Objective To evaluate the therapeutic effects and experience of the tracheal stent implantation for the management of severe tracheal stenosis.Materials Thirteen patients with severe tracheal stenosis of various causes underwent high kilovoltage radiography and computed tomography for evaluating the site,form and extent of the stenosis including 10 at the trachea,1 at the right main bronchus and 2 at left main bronchus.The C2 catheter assisted with ultra-slipping guide wire was inserted into the trachea under fluoroscopy and then a replaced high shoring guide wire was pushed through the stenotic segment and retained the stent. Results All stents were implanted successfully with successful rate 100% together with dyspneic improvements.The mean survival time was 6.2 months for patients with malignant neoplasm.One patient with benign tracheal stenosis has been followed-up for 5 years without restenosis. Conclusions The tracheal stent implantation is an effective means for severe tracheal stenosis.

Objective To analyze changes in lactic acid level in patients with late-onset intracranial hematoma after craniocerebral injury and investigate their relativity.Methods Forty-eight patients with late-onset intracranial hematoma after craniocerebral injury treated in our hospital between May 2009 and December 2012 were enrolled as observation group.There were 32 males and 16 females.Moreover,50 cases checked up in our hospital during the same period were studied as health population controls,including 35 males and 15 females.Level of lactic acid was measured on admission,at the time of definite diagnosis as well as at days 7 and 14 after treatment and compared between groups.Results Level of lactic acid was (1.77 ±0.21) mmol/L in control group and (1.82 ± 0.25) mmol/L in observation group respectively on admission (t =1.070,P ＞ 0.05) ; Level of lactic acid was (3.32 ± 0.89) mmol/L in observation group at the time of definite diagnosis,which increased to (3.74 ± 1.16) mmol/L at days 7 after treatment and decreased to (1.89 ±0.75) mmol/L at days 14 after treatment.When diagnosed and treated for 7 days,level of lactic acid differed significantly between the two groups (P ＜ 0.05).Level of lactic acid related to craniocerebral injury at each time point,but higher correlation coefficient was observed at the time of definite diagnosis and 7 days after treatment with 0.986 and 0.989 respectively.Conclusion Level of lactic acid relates to late-onset intracranial hematoma after craniocerebral injury,which can be used as reference for progression of the disease.

Objective To examine the expression of tight junction protein claudin-5 in blood-spinal cord barrier (BSCB) after spinal cord injury about rat. Methods One hundred-twenty adult male SD rats were randomly divided into blank group (60) and injured group (60). The animal model of spinal cord injury was established using modified Allen method. The expression of claudin-5 in BSCB was examined at 6 h, 12 h, 1 d, 3 d, 5 d and 7 d (five rats per time point). Western blot and RT_PCR were used to detect protein and mRNA expression levels of claudin-5, respectively. Results The success rate of spinal cord injury molding was 81.7%. In injured group, EB content increased gradually over time, reached the peak at the third day(0.9435 ± 0.0813)μg/g and then reduced gradually (P<0.05), EB content was signifi-cantly higher in injured group than in blank group. Claudin-5 mRNA expression in injured group reduced gradually over time and reached the lowest point at the third day(2.871 ± 0.527)and then increased gradually(P<0.05). Claudin-5 mRNA expression was significantly lower in injured group than in blank group(P<0.05). Claudin-5 protein expression in injured group reduced gradually over time, reached the lowest at the third day(0.072 ±0.008)and then increased gradually (P<0.05). Claudin- 5 protein expression was significantly lower in injured group than in blank group(P<0.05). Con-clusions The alteration of claudin-5 expression after SCI may lead to the permeability of BSCB, which may in turn con-tribute to the secondary spinal cord injury.

