Objective:To explore the effect of changes in BMI (ΔBMI) on left ventricular function in early breast cancer patients undergoing anthracycline chemotherapy.Methods:The clinical data of 170 breast cancer patients treated in the Lianyungang Oriental Hospital from January 2018 to October 2021 were retrospectively analyzed. The clinicopathological data and cardiac color doppler ultrasound examination results of the patients were collected. Single-factor and multiple-factor were used to analyze the risk factors of cardiotoxicity in patients after chemotherapy. ΔBMI was calculated and the receiver operating characteristic (ROC) curve was drawn; the cut-off value of the ΔBMI was measured to obtain the diagnostic accuracy.Results:Compared with before chemotherapy, the mean values of BMI, left ventricular end-diastolic volume (EDV), left ventricular end-systolic volume (ESV), left ventricular end-diastolic diameter (LVD), and left ventricular end-systolic diameter (LVS) were increased after chemotherapy, while left ventricular ejection fraction (LVEF) value was decreased. Before and after chemotherapy, the differences between BMI [(22.30±1.88) kg/m 2 vs. (23.59±2.32) kg/m 2] and LVEF [(63.69±4.69)% vs. (59.08±4.28)%] were statistically significant ( t = 3.40 and 4.98, all P < 0.05). The range of ΔBMI was 0-41.3%, and the range of the change of LVEF (ΔLVEF) was 0-15.9%. There was a significant correlation between ΔLVEF and ΔBMI ( r = 0.709, P < 0.001). The incidence of cardiotoxicity was 21.2% (36/170). Logistic regression analysis showed that BMI( OR = 1.639, 95% CI 1.263-2.127, P = 0.000) and ΔBMI ( OR = 1.147, 95% CI 1.071-1.228, P = 0.000) were independent risk factors for cardiotoxicity in early breast cancer patients undergoing anthracycline chemotherapy. According to the cardiotoxicity, the area under the ROC curve of ΔBMI and BMI was 0.757 and 0.687, respectively. When the ΔBMI value was 4.28%, the maximum Youden index was 0.399, the sensitivity was 0.750, and the specificity was 0.649. Conclusion:For breast cancer patients treated with anthracycline chemotherapy, ΔBMI can be used as an effective indicator for predicting cardiotoxicity; when ΔBMI exceeds 4.28%, the risk of cardiotoxicity is high.

Objective To discuss the clinical characteristics for lateral cervical lymph node metastasis in stage cN0 papillary thyroid microcarcinoma and significance and feasibility of preventive dissection,and provide reference for clinical treatment.Methods Reviewd the clinical data of 191 patients with stage cN0 papillary thyroid microcarcinoma patients from Jul.2011 to Dec.2016 underwent surgery in the Department of General Surgery of Lianyungang Oriental Hospital.Assessed the need for preventive cervical lymph node dissection.Chisquare test and logistic regression were used to analyze the relationship between cervical lymph node metastasis and gender,age,tumor number,tumor size,capsule infiltration,single and bilateral tumors,Hashimoto's disease,and central lymph node metastasis.Results The positive rate of cervical lymph node metastasis in papillary thyroid microcarcinoma was 27.9％ (50/191).Univariate analysis showed that the metastasis of the cervical lymph nodes was associated with infiltration of the capsule,Hashimoto disease,and CLN metastasis (all P ＜ 0.05).Multivariate logistic regression analysis showed that the capsule infiltration (OR =7.563,P =0.000),Hashimoto's disease (OR =4.635,P =0.003),and central lymph node metastasis (OR =3.075,P ＜ 0.001) were able to be independent risk factors for cervical lymph node metastasis.When the positive number of lymph node metastasis in the central region was ≥ 2,the positive rate of cervical lymph nodes was significantly increased (P ＜ 0.001).Eleven patients (5.8％) had temporary recurrent laryngeal nerve palsy,29 patients (15.1％) had transient hypoparathyroidism,and no patients with permanent recurrent laryngeal nerve palsy and hypoparathyroidism.Conclusions The removal of the cervical lymph nodes helps to accurately classify the tumor and assess the risk.It is important to choose the postoperative treatment follow-up plan for patients.For patients with capsule infiltration,Hashimoto's disease,and central lymph node metastasis,cervical lymph node dissection should be routinely performed.

