadherin expression. Tube formation assay was used to measure the angiogenesis. Western blotting examined the expression of metastasis, epithelial-mesenchymal transition (EMT) and suppressor of cytokine signaling 3 (SOCS3)/signal transducer and activator of transcription 3 (STAT3) signaling-associated proteins.Results The results revealed that PF4 displayed increased expression in placental villus tissues of RM patients. Serum PF4 level was also elevated in RM patients. PF4 silencing promoted the proliferation, migration, invasion, EMT, and angiogenesis of HTR-8/SVneo cells. Additionally, PF4 knockdown downregulated SOCS3 expression to activate STAT3 signaling. SOCS3 overexpression countervailed the effects of PF4 deficiency on HTR-8/SVneo cells.Conclusion In summary, PF4 participated in the proliferation, migration, invasion, EMT and angiogenesis of trophoblast cells by modulating the SOCS3/STAT3 signaling pathway, indicating that targeting the PF4/SOCS3/STAT3 pathway could be a novel therapy for RM.

Glucagon-like peptide 1 (GLP1), which is mainly processed and cleaved from proglucagon in enteroendocrine cells (EECs) of the intestinal tract, acts on the GLP1 receptor in pancreatic cells to stimulate insulin secretion and to inhibit glucagon secretion. However, GLP1 processing is not fully understood. Here, we show that reticulon 4B (Nogo-B), an endoplasmic reticulum (ER)-resident protein, interacts with the major proglucagon fragment of proglucagon to retain proglucagon on the ER, thereby inhibiting PCSK1-mediated cleavage of proglucagon in the Golgi. Intestinal Nogo-B knockout in male type 2 diabetes mellitus (T2DM) mice increases GLP1 and insulin levels and decreases glucagon levels, thereby alleviating pancreatic injury and insulin resistance. Finally, we identify aberrantly elevated Nogo-B expression and inhibited proglucagon cleavage in EECs from diabetic patients. Our study reveals the subcellular regulatory processes involving Nogo-B during GLP1 production and suggests intestinal Nogo-B as a potential therapeutic target for T2DM. Glucagon-like peptide 1 (GLP1) is processed and cleaved from proglucagon to stimulate insulin secretion. Here, authors show that Nogo-B interacts with proglucagon to retain it on the ER, thereby inhibiting PCSK1-mediated cleavage of proglucagon and secretion of GLP1.

BACKGROUND:Limb body wall complex (LBWC) is a fatal malformation characterized by major defects in the fetal abdominal or thoracic wall, visceral herniation, significant scoliosis or spina bifida, limb deformities, craniofacial deformities, and umbilical cord abnormalities (short or absent umbilical cord). Early diagnosis of this condition is of great clinical significance for clinical intervention and pregnancy decision-making. With the rapid development of fetal ultrasound medicine, early pregnancy (11-13+6 wk) standardized prenatal ultrasound examinations have been widely promoted and applied.AIM:To explore the value of prenatal ultrasound in the diagnosis of fetal LBWC syndrome during early pregnancy.METHODS:The ultrasonographic data and follow-up results of 18 cases of fetal LBWC diagnosed by prenatal ultrasound during early pregnancy (11-13+6 wk) were retrospectively analyzed, and their ultrasonographic characteristics were analyzed.RESULTS:Among the 18 fetuses with limb wall abnormalities, there were spinal dysplasia (18/18, 100%), varying degrees of thoracoschisis and gastroschisis (18/18, 100%), limb dysplasia in 6 cases (6/18, 33%), craniocerebral malformations in 4 cases (4/18, 22%), thickening of the transparent layer of the neck in 5 cases (5/18, 28%), and umbilical cord abnormalities in 18 cases (18/18, 100%), single umbilical artery in 5 cases.CONCLUSION:Prenatal ultrasound in early pregnancy can detect LBWC as early as possible, and correct prenatal evaluation provides important guidance value for pregnancy decision-making and early intervention.

