The importance of cultivating evidence-based consciousness of thinking and implementation capability of specialization postgraduates was analyzed,and experiences and suggestions acquired from the practice of teaching of specialization postgraduates were shared by demonstrating the enlightening of evidence-based consciousness of thinking,the cultivation of evidence-based implementation capability and the establishment of evaluation system,with PBL integrated.

Objective To monitor right heart hemodynamic changes of patients with lung cancer during and after the procedures of pneumonectomy and discuss the effect of pneumonectomy on right heart function and risk of postoperation morbidities. Method 16 patients with lung cancer were randomly selected and the clinical database was queried and Swan-Ganz catheter was applied awake from jugular vein to pulmonary artery ,measuring mean arterial pressure(MAP) ,heart rate(HR) ,central venous pressure(CVP) ,mean pulmonary artery pressure (MPAP),mean pulmonary capllary wedge pressure(MPCWP) ,and eardiaoc output(CO) and calculating cardiac index (CI),left ventricular-stroke work index (LVSWI), right ventricular stroke work index (RVSWI) , and stroke volume index(SVI) instantaneously before anaesthesia, after anaesthesia with single lung ventilation, after pulmonary artery and pulmonary vein occlusion and supine chest dosed during the procedure of pneumonectomy. Pre-and post-operative complications were recored. Results Cardiovascular complications occurred in 6 patients(37.5%) postoperatively. There were no operative or perioperative deaths. MPAP increased significantly after the procedure of pneumonectomy compared with that of preoperation, and MPAP > 26 mm Hg was in 4 patients who got cardiovascular complications postoperatively with morbidity of 100% ,which was "significantly higher than the morbidity of 16.7% (2/12) when MPAP < 25 mm Hg. Conclusion Pneumonectomy has significant effects on right heart hemodynemic changes and as MPAP increases postoperatively, the risk of cardiovascular complications becomes higher.

Animals ; Carcinoma, Hepatocellular ; enzymology ; DNA-Binding Proteins ; Disease Models, Animal ; Liver Neoplasms ; enzymology ; Male ; RNA ; genetics ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar ; Telomerase ; genetics ; metabolism

Abstract: Objective　This paper aims to explore the effect of live attenuated varicella vaccine on the sensitivity of tuberculin skin test(TST), and to provide reference for tuberculin skin test in the future. Methods　TST and emergency varicella vaccine were administered to students in grade one of a high school in Wuxi, Jiangsu province, who had both TB and varicella cases. Independent-samples t test was used to analyze the mean diameter of induration of TST in day 0, day 83 and day 195. The retrospective cohort study was used to analyze the effect of live attenuated varicella vaccine on TST. 　　Results　The mean induration diameter of 45 students who participated in three TST tests on day 0, day 83 and day 195 were analyzed by independent sample t test. On day 0, there was a difference in the mean diameter of TST induration between the unvaccinated and vaccinated groups(1.630±2.837 vs 5.818±4.530) (t=-3.692, P=0.001). On day 83, there was no difference in the mean diameter of TST induration between the two groups(0.001±0.001 vs 0.114±0.533) (t=-1.000, P=0.329). On day 195, there was a difference in the mean diameter of TST induration between the two groups(1.913±3.774 vs 5.023±5.126) (t=-2.309, P=0.026). Moreover, the retrospective cohort study showed that the mean diameter of TST induration changed more significantly after inoculation with varicella vaccine, RR=6.071, 95%CI (1.667-22.116), P<0.05; After inoculation with varicella vaccine, the mean diameter of TST test did not change significantly from day 0 to day 195 with no statistical significance RR=3.474, 95%CI (0.333-36.240), P>0.05. Conclusions　Live attenuated varicella vaccine may temporarily affect the sensitivity of tuberculin skin test.

