Tissue engineering provides urologists a new way to fix or reconstruct the impaired organs.Reconstitution of corporal bodies of penis with engineered tissue substitutes has been applied in animal models.In hypospadias reconstruction,the use of engineered tissue substitutes has been applied clinically.The clinical application of bladder tissue substitutes has been ongoing phase II clinical trial.Great progress has been made in renal replacement therapy with clinical application of human progenitor cells in hemofiltration units,and the engineered intracorporeal renal replacement unit will come true by additional studies.The current status of tissue engineering in clinical practice of urology is reviewed in this paper.

Objective: To investigate the association between the polymorphism of HLA-A, HLA-B genes and pre-eclampsia. Methods: HLA-A, HLA-B genotyping was performed by polymerase chain reaction sequence-specific primer (PCR-SSP) in 119 preeclampsia patients, 117 normal pregnant women and their neonates. Results: The study showed that 16 HLA-A and 39 HLA-B alleles were obtained in pre-eclamptic patients and normal pregnant women. 15 HLA-A and 37 HLA-B alleles were obtained in their neonates. No significant difference was found in maternal or neonatal HLA-A, HLA-B alleles be-tween pre-eclampsia group and control group (Pc>0. 05). The frequencies of HLA-A11, HLA-A24,HLA-B13, HLA-B14, HLA-B15, HLA-B52 maternal/fetus genetic assoications were significantly different between pre-eclampsia group and control group (P<0. 05). Conclusion: Some HLA-A, HLA-B maternal/fetus special bindings may be associated with the susceptibility or protective of pre-eclampsia.

Great difficulties and challenges are existed in the training of clinical type postgraduate of neurosurgery because of the acute onset,server illness and difficult diagnosis of neurosurgical diseases.This paper proposed countermeasures of combing theory with clinical practice and strengthening comprehensive ability after analyzing problems of inadequate professional knowledge,lack of doctor-patient communication and insufficient clinical thinking and innovating ability.The aim was to cultivate the overall quality of postgraduates,making them more qualified for the difficult task of being neurosurgery clinicians.

[ABSTRACT]OBJECTIVETo investigate the efficacy and the related complications of combinedpostauricular methylprednisolone injection and systemic therapy for profound idiopathic sudden hearing loss (ISSNHL). METHODSTotal of 60 patients with ISSNHLwho had received therapy from June 2014 to May 2015 in Beijing Anzhen Hospital affiliated to Capital University of Medical Science,were randomly divided into 2 groups,the systemic application group (30 patients): dexamethasone (DEX) was applied intravenously in dose of 10 mg×5 d, and the postauricular injection group (30 patients): methylprednisolone sodium suecinate was injected subperiosteally near the upper one-thirds of postauricular sulcus every day, 40 mg×5 d.All 60 patients received the same medications for 2 weeks to improve the hearing. Hearing and tympanic membrane were monitered before the injections and two weeks after the termination of injections. SPSS 16.0 software was used to analyze the data.RESULTSThe postauricular injection group: 23 of 30 ears had improvement of hearing. No related complications were reported. The systemic application group: 23 of 31 ears had improvement of hearing (P>0.05) No related complications were reported.CONCLUSIONCombined postauricular methylprednisolone injection and systemic medications therapy can be considered as is an effective therapy for profound idiopathic sudden hearing loss. It can avoid the side-effects of high dose systemic corticostemid treatment. For ISSNHL patients, postauricular methylprednisolone injection may be an appropriate treatment.

Objective To investigate the role of M3 receptor in the effect of penehyclidine hydrochloride(PHC) upregulating β-arrestin-1 expression in lipopolysaccharide(LPS)-induced human pulmonary microvascular endothelial cell(HPMVEC) injury.Methods.M3 shRNA transfected HPMVEC and normal HPMVEC cells were randomly divided into LPS group(A),LPS+pHC group(B),LPS+ M3 shRNA transfection group(C) and PHC+ LPS+ M3 shRNA transfection group(D).The cytoskeleton change was observed by laser scanning confocal.The LDH level in cellular supernate was detected.The VCAM 1 protein expression was examined by immunofluorescence chemistry.β-arrestin-1 protein expression was determined by Western blot and β-arrestin-1mRNA expression was measured by real-time PCR.Results Compared with the group A or C,F-actin cytoskeleton arrangement in the group B or D was neat,the LDH level and VCAM-1 protein expression were decreased,and β-arrestin-1 expression was increased;compared with group A or B,F-actin cytoskeleton arrangement in the group C or D was neat,the LDH level and VCAM-1 protein expression were decreased,while the β-arrestin-1 expression had no obvious change.Conclusion Silence M3 receptor is conducive to reduce LPS-induced HPMVEC injury.But the role of PHC up-regulating β-arrestin-1 expression has no necessary connection with M3 receptor.