Preeclampsia is a potentially life-threatening condition that can arise due to poor placentation and consequent abnormal uterine spiral artery remodeling. Abnormal placentation, in turn, is associated with aberrant trophoblast cell proliferation and apoptosis. Here, we investigated the lncRNA MALAT1 in trophoblast proliferation during early-onset preeclampsia (ePE). MALAT1 levels were examined in placental tissue samples from ePE patients and control patients. The effects and underlying mechanism of MALAT1 on proliferation, migration, invasion and apoptosis were investigated in the first-trimester extravillous trophoblast HTR-8/SVneo cells and the human choriocarcinoma JAR cells. MALAT1 levels were decreased in the placental tissue samples of ePE patients compared with those of control patients, and the levels of MALAT1 were positively correlated with the neonate birth-weight. Knockdown of MALAT1 attenuated the cell viability, proliferation, migration, invasion and the cell cycle progression of trophoblasts, but promoted the apoptosis of trophoblasts. The MALAT1 knockdown promoted miR-101-3p upregulation and VEGFA downregulation. Inhibitor of miR-101-3p increased vascular endothelial growth factor A (VEGFA) expression, and miR-101-3p mimic inhibited VEGFA expression. Luciferase assays showed that miR-101-3p could bind to both MALAT1 and VEGFA. The MALAT1 knockdown-induced induction in the cell vitality and proliferation were attenuated by miR-101-3p inhibitor. We conclude that endogenous MALAT1 promotes proliferation, migration and invasion of trophoblasts by inhibiting the miR-101-3p expression and the subsequent VEGFAupregulation. The reduced MALAT1 level in placental tissue may be involved in the pathogenesis of the ePE.

The development of monocytes in bone marrow is a complex process with multiple steps. We used RNA-seq data to analyze the transcriptome profiles in developing stages of monocytes, including hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), granulocyte–monocyte progenitors (GMPs), and monocytes. We found that genes related to potassium and other cation transmembrane activities and ion binding were upregulated during the differentiation of HSCs into CMPs. Protein transport and membrane surface functional molecules were significantly upregulated in the GMP stage. The CD42RAC and proteasome pathways are significantly upregulated during the development of HSCs into monocytes. Transcription factors Ank1, Runx2, Hmga2, Klf1, Nfia, and Bmyc were upregulated during the differentiation of HSCs into CMPs; Gfi1 and Hmgn2 were highly expressed during the differentiation of CMPs into GMPs; Seventeen transcription factors including Foxo1, Cdkn2d, Foxo3, Ep300, Pias1, Nfkb1, Creb1, Bcl6, Ppp3cb, Stat5b, Nfatc4, Mef2a, Stat6, Ifnar2, Irf7, Irf5, and Cebpb were identified as potentially involved in the development of GMPs into monocytes in mice and humans. In metabolism pathway regulation, HSCs have high glucose, lipid, and nucleic acid metabolism activities; CMPs mainly up regulate the TCA cycle related genes; and GMPs have extremely active metabolisms, with significantly elevated pentose phosphate pathway, TCA cycle, histidine metabolism, and purine metabolism. In the monocyte phase, the tricarboxylic acid (TCA) cycle is reduced, and the anaerobic glycolysis process becomes dominated. Overall, our studies offer the kinetics and maps of gene transcriptional expressions and cell metabolisms during monocyte development in bone marrow.

Changes in population density lead to phenotypic differentiation of solitary and gregarious locusts, which display different resistance to fungal pathogens; however, how to regulate their cellular immune strategies remains unknown. Here, our stochastic simulation of pathogen proliferation suggested that humoral defense always enhanced resistance to fungal pathogens, while phagocytosis sometimes reduced defense against pathogens. Further experimental data proved that gregarious locusts had significantly decreased phagocytosis of hemocytes compared to solitary locusts. Additionally, transcriptional analysis showed that gregarious locusts promoted immune effector expression (gnbp1 and dfp) and reduced phagocytic gene expression (eater) and the cytokine tumor necrosis factor (TNF). Interestingly, higher expression of the cytokine TNF in solitary locusts simultaneously promoted eater expression and inhibited gnbp1 and dfp expression. Moreover, inhibition of TNF increased the survival of solitary locusts, and injection of TNF decreased the survival of gregarious locusts after fungal infection. Therefore, our results indicate that the alerted expression of TNF regulated the immune strategy of locusts to adapt to environmental changes.

