Objective To raise the etiological diagnostic rate of renal colic in remission period with intravenous urography.Methods High-dense intravenous urography with TV monitoring (HIVP-TV) was employed to detect the 48 cases,including 37 cases in remission and 11 cases in attack periods.Results There were signfiicantly differences in imaging time of obstractive sites of injured kidney and ureter between both remission and attack periods(P

Objective To observe the clinical efficacy of acupuncture plus Chinese medicinal fumigation in treating chronic pelvic inflammatory disease (CPID).Method Totally 120 CPID patients were randomized into group A, group B and group C, 40 cases in each group. Group A was intervened by acupuncture plus Chinese medicinal fumigation, group B was by dry acupuncture treatment, while group C was by Chinese medicinal fumigation alone. After 3 treatment courses, the clinical efficacies were observed, and the relapse rates among the cured cases in 8 months after the whole treatment were compared among the 3 groups.Result The total effective rate and recovery rate were respectively 95.0% and 70.0% in group A, versus 82.5% and 45.0% in group B, and 57.5% and 32.5% in group C, and the total effective rate and recovery rate in group A were significantly different from that in group B and group C (P<0.05). The treatment duration for the recovered cases in group A was significantly different from that in group B and C (P<0.05). The relapse rate in the recovered cases in the 8-month follow-up was 10.7% in group A, versus 44.4% in group B and 53.8% in group C, and the relapse rate in group A was markedly lower than that in group B and C (P<0.05).Conclusion Acupuncture plus Chinese medicinal fumigation is an effective method in treating CPID, and its advantages include content efficacy, short treatment duration, and low relapse rate, etc.

BACKGROUND: Prefabricated composite tissue flaps have been used by Bakamjjan for cardiac repair since 1973, but have not been widely used due to technique limitations. Domestic research on prefabricated composite tissue flaps to repair limb bones is rarely reported. OBJECTIVE: To analyze the effects of prefabricated composite tissue flaps in the repair of limb bone and corresponding soft tissue defects. METHODS: New Zealand big rabbit models of bone fracture and soft tissue defect of the extremities were constructed (first operation) and randomly divided into three groups. In group A, prefabricated composite tissue flap was used to treat bone and soft tissue defects of the extremities at 10 days after modeling (second operation). In group B, free femur was used to treat bone and soft tissue defects of the extremities at 10 days after modeling. In group C, the incision was open and sutured with no treatment. General condition, body weight, imaging finding and histological findings were compared between groups. RESULTS AND CONCLUSION: There was 100% survival in all the three groups. Graft displacement was observed in 2 rabbits in the group B, but the deformity healed, which had little effect on the rabbit's mobility. The weight recovery and gain were higher in the group A than in the group B (P < 0.05). The imaging findings showed that a large number of calluses were formed in the group A at 2 weeks after operation, which were bridged in gap at 4 weeks after operation, filled in the defect gap at 8 weeks, and remodeled at 12 weeks. In the group B, a small amount of calluses were formed at 2 weeks after operation, and began to increase at 4 weeks. The femoral cut was obvious. A large number of calluses were formed at 8 weeks after operation, and the defect gap was filled at 12 weeks after operation. In the group C, the callus began to form at 8 weeks after operation, and the defect gap was still present, with osteosclerosis at the two ends. The Lane-Sandhu score was statistically different between the three groups at 8 and 12 weeks after second operation (P < 0.05). Histological observation indicated that a large number of newly formed osteoblasts and bone cells were formed in the group A at 4 weeks after operation, and the tubular structure increased and irregular bone island formed at 8 weeks; new bone formed at 12 weeks, with the presence of the medullary cavity containing yellow bone marrow dominated by adipocytes. In the group B, most of the grafted bones were degraded and absorbed at 4 weeks after operation, and osteoblasts were ossified at 8 weeks. The remaining implanted bones were still visible. Most of the osteoblasts were ossified and became lamellar bones at 12 weeks. In the group C, the defect area was filled with a large amount of fibrous connective tissues at 12 weeks after operation, and there was no bone formation. To conclude, the prefabricated composite tissue flap can be used to repair the bone and soft tissue defects of the extremities, and it has a faster and better therapeutic effect than the traditional free bone repair.

