Objective To explore the transport properties of the radionuclide strontium 90Sr in the soil-plant system,and discuss the accumulation characteristics of strontiumes in different vegetable tissues.Methods Three kinds of vegetables,including Chinese cabbage,radish and celery,were planted in this experiments using stable nuclide 88Sr instead of 90Sr.Strontium concentrations in these kinds of plant and soil were measured with inductively coupled plasma atomic emission spectrometry (ICP-AES),and the transportation factor (TF) of strontium and the concentration ratio (CR) of these plants were calculated.Results The contents of strontium in different tissues of the vegetables increased significantly in response to the strontium concentrations in soil (F =3.75-139.39,P ＜ 0.05).The contents of strontium at 398.33,477.99 and 557.57 mg/kg in different tissues of these vegetables were significantly higher than that in control group (t =-10.49-7.41,P ＜0.05).Except celery stems,there was a positive correlation about contents of the strontium between other tissues of these vegetables and their experimental soils (r =0.88-0.99,t =7.41-15.96,P ＜0.05).Based on dry weight of examples,the TF in each tissue sample of cabbage and radish was higher than 1,and the concentration ratio,for cabbage and radish,was higher in stems than in roots (F =8.22,91.49,P ＜ 0.05).Conclusions Three kinds of vegetables have been shown to have strontium accumulation ability in soil environment.

Objective To discuss the therapeutic strategy and the clinical efficacy of percutaneous cholecystostomy in treating high-risk patients with acute cholecystitis. Methods During the period of Jan. 2006-June 2008,percutaneous cholecystostomy was performed in 27 high-risk patients with acute cholecystitis,consisting of lithic cholecystitis (n = 21) and non-lithic cholecystitis (n = 6). Of 27 patients,percutaneous cholecystostomy via transhepatic approach was performed in 22 and via transperitoneal approach in 5. The 7 F drainage catheter was used. Cholecystography was conducted before the drainage catheter was extracted. Results Percutaneous cholecystostomy was successfully accomplished in all 27 cases,with a technical success rate of 100%. Postoperative patency of gallbladder drainage was obtained in 25 patients,with the relieving or subsiding of abdominal pain and the restoring of temperature and leukocyte account to normal range within 72 hours. In one patient,as the abdominal pain relief was not obvious 72 hours after the procedure,cholecystography was employed and it revealed the obstruction of the drainage catheter. After reopening of the drainage catheter,the abdominal pain was relieved. In another case,cholecystography was carried out because the abdominal pain became worse after the procedure,and minor bile leak was demonstrated. After powerful anti-infective and symptomatic medication,the abdominal pain was alleviated. The drainage catheter was extracted in 25 patients 6-7 weeks after the treatment. Of these 25 patients,12 accepted selective cholecystectomy,7 received percutaneous cholecystolithotomy and 6 with non-lithic cholecystitis did not get any additional surgery. The remaining two patients were living with long-term retention of the indwelling drainage-catheter. Conclusion Percutaneous cholecystostomy is a simple,safe and effective treatment for acute cholecystitis in high-risk patients. This technique is of great value in clinical practice.

Objective To evaluate the role of autophagy in hydrogen-induced reduction of lung injury in septic mice.Methods Sixty pathogen-free healthy male ICR mice,aged 6 weeks,weighing 20-25 g,were divided into 5 groups (n =12 each) using a random number table:sham operation group (group Sh),sepsis group (group Sep),sepsis plus hydrogen group (group Sep+H2),sepsis plus autophagy inhibitor 3-methyladenine (3-MA) group (group Sep+3-MA) and sepsis plus 3-MA plus hydrogen group (group Sep+3-MA+H2).Sepsis was produced by cecal ligation and puncture.At 1 h before operation,3-MA 10 mg/kg was intraperitoneally injected.The mice inhaled 2％ H2 for 1 h starting from 1 and 6 h after operation.Blood samples were collected from the common carotid artery at 24 h after operation for measurement of arterial oxygen partial pressure,and the oxygenation index (OI) was calculated.Pulmonary specimens were obtained for examination of the pathological changes which were scored.Pulnonary mitochondria were isolated for determination of mitochondrial membrane potential (MMP) and ATP content using fluorescence spectrophotometry and a bioluminescence assay,respectively,and the respiratory control rate (RCR) was calculated.The expression of autophagy-related protein microtubule-associated protein 1 light chain 3 (LC3) was determined by Western blot,and the ratio of LC3-Ⅱ to LC3-Ⅰ expression (LC3-Ⅱ/LC3-Ⅰ ratio) was calculated.Results Compared with group Sh,the pathological scores were significantly increased,the OI and contents of mitochondrial RCR,MMP and ATP were decreased,and the LC3-Ⅱ/LC3-Ⅰ ratio was increased in Sep and Sep+H2 groups (P＜0.05).Compared with group Sep,the pathological scores were significantly decreased,the OI and contents of mitochondrial RCR,MMP and ATP were increased,and the LC3-Ⅱ/LC3-Ⅰ ratio was increased in group Sep+H2,and the pathological scores were significantly increased,the OI and contents of mitochondrial RCR,MMP and ATP were decreased,and the LC3-Ⅱ/LC3-Ⅰ ratio was decreased in group Sep+3-MA (P＜0.05),and no significant change was found in each parameter mentioned above in group Sep+3-MA+H2 (P＞0.05).Compared with group Sep+H2,the pathological scores were significantly increased,the OI and contents of mitochondrial RCR,MMP and ATP were decreased,and the LC3-Ⅱ/LC3-Ⅰ ratio was decreased in group Sep+3-MA+H2 (P＜0.05).Conclusion The mechanism by which hydrogen ameliorates lung injury is related to enhanced level of autophagy in septic mice.