Background Preeclampsia (PE) is a complex pregnancy-related disease that endangers the safety of maternal and fetal. The purpose of this study is to reveal the pathogenesis of preeclampsia and discover new predictors from the perspective of peptidomics. The umbilical cord blood of PE and control group was analyzed by peptidomics. A peptide named Regulation of Proliferation Process in Preeclampsia (ROPPIP) was screened out to explore its role in the proliferation, migration and apoptosis of trophoblast cells in preeclampsia. Methods We compared and analyzed the umbilical cord blood of patients with PE and normal pregnant women using liquid chromatography-tandem mass spectrometry (LC-MS). hTR-8/Svneo cells cultured in vitro were divided into ROPPIP group and a disordered peptide group as control. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, Transwell chamber assays and western blot analysis were performed to detect cell proliferation, invasion, migration and apoptosis, in addition to the expression of Matrix metalloproteinase-2 (MMP2), nuclear associated antigen Ki67, B-cell lymphoma-2 (Bcl2), Caspase 3, and β-actin protein. Results We identified 133 differential peptides. Of these, 51 were up-regulated while 82 were down-regulated. the polypeptide SFGVRMATASPTDGNV with low differential expression in the serum of PE patients was selected for the study, we named the polypeptide as Regulation of Proliferation Process in PE (ROPPIP). The experiment shows that ROPPIP can up-regulate the expression levels of MMP2, Ki67, and Bcl2 in HTR-8/Svneo cells, down-regulate the expression of caspase-3, promote the proliferation and migration of HTR-8/Svneo cells and inhibit the apoptosis induced by cisplatin, the activation of the phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway may be associated with the function of ROPPIP. Conclusions ROPPIP promotes HTR-8/Svneo cells migration and proliferation, and inhibits apoptosis, by regulating the activation of the PI3K/AKT/mTOR signaling pathway.

目的 研究二甲双胍对糖尿病伴亚临床甲状腺功能减退患者甲状腺功能的影响.方法 检索CNKI、万方、维普、PubMed、Web of Science、CBM数据库,检索时间为建库至2020年12月.搜集有关二甲双胍治疗糖尿病伴亚临床甲状腺功能减退患者的随机对照试验(RCT),由2名研究者根据入选及排除标准筛选文献,提取数据后采用RevMan 5.3软件进行Meta分析.结果 共纳入6个RCT,包括601例患者.Meta分析结果显示,与对照组比较,二甲双胍可以明显降低血清促甲状腺激素(TSH)水平(MD=-1.25,95％CI:-1.75～-0.74,P<0.00001);但观察组和对照组的血清游离三碘甲状腺原氨酸(FT3)和血清游离甲状腺素(FT4)水平比较,差异无统计学意义(P>0.05).结论 二甲双胍可以明显降低糖尿病伴亚临床甲状腺功能减退患者的血清TSH水平,不影响FT3和FT4的水平.

目的 比较甘精胰岛素300 U/ml(Gla-300)与100 U/ml(Gla-100)治疗非胰岛素类降糖药血糖控制不佳中国T2DM患者的疗效和安全性.方法 本研究为EDITION AP(NCT02855684)中国亚组分析,在这项开放标签、随机对照的临床试验中,非Ins类降糖药物血糖控制不佳的474例中国T2DM患者按2:1比例随机予Gla-300(n=315)或Gla-100(n=159)治疗,观察两组26周时的疗效和安全性指标.结果 两组自基线至治疗26周时HbA1c降幅的最小二乘均值差为0.05％,达到非劣效性评估终点.26周治疗期间,Gla-300组发生至少1次重度和/或证实夜间低血糖患者比例低于Gla-100组(31.5％vs 42.0％,P=0.03).两组其余疗效和安全性指标差异无统计学意义.结论Gla-300治疗26周降低HbA1c效果与Gla-100相似,发生夜间低血糖风险更低.