OBJECTIVE: To probe the correlation between the postmortem interval (PMI) and the DNA degradation of costicartilage and dental pulp cells in human being after death, and to seek a new method for estimating PMI. METHODS: The image cytometry was used to measure the DNA degradation under different ambient temperatures (30-35 degrees C, 15-20 degrees C) in 0-15 days after death. RESULTS: The average DNA content of two kinds of tissue was degradated with the prolongation of PMI. But there was a plateau period of 0-4 days for dental pulp cells of human being in 15-20 degrees C. There was a high negative correlativity P<0.01 between the average DNA content and PMI. CONCLUSION PMI could be estimated accurately according to the DNA degradation of costicartilage and dental pulp cells in human being after death.
Adolescent ; Adult ; Autopsy ; Cartilage/metabolism* ; DNA/metabolism* ; Dental Pulp/cytology* ; Female ; Forensic Pathology/methods* ; Humans ; Image Processing, Computer-Assisted/methods* ; Male ; Middle Aged ; Postmortem Changes ; Ribs/metabolism* ; Temperature ; Time Factors ; Young Adult

ObjectiveTo investigate the role and mechanism of hyodeoxycholic acid （HDCA） in the progression of metabolic associated fatty liver disease （MAFLD）， and to provide a new theoretical basis for further clarifying the pathogenesis of MAFLD. MethodsL02 hepatocytes were used as experimental cells， and palmitic acid was used to induce steatosis in L02 cells. The farnesoid X receptor （FXR） siRNA interference chain technique was used to construct a hepatocyte cell line with low FXR expression. CCK8 assay was used to observe the effect of HDCA on L02 steatosis hepatocytes at different concentrations （0， 100， 200， 300， and 400 μmol/L） and time points （12， 24， 36， and 48 hours）. The method of qRT-PCR was used to measure the mRNA expression levels of FXR， proliferating cell nuclear antigen （PCNA）， Cyclin D1， phosphatidylinositol 3-kinase （PI3K）， and protein kinase-B （AKT）， and Western blot was used to measure the protein expression levels of FXR， Cyclin D1， PCNA， PI3K， phosphorylated PI3K （p-PI3K）， AKT， and phosphorylated （p-AKT）. A one-way analysis of variance was used for comparison of normally distributed continuous data with homogeneity of variance between multiple groups， and the Tukey HSD test was used for further comparison between two groups； the Welch analysis of variance was used for comparison of normally distributed continuous data with heterogeneity of variance between multiple groups， and the Games-Howell test was used for further comparison between two groups. The independent-samples t test was used for comparison between two groups. ResultsCCK8 assay showed a significant reduction in the viability of L02 cells and steatosis hepatocytes treated by 300 μmol/L HDCA （P<0.05）， and qRT-PCR showed a significant increase in the mRNA expression level of FXR and significant reductions in the mRNA expression levels of PCNA， Cyclin D1， PI3K， and AKT （all P<0.05）. Western blot showed a significant increase in the protein expression level of FRX （P<0.05）， and after interference of FXR expression in L02 cells， there were significant increases in the protein expression levels of PCNA， PI3K， p-PI3K， AKT， and p-AKT （all P<0.05）. ConclusionHDCA inhibits the PI3K/AKT signaling pathway by upregulating FXR expression， thereby inducing a reduction in the viability of steatosis hepatocytes.

OBJECTIVEOur research was aim to investigate the effect of microRNA-328 (miR-328) on proliferation of chronic myeloid leukemia(CML) cell K562 and the mediated effect of C/EBPα.