Standard treatment for resectable IIIa/N2 non-small-cell lung cancer (NSCLC) is still under debate. Optional treatments include chemotherapy, radiotherapy and surgery, other options include target therapy and immunotherapy. Multidisciplinary treatment has therefore been emphasized by various clinical trials, including bimodality strategy which has been defined as chemotherapy plus surgery or chemotherapy plus radiotherapy, and trimodality treatment which refers to chemotherapy plus surgery and radiotherapy. However, there is still no consensus on the optimal strategy on treating resectable IIIa/N2 NSCLC. Therefore, we reviewed a series of phase II and III clinical trials as well as some meta-analyses and case reports to compare the efficacy of different strategies on survival of cN2 NSCLC, and concluded that for resectable IIIa/N2 NSCLC surgery is recommended, and that strategy of chemotherapy plus surgery may not achieve better survival than that of chemotherapy plus radiotherapy. Size of tumor as well as lymph nodes should be taken into account when choosing optimal therapy, so that promising individualized strategy could be given to patients with resectable stage IIIa/N2 NSCLC.
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Clinical Trials as Topic ; Combined Modality Therapy ; Humans ; Lung Neoplasms ; drug therapy ; radiotherapy ; surgery ; therapy ; Meta-Analysis as Topic ; Neoplasm Staging ; Treatment Outcome

Objective To study the effect of microRNA-204 (miR-204) on the biological characteristics of breast cancer cells.Methods Real-time PCR was used to detect the expression of miR-204 in human breast cancer cell MDA-MB-231 after transfection of miR-204 mimics and inhibitor for 48 h.Flow cytometry was used to analyse the effect of miR-204 on the proliferation and apoptosis of MDA-MB-231 cells.The effect of miR-204 on the migration of MDA-MB-231 cells was detected by Transwell migration assay.Results Real-time PCR analysis showed that miR-204 mimics and inhibitors had significant effect compared with normal control group(P<0.01).Flow cytometry analysis showed that compared with normal control group,the number of G1 phase cells of miR-204 mimics group was significantly decreased(P<0.01),while the number of G2/M cells of miR-204 mimics group was significantly increased(P<0.01).In contrast,the number of G1 phase cells of miR-204 inhibitor group was significantly increased(P<0.01),while the number of G2/M cells of miR-204 inhibitor group was significantly decreased(P<0.01).miR-204 mimics group significantly promoted apoptosis,while the inhibitor group significantly inhibited apoptosis(P<0.01).Transwell migration analysis showed that the number of cells of miR-204 mimics group were significantly reduced,while the number of cells was significantly increased in the inhibitor group(P<0.01).Conclusion We find miR-204,which can promote cell apoptosis and inhibit cell proliferation and migration,is a negative factor in the breast cancer cell line MDA-MB-231.

OBJECTIVE To investigate the effect of mono-2-ethylhexyl phthalate(MEHP) on proliferation of primary neural stem cells(NSCs)of rats and NE-4C cells of mice and on the migration of NE-4C cells and the mechanism. METHODS NE-4C or NSCs were treated with MEHP 1,10,100 and 1000 μmol · L-1 for 72 h,respectively. The cytotoxicity was estimated with the cell counting kit-8 (CCK-8). Cell proliferation was analyzed by EdU assay. The mRNA expression levels of the glucocorticoid receptor(GR),signal transducer and activator of transcription 3(Stat3)and sex determining region Y (SRY)-box 2(Sox2) were detected by qRT-PCR. The protein expression levels of total GR,GRβ, Sox2,Stat3 and p-Stat3 were measured by Western blotting. RESULTS Cell viability of NE-4C cells and NSCs at MEHP 1000μmol·L-1 was significantly decreased,which was 70.3%and 40.0%of the control group, respectively. EdU assay showed that MEHP 100 μmol · L-1 decreased NE-4C cells and NSCs by 74.8%and 12.0%(P<0.05)compared with control. The effect of MEHP on the cell migration of NE-4C was evidenced by the fact that the migration was obviously reduced to (63.4±2.0)%(P<0.05)after treatment with MEHP 100μmol · L-1 for 72 h. The mRNA expression levels associated with proliferation and migration in NE-4C of GR,Stat3 and Sox2 in MEHP 100 μmol · L-1 group were down-regulated to 49.8%,26.0% and 14.0%of control(P<0.05). At MEHP 100μmol · L-1,mRNA of GR, Stat3 and Sox2 in NSCs declined to 10.0%,14.0% and 15.3% of normal control. Western blotting results revealed that protein expressions of GR,GRβ,Sox2 and p-Stat3 were remarkably inhibited by MEHP 100 μmol · L-1 in that the relative expression of NE-4C was 0.92 ± 0.17,0.87 ± 0.35,0.81 ± 0.22 and 0.62 ± 0.24(P<0.05). The corresponding protein expression in NSCs was 0.82 ± 0.20,0.56 ± 0.12,0.84 ± 0.36 and 0.53 ± 0.20(P<0.05)when the cells were treated with MEHP 100μmol · L-1 for 72 h. CONCLUSION MEHP can inhibit the proliferation and migration of NE-4C cells and NSCs possibly by decreasing Stat3 and Sox2 that are mediated by GRβ.