Objective To evaluate the relationship between the endogenous protection induced by autophagy against acute lung injury and inflammatory responses in the septic mice.Methods A total of 130 pathogen-free male C57BL/6 mice,aged 6 weeks,weighing 20-25 g,were randomly divided into 5 groups (n =26 each) using a random number table:sham operation group (group S),sepsis group (group Sep),autophagy inducer rapamycin group (group Rap),autophagy inhibitor 3-methyladenine (3-MA) group (group 3-MA),and lysosome inhibitor bafilomycin group (group Baf).Sepsis was produced by cecal ligation and puncture in chloral hydrate-anesthetized mice.Rapamycin 10 mg/kg,3-MA 15 mg/kg,and bafilomycin 1 mg/kg were injected intraperitoneally at 1 h after operation in Rap,3-MA and Baf groups,respectively.Twenty mice in each group were selected and observed for the survival at 7 days after operation,and the 7-day survival rate was calculated.Six mice in each group were selected,and arterial blood samples were obtained at 24 h after operation,the mice were then sacrificed,and lung tissues were obtained for determination of the levels of tumor necrosis factor-alpha (TNF-α),high-mobility group box 1 (HMGB1),interleukin-6 (IL-6),IL-10 and monocyte chemotactic protein-1 (MCP-1) in serum and lung tissues by enzyme-linked immunosorbent assay.The expression of autophagy-related proteins microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ),Beclin-1 and lysosomal-associated membrane protein 2 (LAMP2),and Ras-related protein 7 (Rab7) in lung tissues was detected by Western blot.Results Compared with group S,the 7-day survival rate was significantly decreased,and the levels of TNF-α,HMGB1,IL-6,IL-10 and MCP-1 in serum and lung tissues and LC3 Ⅱ,Beclin-1,LAMP2 and Rab7 in lung tissues were significantly increased in group Sep (P＜0.05).Compared with group Sep,the 7-day survival rate and levels of IL-10,LAMP2 and Rab7 in serum and lung tissues were significantly increased in group Rap and decreased in 3-MA and Baf groups,and the levels of TNF-α,HMGB1,IL-6 and MCP1 in serum and lung tissues were significantly decreased in group Rap and increased in 3-MA and Baf groups,and the levels of LC3 Ⅱ and Beclin-1 in lung tissues were significantly increased in Rap and Baf groups and decreased in group 3-MA (P＜0.05).Conclusion Autophagy-induced endogenous protection against acute lung injury is related to inhibition of inflammatory responses in the septic mice.