METHODSThe eukaryotic expression vectors of miR-328 targeting gene and suppressor gene (hsa-miR-328 and hsa-miR-328-inhibitor) were constructed, and transfected into K562 cells respectively. The mRNA expression levels of miR-328 and C/EBP α were detected by real-time fluorescence quantitative RT-PCR; C/EBP α protein expression was detected by Western blot; CCK-8 was used to estimate the cell viability.

RESULTSThe recombinant genes of hsa-miR-328 and hsa-miR-328-inhibitor were successfully constructed and transfected into K562 cells. Fluorescent cells were observed after 24 h, and the visible fluorescence cells were gradually increased after 48 h or 72 h, the miR-328 showed no effect on the mRNA expression of C/EBPα detected by RT-PCR. Meanwhile, miR-328 showed recovering effect on C/EBPα translation and inhibition of K562 cells proliferation.

CONCLUSIONmiR-328 has been successfully constructed and transfected into K562 cells, miR-328 inhibits the proliferation of K562 cells by up-regulation of C/EBPα.

CCAAT-Enhancer-Binding Protein-alpha ; Cell Proliferation ; Cell Survival ; Humans ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; MicroRNAs ; Transfection ; Up-Regulation

OBJECTIVETo investigate the relationship between aldose reductase like protein (ARL-1) gene overexpressed in HCC cells and drug-resistance of the cell to drugs containing carbonyl group.

METHODSTo establish ARL-1 stable expression positive cell line, eukaryotic expression vectors containing ARL-1 gene cDNA were transfected into Hep cell mediated by lipofect AMINE. The positive monoclones were determined by PCR and RT-PCR, respectively. Then MTT assay was used to study the drug resistance ability of the cells to drugs containing carbonyl after incubating three days with those drugs.

RESULTSAfter ARL-1 gene transfection mediated by lipofect AMINE, one positive monoclonal cell overexpressing ARL-1 gene was selected. Compared with the control cell group, drug resistance ability of the positive cells to ADM and MMC which contain carbonyl group increased 2.3 and 3.17 fold, respectively (t=6.39, P=0.016 in ADM group and t=30.06, P=0.001 in MMC group). In the same time, drug resistance ability to 5-FU which has no carbonyl group had no statistical difference between positive monoclonal cell group and control cell group (t=0.684, P=0.531).

CONCLUSIONSThe Hep ARL-1 positive cell line with stable expression of ARL-1 gene has been established successfully and the up-regulation of ARL-1 gene may plays an important role in drug resistance of the cells to anticancer drugs containing carbonyl group.

Aldehyde Reductase ; genetics ; metabolism ; Antineoplastic Agents ; pharmacology ; Doxorubicin ; pharmacology ; Drug Resistance, Neoplasm ; genetics ; physiology ; Fluorouracil ; pharmacology ; Humans ; Inhibitory Concentration 50 ; Mitomycin ; pharmacology ; Transfection ; Tumor Cells, Cultured ; drug effects

Migrations of orthopedic wires to cardiovascular system are uncommon and rarely reported. We report a case of right ventricle embolization with the Kirschner wire that was used for right 2nd rib osteosynthesis 2 years and 8 months previously in a 50-year-old man. The patient was asymptomatic and migration of the Kirschner wire was discovered by routine chest X-ray. An 8 cm-long Kirschner wire was successfully retrieved from the right ventricle. The treatment strategy for Kirschner wire removal from right ventricle is discussed.
Bone Wires ; adverse effects ; Embolism ; etiology ; Foreign-Body Migration ; Heart Ventricles ; Humans ; Male ; Middle Aged ; Rib Fractures ; surgery ; Ribs

OBJECTIVETo study the features of vascular smooth muscle cell (VSMC) proliferation induced by endothelin-1 (ET-1).

METHODSVSMCs of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats were cultured and treated with ET-1. Basic fibroblast growth factor (bFGF) gene expression was measured using both Northern blot and an enzyme-linked immunoassay.