Objective To investigate the consensus and controversies on the delineation of radiotherapy target volume for patients with locally advanced non-small cell lung cancer (LA-NSCLC).Methods Questionnaires including 15 questions on the delineation of radiotherapy target volume of NSCLC were sent to 12 radiation departments in China in November 2015.A patient with LA-NSCLC was selected by Fudan University Shanghai Cancer Center, and simulation CT images and medical history data were sent to the 12 radiation departments.Twelve radiation oncologists from the 12 radiation departments showed and explained the delineation of radiotherapy target volume of their own, and the patient was discussed by all experts in the sixth multidisciplinary summit forum of precise radiotherapy and chemotherapy for tumor and lung cancer.Results All receivers of the questionnaire answered the questions.The standard lung window width/level for the delineation of lung cancer was 800-1600/-600 to-750 HU, and the mediastinum window was 350-400/20-40 HU.Respiratory movement was measured by stimulator, 4D-CT, and stimulator+4D-CT with 2-5 mm expansion based on experience.The primary clinical target volume (CTV) was defined as gross target volume (GTV) plus 5-6 mm for squamous carcinoma/5-8 mm for adenocarcinoma.The metastatic lesion of mediastinal lymph nodes was delineated as 5 mm plus primary lesion in 6 departments and as primary lesion in another 6 departments.Of the 12 departments, 10 applied 5 mm of set-up error, 1 applied 3 mm, and 1 applied 4-6 mm.For V20 of the lungs, 10 departments defined it as<30%, 1 as<35%, and 1 as 28%.Nine departments defined the radiation dose of concurrent chemoradiotherapy (CCRT) for LA-NSCLC as 60 Gy in 30 fractions, 62.7 Gy in 33 fractions in 1 department, 50-60 Gy in 25-30 fractions in 1 department, and 60-70 Gy in 25-30 fractions in 1 department.For the delineation of target volume for the LA-NSCLC patient treated with CCRT, the primary planning target volume (PTV) was defined as GTV plus organ movement (IGTV) and set-up error (GTV→IGTV→PTV) in 3 departments, as CTV plus organ movement (ITV) and set-up error (GTV→CTV→ITV→PTV) in 8 departments, and as CTV plus set-up error/IGTV plus 5-6 mm for squamous carcinoma/5-8 mm for adenocarcinoma (CTV) and set-up error (GTV→CTV→PTV/GTV→IGTV→CTV→PTV) in 1 department.For the delineation of PTV in the mediastinal lymph node, GTV→IGTV→PTV was performed in 3 departments, GTV→CTV→ITV→PTV in 8 departments, and GTV→CTV→PTV in 1 department.For 10%-100% patients with LA-NSCLC, the radiation field needed to be replanned when 38-50 Gy was completed.There was no unified standard for the optimal standardized uptake value (SUV) of positron emission tomography (PET)-computed tomography (CT) simulation and delineation.Seven departments had applied magnetic resonance imaging (MRI) simulation and 10 departments had applied stereotactic body radiation therapy (SBRT) for the treatment of early-stage NSCLC.For the delineation of PTV for early-stage NSCLC (T1-2N0M0), GTV→IGTV→PTV was performed in 5 departments, IGTV→PTV in 3 departments, and GTV→CTV→ITV→PTV in 2 departments.In all the 12 departments, peripheral early-stage NSCLC was given 6.0-12.5 Gy/fraction, 3-12 fractions and central early-stage NSCLC was given 4.6-10.0 Gy/fraction, 5-10 fractions.The results of discussion on the delineation of target volume for the patient were as follows:respiratory movements should be measured by 4D-CT or simulator;the lung window width/level is 1600/-600 HU and the mediastinal window width/level is 400/20 HU;the primary controversy is whether the involved-field irradiation or elective nodal irradiation should be used for the delineation of CTVnd in the mediastinal lymph node.Conclusions Basic consensus is reached for the delineation of target volume in LANSCLC in these aspects:lung window width/level, respiratory movements and set-up error, primary lesion delineation, the radiation dose in CCRT, and the optimal time for replanning the radiation field.There are controversies on the optimal SUV in the delineation of target volume based on PET-CT simulation, the optimal dose fractionation in SBRT for early-stage NSCLC, and the delineation of CTVnd.