OBJECTIVE To investigate the effect of curcumin on proliferation of neural stem cells (NSCs) of rats and the mechanism. METHODS NSCs derived from the forebrain of rat E15 embryos were cultured in vitro and identified by neuroepithelial stem cell protein ( nestin and SOX2) staining. NSCs were treated with curcumin 0.1, 0.5, 2.5, 12.5 and 62.5 μmol.L-1 for 24 h, respectively. The cyto-toxicity was estimated by measuring the release of lactate dehydrogenase(LDH). Cell viability and prolif-eration were analyzed respectively by MTT and BrdU assay. The mRNA expression levels of glucocorti-coid receptor (GR), Stat3, Notch1 and p21 were detected by qRT-PCR. The protein expression levels of total GR, Stat3 and phosphorylated Stat3 were measured by Western blotting. RESULTS The primary neural stem cells were identified as NSCs. Curcumin 12.5 and 62.5 μmol.L-1 had cell cytotoxicity( P<0.05). Cell viability assay indicated that curcumin 0.5 and 2.5 μmol.L-1 enhanced NSCs viability( P <0.05), but in 62.5 μmol.L-1 group the cell cytotoxicity was inhibited(P<0.05). Curcumin 0.1, 0.5 and 2.5 μmol.L-1 increased NSCs proliferation ( P < 0. 05), whereas 12. 5 and 62. 5 μmol.L-1 caused a decrease in NSCs proliferation(P<0.05). The mRNA expression level of GR in 0.5 μmol.L-1 group was significantly reduced( P<0.05). Western blotting analysis revealed that the protein expression of GR, Stat3 and p-Stat3 was inhibited by curcumin in 0.5 μmol.L-1 group(P<0.05). CONCLUSION Curcumin stimulates NSCs proliferation, possibly by inhibiting GR mRNA and related protein expression.

Objective: To explore the dynamic regulation of histone acetylases p300 and p300/CBP associated factor (PCAF) on cardiac development gene NKX2.5 during cardio-genesis and to provide the new theoretical basis to clarify the regulatory mechanism for cardio-genesis in fetal mice.
Methods: Our research included 4 groups of cardiac tissues: Embryo (EB) 14.5 days group,n=10, EB 16.5 days group, n=10 and Neonatal 0.5 day group,n=5, Neonatal 7 days group,n=3. Immunoprecipitation was performed in myocardial tissues using anti-p300, anti-PCAF and anti-H3K9ac antibodies to retrieve p300, PCAF and H3K9ac binding DNA, the speciifc DNA sequences were ampliifed by real-time PCR to detect and the binding levels of p300, PCAF and the acetylation level of H3K9ac in NKX2.5 promoter sequence. In addition, the mRNA expression of NKX2.5 was examined by RT-PCR.
Results: The binding levels of p300 and PCAF had the timing consequence at different stage of cardio-genesis. The binding level of p300 in EB 16.5 days group (0.063 ± 0.021), Neonatal 0.5 day group (0.019 ± 0.008), Neonatal 7 days group (0.011 ± 0.003) were all lower than that in EB 14.5 days group (0.231 ± 0.033), and in Neonatal 0.5 day group and Neonatal 7 days group were lower than EB 16.5 days group, allP<0.05. The binding level of PCAF in EB 16.5 days group (0.063 ± 0.021), Neonatal 0.5 day group (0.019 ± 0.008), Neonatal 7 days group (0.011 ± 0.003) were all lower than that in EB 14.5 days group (0.185 ± 0.023), allP<0.05. The H3K9ac acetylation level and NKX2.5 mRNA expression level had the timing consequence at different stage of cardio-genesis. H3K9ac acetylation level in EB 16.5 days group (0.098 ± 0.014), Neonatal 0.5 day group (0.074 ± 0.010), Neonatal 7 days group (0.045 ± 0.014) were all lower than that in EB 14.5 days group (0.119 ± 0.020), and in Neonatal 7 days group was lower than EB 16.5 days group, allP<0.05. The NKX2.5 mRNA expression level in EB 16.5 days group (0.701 ± 0.181), Neonatal 0.5 day group (0.502 ± 0.159), Neonatal 7 days group (0.529 ± 0.13) were all lower than that in EB 14.5 days group (1.000 ± 0.130), allP<0.05.
Conclusion: Histone acetylases p300 and PCAF may dynamically regulate H3K9ac acetylation in NKX2.5 promoter sequence, and the mRNA of NKX2.5 was dynamically expressed during cardio-genesis in experimental fetal mice.