RESULTSET-1 resulted in an increase in bFGF transcripts at 8 - 24 h; bFGF levels were significantly higher in VSMCs treated with ET-1 than in those not treated. However, VSMCs growth responses in SHR and WKY were different. Smooth muscle cells of SHR were hyper-responsive to ET-1. Maximal bFGF mRNA levels were elevated 3.5-fold at 4 h of stimulation in WKY and 8-fold at 8h in SHR4. Moreover, the proliferation of VSMCs induced by ET-1 was inhibited by antisense phosphorothioate oligodeoxynucleotides (10 micromol/L AS-bFGF) but not sense bFGF oligomers at the same concentrations, being reduced by 80% in SHR and 40% in WKY vs control, respectively. Furthermore, the effect of AS-bFGF oligomers on SHR SMC proliferation is significantly greater than on WKY SMC proliferation.

CONCLUSIONET-1 may be required for exaggerated vascular growth responses in SHR and bFGF may be involved.

Animals ; Cell Division ; drug effects ; Cells, Cultured ; DNA, Antisense ; pharmacology ; Dose-Response Relationship, Drug ; Endothelin-1 ; pharmacology ; Fibroblast Growth Factor 2 ; genetics ; Gene Expression Regulation ; drug effects ; Muscle, Smooth, Vascular ; cytology ; drug effects ; metabolism ; Oligonucleotides ; pharmacology ; RNA, Messenger ; drug effects ; genetics ; metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Time Factors

Objective: To construct 3β-HSD gene shRNA lentivirus interference vecto, then transfect into human MCF-7 cells, and construct cell line with 3β-HSD gene silencing, finally to study the effects of 3β-HSD on apoptosis induced by di- (2-ethylhexyl) phthalate (DEHP) . Methods: According to the mRNA sequence of 3β-HSD gene provided by GenBank, three interference sequences were designed and connected to PLVX-shRNA2-puro after annealing. The recombinant lentivirus vector was transfected into 293FT cells, the virus supernatants were collected and infected with MCF-7 cells. After puromycin screening, MCF-7 cells with 3β-HSD gene silencing were constructed. The cells with 3β-HSD gene silencing were identified by real-time quantitative PCR and western blot. Then the 3β-HSD gene silencing cells and MCF-7 cells were treated at various doses of DEHP for 24 hours to detect the gene expression and protein expression of apoptosis genes including Bax, Caspase-3 and Caspase-8. Results: The interference sequence of 3β-HSD gene inserted into lentivirus vector PLVX-shRNA2-puro is consistent with the designed sequence. 3β-HSD gene expression level in MCF-7 cells with 3β-HSD gene silencing was 77% lower than than that of control MCF-7 cells. 3β-HSD protein level in MCF-7 cells with 3β-HSD gene silencing was 74% lower than that of control MCF-7 cells. After DEHP treatment in MCF-7 cells with 3β-HSD gene silencing and control MCF-7 cells, qRT-PCR results showed that Bax gene expression levels increased by 28%-54%, Caspase-3 gene increased by 13%-49%, Caspase-8 gene increased by 21%-70% in MCF-7 cells when compared with the control group. Additionally, in the 3β-HSD gene silencing cells, Bax gene expression level decreased by 11%-28%, Caspase-3 gene expression decreased by 12%-23%, Caspase-8 gene expression decreased by 11%-34%, compared with the same treatment group of MCF-7 cells. Western blot results showed that Bax protein expression level increased by 28%-61%, Caspase-3 protein expression level increased by 40%-48%, Caspase-8 protein increased by 31%-84% in MCF-7 cells when compared with the control group. In 3β-HSD gene silencing cells, Bax protein expression level increased by 11%-27%, Caspase-3 protein increased by 21%-40%, Caspase-8 protein increased by 12%-25%, compared with the same treatment group of MCF-7 cells. Conclusion The stable 3β-HSD gene silencing cell line are successfully constructed in this study. DEHP can induce increased expression of apoptotic gene and protein. Silencing of 3β-HSD gene can inhibit the activation of apoptotic gene by DEHP in a certain degree.