Objective To investigate the clinical distribution and antimicrobial resistance of Streptococcus agalactiae(S.agalactiae) in neonatal intensive care unit(NICU), and provide reference for antimicrobial use and intervention measures.Methods Specimens from neonates in the NICU of a hospital in 2010-2014 were collected, the department sources and antimicrobial susceptibility testing results of 62 strains of S.agalactiae isolated from children were analyzed.Results 62 strains of S.agalactiae were mainly distributed at full-term NICU, accounting for 64.52％;the main source of specimens was blood, accounting for 90.33％, followed, by cerebrospinal fluid (6.45％), sputum, and secretion(both were 1.61％).S.agalactiae had the highest resistance rate to tetracycline(79.03％);resistance rates to erythromycin and clindamycin were both 74.19％, resistance rate to levofloxacin was 40.32％, susceptibility rates to penicillin and ampicillin were both 100％.Conclusion S.agalactiae infection mainly occurred in neonates in full-term NICU, and has high resistance rate to multiple antimicrobial agents, penicillin and ampicillin can be used as the preferred antimicrobial agents for the treatment of S.agalactiae infection.

Objective To explore the clinical application and value of percutaneous treatment of pancreatic pseudocysts guided by CT.Methods The percutaneous external draining of pancreatic pseudocyst caused by various causes was performed under CT guidance in 29 cases, including 21 males and 8 females, age from 22 to 71 years, average (48.2?13.6) years. After the point, the angle,and the depth of puncture were measured on CT images, pseudocyst puncture and catheterization of external draining were made and followed up. Results 30 procedures of puncture in 29 lesions were done, the successful rate was 100%. Puncture path included frontal in 17 cases(18 times of puncture), lateral in 8 cases ; back in 4 cases, and 30 drainage catheters were placed. All cases were followed up except one case, follow up time ranged from 1 to 20 months [average (8 07?4 04) months]. Following disappearance of pseudocyst, catheters were extracted in 19 cases except 2 cases with pseudocyst recurrance. Follow up time from 4 to 14 months[average (8.29?4.03) months]. 5 cases had surgerical operations again after draining 1-4 months, 4 cases were still being followed up. The effective rate of therapy was 65.52%(19/29). Conclusion The technique of percutaneous catheter external draining of pancreatic pseudocyst guided by CT is mildly invasive and simple, and has high successful rate.

OBJECTIVEA multi-center randomized phase III clinical trial was designed to evaluate the efficacy, clinical benefit response (CBR) and toxicity profile of germcitabine (GEM) or GEM plus cisplatin (CDDP) for locally advanced (LAPC) or metastatic pancreatic cancer (MPC).

METHODSFrom July 2000 to May 2001, 42 untreated patients with LAPC or MPC were collected and randomized into two groups: Arm A-GEM 20 patients and Arm B-GEM + CDDP 22 patients. Eligibility criteria were: cytologically and pathologically proven pancreatic carcinoma, Karnosky performance status (KPS) 60 - 80, age 18 - 75 yrs, adequate hematological, renal and liver function, measurable disease, and controllable pain. For Arm A patients, weekly dose of GEM 1 000 mg/m(2)/w for 7 times followed by a week rest. Then weekly GEM at the same dose for 3 times every 4 weeks. Arm B patients were given weekly dose of GEM 1 000 mg/m(2)/w for 3 times every 4 weeks combined with CDDP 60 mg/m(2) on D15 for 3 cycles.

RESULTSThirty-four patients were available for objective response (Arm A 16 and Arm B 18) and 36 (Arm A 16 and Arm B 20) for CBR evaluation. In Arm A and Arm B, PR 1 (6.3%) and 2 (11%), MR 4 (25%) and 3 (16.7%), SD 7 (43.8%) and 8 (44.4%), PD 4 (25%) and 5 (27.8%), PR + MR 31.3% and 27.8%, PR + MR + SD 75% and 72.2% were observed. Positive CBR was 14/16 (87.5%) in Arm A and 14/20 (70.0%) in Arm B. The negative results was 2/16 (12.5%) in Arm A and 6/20 (30.0%) in Arm B. The median time of disease progression was not yet available at present. The 3-month survival rate of both Arm A and B was 100%, the 6-month survival rates of Arm A and B were 81.3% and 61.6% and the 12-month survival rates of Arm A and B was 31.3% and 11.1%, with median survivals of 273 and 217 days. The incidence of hematological and non-hematological toxicity of Arm A was lower than that of Arm B without statistical significance. The toxicity ranging from being mild to moderate was manageable.

CONCLUSIONGEM or GEM plus CDDP is able to lead to a moderate objective response rate, also significantly improve the quality of life in patients with locally advanced or metastatic pancreatic cancer patients, prolonging the survival time with tolerable toxicity.