Objective To study the radioprotective effects of ultra-small carbon quantum dots (CQDs) in mice in vivo,and to reveal the protective mechanism,as well as to study the body immune response to CQDs and the toxicity in vivo.Methods Mice were injected with different concentrations of CQDs solution.Mice models of systemic radiation injury were constructed by high dose gamma rays radiation.The 30-days survival rate,bone marrow DNA,femoral bone marrow nucleated cells (BMNC),tissue superoxide dismutase (SOD) and malondialdehyde (MDA) were measured to evaluate the radioprotective effects of CQDs,and to investigate the possible protective mechanism.The toxicity of CQDs in vivo was studied by measuring the changes of body weight,liver index and spleen index before and after injections of CQDs in mice.Results CQDs showed obvious radioprotective effects on mice in vivo.Compared with the control group,the 30-days survival rate of irradiated mice treated with CQDs increased from 0％ to 40％.CQDs could effectively reduce the hematopoietic system damages caused by radiation,and increase the level of bone marrow DNA,femur BMNC,liver and lung SOD,as well as reduce the production of MDA in liver and lung.The results of immunological reaction tests showed that CQDs had less toxicity in vivo and did not trigger the body immune response.Conclusions CQDs has tremendous application prospects in the field of radiation protection.This study can provide new ideas for the application of new nano-materials in medical field.

Objective To investigate the application of ultrasonic examination for patients with liver cirrhosis after transjugular intrahepatic portosystemic shunt (TIPS) in the stents in artificial channel (SIAC) and portal vein (PV).Methods The clinical data of 28 patients who were admitted into our hospital from January 2013 to February 2017 and received TIPS were analyzed.Scanned the stents in artificial channel and portal vein and their inner diameter through transabdominal probe,and then measured the blood flow velocity by doppler.ResultsAfter TIPS,the SIAC of cirrhosis patients showed parallel tubular high echo,smooth wall and clear vessel lumen.And the inner diameter of SIAC was (5.93±0.76)mm,the blood flow velocity was (97.14±28.46)cm/s,and the 95% reference value was 4.45 mm~7.41 mm and 41.36~152.92 cm/s respectively.And the inner diameter of PV was (12.40 mm±2.90)mm,the blood flow velocity was (38.33 cm±16.01)cm/s,and the 95% reference value was 6.72~18.08 mm and 22.32~49.34 cm/s respectively.Conclusion Ultrasonography can give objective evaluation of whether SIAC and PV is unobstructed after TIPS,and it can get their parameters of inner diameter and velocity.As a result, ultrasonography can be regard as a perfect means for follow-up checkup.

Objective To study the effects of methylprednisolone on the permeability of blood-spinal cord barrier (BSCB) and claudin-5 expression after spinal cord injury in rats. Methods The rat model of spinal cord injury was estab?lished using modified Allen method. SD rats were randomly divided into sham-operated group, spinal cord injury group and methylprednisolone pretreatment group. The permeability of BSCB and expression of claudin–5 were assessed at 12 h, 1, 3, 5, and 7 d after the onset of spinal cord injury (five animals per each time point). RT-PCR and Western blot were used to detect the expression of claudin-5. Results The success rate of the model was 84.0%. EB content was sig?nificantly higher in spinal cord injury group than in sham-operated group at each time point (F value 27.732,P<0.05). EB content was lower in methylprednisolone pretreatment group than in spinal cord injury group (F value 48.149,P<0.05). The mRNA expression of claudin-5 was lower in spinal cord injury group than sham-operated group at each time point (F value 12.248,P<0.05). The mRNA expression of claudin–5 was higher in methylprednisolone pretreatment group than in spinal cord injury group at each time point (Fvalue 15.316,P<0.05). The protein expression of claudin-5 was lower in spinal cord injury group than in sham operated group at each time point (Fvalue 18.108,P<0.05). The pro?tein expression of Claudin-5 was higher in methylprednisolone pretreatment group than spinal cord injury group at each time point (F value 20.247,P<0.05). Conclusions Methylprednisolone improves permeability of BSCB after spinal cord injury probably through enhancing claudin-5 expression in rats.
was lower in spinal cord injury group than in sham operated group at each time point (Fvalue 18.108,P<0.05). The pro?tein expression of Claudin-5 was higher in methylprednisolone pretreatment group than spinal cord injury group at each time point (F value 20.247,P<0.05). Conclusions Methylprednisolone improves permeability of BSCB after spinal cord injury probably through enhancing claudin-5 expression in rats.

