Hepatocellular carcinoma (HCC)is a common malignant tumor in the world,and surgical resection and liver transplantation are two radical treatment modalities,but only 10%-20%of all patients can receive such treatments.In recent years,local therapies including radiofrequency ablation,microwave ablation,cryoablation,and the irreversible electroporation ablation which appeared recently have gradu-ally become the alternative therapies for the patients who are unable to undergo surgery.In addition to local tumor growth control and im-provement in survival outcomes,the ablation technology also helps to downgrade tumor for secondary resection.This article focuses on the re-search progress in radiofrequency ablation alone and in combination with other therapies in the treatment of HCC,compares radiofrequency ablation with other local ablative therapies,and briefly introduces the application of intelligent navigation technology in adjuvant ablation. With the development of medical imaging and progress in related fields,the ablation technology will be widely applied in clinical practice in the future.

Based on the translational research measurement and backtracking model put forward in this paper,it takes the new drug approved to enter into the market by American FDA from 2006-2015 as the fundamental data to measure the knowledge relations among new drug products-core patent-scientific paper-fund assistance,and puts forward the policies and suggestions for promoting innovation of pharmaceutical products in China.

Purpose To establish a golden hamster model of intrahepatic cholangiocarcinoma (ICC) using BOP [N-nitrosobis (2-oxo-propyl) amine] and to explore the protein expression of Wisp-1,β-catenin, TGF-β1 and Smad4 in ICC and their relationship with the tumorigenesis. Methods 57 female golden hamsters aged 8 to 9 weeks (39 in experimental group, 18 in control group), the experi-mental animals were subjected to subcutaneous injection of BOP, the control group was injected with saline. The liver was removed and paraffin sections were prepared for histopathological observation. The protein expression of Wisp-1,β-catenin, TGF-β1 and Smad4 was detected by immunohistochemistry (IHC) in these blocks. Results Most of the animals in the experimental group (29/39) developed ICC, part of the animal (8/39) developed bile duct dysplasia, 1 developed focal bile duct hyperplasia, and 1 was not found bile duct hyperplasia. The positive expression rates of four protein markers in ICC, bile duct dysplasia and normal intrahepatic bile duct tissues were Wisp-1,79. 3%, 87. 5% and 5. 0%,β-catenin, 96. 6%, 100. 0% and 15. 0%, Smad4, 96. 6%, 100. 0% and 25. 0%, TGF-β1, 62. 1%, 12. 5% and 5. 0%, respectively. The positive expression rates of Wisp-1, beta-catenin and Smad4 protein in both the ICC and the tissue of bile duct dysplasia were higher than that of normal intrahepatic bile duct tissue ( P<0. 001 ) , The positive ex-pression of TGF-β1 in the ICC tissue was higher than that of normal intrahepatic bile duct tissue and bile duct dysplasia (P<0. 001). Conclusions The study showed that BOP can induce a golden hamster model of ICC and provides a reliable animal model for the study of ICC. The high expression of Wisp-1,β-catenin, TGF-β1 and Smad4 in BOP-induced intrahepatic cholangiocarcinoma is closely re-lated to occurrence, development and infiltration of ICC.

Analyzed in this paper are the methods and their operability and efficiency for assessing the impact of papers on clinical research in view of evidence-based medicine, including citation analysis based on the clinical practice guidelines and evidence-based medicine database and comparative analysis of clinical trials registry data-base, with the model for assessing the impact of papers on clinical research in view of evidence-based medicine proposed.

Objective To evaluate the effect of naringenin on KIM-1 expression in rats with renal interstitial fibrosis caused by unilateral ureteral obstruction(UUO).Methods 24 SD male rats were randomly divided into Sham group,UUO group and naringe-nin group(Nar group),respectively.Rats in UUO group and Nar group got UUO to establish renal interstitial fibrosis models. Rats in Sham group only free but not ligated and cut ureters.Rats were administered saline and naringenin 25 mg/(kg·d)for 14 days.Then,24 h urine samples were collected before the rats were killed,and KIM-1 in these samples were measured by ELISA. Specimens were obtained from obstructive renal,the pathological change of renal tubule and interstitial were observe by HE and Masson staining.Moreover,the tubulointerstitial damage index was scored and the expression of KIM-1 in renal tissue was examined by immunohistochemical staining.Results Compared with Sham group,the tubulointerstitial damage index of UUO group significantly increased(P <0.05),contents of KIM-1 in urine and renal tissues also significantly increased(P <0.05).Com-pared with UUO group,the tubulointerstitial damage index score of Nar group alleviated(P <0.01),contents of KIM-1 in urine and renal tissues also reduced(P <0.05 ).Correlation analysis showed that there was positive correlation between KIM-1 in urine and renal tissues and TDI(r=0.862,0.866,P <0.01).Conclusion Naringenin can relieve renal interstitial fibrosis and reduce the content of KIM-1.