Adult ; Aged ; Antimetabolites, Antineoplastic ; adverse effects ; therapeutic use ; Antineoplastic Agents ; adverse effects ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; adverse effects ; therapeutic use ; CA-19-9 Antigen ; analysis ; Cisplatin ; adverse effects ; therapeutic use ; Deoxycytidine ; adverse effects ; analogs & derivatives ; therapeutic use ; Female ; Humans ; Male ; Middle Aged ; Pancreatic Neoplasms ; drug therapy ; mortality ; Survival Rate ; Treatment Outcome

Laparoscopic pancreaticoduodenectomy (LPD) is one of the most complicated operations in laparoscopic field.After been widely reported nowadays, LPD has been cautiously regarded as feasible and safe for radically resection.At present, several large pancreatic surgery centers in China have successively carried out this kind of surgery, with over one thousand cases in all.However, partly due to its complexity and steep learning curve, this procedure only remains limited to a few selected large pancreatic centers.Large sample prospective random control test studies are still required.We suggest that in China, LPD should only be developed steadily and step by step by highly skilled open and laparoscopic surgeons who have minimally invasive concept, contrary to fears and could grasp technical expertise.

The insulinoma, which is the most common pancreatic neuroendocrine tumor, can be misdiagnosed and mistreated easily.Recently, the misdiagnosis rate has decreased significantly owing to the establishment of diagnosis and treatment system.However, the misconception about its diagnosis and treatment still exists because the diagnosis and treatment level varies greatly among different centers.This article aims to summarize the experience in the diagnosis and treatment of insulinoma in Peking Union Medical College Hospital, and introduce the qualitative and localization diagnosis, surgical and interventional treatment and perioperative management about insulinoma, so as to standardize the diagnosis and treatment procedure in China.

Pancreaticoduodenectomy is cumbersome and difficult to operate,with a long operative time and high risk of postoperative complications,thus it is one of the most complicated operations among general surgery.With the popularization and progress of minimally invasive techniques,minimally invasive pancreaticoduodenectomy (MIPD) has obtained a well developing.It has been confirmed that MIPD is noninferior or even superior to the traditional open pancreaticoduodenectomy in term of the feasibility,safety and effects of radical cure.However,the relevant conclusions are mostly from single-center retrospective studies,without high-quality evidence support.The authors has reviewed the recent research progress of MIPD in the indications and contraindications,safety,feasibility and tumor curative effect,and illustrated the current status and prospects of MIPD with clinical experience and related literature,contributing to the standardization of MIPD in China.

Objective: To test the expression of miR-1178 in pancreatic cancer and study its clinicopathological significance and mechanism. Methods: The expression of miR-1178 in 87 paired paraffin pancreatic ductal adenocarcinoma specimens and adjacent non- cancerous pancreatic tissue diagnosed by Pathology Department of Peking Union Medical College Hospital was detected by hybridization in situ. The relationship between the expression of miR-1178 and clinicopathological characters was analyzed.miR-1178 mimics and inhibitor were used to further detect the close relationship among miR-1178 and cancer invasion. Establish a nude mice subcutaneously transplanted tumor model, 4 weeks after vaccination for tumor volume and weight measurement.Student t-test, rank sum test, and χ² test was used respectively to compare the data between two groups. Cox regression was adopted to improve the single factor and multiple factors analysis. Results: The results of hybridization in situ showed the expression of miR-1178 was increased in 72 cases with pancreatic cancer compared to that in paired normal pancreatic tissues (50/72 vs. 11/72, χ²=43.26, P<0.05). miR-1178 expression was positively associated with tumor lymph node stage (χ²=4.189, P=0.041). Univariate and multivariate analysis revealed that miR-1178 was an independent adverse prognostic indicator for patients with pancreatic cancer (HR=2.364, 95%CI: 1.114-5.019, P=0.025). Transwell assay indicated the over-expression of miR-1178 increased the number of AsPC-1 cells that penetrated the ECM-coated membrane (177.0±19.8 vs. 119.7±15.9)(χ²=8.21, P<0.05). For the in vivo experiment, overexpression of miR-1178 significantly promoted tumor growth, compared with control group (tumor volume: (5 122.4±760.2)mm³ vs. (1 976.8±601.8)mm³, t=2.413, P<0.05; tumor weight: (1.55±0.21)g vs. (0.67±0.17)g, t=2.960, P<0.05). Over-expression of miR-1178 down-regulated the expression of Stub1 and elevated the expression of FAK/MMP-9 signal pathway(P<0.05). Conclusions MiR-1178 is overexpressed in pancreatic cancer, and is effective for predicting patients′ prognosis. MiR-1178 regulate Stub1/FAK/MMP-9 signal pathway and promote the invasion of AsPC-1 cells.