Objective To evaluate the role of adenosine A1 receptors in hippocampal neurons in the cognitive dysfunction caused by isoflurane anesthesia in aged mice.Methods Sixteen male adenosine A1 receptor gene knockout homozygote mice (gene knockout mice) and 16 male wild-type mice,aged 18-22 months,weighing 27-32 g,were studied.Each type of mice was randomly divided into 2 groups (n=8 each) using a random number table:control group (group C) and isoflurane anesthesia group (group Ⅰ).Mice inhaled 1.4％ isoflurane in 100％ O2 for 2 h in group Ⅰ,and 100％ O2 for 2 h in group C.All the mice underwent Morris water maze test at 24 h after isoflurane or O2 inhalation.After the test,the mice were sacrificed and the hippocampal tissues were harvested to determine the number of β-amyloid1-42 (Aβ1-42) plaques (using immunohistochemistry) and expression of phosphorylated tau (p-tau) protein,and 2B subunit-containing N-methyl-D-aspartate receptors (NR2B) (by Western blot analysis).Results Compared with group C of wild type mice,the escape latency was significantly prolonged,the number of Aβ1-42 plaques was enlarged,the expression of p-tau protein was up-regulated,and the expression of N R2B was down-regulated in group Ⅰ of wild type mice.Compared with group Ⅰ of wild type mice,the escape latency was significantly shortened,the number of Aβ1-42 plaques was decreased,the expression of p-tau protein was down-regulated,and the expression of NR2B was up-regulated in group Ⅰ of gene knockout mice.There was no significant difference in the parameters mentioned above between group Ⅰ and group C of gene knockout mice.Conclusion Adenosine A1 receptors in hippocampal neurons mediate isoflurane anesthesia-induced cognitive dysfunction in aged mice,and the mechanism may be related to promotion of deposition of Aβ,phosphorylation of tau protein and inhibition of activities of NR2B.

OBJECTIVETo evaluate the effect of different immune status on the incidence of hepatic lesions in patients with hepatitis B virus (HBV) infection undergoing anti-tuberculosis therapy.

METHODSThe PubMed (1966-2013), Embase (1966-2013), Wanfang (1998-2013), Chinese National Knowledge Infrastructure (CNKI; 1997-2013), and Chinese Biomedical (CBMdisc; 1860-2013) literature databases were searched for case-control studies of hepatic lesions in patients undergoing anti-tuberculosis therapy with or without concomitant HBV infection. The HBV patients were divided into subgroups according to hepatitis B e antigen (HBeAg) positivity or negativity, all members of the control group were HBsAg⁻. The data from all 7 studies included in the meta-analysis were extracted and analysed using RevMan5.2 soft-ware.

RESULTSPatients with HBV infection who were undergoing anti-tuberculosis therapy had a higher risk factor than the control patients (OR =5.81, 95% CI =[4.26, 7.39]). The HBV patients with HBeAg positivity who were undergoing anti-tuberculosis therapy had a high risk factor than the HBV patients with HBeAg negativity (OR =2.56, 95% CI=[1.90, 3.44]).

CONCLUSIONHBV infection is a risk factor for hepatic lesions when undergoing anti-tuberculosis therapy, and HBeAg-positive status may put a patient at higher risk.

Antitubercular Agents ; adverse effects ; therapeutic use ; Hepatitis B ; complications ; pathology ; Hepatitis B e Antigens ; blood ; Humans ; Liver ; drug effects ; pathology ; Tuberculosis ; complications ; drug therapy ; pathology

Bisphosphonate-Associated Osteonecrosis of the Jaw ; Humans