Objective To investigate the correlation of angiotensin Ⅱ type 1 receptor (AT1R) gene polymorphism with AT1R expression levels and brain edema after hypertensive intracerebral hemorrhage .Methods 45 operative patients with hypertensive intracerebral hemorrhage in the Affiliated Yongchuan Hospital of Chongqing Medical Univercity from December 2011 to August 2012 were collected as the experimental group and 45 operative patients with refractory epilepsy weres selected as the control group .The venous blood in the two groups were collected for detecting the AT 1R gene polymorphism ;The brain tissue was taken from lesions in operation ,then AT1R mRNA concentration was determined by RT-PCR and the AT1R protein level was determined by Western blot ;Head CT was performed on postoperative 1 ,3 ,5 d;the degree of cerebral edema was reflected by CT value . Results The levels of two kinds of genotype AT1R mRNA in the experimental group had no statistically significant difference(P>0 .05);the operative area CT value of AC genotype was significantly lower than that of AA genotype with statistical difference (P<0 .05);the ATIRmRNA of various genotypes ,protein level and cerebral edema in the control group had no statistical differences . Conclusion The AT 1R gene polymorphism has no obvious correlation with the concentration expression of AT 1R mRNA in the brain tis-sue;there is correlation between AT 1R protein level and AT 1R protein level and the cerebral edema degree in the brain tissue .

AIM: To observe the effects of cimetidine(Cim) on platelet function and thrombosis. METHODS: After incubated with Cim in vitro , rat platelets were activated with ADP or thrombin. The platelet aggregation, platelet malondialdehyde(MDA) formation, platelet intracellular free calcium([Ca 2+ ] i), and thromboxane B 2 (TXB 2) were measured. The effects of Cim on electric-induced thrombosis in rat carotid artery were examined. RESULTS: Cim potentiated ADP induced platelet aggregation , increased the thrombin induced [Ca 2+ ] i and MDA formation, decreased TXB 2. Also, Cim shortened the duration of electric-stimulated occlution time in rat carotid artery. CONCLUSION: Cim increased platelet function and accelerated thrombosis.

Aim To investigate effects of chlorzoxazone on survival and apoptosis of HepG2 cells.Methods The necrosis of HepG2 cells was evaluated by measurement of LDH release.The effects of chlorzoxazone on survival of HepG2 cells were assayed by MTT dyereduction.The effects of chlorzoxazone on cell apoptosis was analyzed by TUNEL method.The ultrastructure of HepG2 cells was observed by transmission electron microscope.Results Chlorzoxazone at concentrations of 100～500 ?mol?L-1 inhibited survival ratios of HepG2 cells in a dose-dependent manner significantly.Typical apoptotic changes were observed in HepG2 cells under the fluorescence microscope and transmission electron microscope.Apoptosis of HepG2 cells was induced after treatment of chlorzoxazone at concentrations from 100 ?mol?L-1 to 500 ?mol?L-1 for 48h,which showed obvious concentration-effect relationship.The apoptotic ratios of HepG2 cells were also increased when chlorzoxazone(100,200,300 and 500 ?mol?L-1) was treated for 24,48 and 72 h,which showed obvious time-effect relationship.Conclusion Chlorzoxazone inhibited HepG2 cells survival and induced cell apoptosis.

ObjectiveTo evaluate the technical feasibility of animal model of avascular necrosis of femoral head (ANFH)with transcatheter arterial embolization (TAE).MethodsTwenty experimental pigs were randomly divided into experimental group and control group (each n= 10).Experimental group:A 5F Cobra catheter was inserted into left femoral artery,and the feeding arteries of femoral head were superselectively inserted.The feeding arteries were embolismed through transcatheter arterial injecting the segments of silk measuring about 500μm.Control group:The arterial embolization was not performed,and the other treatment was identical to experimental group.The articulation of hip in all pigs underwent plain X-ray examination,CT and MR scanning 2 weeks and 4 weeks after treatment,respectively.Histological examination was made in 4 weeks to evaluate volume of bone trabecula (TBV) and percentage of bone lacuna (PBL) at unit area under microscope.The data were compared between the two groups.Results In experimental group,CT and MRI showed swolling in hip soft tissue and high T1 in hip joint cavity,while no obvious abnormalities were found in plain X-ray film 2 weeks after feeding arteries were embolized.Four weeks after feeding arteries embolization,plain X-ray film,CT and MR showed typical necrosis of femoral head in the experimental group,while no obvious abnormalities were found in control group.The histology examination revealed there were obvious karyopyknosis and anachromasis in the bone cells.The quantity of bone cells decreased obviously or disappeared.PBL increased and TBV decreased significantly compared with those of control group (P＜0.05).ConclusionThe animal model of ANFH in pigs can be induced by TAE.It can preferably mimic the pathological situation of ANFH.