The modulation of ACh on delayed rectifier-like potassium currents (I(K)) was studied in freshly dissociated cerebral cortical neurons using the whole-cell patch-clamp technique. Wistar rats between 10- and 14-day old of both sexes were used. After rats were decapitated, their brains were quickly removed, iced, and then manually cut into 400 mum slices. Slices were then incubated for 0.5 h at 32 degrees C in a buffered artificial cerebrospinal fluid (ACSF) bubbled with 95% O2, 5% CO2. Slices were then removed into buffered ACSF containing protease (0.5 mg/ml) at 32 degrees C. After 30 min of enzyme digestion, tissue was rinsed three times in the buffered saline. Then the enzyme-treated slices were mechanically dissociated with a graded series of fire-polished Pasteur pipettes. The cell suspension was then plated into a 35 mm dish and placed on the stage of a Olympus inverted microscope. For whole-cell recordings of currents, standard voltage-clamp techniques were used. Neurons were held at -80 mV, and the I(K) was evoked by 2 000 ms depolarizing voltage commands to potential between -40 mV and +60 mV in 10 mV steps applied at a frequency of 0.5 Hz. It was found that the inhibitory effect of ACh (0.1, 1, 10, 100 mumol/L) on I(K) was dose-dependent. It was also found that ACh affected the activation process of I(K) significantly, i.e., the activation curve of I(K) was characterized by half-activation potential of (-41.8+/-9.7) mV and a slope factor of (30.7+/-7.2) mV in the cortical neurons and they were changed to (-122.4+/-38.6) mV and (42.4+/-7.0) mV, respectively, after giving ACh (10 mumol/L). Tubocurarine (100 mumol/L) antagonized the inhibitory effect of ACh on I(K), and the drop of currents varied from the control value of (36.5+/-7..8)% to (16.9+/-13.8)% (n=8, P<0.01). 4-DAMP (10 mumol/L) blocked the inhibitory effect of ACh on I(K), and the currents reduced from the control value of (36.5+/-7.8)% to (26.8+/-4.7) % (n=6, P<0.05). Pirenzepin did not antagonize the inhibition of ACh on I(K) (n=7, P>0.05). Chelerythrine (20 mumol/L) blocked the inhibitory effect of ACh on I(K) and the currents reduced from the control value of (36.5+/-7.8)% to (11.7+/-17.3)% (n=6, P<0.05). On the contrary, PDBu (10 mumol/L) strengthened the inhibition of ACh on I(K) and the drop of currents changed from the control value of (36.5+/-7.8)% to (59.2+/-14.0)% (n=5, P<0.05). PDBu abolished the antagonism of chelerythrine on ACh in cortical neurons. It is suggested that the ACh-induced depolarization of neurons in the cortex is attributed to the inhibition of I(K) that is most likely evoked by the activation of nicotinic ACh receptors and muscarinic M3 receptor via protein kinase C (PKC) signal transduction pathway.
Acetylcholine ; physiology ; Animals ; Cell Separation ; Delayed Rectifier Potassium Channels ; antagonists & inhibitors ; Female ; Male ; Neurons ; metabolism ; physiology ; Patch-Clamp Techniques ; Protein Kinase C ; metabolism ; physiology ; Rats ; Rats, Wistar ; Receptor, Muscarinic M3 ; metabolism ; Receptors, Nicotinic ; metabolism ; Signal Transduction ; physiology ; Somatosensory Cortex ; cytology ; physiology

OBJECTIVETo explore the effect of 2-methoxyestradiol (2ME2) and arsenic trioxide (As2O3) on the apoptosis related gene expression in multiple myeloma cell line CZ-1.

METHODSTotal RNA was isolated from CZ-1 cells which had been treated with 2ME2 and As2O3 at an apoptosis-inducing concentration and reverse-transcribed into a cDNA probe labeled with Bio-16-dUTP, and then hybridized it with a microarray containing up to 96 key genes involved in apoptosis. The gene expression profile of the 2ME2 and As2O3 treated CZ-1 cells were analyzed with GEArray Analyzer software. The microarray results were confirmed by RT-PCR.

RESULTSAs2O3 treatment caused the alteration in the expression of 52 genes (54.2% of total genes on microarray). Among them, 42 (80.8%) were upregulated and 10 (19.2%) were downregulated. The upregulated genes were mainly involved in caspases family, P53 and ATM pathway, death effector domain family, TNF receptor family and CIDE family. 2ME2 treatment resulted in the alteration of 42 genes (43.8% of the total genes on microarray). Of them, 32 (76.2%) were downregulated and 10 (23.8%) were upregulated. The downregulated genes mainly belonged to bcl-2 family, inhibitor of apoptosis protein family (IAP), TRAF family, TNF ligand family, and CARD family.

