ABSTRACT
Objective To analyze the incidence and causes of stillbirth in 11 hospitals of Guangdong province, and to explore the appropriate interventions. Methods Clinical data of stillbirth in 11 hospitals of Guangdong province were collected from January 2014 to December 2016. The gestational weeks,causes,maternal conditions and other factors were analyzed.Results (1)From 2014 to 2016,103 472 newborns were delivered in the 11 hospitals,and the number of stillbirth was 2 204,with the incidence of 2.13%. Among them, 0.71%(738/103 472) was therapeutic induction, 1.42%(1 066/103 472) was natural stillbirth.At different gestational age(<28 weeks,28-<37 weeks and≥37 weeks),the incidence of stillbirth was 55.63% (1 226/2 204), 28.45% (627/2 204) and 15.92% (351/2 204), respectively, with statistically significant difference (P<0.01). (2) For stillbirth<28 weeks, the first reason was therapeutic induction, accounting for 53.34%(654/1 226).For stillbirth during 28-37 weeks,pre-eclampsia was the major cause, accounting for 40.67% (255/627). And for full-term stillbirth, the causes were umbilical cord factors (19.37%, 68/351), abnormal labor (17.09%, 60/351). (3) In all the stillbirth cases, the incidence of fetal growth restriction (FGR) <28 weeks was significantly higher than that during 28-37 weeks [23.49%(288/1 226)vs 18.02%(113/627), P<0.01]. (4) The stillbirth rate during labor was significantly higher in women ≥35 years old than in younger women [63.88%(191/299)vs 36.12%(108/299);χ2=9.346, P=0.000]. For the causes of stillbirth during labor, the incidence of severe maternal obstetrical complications [61.11%(33/54)vs 38.89%(21/54);χ2=3.323,P=0.002],abnormal labor[65.82%(52/79)vs 34.18%(27/79);χ2=4.067,P=0.001]and abnormal fetal position[66.63%(26/39)vs 33.37%(13/39);χ2=3.002,P=0.013] were higher in women ≥35 years old than in younger women. (5) Cesarean section during labor accounted for 33.77%(101/299)of stillbirth,including 76 cases of emergency cesarean section or converted to cesarean section during labor. Conclusions (1) The incidence of stillbirth in the 11 hospitals is high, and the causes are different at different gestational ages, therefore,different interventions are needed to reduce the incidence in different gestational weeks. Supervision of therapeutic induction should be strengthened <28 gestational weeks;standard management of pregnancy might decrease the occurrence of natural death ≥28 weeks. (2) Attention should be paid to fetal body weight during pregnancy, especially FGR. (3) The stillbirth rate is high in elderly pregnant women, so it is important to strengthen the management of the elderly pregnant women.
ABSTRACT
Objective To investigate the production and mechanism of chemokine (C-C motif) ligand 5 (CCL5) by macrophages in U14 cervical cancer-bearing mice during infection. Methods The U14 cervical cancer cells were injected in C57BL/6 mice to induce tumor-bearing condition. Lipopolysaccharide (LPS) was injected into C57BL/6 mice to induce infection. The protein expression of CCL5 in the serum and the CCL5 mRNA expression in inflammatory cells were measured by ELISA and fluorescence quantitative-PCR in four groups. Macrophages were induced in the tumor conditioned medium (TCM) which extracted from mice serum. The protein expression levels of CCL5, prostaglandin E2 (PGE2) and cyclic adenosine monophosphate (cAMP) in the medium and CCL5, PGE2 and cAMP mRNA expression in the macrophages were detected in different groups. In order to determine whether the inhibition was related to PGE2, selective cyclooxygenase 2(COX-2) inhibitor NS398 was used to reverse this phenomenon and protein kinase A (PKA) inhibitor H89 demonstrated the mechanism through blocking cAMP/PKA signaling pathway. Results (1) The protein and mRNA level of CCL5 in tumor-bearing mice were respectively (151±35) pg/ml and 1.0, which were lower than those in the tumor-free mice (691 ± 85) pg/ml and 4.5 ± 0.8, there were significant difference between them (all P<0.05). The protein and mRNA level of PGE2 in tumor-bearing mice were (1 198±83) pg/ml and 5.8±0.8, which were higher than those in the tumor-free mice (187±25) pg/ml and 1.0, the difference were significant (all P<0.05). The protein and mRNA level of CCL5 in tumor-free+LPS mice were (4 049±141) pg/ml and 31.5±2.0, which were higher than those in the tumor-bearing+LPS mice (1 951±71) pg/ml and 12.1±2.8, the difference were also significant (P<0.05). The protein and mRNA level of PGE2 in tumor-free+LPS mice were (676±70) pg/ml and 3.4±0.4, which were lower than those in tumor-bearing+LPS mice (2 550±382) pg/ml and 11.6±0.9, the difference were also significant (all P<0.05). (2) Macrophages were cultured in vitro using TCM derived from mice. The protein and mRNA level of CCL5 in tumor-bearing mice TCM were respectively (1 626 ± 177) pg/ml and 28.6 ± 1.2, which were higher than those in the tumor-free mice TCM [(27 ± 3) pg/ml and 1.0], there were significant difference (P<0.05). The protein and mRNA level of PGE2 in tumor-bearing mice TCM were (790 ± 156) pg/ml and 1.7 ± 