AIMS:To determine the relationship between thyroid markers during pregnancy and gestational diabetes mellitus (GDM) or post-partum glucose metabolism.MATERIALS AND METHODS:Based on pregnancy 75-g oral glucose tolerance test (OGTT) results, 1467 subjects were grouped into normal glucose tolerance (NGTp; n = 768) and GDM (n = 699) groups. Furthermore, based on post-partum 75-g OGTT results, 286 GDM subjects, screened for glucose metabolism after delivery, were grouped into NGTd (n = 241) and abnormal glucose tolerance (AGT; n = 45) groups.RESULTS:Maternal age, family history of diabetes, acanthosis nigricans, previous adverse pregnancy outcomes and caesarean section incidence, and thyroid positive antibody rates were higher in the GDM group than in the NGTp group. In the first trimester, free triiodothyronine (FT3), thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb) levels were higher in the GDM group than in the NGTp group. In the second trimester, free thyroxine (FT4) levels were lower and TPOAb and TgAb levels were higher in the GDM group than in the NGTp group. After adjusting for confounding factors, FT3, TPOAb and TgAb (first trimester), and FT4, TPOAb and TgAb (second trimester) were risk factors for GDM. TPOAb and TgAb levels were higher in the AGT group than in the NGTd group and were potential predictors of abnormal post-partum glucose tolerance.CONCLUSIONS:GDM risk significantly increased with increased FT3 (first trimester), TPOAb and TgAb (first and second trimesters) or with decreased FT4 (second trimester). Presence of thyroid antibodies predicted post-partum glucose abnormalities in subjects with GDM.

Objective:To explore the efficacy and safety of biphasic insulin aspart 30 (UBLIN ?30) in treatment of diabetic patients. Methods:A multicenter, randomized, open-labeled and positive control clinical trial included the patients with type 1 or type 2 diabetes mellitus having poor glucose control after using premixed insulin monotherapy or combine with 1 or 2 oral antidiabetic drugs. All patients were treated with UBLIN ?30 or NovoMix ?30 for 24 weeks in two groups by a ratio of 1∶1. The decreased value and qualification rates of glycated hemoglobin A 1c(HbA 1c), fasting blood glucose (FPG) and 2-hour postprandial plasma glucose (2hPG), the incidence of hypoglycemic and the adverse events were compared at the end of 24 weeks. Analysis of variance (ANOVA) test, t test and Wilcoxon test were used. Results:All of 668 cases were included in the trial, but 618 cases were in complete conformity to the design plan (305 cases received UBLIN ?30 therapy and 313 cases received NovoMix ?30 therapy). At the end of 24-week treatment period, HbA 1c in UBLIN ?30 group and NovoMix ?30 group decreased by (1.38±1.33)% and (1.37±1.53)%, respectively, compared with the pre-treatment period, and the differences in the post-treatment change values were not statistically significant ( P>0.05). FPG decreased by (2.28±3.76) mmol/L and (1.67±3.55) mmol/L in the two groups, respectively, and the difference between groups in the decreasing values was statistically significant ( P=0.03). The 2hPG decreased by (3.22±5.38) mmol/L and (2.78±4.83) mmol/L in UBLIN ?30 group and NovoMix ?30 group, respectively, and the difference in the decrease was not statistically significant ( P=0.27). Moreover, the incidence of hypoglycemic events was 45.6% (151/331) and 43.8% (146/333) in UBLIN ?30 group and NovoMix ?30 group, respectively, and the incidence of other adverse reactions was 0.9% (3/331) and 0.9% (3/333), respectively. Conclusions:UBLIN ?30 provided similar glycemic control and safety profiles to NovoMix ?30, indicating that UBLIN ?30 is a suitable therapeutic option in clinical practice.

Objective:To explore the relationship between serum serine protease inhibitor B1 (SerpinB1) and the risk of gestational diabetes mellitus (GDM).Methods:A total of 328 pregnant women who were checked up in the clinic of Shengjing Hospital of China Medical University from 2016 to 2018 were divided into two groups according to GDM diagnostic criteria: normal (NC) group ( n=155) and GDM group ( n=173). The correlations between serum SerpinB1 level and glucose and lipid metabolism indexes were analyzed in 5-12 weeks, 13-23 weeks, 24-28 weeks and 29-37 weeks of pregnancy. The pregnant women who did not have GDM at 5-12 weeks of gestation but diagnosed GDM after 24 weeks of pregnancy were selected as GDM-A group ( n=18). The pregnant women who did not have GDM at 13-23 weeks of gestation but diagnosed GDM after 24 weeks of pregnancy were selected as GDM-B group ( n=26). Logistic regression was used to analyze the risk factors of GDM during pregnancy. Receiver operating characteristic (ROC) curve predicted the cut-off value of serum SerpinB1 levels affecting the occurrence of GDM after 24 weeks of pregnancy. Results:In the GDM group, the serum SerpinB1 level at 5-12 weeks gestation, 13-23 weeks gestation, 24-28 weeks gestation of pregnancy was significantly higher than that in the NC group ( P<0.05). At 24-28 weeks of gestation, the level of serum SerpinB1 was positively correlated with LDL-C（ r=0.786, P<0.05） and negatively correlated with fasting insulin and HOMA-IR( r=-0.724 and -0.680 respectively, P<0.05). After correcting the confounding factors such as gestational age, pre-pregnant BMI, acanthosis nigricans and triglycerides, etc, serum SerpinB1 level at 13-23 weeks gestation was still an independent risk factor for GDM after 24 weeks of pregnancy (OR=1.573, 95%CI was 1.035 to 2.228, P<0.05). The area under the ROC curve of GDM was 0.631 ( P<0.05). Conclusions:Elevated serum SerpinB1 levels at 13-23 weeks of pregnancy is related to the risk of GDM occurrence after 24 weeks of pregnancy, which may be a serological marker before the occurrence of GDM.

