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Introduction: During normal pregnancy, changes in the gut microbiota (GM) in response to physiological alterations in hormonal secretion, immune functions and homeostasis have received extensive attention. However, the dynamic changes in the GM during three consecutive trimesters of pregnancy and their relationship with glucose and lipid metabolism have not been reported. In this study, we aimed to investigate the dynamic changes in the diversity and species of the GM during three consecutive trimesters in women who naturally conceived, and their relationships with abnormal fasting blood glucose (FBG) and serum lipid levels. Methods: A total of 30 pregnant women without any known chronic or autoimmune inflammatory disease history before pregnancy were enrolled during the first trimester. Serum and stool samples were collected during the first trimester, the second trimester, and the third trimester. Serum samples were tested for FBG and blood lipid levels, and stool specimens were analyzed by 16S rDNA sequencing. Results: The abundance ratio of bacteroidetes/firmicutes showed an increasing tendency in most of the subjects (19/30, 63.3%) from the first to the third trimester. LEfSe analysis showed that the abundance of Bilophilawas significantly increased from the first to the third trimester. In addition, at the genus level, the increased relative abundance of Mitsuokella, Clostridium sensu stricto and Weissellawere potentially involved in the development of high FBG during pregnancy. The raised relative abundance of Corynebacterium, Rothiaand Granulicatellapotentially contributed to the occurrence of dyslipidemia during pregnancy. Conclusions: There are dynamic changes in the GM during the three trimesters, and the alterations in some bacterium abundance may contribute to the development of high FBG and dyslipidemia during pregnancy. Monitoring enterotypes and correcting dysbiosis in the first trimester may become new strategies for predicting and preventing glucolipid metabolism disorders during pregnancy.

Controlling the photoactive layer morphology towards nanoscale bi-continuous donor/acceptor interpenetrating networks is a key issue to build high-performance organic solar cells (OSCs). Due to the distinct properties between donor and acceptor materials, casting an active layer from a single solvent solution usually results in either insufficient or excessive phase separation that reduces the device performance. In comparison to the fullerene acceptors with closed-cage structures, the currently dominant non-fullerene acceptors possess the similar anisotropic π-π interactions with p-type organic semiconductor donors, giving rise to the complexity of the morphology regulation. Herein, we employ 4,4′-dimethoxyoctafluorobiphenyl (OFP) with strong crystallinity as a volatile solid additive to optimize the active layer morphology of OSCs. The synergistic effect of 1-chloronaphthalene (CN) and OFP as dual additives shows supreme capability on optimizing the morphology over the conventional additive of CN, which is in favor of improving charge transport and suppressing charge recombination for higher fill factors in various systems. In particular, the PTQ10:m-BTP-C6Ph-based device processed by the additive showed a remarkable power-conversion efficiency (PCE) of 17.74%, whereas the control device processed by CN additive yielded a relatively lower PCE of 16.45%.

This study explored whether circulating exosomes effectively participate in the inflammatory response in Hashimoto thyroiditis (HT).

MicroRNA-326 (miR-326), as a member of the microRNA (miRNA) family, which includes endogenous single-stranded, conserved, noncoding small RNAs, has been reported to play important roles in autoimmune diseases such as multiple sclerosis and systemic lupus erythematosus. However, few studies of the role of miR-326 in autoimmune thyroiditis (AIT) have been published. Here, we explored the roles of miR-326 and the involved pathway in iodine-induced AIT. NOD.H-2h4mice, which are a model of human AIT, were randomly divided into a normal water control group and a high-iodine group. Mice in the high-iodine group were administered 0.05% NaI (~1000 times the normal daily iodine intake), and mice in the control group received sterile water. Furthermore, we evaluated small interfering RNA (siRNA) interference in spleen mononuclear cell experiments in vitro. In this study, we found that Th17 cells were significantly increased with a high expression of miR-326 in an iodine-induced thyroiditis NOD.H-2h4mouse model. In addition, the expression of Ets-1 protein, a negative regulator of Th17 differentiation, was significantly decreased. Intriguingly, our analysis showed that Ets-1 protein expression was negatively correlated with miR-326 levels in AIT mice (r= −0.814, p< 0.01). Our study indicated that miR-326 inhibited Ets-1 protein expression and promoted the differentiation of Th17 cells during the onset and development of AIT. The addition of a miR-326 inhibitor reversed Th17 cell production and Ets-1 protein expression, supporting this hypothesis. The results of our study suggest that miR-326 may target the Ets-1 protein to contribute to iodide-induced thyroiditis, providing a new theoretical basis for the use of miRNA targeting therapy for the treatment of autoimmune diseases.

Expression of the oncogene Twist1 is correlated with tumor development and metastasis. Recent studies have suggested that the epithelial-to-mesenchymal transition (EMT) is necessary for tumor progression and metastases. Little is known concerning the role of Twist1 and EMT in thyroid cancer. In the present work, the expression levels of Twist1 and one marker of EMT, vimentin, were measured in papillary thyroid carcinoma (PTC). The results showed Twist1 expression to be correlated only with cancer lymph node metastases (P= 0.004) and not with other clinicopathological indicators. Moreover, Twist1 expression was positively correlated with the expression of vimentin (r= 0.408, P= 0.003). In vitro studies further indicated that reducing Twist1 expression using short hairpin RNA against Twist1 can decrease the invasive and metastatic properties of PTC cells and that the down-regulation of Twist1 can reverse EMT by increasing the expression of E-cadherin and down-regulating the expression of vimentin in the PTC cell line IHH-4. To investigate the effects on Twist1, the PTC cell lines TPC-1 and BCPAP were treated with TNF-α, resulting in Twist1 up-regulation that was dependent on NF-κB activation. After the inhibition of NF-κB activity with Bay11-7082, the Twist1 mRNA and protein levels could not be increased. The decline in the Twist1 mRNA and protein levels rendered the cancer cells less invasive. Thus, we conclude that Twist1 plays an important role in the EMT of PTC via the NF-κB pathway.

In this study, we researched the pattern of thyroid function of subclinical hypothyroid (SCH) women with levothyroxine (LT4) throughout pregnancy and determined the optimal dosages of LT4for such women. 56 SCH pregnant women were followed regularly prospectively. They were divided into three groups: group A (n= 29. Baseline TSH between 2.5 and 5.0 mIU/L) received 50 μg/day of LT4; group B (n= 17. Baseline TSH between 5.0 and 8.0 mIU/L) received 75 μg/day of L-T4; group C (n= 10. Baseline TSH >8.0 mIU/L) received 100 μg/day of LT4. All the patients started LT4therapy around the 8th gestational week. Serum TSH, free T4, and free T3were measured at 4-week intervals throughout pregnancy. Among the thyroid function indexes, serum TSH changed quickly and decreased significantly 4 weeks after LT4therapy. The change of serum FT4responded drastically at the 12th gestational week. We also found that serum FT3did not change much after LT4therapy. 50, 75, and 100 μg/day can maintain serum TSH level of 79.3, 82.4, and 90.0 % of SCH women in definitive therapeutic goal in group A, B, and C, respectively. The LT4dose need to be adjusted one or more times in 20.7, 17.6, and 10.0 % of the SCH women in group A, B, and C, respectively. The different LT4dose can be chosen according to the baseline TSH levels of SCH women. The constant LT4dose can maintain serum TSH levels of 79.3–90 % patients in the ideal range. A small part of patients require adjust therapy also during the second and third trimester. Therefore, careful follow-up of SCH pregnant women should be taken, and thyroid function should be tested every month until the end of pregnancy.

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