Objective To evaluate the role of p38MAPK signaling pathway in the up-regulation of heme oxygenase-1 (HO-1) expression during hemorrhagic shock and resuscitation (HSR)-induced acute lung injury (ALI) in mice. Methods Thirty-two C3H/HeN (wild-type) mice, aged 10-12 weeks, weighing 20-25 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S); group HSR; FR167653 (a p38MAPK inhibitor) group (group FR) and FR167653 + HSR group (group FR + HSR). HSR was induced according to the methods described by Ayala et al. MAP was reduced to 35-45 mm Hg and maintained for 60 min.Then the animals were resuscitated with transfusion of the shed blood and lactated Ringer's solution equivalent to the volume of shed blood. FR167653 5 mg/kg was injected intravenosly in group FR. FR167653 5 mg/kg was injected intravenously 30 min before blood-letting in group FR + HSR. The animals were sacrificed by exsanguination at 6 h after resuscitation. The lungs were immediately removed for microscopic examination. The W/D lung weight ratio was calculated and the levels of myeloperoxidase (MPO), IL-10, IL-6 and HO-1 and activated p38MAPK were determined (by ELISA).Results Compared with group S, the pathological score, W/D ratio, the levels of MPO, IL-10, IL-6 and HO-1 and the level of activated p38MAPK were significantly increased in group HSR, the pathological score, W/D ratio and the level of HO-1 were significantly increased in group HSR + FR ( P ＜ 0.01) .Compared with group HSR, the pathological score, W/D ratio, the levels of MPO, IL-10, IL-6 and HO-1 and activated p38MAPK were significantly decreased in group HSR + FR ( P ＜ 0.01 ). Conclusion p38MAPK signaling pathway mediates the up-regulation of HO-1 expression during HSR-induced ALI in mice.

Objective To explore the effects of penehyclidine hydrochloride (PHC) on the withdrawal syndrome and conditioned place preference(CPP) of morphine dependent rats. Methods ( 1 ) Forty-eight male SD rats were randomly assigned to 6 groups with one of 8 rats:morphine dependent group (MOR group) ,naloxone precipitated withdrawal group ( NAL group) ,PHC treatment groups ( PHC1,2,3 ) ,normal saline control group ( NS group). Subcutaneous injection of morphine in gradually increasing doses for 5 days (from 10 to 50 mg/kg ,two times daily) to establish the model of morphine physical dependent rats. The withdrawal syndrome was precipitated by naloxone (5 mg/kg,sc) and treated with PHC in various doses (0.5,1.0,1.5 mg/kg ,ip ) 30 min before haloxone-precipitated withdrawal. The body weight loss and withdrawal syndrome were observed respectively in 20 minutes. (2) 40 male SD rats were randomly assigned to 5 groups with one of 8 rats: morphine dependent group (MOR group) ,PHC treatment groups (PHC1 ,2,3 ) ,normal saline control group (NS group). The morphine conditioned place preference was induced by alternate subcutaneous injection of morphine for 7 days in rats ( 10mg/kg,once daily,8:00 AM) and saline( 16:00 PM). At d8,the rats were received the CPP test. The rats of PHC groups were treated with PHC (0.5,1.0,1.5 mg/kg , ip) prior to the CPP test, whereas the rats were treated with saline in MOR and NS group. Results (1) Theweight loss((8.53 ±l.20)g,(7.36±l.06)g,(5.40±1.79 ) g vs ( 12.63 ± 2.22 ) g, F = 83.16, P ＜ 0.01 ) and score precipitated withdrawal symptoms ( 25.36 ± 3.11,21.38±3.50,17.06±1.78 vs 31.69 ±2.76, F=256.56, P＜0.01)of morphine withdrawal rats was obviously alleviated by ip PHC in dose-related manner before naloxone-precipitated withdrawal. (2) There were significant differences in the times spent in the drug-paired side (gray area) between MOR and PHC groups( (529 ± 83 )s,(460 ± 107 ) s, (418 ± 97 ) s vs ( 643 ± 111 ) s, F = 13.22, P ＜ 0.01 ), and also in dose-related manner. Conclusion PHC could significantly inhibit the withdrawal syndrome and the expression of CPP on morphine dependent rats in a dose-dependent manner.