Objective To promote the development of precision medicine and gene sequencing technologies in China by analyzing the innovation situation in gene sequencing technologies.Methods An innovation situation research analysis frame was established with scientific literature and patent information as its basic data.The innovation situation in gene sequencing technologies was analyzed in aspects of scientific research and technical R & D.Results The research on gene sequencing technologies and technical R & D were focused on tumor diagnosis and treatment,plant gene sequencing,identification of HIV and gastrointestinal flora.Single cell genome amplification technology has greatly promoted the development of gene sequencing technologies.Conclusion The level of gene sequencing technologies and technical R & D in China is approaching to that in the world.

Objective To explore the effects of excise-induced fatigue on the microloop plasticity of prefrontal cortex through observing the expression of parvalbumin positive neurons in prefrontal cortexes of rats induced by exhaustive exercise,so as to find out the possible mechanism of the central regulation of exercise-induced fatigue by measuring the expression of NMDAR2B receptors.Methods Thirty-six Wistar rats were randomly divided into an exhausted group (E),a repeated exhaustion group (RE) and a control group (CG),each of 12.For group E,the adjusted Bedford incremental load of treadmill exercise program was employed:the initial treadmill speed was 8.2 m/min,lasting for 15 minutes,then increased to 15 m/min for another 15 minutes,and finally increased to 20 m/min till exhaustion.For RE group,they were given continuous treadmill exercises to exhaustion for consecutive 7 days.The immunofluorescence technique was used to observe the expression of PV+ interneurons after exhausted treadmill running.The Western blotting technique was used to determine the expression of NMDAR2B in the tissue of the prefrontal cortex.Results After the exhausted treadmill running,the expression of PV+ interneurons in the prefrontal cortexes of both E and RE groups increased significantly compared with the control group(P＜0.01).The immunofluorescence results indicated that NMDAR2B positive neurons were seen in group E,but not obviously in group CG and RE.The Western blotting showed that compared with CG group the protein expression of NMDAR2B in prefrontal cortexes of group E was relatively high,and that of group RE was relatively low,but without significant difference (P＞0.05).The running distance and prefrontal cortex NMDAR2B expression were found negatively correlated (P＜ 0.01).Conclusions Exhaustive exercises have an impact on the plasticity in rats' prefrontal cortex neural network through regulating the local loop of PV positive neurons.This plasticity of the prefrontal cortex is involved in the regulation of central fatigue.The present study might provide morphological basis for the research of central mechanism of the exercise-induced fatigue.

Objective:To investigate the roles of apoptosis-associated speck-like protein containing CARD(ASC),one of differentially expressed proteins in neutrophil death induced by ONO-AE-248.Methods:Human neutrophils were cultured in vitro with or without ONO-AE-248(5?10-5 mol/L).The expression of ASC mRNA was detected by RT-PCR.PMN proteins were extracted at 12 h and then separated by 2D electrophoresis.20 differentially expressed proteins were selected and determined by PDQest 2-DE software.Results:ONO-AE-248 decreased the expression of ASC mRNA strikingly in 2 hours;ASC was one of the important differentially expressed proteins between spontaneous apoptosis and non-apoptosis programmed cell death induced by ONO-AE-248 in 12 hour and ASC protein point was weaker in ONO-AE-248 group.Conclusion:ASC might act as double switch that leads to apoptosis of neutrophils in the high expression and removes the forbiddance of pathway of ONO-AE-248 signals in the low expression,resulting in non-apoptosis programmed cell death of neutrophils.

Using the APAAP method, we detected IL 4 producing cells in the peripheral blood of 9 patients with multiple myeloma and 11 normal subjects and lound that positive cell in MM (7.6%?2.1%) were significantly less as compared to normal subjects (15.36% ?4.1%), (P

Objective To analyse the clinical characteristics,gene mutation and enzymatic activity of αgalactosidase A(α-GalA)in a 15-year-old male patient with typical Fabry disease,whose mother was without any clinical manifestations.Methods Clinical features and laboratory data were collected from the patient and his mother.Genomie DNA was extracted from peripheral blood of the patient.his mother,and a healthy control subject.Seven exons of the GLA gene were amplified by PCR.PCR products were purified.cloned into T vector,and then sequenced.The enzymatic activity of α-GalA Was measured by fluorimetrie substrate assay. Results DNA sequencing results showed that a missense mutation of 10036-10038delAAG in exon 7 WaS identified in the patient,resulting in the replacement of 374 lysine and 375 glyeine by arginine,which Was not previously reported.The patient Was a hemizygote with gene mutation,his mother WaS a heterozygote carrying gene mutation,and the healthy control without mutation.α-GalA enzymatic activity assay showed that the enzymatic activity of the patient with GLA gene mutation was only 50%of the healthy control subject,while the enzymatic activity of the patient's mother Was about 70%of the heahhy control SObject.Conclusiolls Detecting GLA gene mutation and α-GalA enzymatic activity in patients with Fabry disease who have been clinically diagnosed seelns to be helpful in finding other patients in the family and in further understanding the molecular pathogenesis of that disease.