Objective Mechanisms of pulmonary vein isolation (PVI) for atrial fibrillation remain controversy.This study aimed to investigate the impact of PVI on vagal modulation to atria.Methods Eighteen adult mongrel dogs under general anesthesia were randomly divided into two groups.Bilateral cervical sympathovagal trunks were decentralized and sympathetic effects was blocked by metoprolol administration.Atrial electrical remodeling (AER) was established by rapid right atrial pacing at the rate of 600 bpm for 30 minutes.PVI was performed in group A.Atrial effective refractory period (ERP),vulnerability window (VW) of atrial fibrillation,and sinus rhythm cycle length (SCL) were measured at baseline and during vagal stimulation before and after atrial rapid pacing with and without PVI at fight atrial appendage (RAA),left atrial appendage (LAA),distal coronary sinus (CSd) and proximal coronary sinus (CSp).Results (1) Effects of PVI on vagal modulation:Shortening of SCL during vagal stimulation decreased significantly after PVI compared with that before PVI in group A (P＜0.001).Shortening of ERP during vagal stimulation decreaseed significantly after PVI compared with that before PVI (P＜0.05).VW of atrial fibrillation during vagal stimulation decreased significantly after PVI compared with that before PVI (P＜0.05).(2) Effects of PVI on AER:shortening of ERP before and after atrial rapid pacing increased significantly at baseline and vagal stimulation in group B compared with that in group A (P＜0.05).VW during vagal stimulation increased significantly after atrial rapid pacing in group B (P＜0.05).Conclusion PVI attenuates the vagal modulation to the atria,thereby decreases the susceptibility to atrial fibrillation mediated by vagal activity.PVI releases AER,which maybe contributes to the vagal denervation.Our study indicates that PVI not only can eradicate triggered foci but also modify substrates for AF.(J Geriatr Cardiol 2008;5:28-32)

The Long-term Thromboembolic Event Analysis in Atrial Fibrillation Patients With Radiofrequency Catheter Ablation
Objective: To observe the thromboembolic event in atrial fibrillation (AF) patients with long-term successful radiofrequency catheter ablation (RFCA), and to study the relationship between thromboembolic event and CHA2DS2-VASC score in order to guide the anticoagulation strategy for AF patients.
Methods: A total of 321 AF patients who received RFCA in our hospital from 2000-01 to 2009-05 were studied. There were 261 patients with paroxysmal AF and 60 with persistent AF, they were followed-up for (66.7±26.9) months. The patients were divided into 2 groups according to AF recurrence condition as Non-recurrence group, n=204 and Recurrence group, n=117. The relationship between thromboembolic event and CHA2DS2-VASC score was studied.
Results: The Non-recurrence group had significantly lower rate of thromboembolism than that in Recurrence group (1.96% vs 7.69%), P=0.017. In both groups, the patients with CHA2DS2-VASC score < 2 had much lower rate of thromboembolism than those with CHA2DS2-VASC score ≥ 2, (0% vs 5%), P=0.023 and (4.45% vs 17.24%), P=0.041. The patients with CHA2DS2-VASC score<2 in Non-recurrence group had lower rate of thromboembolism than those in Recurrence group (0%vs 4.45%), P=0.029. The rate of thromboembolism had no statistic meaning between 2 groups in patients with CHA2DS2-VASC score≥2 (5%vs 17.24%), P=0.054.
Conclusion: The AF patients who received RFCA without AF recurrence in long-term follow-up had the lower rate of thromboembolic event, CHA2DS2-VASC score was important for evaluating such event. The patients with CHA2DS2-VASC score < 2 could consider stopping warfarin anticoagulation, while the patients with CHA2DS2-VASC score ≥ 2 might be beneifted for warfarin anticoagulation.

Objective To evaluate the effect of inhaling hydrogen (H2) on proteomics during acute lung injury in septic mice.Methods Sixty male ICR mice,aged 6 weeks,weighing 20-25 g,were divided into 4 groups (n=15 each) using a random number table:sham operation group (Sh group),sham operation plus H2 group (Sh+H2 group),sepsis group (S group) and sepsis plus H2 group (S+H2 group).Sepsis was produced by cecal ligation and puncture.The mice in Sh+H2 and S+H2 groups inhaled 2％ H2 for 1 h starting from 1 and 6 h after operation.At 24 h after operation,lungs were removed for identification of proteins by isobaric tags for relative and absolute quantification and liquid chromatography-tandem mass spectrometry analysis,and the differentially expressed proteins were screened.The differentially expressed proteins were used for KEGG pathway enrichment analysis and STRING protein-protein interaction networks analysis.Western blot was used to confirm the 4 differentially expressed proteins semaphorin 7A,transferrin,OTULIN and mitogen-activated protein kinase kinase kinase 1.Results A total of 4 472 quantifiable proteins were identified.A total of 192 proteins which were related to acute lung injury during H2 inhalationinduced reduction of sepsis were identified.The 192 proteins involved phosphatidylinositol 3-kinase/serine0threonine kinase signaling pathway,chemokine signaling pathway,hypoxia-inducible factor 1 signaling pathway,complement and coagulation cascades,peroxisome proliferator-activated receptor signaling pathway and proteins including ribosome proteins,myosin and troponin,collagen and adhesion-related proteins,coagulation-related proteins found in STRING protein-protein interaction networks.Conclusion Inhaling H2 can induce changes in the expression of 192 proteins,which may be the mechanism of lung protection in septic mice.