Objective: To investigate the expression of KLK7 in pancreatic cancer and its clinical significance. Methods: Immunohistochemistry was used to detect the expression of KLK7 protein in pancreatic cancer tissue microarray with 92 samples. Statistical analysis of the relationship between KLK7 and clinicopathological characteristics was finished. Pancreatic cancer cell lines were infected with lentiviuses in order to get cells with KLK7 stable overexpression.KLK7-siRNA was transfected into pancreatic cancer cells to knock down KLK7.Cell proliferation and chemosensitivity were detected by CCK-8 assay; Cell invasion and migration abilities were detected by Transwell assay. At the same time, subcutaneous xenograft tumor models were established in nude mice to observe the effect of KLK7 on tumor growth in nude mice. Data were statistically analyzed by rank sum test, χ² test and Logistic regression analysis. Results: The expression level of KLK7 in pancreatic cancer tissues was higher than that in paired adjacent tissues (P<0.05). KLK7 expression was correlated with vascular invasion(χ²=7.535, P<0.05). Further univariate and multivariate analysis showed that KLK7 expression was an independent risk factor for vascular invasion of pancreatic cancer(χ²=7.535, P<0.05). The overexpression of KLK7 in pancreatic cancer cell lines BxPC-3 and CFPAC can increase their proliferation abilities, reduce the chemosensitivity and promote their migration and invasion behaviour; The results of in vivo experiments showed that the volume of subcutaneously transplanted tumors in the overexpressing KLK7 group was significantly larger than that in the control group (t=4.479, P<0.05). The group of overexpressing KLK7 showed greater tumor weight than the control group(t=2.831, P<0.05). Conclusions The expression level of KLK7 in pancreatic ductal adenocarcinoma was higher than that in paired adjacent tissues and it is an independent risk factor for vascular invasion of pancreatic cancer.KLK7 can promote the proliferation of pancreatic cancer cells, reduce the chemosensitivity and increase the invasion and migration of pancreatic cancer cells.

Pancreatic neuroendocrine tumors are a group of rare neoplasms originating from the neuroendocrine cells of pancreas.They can be classified into functioning or non-functioning groups according to hormone secretion.Due to the application of high-resolution imaging techniques,the incidence of incidental non-functioning pancreatic neuroendocrine tumors has been rising for decades.Although the optimal prognosis,nonfunctioning pancreatic neuroendocrine tumor are heterogeneous,and the complication morbidity is high.So controversy still exists for the choice of treatment approach.This article aims to summarize and analyze the progress and current controversy about the treatment of incidental non-functioning pancreatic neuroendocrine tumors,and discuss about the appropriate treatment choice for patients.

Objectives To examine the expression of the long coding RNA GSTM3TV2 in pancreatic cancer tissues and to examine its role and mechanism in chemoresistance of pancreatic cancer cells. Methods The expression of lncRNA GSTM3TV2 in 15 pancreatic cancer specimens and corresponding adjacent to cancer tissue samples diagnosed by Department of Pathology, Peking Union Medical College Hospital was detected by real?time PCR.And the expressions of GSTM3TV2 in pancreatic cancer cell AsPC?1,BxPC?3,MIAPaCa?2,PanC?1,SU86.86,T3M4,and chemoresistant cells AsPC?1/GR and MIAPaCa?2/GR, and human pancreatic nestin?expressing cells hTERT?HPNE were detected. Pancreatic cancer cell lines were transfected with GSTM3TV2?pcDNA3.1(+)in order to get cells with GSTM3TV2 overexpression.GSTM3TV2?siRNA was transfected into pancreatic cancer cells to knock down GSTM3TV2. The cell chemoresistance was measured by CCK?8 and flow cytometry assay when incubated with nab?paclitaxel. At the same time, subcutaneous xenograft tumor models were established in nude mice to observe the effect of GSTM3TV2 on chemoresistance of tumor growth in nude mice.Western blot assay was also performed to detect the molecular mechanism of chemoresistance of GSTM3TV2. Results Comparing toadjacent tissues(0.084 ± 0.019), GSTM3TV2 expression was significantly upregulated in the pancreatic cancer tissues(0.493 ± 0.084) (t=5.146, P<0.05). GSTM3TV2 expression were higher in the chemotherapy resistance pancreatic cancer cells AsPC?1/GR(210.799±19.788) and MIAPaCa?2/GR(122.408±23.419) than that in the AsPC?1(3.793±0.615) and the MIAPaCa?2(5.179±1.095)(t=21.800,P<0.05;t=-18.490,P<0.05). The results of in vivo experiments showed that the volume of subcutaneously transplanted tumors in the overexpressing GSTM3TV2 group ((1 059.609±102.498)mm3) was significantly larger than that in the control group((566.414±81.087) mm3) by treated with nab?paclitaxel(t=4.230,P<0.05).Meanwhile,GSTM3TV2 could promote the expression of Cyclin D1, CDK6, Cyclin E1, Vimentin, N?cadherin, ZEB1, Snail and Slug; but decrease cleaved caspase?3,cleaved PARP in pancreatic cancer cells.Conclusions The expression level of GSTM3TV2 in pancreatic canceris higher than that in paired adjacent tissues. GSTM3TV2 may act as an oncogene to promote chemoresistance in pancreatic cancer through regulation of cell proliferation,apoptosis, and epithelial?mesenchymal transition.