0.3, which were higher than those in the tumor-free mice TCM [(448 ± 115) pg/ml, 1.0], the difference were significant (all P<0.05). The protein and mRNA level of cAMP in tumor-bearing mice TCM were (164 ± 30) pg/ml and 1.6 ± 0.3, which weres higher than those in the tumor-free mice TCM [(118 ± 25) pg/ml,1.0], the difference were significant (all P<0.05). The protein and mRNA level of CCL5 in tumor-free + LPS mice TCM were (10 475 ± 742) pg/ml and 212.0 ± 5.7, which were higher than those in the tumor-bearing+LPS mice TCM [(6 375±530) pg/ml, 142.3±2.5], the difference were significant (all P<0.05). The protein and mRNA level of PGE2 in tumor-free+LPS mice TCM were (2 438±95) pg/ml and 4.3±0.7, which weres lower than those in the tumor-bearing + LPS mice TCM [(3 441 ± 163) pg/ml, 5.9 ± 0.3], the difference were significant (all P<0.05). The protein and mRNA level of cAMP in tumor-free+LPS mice TCM were (340 ± 13) pg/ml and 4.1 ± 0.4, which were lower than those in the tumor-bearing + LPS mice TCM [(542 ± 42) pg/ml, 5.4 ± 0.5], the difference were significant (all P<0.05). (3) Using COX-2 inhibitor NS398 in the tumor-bearing+LPS mice, the protein and mRNA level of CCL5, PGE2 and cAMP were (7 691±269) pg/ml and 159.0±8.9, (2 820±152) pg/ml and 4.9 ± 0.3, (465 ± 8) pg/ml and 4.3 ± 0.4, respectively, and there were significant difference (all P<0.05), compared to before treatment. Using PKA inhibitor H89 in the tumor-bearing+LPS mice, the protein and mRNA level of CCL5, PGE2 and cAMP were (8 375±520) pg/ml and 177.0±8.8, (2 650±35) pg/ml and 4.7 ± 0.4, (368 ± 13) pg/ml and 3.1 ± 0.7, respectively, and there were significant difference (all P<0.05), compared to before treatment. Conclusion TCM of U14 cells activated macrophages to release PGE2 could inhibit the expression of CCL5 levels by cAMP/PKA signaling pathway.
ABSTRACT
Objective To detect the immune effect of FbaAmAb2 against the surface protein of group A Straptococcus (GAS),and explore the pathogenesis and therapy of GAS infections.Methods By subclonal and bacterial ELISA,the positive hybridoma cells were screened that can produce better titers of FbaAmAb2 against GAS-surface FbaA protein,and were injected into the peritoneal cavities of BALB/c mice to produce ascites.The collected ascites were performed to dilute,as follows,original ascite,1:2,1:4,1:8,and 1:16 to test tube agglutination.Based on the results,we selected appropriate dilution to passively immunize mice,and then challenged the mice with GAS,evaluating FbaAmAb2 neutralizing ability with GAS in mice by the survival rate of the immunized mice.Whether FbaAmAb2 could inhibit the binding of factor H to GAS was confirmed by the invasive inhibition assay.Results The IgG titer of bacteria solution ELISA is 1:160 and the titer of tube agglutination is 1∶8.The protect rates of FbaAmAb2 on preventing mice with GAS infections are as follows:66.67％ in original ascite and 1:2 diluted groups,and 50％ in 1:4 diluted group.Mice in each experimental group were evoked significantly protective immune responses compared with the PBS control by SPSS analysis.FbaAmAb2 can competitively inhibit factor H binding to the surface proteins FbaA of GAS,which decreased the entry of GAS into the cytoplasm of human epithelial cells through the binding of factor H.Conclusion FbaAmAb2 is promising to be used in emergent prevention or the clinical therapy for GAS infection and it is promising starting points for pharmacologic targeting and further development of new therapeutic agents for GAS.
ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of the traditional Chinese drugs, Shuganyishen, on Ishikawa cell line.</p><p><b>METHOD</b>Rat blood serum was prepared by using Chinese drugs serum pharmacology method, in which, Shuganyishen was contained or not contained. Ishikawa cells were subjected into five groups: (1) normal cells group (NCG), (2) rat blood serum without Shuganyishen group (NSGG) as negative control, (3) Shuganyishen group (SGG), (4) Cisplatin group (DDPG) as positive control, and (5) Shuganyishen with Cisplatin group (S&CG). MTT assay was used to evaluate the inhibition effect on cell growth in each group. The mRNA expression of estrogen receptor alpha and beta (ERalpha and ERbeta) in each group was detected by RT-PCR.</p><p><b>RESULT</b>Effective inhibition of cell growth was found in the groups of SGG and S&CG, respectively (P < 0.05), which had no significant difference from positive control by MTT. The mRNA expression of ERbeta was slightly going up, while the expression of ERalpha was hardly effected in SGG by RT-PCR. Interestingly in S&CG, the mRNA expression of ERalpha was significantly down-regulated (P < 0.05), but the mRNA expression of ERbeta remained no change. As the positive control, the mRNA expression of ERalpha and ERbeta was significantly down-regulated in DDPG (P < 0.5).</p><p><b>CONCLUSION</b>Traditional Chinese drugs, Shuganyishen, may inhibit Ishikawa cell growth and had no effects on the expression of ERalpha, furthermore, can reverse the inhibition of ERbeta expression by Cisplatin.</p>
