Objective To explore the influence of sodium oxamate on the radiaosensitivity of hypoxic nasopharyngeal carcinoma CNE2 cells. Methods The production of lactate and angiotensin Ⅱ in CNE2 with or without sodium oxamate treatment was detected by lactate assay kit and angiotensin Ⅱ ELISA kit. Cell growth of hypoxic CNE2 with or without sodium oxamate treatment was measured in vitro by MTT method. Radiosensitivity of hypoxic CNE2 with or without sodium oxamate treatment was tested by clone formation assay. Results Lactate and angiotensin Ⅱ production of CNE2 cells treated with sodium oxalate was inhibited. Sodium oxalate inhibited the proliferation of hypoxic CNE2 cells. The radiosensitivity of hypoxic CNE2 cells treated with sodium oxalate was largely improved. Conclusions Sodium oxalate inhibits the proliferation of CNE2 cells in hypoxic condition and significantly enhances the radiosensitivity of hypoxic CNE2 cells. The mechanism may be involved in its inhibiting of angiotensinⅡproduction.

Objective To investigate the clinical performance of ultrasound screening for fetal structural anomalies at 11-13+6 weeks of gestation and to evaluate the relation of structural anomalies with karyotypes and copy number variations. Methods A retrospective analysis was conducted on fetuses with structural anomalies detected by ultrasound examination at 11-13+6 gestational weeks in First Affiliated Hospital of Sun Yat-Sen University from January 2013 to December 2017. Karyotype and chromosomal microarray analysis(CMA) were offered to these fetuses and ultrasound scans were repeated at 16-18 gestational weeks. All fetuses were followed up to termination or birth. Fisher's exact test was used for statistical analysis. Results A total of 362 fetuses with structural anomalies were studied including 101 (27.9%) fatal malformations, 253 (69.9%) major malformations and eight (0.2%) minor malformations. Cardiac malformation (32.6%, 118/362), central nervous system anomalies (24.9%, 90/362) and anterior abdominal wall defects (20.9%, 76/362) were the three most common abnormalities. Invasive prenatal test was performed in 107 cases including 25 fatal, 79 major and three minor malformations. Thirty (28%) out of the 107 cases had abnormal karyotypes, which were chromosomal aneuploidies (n=28) and chromosomal fragment abnormalities (n=2). Among the 99 cases received CMA, 25 had abnormal karyotypes, and copy number variations were identified in eight [three (4.05%) were pathogenic variations] out of the rest 74 with normal karyotypes. The incidence of chromosomal abnormalities in fetuses with major malformations was higher than that of fetuses with fatal malformation [32.9% (26/79) vs 12.0% (3/25), P=0.045]. Altogether, 117 cases repeated second-trimester ultrasound among which 16 (13.7%) were normal; 19 (16.2%) had cardiac defect which was discordant with the first-trimester evaluation and five (4.2%) were found to have additional malformations. Diagnosis of the other 77 cases were consistent with the first-trimester ultrasound findings. After the second-trimester ultrasound scanning, 49 pregnancies were terminated; 39 twin pregnancies and four triplet pregnancies underwent selective fetal reduction; 25 continued to delivery with good neonatal outcomes. Out of the 23 699 cases without abnormal ultrasound findings at 11-13+6 gestational weeks, 20 182 (85.2%) were successfully followed up, among which structural abnormalities were found in 178 during the second trimester and in 31 after birth. Conclusions A detailed ultrasound examination at 11-13+6 weeks of gestation is important to identify fetal structural defects. However, it could not replace the second-trimester ultrasound. There is a high risk of chromosomal abnormalities in fetuses with early-detected structural defects. CMA is able to identify pathogenic copy number variations with a relatively low detection rate.