CONCLUSION2ME2 and As2O3 induce the CZ-1 cells apoptosis by different pathways. As2O3 mainly induces upregulation of proapoptotic genes, and 2ME2 downregulation of anti-apoptotic genes expression.

Apoptosis ; drug effects ; genetics ; Arsenicals ; pharmacology ; Cell Line, Tumor ; Estradiol ; analogs & derivatives ; pharmacology ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Multiple Myeloma ; genetics ; pathology ; Oligonucleotide Array Sequence Analysis ; Oxides ; pharmacology ; Reverse Transcriptase Polymerase Chain Reaction ; Tubulin Modulators ; pharmacology

15 scores were randomly divided into therapeutic group (30 cases)and control group(30 cases).The two groups were treated with the same conventional therapy. From the 1st day of admission,Xuebijing injection 80 ml was given by intravenous drip once for every 12 hours for 7 days to the therapeutic group.The level of tumor necrosis factor-?(TNF-?),interleukin-1?(IL-1?),IL-6,IL-10,and APACHEⅡscore were tested on 1,3,5 and 7 days after admission.The case fatality and incidences rates of sepsis and MODS in both groups were recorded.Results Compared with the control group,APACHEⅡscore,TNF-?,IL-1?,IL-6 and IL-10 of the therapeutic group were lower significantly on the 3rd day after admission,especially on the 5th day(all P

AIMTo study the effect of Nociceptin/orphanin FQ (N/OFQ) on transient outward potassium (I(A)) in rat cerebral cortical neurons and its kinetic mechanism.

METHODSThe effects of N/OFQ on I(A) were investigated by using the whole cell patch clamp technique in acutely dissociated rat cerebral cortical neurons.

RESULTS(1) At the voltage of + 60 mV, 0.1 micromol/L N/OFQ made I(A) decreased from (5356.1 +/- 361.6) pA to (4113.3 +/- 312.7) pA (P < 0.01, n = 10) and the percent inhibition was 23.2% +/- 2.2%. (2) (N/OFQ made I-V curve of I(A) decreased significantly (P < 0.01, n = 10).(3) 0.1 micromol/L N/OFQ shifted the activation curve of I(A) to positive potential from (-9.2 +/- 2.5)mV to (30.6 +/- 3.7) mV (P < 0.01, n = 8) and changed the slope factor(kappa) of the activation curve from (20.4 +/- 2.3) mV to (22.6 +/- 2.1) mV (P > 0.05, n = 8). (4) 0.1 micromol/L N/OFQ caused a significant hyperpolarizing shift of the inactivation curve from (-64.1 +/- 3.2) mV to (-55.9 +/- 1.9) mV (P < 0.05, n = 5), without significant effect on kappa of the inactivation curve.

CONCLUSION0.1 micromol/L N/OFQ has a significant inhibition on I(A) and shift the activation and inactivation curve to depolarization in cerebral parietal cortical neurons of rats.

Animals ; Cerebral Cortex ; physiology ; Female ; Male ; Neurons ; physiology ; Opioid Peptides ; physiology ; Parietal Lobe ; physiology ; Potassium Channel Blockers ; Potassium Channels ; physiology ; Rats ; Rats, Wistar

OBJECTIVETo study the genetic etiology of an autosomal dominant dentinogenesis imperfecta in a Chinese family.

METHODSThe molecular change of the disease in the family was analyzed through the clinical examination, linkage analysis, mutational screening of the DSPP gene and restriction fragment length polymorphism analysis.

RESULTSThe disease related gene was completely linked with microsatellite marker D4S1534. We found a novel mutation in the first exon of the DSPP gene (c.49C>T, p.Pro17Ser). All patients in the family had the mutation, while this mutation was not observed in the normal individuals of this family and 100 unrelated controls.

CONCLUSIONThe p.Pro17Ser identified in the family was a new pathogenic mutation. Our finding provided further understanding of the molecular mechanism of dentinogenesis imperfecta.

Amino Acid Sequence ; Asian Continental Ancestry Group ; genetics ; Base Sequence ; Dentinogenesis Imperfecta ; genetics ; Exons ; Extracellular Matrix Proteins ; genetics ; Female ; Humans ; Male ; Microsatellite Repeats ; Molecular Sequence Data ; Mutation ; Pedigree ; Phosphoproteins ; Sialoglycoproteins ; Young Adult