Objective To investigate and establish thyroid function reference range during 3 pregnant stages in Chaoshan area:thyrotropin (TSH),free thyroxin (FT4).Methods 863 healthy pregnant women visited antenatal clinic in the Second Affiliated Hospital were included in this study.By detecting serum levels of TSH,FT4,thyroglobulin antibody (TgAb),and thyroid peroxi-dase antibody (TPOAb)in these women,the euthyroid reference ranges of serum TSH and FT4 in different pregnant stages were established based on the standards of the United States National Institute of Clinical Biochemical (NACB)guidelines.Results The ranges of serum TSH in the first,second and third trimester of pregnancy were 0.13-3.93 mIU/L,0.14-4.55mlU/L,and 0.42-3.85 mIU/L,respectively.The ranges of serum FT4 levels in these 3 stages were 12.00-23.34 pmol/L,6.27-12.65pmol/ L, and 9.80-18.20 pmol/L,respectively.The range of serum TSH levels in our study were similar with the reference range recom-mended by the guidelines in China,but were different compared with the American Thyroid Association (ATA)guidelines.Conclu-sion TSH,FT4 levels show dynamic changes during different stages of pregnancy.The thyroid function ranges of healthy pregnant women in Chaoshan area are quite different compared with non-pregnant population and pregnant women in distinct area.Due to the differences of diet,iodine intake,economy and culture in Chaoshan area,regional thyroid function reference ranges specific for differ-ent stages of pregnant women should be established.

AIM:To observe the effect of B-HT933, a selective α2-adrenoceptor agonist, on lipopolysaccha-ride ( LPS )-induced TNF-αproduction in neonatal rat cardiomyocytes and to explore the underlying mechanisms . METHODS:The neonatal rat cardiomyocytes were cultured .The localization of α2A-adrenoceptor in the cardiomyocytes was examined by immunofluorescence staining .The cardiomyocytes were exposed to LPS or/and B-HT933 for different time.The level of TNF-αin the supernatants and the mRNA expression of TNF-αwere detected by ELISA and real-time PCR, respectively.In addition, LPS-associated signal molecules in the cardiomyocytes were also examined by Western blotting.RESULTS: Immunofluorescence staining showed that α2A-adrenoceptors were localized in the cardiomyocytes . LPS stimulated TNF-αproduction in the cardiomyocytes in a dose and time-dependent manner .B-HT933 pretreatment sig-nificantly inhibited the expression of TNF-αat mRNA and protein levels in LPS-treated cardiomyocytes .Furthermore, LPS exposure induced IκBαand p38 phosphorylation in cardiomyocytes and only IκBαphosphorylation was prevented by B-HT933 treatment.CONCLUSION:α2A-adrenoceptors are present in neonatal rat cardiomyocytes and its agonist B -HT933 inhibits LPS-induced TNF-αproduction in cardiomyocytes via suppressing IκBαphosphorylation .

As an important part of tumor microenvironment, neutrophils are poorly understood due to their spatiotemporal heterogeneity in tumorigenesis. Here we defined, at single-cell resolution, CD44-CXCR2- neutrophils as tumor-specific neutrophils (tsNeus) in both mouse and human gastric cancer (GC). We uncovered a Hippo regulon in neutrophils with unique YAP signature genes (e.g., ICAM1, CD14, EGR1) distinct from those identified in epithelial and/or cancer cells. Importantly, knockout of YAP/TAZ in neutrophils impaired their differentiation into CD54+ tsNeus and reduced their antitumor activity, leading to accelerated GC progression. Moreover, the relative amounts of CD54+ tsNeus were found to be negatively associated with GC progression and positively associated with patient survival. Interestingly, GC patients receiving neoadjuvant chemotherapy had increased numbers of CD54+ tsNeus. Furthermore, pharmacologically enhancing YAP activity selectively activated neutrophils to suppress refractory GC, with no significant inflammation-related side effects. Thus, our work characterized tumor-specific neutrophils in GC and revealed an essential role of YAP/TAZ-CD54 axis in tsNeus, opening a new possibility to develop neutrophil-based antitumor therapeutics.
Humans ; Animals ; Mice ; Adaptor Proteins, Signal Transducing/metabolism* ; Transcription Factors/metabolism* ; Stomach Neoplasms/pathology* ; Neutrophils/pathology* ; Signal Transduction/genetics* ; YAP-Signaling Proteins ; Tumor Microenvironment ; Hyaluronan Receptors/genetics*