目的 探讨脂肪来源干细胞(adipose derived stem cells,ADSCs)与富血小板血浆(platelet rich plasma,PRP)联合应用对糖尿病大鼠创面胶原蛋白表达的影响.方法 采用链脲佐菌素诱导糖尿病大鼠模型并造成创面.以0.3 ml PBS干预的正常大鼠对照组和高血糖大鼠糖尿病组;分别以1×106/ml ADSCs、0.3 ml PRP和1×106/ml ADSCs+0.3 ml PRP干预的高血糖大鼠,并分为ADSCs组、PRP组和ADSCs-PRP组(n=6).术后第3、7、14天观察创面愈合情况,组织学检查胶原生成情况,PCR检测第7天创面Col la1、波形蛋白(vimentin,Vim)的表达情况.结果 糖尿病组胶原最少愈合最慢,ADSCs-PRP组优于ADSCs及PRP组.Realtime PCR显示糖尿病组Col 1a1、Vim相对表达量最低,ADSCs-PRP组改善最大.结论 ADSCs-PRP可有效提高糖尿病伤口胶原蛋白的合成,优于单独干预,可能的作用机制为上调Col 1a1、Vim的表达.

Spaceflight-associated immune system weakening ultimately limits the ability of humans to expand their presence beyond the earth's orbit. A mechanistic study of microgravity-regulated immune cell function is necessary to overcome this challenge. Here, we demonstrate that both spaceflight (real) and simulated microgravity significantly reduce macrophage differentiation, decrease macrophage quantity and functional polarization, and lead to metabolic reprogramming, as demonstrated by changes in gene expression profiles. Moreover, we identified RAS/ERK/NFκB as a major microgravity-regulated pathway. Exogenous ERK and NFκB activators significantly counteracted the effect of microgravity on macrophage differentiation. In addition, microgravity also affects the p53 pathway, which we verified by RT-qPCR and Western blot. Collectively, our data reveal a new mechanism for the effects of microgravity on macrophage development and provide potential molecular targets for the prevention or treatment of macrophage differentiation deficiency in spaceflight.

目的:探讨亚临床甲状腺功能减退(SCH)对胰岛素抵抗和胰岛B细胞功能的影响.方法:共有92名中学生志愿者行75 g口服葡萄糖刺激胰岛素释放试验(OGIRT),同时测定甲状腺功能.采用HOMA-IR、松田指数(MI)等指标评价胰岛素抵抗.胰岛B细胞功能的评估包括HOMA-β,血胰岛素/葡萄糖之值,以及多种由OGIRT计算出的参数.结果:SCH组较甲状腺功能正常(ET)组OGIRT后120 min血糖显著升高[(7.39 ± 1.07)mmol·L-1 vs(6.53 ± 1.24)mmol·L-1,P=0.021],糖耐量异常的发生率显著升高(53.85 vs 18.99,P=0.017).SCH组的MI显著降低(33.33 ± 10.32 vs 59.59 ± 27.18,P=0.001),HOMA-IR显著升高[7.61(5.62～9.66)vs 4.04(2.96～5.87),P=0.002].SCH组较ET组HOMA-β显著升高[318.52(285.87～387.69)vs 217.69(143.79～302.01),P =0.001],两组间糖负荷后胰岛素曲线下面积较空腹的增量(ΔAUCins),以及其与血糖曲线下面积增量的比值(ΔAUCins/ΔAUCglu)差异无统计学意义,反映胰岛素早相分泌的ΔAUCins30/ΔAUCglu30差异也无统计学意义.结论:SCH较ET者血糖升高,糖耐量异常发生率升高,存在着更为严重的胰岛素抵抗,空腹胰岛素分泌增加,而糖负荷后的胰岛素分泌没有差异.

