Only a few epidemiological studies have focused on the correlation between prenatal exposure to polybrominated diphenyl ethers (PBDEs) and infant birth outcomes (IBO), and the results of these epidemiological studies are contradictory. The objective of this study was to assess the correlation between prenatal exposure to PBDEs (PEP) and IBO (i.e., birth weight) in an analysis of epidemiological studies and an experimental animals study. We searched databases of the medical literature (PubMed, Excerpta Medica Database, Cochrane Library, and China National Knowledge Infrastructure) for articles and pooled the results of the included epidemiological studies. In parallel, birth outcomes (i.e., birth weights of pups) were collected from female Sprague-Dawley (SD) rats exposed to decabromodiphenyl ether (DecaBDE) in the diet from five weeks of age to delivery. A significant negative relationship was found between human PBDE burden and birth weight in the analysis of seven epidemiological studies based on a random-effects model (β = −50.598; 95% confidence interval (CI) −95.914, −5.282; I² = 11.8%; p = 0.029). In the experimental animal study, a significant decrease in birth weight in the DecaBDE-treated group was also observed (5.26 ± 0.39 vs. 5.8 ± 0.58, p = 0.0132). The results of our study contribute to increasing evidence suggesting that PEP adversely impacts IBO, especially birth weight.

Background: Dysregulated DNA methylation in lymphocytes has been linked to autoimmune disorders. The aims of this study were to identify global DNA methylation patterns in patients with autoimmune thyroid diseases (AITDs) and to observe methylation changes after treatment for these conditions. Methods: We conducted a cross-sectional study design including the following patients: 51 with newly diagnosed Graves’ disease (GD), 28 with autoimmune hypothyroidism (AIT), 29 with positive thyroid autoantibodies (pTAb) and 39 matched healthy volunteers. Forty GD patients treated with radioiodine or antithyroid drugs and 28 AIT patients treated with L-thyroxine were followed for 3 months. Serum free triiodothyronine (FT3), free thyroxine (FT4), thyrotropin (TSH), thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TgAb) and thyrotropin receptor antibody (TRAb) were assayed using electrochemiluminescent immunoassays. CD3+ T and CD19+ B cells were separated by flow cytometry for total DNA and RNA extraction. Global DNA methylation levels were determined by absorptiometry using a methylation quantification kit. DNA methyltransferase (DNMT) expression levels were detected by real-time PCR. Results: Hypomethylation and down-regulated DNMT1 expression in T and B lymphocytes were observed in the newly diagnosed GD patients. Neither the AIT patients nor the pTAb patients exhibited differences in their global DNA methylation status or DNMT mRNA levels compared with healthy controls. Antithyroid drugs restored global methylation and DNMT1 expression in both T and B lymphocytes, whereas radioiodine therapy affected only T cells. L-thyroxine replacement did not alter the methylation or DNMT expression levels in lymphocytes. The global methylation levels of B cells were negatively correlated with the serum TPOAbs in AITD patients. Conclusions: Hyperthyroid patients with newly diagnosed GD had global hypomethylation and lower DNMT1 expression in T and B lymphocytes. The results provide the first demonstration that antithyroid drugs or radioiodine treatment restores global DNA methylation and DNMT1 expression with concurrent relief of hyperthyroidism.

Objective: Gestational diabetes mellitus (GDM) is characterized by glucose intolerance during gestation. It is associated with a series of maternal and foetal complications. Interleukin (IL)-34 is a recently discovered pro-inflammatory cytokine that functions as a ligand for colony-stimulating factor-1 receptor (CSF-1R). The contribution of IL-34 in the development of multiple chronic inflammatory diseases and autoimmune diseases has been recently discovered. The aim of this study was to evaluate whether IL-34 participates in the pathogenesis of GDM. Method: A total of 120 women were enrolled in this study, which included 60 GDM patients and age- and sex-matched healthy pregnant women. The expression of IL-34 in serum, cord blood and placental tissues was analysed by ELISA and Western blot assays. The association between IL-34 levels and clinical features was also studied. We additionally evaluated the effect of recombinant mouse IL-34 (rmIL-34) on apoptosis and pancreatic β cell function. Results: We found that IL-34 expression is highly increased in serum, cord blood and placental tissues in patients with GDM. In addition, there was a positive association between serum IL-34 and insulin resistance and glucose concentrations. Our data also revealed that IL-34 contributes to the apoptosis of pancreatic β cells in GDM caused by CSF-1R. Furthermore, functional studies found that IL-34 inhibited pancreatic β cell function and cell viability, while CSF-1R inhibitor blocked this effect. Conclusion: IL-34 plays a crucial role in the development of GDM by targeting CSF-1R, insulin production and β cell function.

Migraine is a chronic headache disease, which ranks second in years lost due to disability. However, the mechanism of migraines is still not clear. In migraine patients, fasting can trigger headache attacks. We explored the probable mechanism of why fasting can induce headaches. Nitroglycerin (NTG) was used to induce acute migraine attacks in mice. Primary astrocytes were used to study the pathophysiological mechanism and a Seahorse analyzer was used to detect mitochondrial function. NTG induced more serious headaches in the fasting group. Both the head-scratching times and climbing-cage times in the fasting group were higher than those in normal-diet group. More ROS and inflammatory factors, such as IL-6 and IL-1β, were induced in low-glucose conditions. Seahorse showed that the basal oxygen consumption rate (OCR) and OCR for ATP production were lower in mice who had received NTG with low glucose levels than in other groups. The activity of AMPK was inhibited in this group, which may explain the Seahorse results. We concluded that in the low-glucose state, astrocytes produce more inflammatory factors, ROS, which may be a result of mitochondrial metabolism dysfunction. Improving mitochondrial function and supplying enough substrates may be an option for relieving migraine attacks.