Objective To investigate the effects of galantamine on the myocardial ischemia-reperfusion (I/R) injury in rats and the possible mechanism.Methods Fifty male SD rats weighing 225-275 g were randomly assigned into 5 groups (n =10 each):sham operation group (group SH); I/R group; galantamine + I/R group (group GAL); M receptor antagonist atropine + galantamine + I/R group (group AT); vagus nerve cut-off + galantamine + I/R group (group VGT).Myocardial I/R was induced by occlusion of left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion.Normal saline 2 ml/kg was slowly injected via the femoral vein at 30 min before ischemia in groups SH and I/R.Galantamine 4 mg/kg was slowly injected via the femoral vein at 30 min before ischemia in group GAL.Atropine 4 mg/kg was slowly injected via the femoral vein at 45 min before ischemia in group AT and the other procedures were the same as those in group GAL.Bilateral cervical vagus nerves were cut off at 45 min before ischemia in group VGT and the other procedures were the same as those in group GAL.At the end of reperfusion,the hearts were removed for determination of myocardial infarct size,MPO and SOD activities,and MDA contents.Results The myocardial infarct size was significantly larger,the MPO activity and MDA content were significantly higher,and the SOD activity was significantly lower in group I/R than in group SH,and in groups AT and VGT than in group GAL (P ＜ 0.05).The myocardial infarct size was significantly smaller,the MDA content and MPO activity were significantly lower,and the SOD activity was significantly higher in group GAL than in group I/R P ＜ 0.05).Conclusion Galantamine has protective effect on myocardium against I/R injury and regulation of peripheral vagus nerve tension may be involved in the mechanism.

Objective To investigate the effects of penehyclidine hydrochloride ( PHC) on lipopolysaccharide (LPS) -induced endothelial cells injury and its mechanism. Methods ECV-304 was cultured in RPMI1640 in a 5% humidified CO2 atmosphere at 37 ℃. Then cultured cells were used to assess the following treatments: control group, LPS group (1 μg/mL) and PHC group(2 μg/mL). At the end of the experiments, supernatant was collected for determination of lactate dehydrogenase ( LDH), and cells were collected for determination of malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) levels. And extracellular regulated kinasel/2( ERKl/2)and JNK MAPK (mitogen-activated protein kinases, MAPK) protein expressions were determined using Western blot technique. Analysis of variance (ANOVA) was used for statistical analysis to compare values among all groups. A significant difference was presumed for a probability value < 0.05. Results Compared with control group, LDH leakage [(1642 ± 367) U/L vs (169±33)U/L], the contents of MDA[(13. 2 ± 1. 2) nmol/L vs (7. 2 ±0. 8)nmol/mL] and NO levels [(143.2 ± 10.3) μmol/L vs(85.5 ±4.1) μmol/L], expressions of ERK1/2 and JNK were remarkably increased and SOD activities[(41.2 ±2.7) U/mL vs (61. 1 ±2.8) U/mL] were obviously decreased in LPS group. PHC markedly decreased LDH leakage [(392 ±90) U/L], MDA contents [(8. 6 ± 1. 3) nmol/ mL] and NO levels [(92.1 ±6.6) μmol/L], ERK1/2 activation and enhanced SOD activities [(58.0± 3.0) U/mL]. Conclusions PHC could protect endothelial cells against LPS-induced cell injury. The effect of PHC is likely mediated through inhibition of ERK1/2 MAPK activation.

Zebrafish was selected as model animal, and glucocorticoid dexamethasone was used as a model compound to establish a rapid and high efficient osteopenia model. Zebrafish larvae at 4 days post fertilization (dpf) were exposed to a serial concentrations of dexamethasone solutions, and 0.5% DMSO was selected as the vehicle control group. All groups were incubated in 24-well plates (28.5 degrees C) until 9 dpf. In addition, effects of 10 micromol x L(-1) dexamethasone on preventing against osteopenia induced by etidronate disodium were also investigated. Zebrafish bones at 9 dpf were stained with alizarin red. Quantitative analysis of the stained area was performed by microscopic inspection and digital imaging methods to reflect the amount of bone mineralization. Results showed that dexamethasone group at 2.5, 10 and 25 micromol x L(-1) can decrease the staining area and the staining optical density values of zebrafish head bones when compared with the vehicle control group (0.5% DMSO), which suggested that dexamethasone can significantly reduce the zebrafish mineralized bone and the bone mineral density. Results also showed that 15 and 30 microg x mL(-1) etidronate disodium can increase the mineralized matrix of zebrafish head bone and prevent against osteopenia induced by dexamethasone. In conclusion, the study indicated that zebrafish can be an idea osteopenia model induced by dexamethasone.