Objective: The present study aimed to investigate the adverse effects of the anti-thyroid drugs (ATD) propylthiouracil (PTU) and methimazole (MMI)/carbimazole (CMZ) in treating hyperthyroidism. Method: Qualitative analysis was performed for studies identified in literature search up to April 20, 2019, and 30 studies were selected for meta-analysis. The study designs included case-control studies, randomized controlled trials, and retrospective cohort studies. Patients were in four age groups: childhood, gestating mothers, older adults, and other ages, and all were receiving PTU or MMI/CMZ. Adverse reactions to MMI/CMZ and PTU were evaluated and compared. Results: Odds of liver function injury was higher in the PTU group than in the MMI/CMZ group (odds ratio [OR] 2.40; 95% Confidence Interval [CI] 1.16 to 4.96; P=0.02).Odds of elevated transaminase was much higher in the PTU group than in the MMI/CMZ group (OR 3.96; 95%CI 2.49 to 6.28; P<0.00001). No significant between-group differences were found in odds of elevated bilirubin, agranulocytosis, rash and urticaria; incidence of other adverse events; or in children. Odds of birth defects during the first trimester of pregnancy was higher in the MMI/CMZ group than in the PTU group (OR 1.29; 95%CI 1.09 to 1.53; P=0.003). Conclusion: The impact of PTU on liver injury and transaminase levels is greater than that of MMI/CMZ, but no significant between-group differences are found in the drugs' effects on bilirubin, agranulocytosis and rash, urticaria, or in children. In treating pregnancy-related hyperthyroidism, PTU should be used in the first trimester and MMI reserved for use in late pregnancy.

妊娠期糖尿病(GDM)是指妊娠期间发生的轻度的糖代谢异常,但血糖未达到显性糖尿病的水平,占孕期糖尿病的80％～90％,易导致妊娠不良结局[1].妊娠期糖尿病产后是2型糖尿病发病的高危人群且子代发生肥胖、糖耐量异常和2型糖尿病等代谢相关疾病风险增加,严重影响人类的健康[2].

Type 2 diabetes is a chronic inflammatory process associated with insulin dysfunction and insulin resistance. Neutrophils release neutrophil extracellular traps (NETs) in inflammatory condition, which is associated with the progression of the disease. As an endogenous secreted protein, elastase inhibitor (SerpinB1) can effectively inhibit the effect of this structure in islet cell function and insulin signaling pathway, and also promote the proliferation of islet β cells. This article aims to investigate the relationship between NETs and its inhibitor SerpinB1 and type 2 diabetes.

Chronic exposure of pancreatic β-cells to excess free fatty acids is thought to contribute to type 2 diabetes pathogenesis in obesity by impairing β-cell function and even leading to apoptosis. In β-cells, lipid droplet-associated protein perilipin 5 (PLIN5) has been shown to enhance insulin secretion by regulating intracellular lipid metabolism; the roles of PLIN5 in response to lipotoxicity remain poorly understood. INS-1 β-cells were transfected with PLIN5-overexpression adenovirus (Ad-PLIN5) and treated with palmitate. C57BL/6 J male mice were fed with high fat diet and tail intravenous injected with adeno-associated virus overexpressing PLIN5 (AAV-PLIN5) in β-cells. Our data showed that palmitate and PPAR agonists including WY14643 (PPARα), GW501516 (PPARβ/δ), rosiglitazone (PPARγ) in vitro all induced PLIN5 expression in INS-1 cells. Under palmitate overload, although upregulating PLIN5 promoted lipid droplet storage, it alleviated lipotoxicity in INS-1 β-cells with improved cell viability, cell apoptosis and β-cell function. The protection role of PLIN5 in β-cell function observed in cell experiments were further verified in in vivo study indicated by mitigated glucose intolerance in high fat diet fed mice with β-cell-specific overexpression of PLIN5. Mechanistic experiments revealed that enhanced FAO induced by elevation of PLIN5, followed by decreased ER stress may be a major mechanism responsible for alleviation of lipotoxicity observed in the present study. Our finding substantiated the important role of PLIN5 in protection against lipotoxicity in β-cells.