Objective: To investigate the effects of curcumin on pneumococcal pneumonia-induced pneumonia, apoptosis and p38 MAPK expression in infant mice. Methods: A total of 60 male infant C57BL/6 mice at three weeks of age were randomly divided into 6 groups: control group, model group, high-dose curcumin treatment group, middle-dose curcumin treatment group, low-dose curcumin treatment group and SB203580 treatment group. The Curcumin and SB203580 were intraperitoneally applied at doses of 200, 60, and 20 mg/kg (for curcumin) and 100 mg/kg (for SB203580) from two days before bacterial infection to three days post-infection. The control group and model group were intraperitoneally injected with an equal volume of saline. The model group, curcumin treatment groups and SB203580 treatment group were transnasally inoculated with approximately 10⁶ CFU/ml of pneumococcal pneumonia in 50 μl of PBS applied to the tip of the nose to establish the experimental pneumococcal pneumonia. Subsequently, all the mice were killed and lung tissues were harvested for hematoxylin-eosin staining, calculation of lung score indexes, measurement of IL-1β and TNF-α contents by ELISA, and measurement of Bax, Bcl-2and p38 MAPK expression by Western blot. Results: Compared to the model group, the edema score (0.50 ± 0.10, 1.51 ± 0.16, 1.38±0.11, vs. 2.50 ± 0.20), hemorrhage score (0.32 ± 0.09, 1.01 ± 0.11, 0.85±0.09 vs. 1.80 ± 0.20), inflammatory cell infiltrate score (0.35 ± 0.09, 1.61 ± 0.16, 1.52±0.10 vs. 3.21 ± 0.22), small airway damage score (0.12 ± 0.03, 0.53 ± 0.14, 0.50±0.04 vs. 1.12 ± 0.19) in the medium-, high-dose group and SB203580 treatment group significantly decreased (P<0.01). Compared to the model group, the contents of IL-1β (20.38 ± 1.69 pg/ml, 25.73 ± 2.08 pg/ml vs. 40.22 ± 5.70 pg/ml) and TNF-α (160.39 ± 15.81 pg/ml, 198.67 ± 18.97 pg/ml vs. 282.22 ± 25.30 pg/ml), Bax/Bcl-2 (0.31 ± 0.05, 0.53 ± 0.06 vs. 1.79 ± 0.17) and expression of phosphorylated p38 MAPK (0.69 ± 0.05, 0.81 ± 0.07 vs. 1.71 ± 0.14) in the high-dose group and SB203580 treeatment group significantly decreased (P<0.01). Conclusions Curcumin can inhibit the inflammatory response and cellular apoptosis in the lungs of mice with pneumococcal pneumonia, and the mechanisms maybe related to its inhibition of p38 MAPK expression.

Objective: To explore the association between single nucleotide polymorphism rs12632942 in SCN10A exon and oxaliplatin-induced peripheral neuropathy (OXLIPN) in colorectal cancer (CRC) patients receiving chemotherapy. Methods:Atotal of 319 cases of blood samples from CRC patients receiving chemotherapy regimen with Oxaliplatin (OXL) were collected from the Second Affiliated Hospital of Guangzhou Medical University, the Second Affiliated Hospital of Nanchang University, and Guangzhou Baiyun District Hospital of Chinese Medicine during January 2011 and June 2013. DNAwas routinely extracted, and PCR amplification was performed to analyze the genotype of rs12632942; and OXLIPN of patients was also evaluated. The association between rs12632942 genotype and OXLIPN was analyzed by χ2 test and multivariate logistic regression model. Results: The genotypes of rs12632942 of 319 CRC patients:AAof 134 cases,AG of 156 cases and GG of 29 cases; and the genotype distribution of rs12632942 was in accordance with Hardy-Weinberg equiliberum (P>0.05). χ2 test showed that rs12632942AG+GG genotype was associated with Ⅱ-Ⅳ degree OXLIPN (P<0.01). Multivariate logistic regression model showed that rs12632942 AG + GG genotype was an independent risk factor for Ⅱ-Ⅳ degree OXLIPN（OR=2.044； 95%CI=1.231-3.392; P<0.01） . Conclusion: Colorectal cancer patients with SCN10A exon polymorphism rs12632942AG + GG genotype were susceptible to Ⅱ-Ⅳ degree OXLIPN.