Objective To evaluate the effect of hydrogen on mitochondrial dynamics during endotoxin-induced damage to human umbilical vein endothelial cells (HUVECs).Methods HUVECs cultured in vitro were seeded in the culture plate and divided into 4 groups using a random number table:control group (group C),hydrogen-saturated culture medium group (H group),endotoxin group (group E) and endotoxin + hydrogen-saturated culture medium group (group E+H).The cells were cultured in the plain culture medium in C and E groups.The cells were cultured in the hydrogen-saturated culture medium containing lipopolysaccharide (LPS) with the final concentration of 10 μg/ml in H and E+H groups.At 2,8 and 24 h of culture or incubation with LPS,the cell viability was detected by methyl thiazolyl tetrazolium assay,the intracellular ATP content was measured using the phosphomolybdic acid colorimetric method,and the expression of dynamin-related protein 1 (DRP1) was detected by using Western blot.The expression of DRP1 was detected by immunofluorescence at 8 h of incubation with LPS.Results Compared with group C,the cell viability and ATP content were significantly decreased,and the expression of DRP1 was up-regulated at each incubation time point in E and E +H groups (P＜0.05),and no significant change was found in the parameters mentioned above in group H (P＞0.05).Compared with group E,the cell viability and ATP content were significantly increased,and the expression of DRP1 was down-regulated at each incubation time point in group E+H (P＜0.05).Conclusion The mechanism by which hydrogen reduces endotoxin-induced damage to HUVECs is related to down-regulation of DRP1 expression and inhibition of excessive mitochondrial fission.

Background Atrial electrical remodeling(AER)plays an important role in the pathogenesis and maintenance of atrialfibrillation.However,little is known about modulation of vagal activilty to AER.This study aimed to investigate the relationshipbetween vagal moduation and AER. Methods Twenty four adult mongrel dogs under general anesthesia were randomized into 3groups.Sympathetic activity was blocked by administration of metoprolol in 3 groups.The changes in vagal modulation to atria afterAER were observed in 10 dogs without vagal interruption in group A.The effects of vagal intervention on AER were investigated in 8dogs with administration of atropine in group B.The impact of aggressively vagal activity on AER was studied in 6 dogs with bilateralcervical vag sympathetic trunLks stimulation during AER in group C.Bilateral cervicall vagosympathetic trunks were decentralized.Multipolar catheters wereplaced into high right atria(RA),coronary sinus(CS)and rightventricle(RV).AER was induced by 600 bpmpacing through RA catheter for 30 minutes.Attial effective refractory period(ERP)and vulnerability window (VW)of atrial fibrillationwere measured with and without vagal stimulation before and after AER.Results In group A,ERP decreased significantly at baselineand during vagal stimulation after AER compared with that beforeAER(all P＜0.05).In group B,ERP remaind unchanged at baselineand vagal stimulation after AER compared with tbat before AER (all P＞0.05).In group C,ERP shortened significantly at baseline andvagal stimulation after AER compared with that before AER(all P＜0.05).ERP shortening after AER in Groups A and C increasedsignificantly than that in group B (all P＜0.05).Atrial fibrillation could not be induced at baseline(VW close to 0) before and after AERin three groups.VW became widen significantly during vagal stimulation after AER compared with that before AER in Groups A and C(all P＜0.05),while VW remained unchanged in group B (VW close to 0).Conclusions Short-term AER results in the decrease inERP.AER is accompanied by the increases in atrial vagal modulation.The increased vagal activity and vagal stimulation promote AER,thereby increase the susceptibility to atrial fibrillation.The interrupted vagal activity attenuates AER.thereby suppresses the atriaIfibrillation mediated by vagal stimutlation.

The school-age boy was admitted to Tianjin Children's Hospital for "fever and cough for 6 days".After detail examinations,the diagnosis of severe Mycoplasma pneumoniae pneumonia was proved.Treatments:anti-infection with Azithromycin and Meropenem;the obstruction of air way was relieved;assisted with symptomatic and supportive treatment.During the treatment,disorder of consciousness and hemiplegia of right limbs occurred,cerebral infarction was proved later by magnetic resonance angiography(MRA).Severe Mycoplasma pneumoniae pneumonia complicated with cerebral infarction is clinically rare with a high morbidity and mortality.Attention should be paid to body examination and Laboratory test.Multi-disciplinary cooperation is helpful.