Objective To investigate the effect of diuretic (furosemide) therapy on kidney injury induced by melamine and cyanuric acid in rats. Methods 36 male Spragne Dawley rats were random disided into 3 groups. Group A was treated with 2mL of water daily, group B was treated with melamine and cyanuric acid ( each 100 mg/kg) daily for 4 days and then 2ml of water daily, group C was treated with the same as group B at the first 4 days and then treatment with furosemide (20mg/kg) daily. Samples of blood and 24h urine were collected to detective biochemical indexes, and kidney sections were performed on days 4 and 11 ( each end point, n = 6). The kidneys were observed with histopathology and renal crystal deposition scores were determined. Results On the 4th day, group B and group C were resulted in acute kidney injury such as oliguria [ ( 3. 39 ± 1.02 ) ml, ( 3. 20 ± 0. 86 ) ml ] and high serum creatinine [ ( 153.54 ±27. 08)μmol/L, (160. 11 ± 19. 55)μmol/L] and renal melamine cyanurate crystal were found in the renal tissues. On the 11th day, the renal crystal deposition score in the rats was reduced by 9. 52% ( P >0. 05). Compared with those of the 4th day in group B, it reduced by 63.63%( P <0.05) in group C. Urine volume were increased significantly compared with those of the 4th day( P < 0. 05 ) in group C [ from (3.20±0. 86)ml to (25.96 ±5.97)ml] and group B [ from(3. 39 ± 1.02)ml to (8. 57 ± 1.66)ml] , and Urine volume in group C was increased significantly more than that in group B ( P < 0. 05 ). The serum creatinine was obviously reduced as compared with those of the 4th day in group B and C( P <0.05), from[ (153. 54±27.08) μmol/L] to [ ( 106. 10 ±5.53) μmol/L] in group B and from [ ( 160. 11 ± 19. 55) μmol/L] to [ (67. 17 ± 12. 80 ) μmol/L] in group C, but the serum creatinine in group B was still higher than that in group A and C ( P < 0. 05). Conclusions Furosemide can attenuate the damage of acute kidney injury induced by melamine and cyanuric acid.

Objective To investigate the clinical effect of acupoint catgut embedding therapy combined with Buzhong Decoction in the treatment of depression for spleen qi stagnation type gastroptosis. Methods From November 2015 to October 2017 due to ptosis of the stomach (spleen qi stagnation type) and on the basis of study, 60 patients in our hospital were randomly divided into two groups. 30 cases of control group was given Buzhongyiqi pill treatment and the observation group of 30 cases was given acupoint catgut embedding therapy combined with Buzhong Decoction for depression. Results After treatment, the observation group's lassitude, anorexia, abdominal distension and symptom score lower than the control group; total efficiency of observation group was 93. 33％ higher than that of the control group (28/30), 70％ (21/30). The difference was obvious, P＜0. 05. Conclusion Buzhong Decoction in treating gastroptosis for depression with catgut embedding(spleen qi stagnation type) has significant effects, which can effectively relieve the clinical symptoms and is worthy of promotion.

OBJECTIVE: To diagnose a 46,XN,del(11)(q14q22) fetus by non-invasive prenatal testing (NIPT), karyotype analysis and whole genome sequencing (WGS). METHODS: Peripheral blood sample of the gravida was taken for NIPT screening. Blood samples of the gravida, her husband, and umbilical cord blood were also taken for chromosome karyotyping and whole genome sequencing (WGS). RESULTS: NIPT screening indicated the fetus has carried partial deletion of chromosome 11, while no chromosomal abnormality was found with the cord blood sample due to the low resolution of G-banding analysis. WGS analysis of the cord blood indicated 46,XN,del(11q14.3q22.1). seq[GRCh37/hg19] (90 623 404-97 469 319)×1, 6.85 Mb. The karyotype of the fetus was eventually determined as 46,XN,del(11)(q14q22). Karyotyping analysis suggested that the gravida and her husband were 46,XX,del(11)(q14q22)[8]/46,XX[92] and 46,XY, respectively. However, neither of them was found to harbor the del(11)(q14q22) by WGS. CONCLUSION The abnormal karyotype of the fetus has derived from its mother's low percentage mosaicism. Combined NIPT, karyotyping analysis and WGS can detect chromosomal disorders with accuracy.

Objective To observe the changes of short-chain acyl-CoA dehydrogenase (SCAD) expression on human umbilical vein endothelial cell (HUVEC) apoptosis and investigate its relationship with apoptosis. Methods The HUVEC was cultured normally for 2-3 days. The apoptotic model of HUVEC was established by tert-butyl hydrogen peroxide (tBHP). The HUVEC was treated by different concentrations of tBHP (0, 10, 20, 30, 40, 50 μmol/L) for 12 hours and different time (0, 3, 6, 9, 12 hours) with 50 μmol/L tBHP to establish the apoptotic model of HUVEC. The cell viability was detected by methyl thiazolyl tetrazolium (MTT), the mRNA expression of SCAD was determined by real-time polymerase chain reaction (PCR), the protein expression of SCAD was achieved by Western Blot. The best concentrate and time were determined to interfere the HUVEC to achieve the apoptotic model of HUVEC. The SCAD gene of HUVEC was knocked down by RNA interference sequence (siRNA274, siRNA414, siRNA679). The mRNA expression of SCAD, the protein expression of SCAD and the activity of SCAD enzyme were detected to achieve the best RNA interference sequence. The HUVEC was intervened by the best RNA interference sequence and tBHP. The cell activity and apoptosis rate, the enzyme activity of SCAD, the mRNA and protein expression of SCAD, the contents of reactive oxygen species (ROS), aderosine triphosphate (ATP) and free fatty acid (FFA) were detected to observe the effect of SCAD on apoptosis of HUVEC. Results ① The cell viability, the mRNA expression and the protein expression of SCAD were decreased gradually in a concentration and time dependent manner with the increase of tBHP concentration and the prolongation of intervention time. The decline was most significant in the group of the 50 μmol/L tBHP to interfere HUVEC for 12 hours. ② The siRNA679 transfection was the most significant in reducing SCAD mRNA and protein expressions among the three interference sequences (siRNA274, siRNA414, siRNA679). ③ Compare with blank control group, the cell viability was significantly decreased in the siRNA679 group (A value: 0.48±0.09 vs. 1.00±0.09, P < 0.01), the apoptotic rate of HUVEC was significantly increased [(29.96±2.09)% vs. (2.90±1.90)%, P < 0.01], the expression of SCAD mRNA and SCAD protein, the activity of SCAD enzyme and the content of ATP were significantly decreased [SCAD mRNA (2-ΔΔCt): 0.50±0.16 vs. 1.34±0.12, SCAD/α-Tubulin: 0.67±0.11 vs. 1.00±0.06, the activity of SCAD enzyme (kU/g): 0.38±0.04 vs. 0.53±0.04, the content of ATP (μmol/g): 0.14±0.02 vs. 0.19±0.01, all P < 0.05], the contents of FFA and ROS were significantly increased [FFA (nmol/g): 0.84±0.07 vs. 0.47±0.04, ROS (average fluorescence intensity): 647.5±23.7 vs. 434.2±46.5, both P < 0.01]. Meanwhile, SCAD siRNA treatment triggered the same apoptosis as HUVEC treated with tBHP. Conclusions Down-regulation of SCAD may play an important role in HUVEC apoptosis. Increase in the expression of SCAD may become an important part in intervening HUVEC apoptosis.