Purpose: Hungry bone syndrome after parathyroidectomy is an important clinical problem in patients on maintenance hemodialysis. We examined the effect of an enhanced recovery after surgery (ERAS) program on the incidence of hungry bone syndrome after parathyroidectomy in this population. Methods: This single-institution, retrospective study analyzed 108 patients on hemodialysis who underwent parathyroidectomy for secondary hyperparathyroidism. Patients were classified into the pre-ERAS (n = 52) and post-ERAS (n = 56) groups. The ERAS program identified high-risk patients and enforced aggressive measures to normalize calcium levels following parathyroidectomy. Results: There was no significant difference in age, sex, body weight, presenting symptoms, preoperative calcium and alkaline phosphatase levels, postoperative intact parathyroid levels, postoperative calcium levels at 1 and 24 hours after parathyroidectomy, and 30-day readmission rates between the groups. The post-ERAS group had significantly higher levels of postoperative calcium at 48 and 72 hours after parathyroidectomy, but a lower incidence of hungry bone syndrome and shorter postoperative length of stay. Patients with hungry bone syndrome had higher preoperative levels of alkaline phosphatase and intact parathyroid, longer postoperative length of stay, and were less likely to have been part of the ERAS program. High preoperative alkaline phosphatase levels and absence of the ERAS program were independent risk factors for hungry bone syndrome after parathyroidectomy. Conclusion The ERAS program reduced the incidence of hungry bone syndrome and shortened the postoperative length of stay in patients on maintenance hemodialysis who underwent parathyroidectomy for secondary hyperparathyroidism.

【Objective】 To observe the effects of hsa-miR-124-3p.1 in inhibiting epithelial-mesenchymal transition （EMT）， migration and invasion of human gastric cancer cells induced by transforming growth factor β1 （TGF-β1） by targeting tumor necrosis factor receptor-associated factor 6 （TRAF6）. 【Methods】 A total of 43 gastric cancer tissues and 43 normal para-carcinoma tissues were collected. The human gastric mucosal epithelial cells GES-1 and gastric cancer cells （NCI-N87， MGC-803， BGC-823， SGC-7901， and MKN-45） were cultured. The expressions of miR-124-3p.1 and TRAF6 in tissues and cells were detected by fluorescent quantitative PCR and Western blotting. The targeted relationship between miR-124-3p.1 and TRAF6 was verified by dual-luciferase reporter gene system assay. SGC-7901 cell lines with miR-124-3p.1 and TRAF6 overexpression were constructed. The cells were induced by TGF-β1. The invasion and migration abilities of the cells were evaluated by Transwell chamber assay and scratch test. 【Results】 Compared with normal para-carcinoma tissues and normal gastric mucosal cells， the expression of miR-124-3p.1 was downregulated， while the expressions of TRAF6 mRNA and protein were upregulated in gastric cancer tissues and cells （P<0.05）. Compared with control group， expression of E-cadherin in cells was downregulated， expressions of N-cadherin and Vimentin were upregulated， invasion and migration rates of cells were increased in TGF-β1 group （P<0.05）. Compared with TGF-β1 group， after cells were transfected with miR-124-3p.1 mimic， the expression of E-cadherin was upregulated， the expressions of N-cadherin and Vimentin were down-regulated， and invasion and migration rates of cells were decreased （P<0.05）. Compared with miR-124-3p.1 mimic group， invasion and migration rates of cells were increased in TGF-β1+mimic+TRAF6 group， expressions of TRAF6， N-cadherin and Vimentin were up-regulated， and the expression of E-cadherin was down-regulated （P<0.05）. 【Conclusion】 hsa-miR-124-3p.1 is lowly expressed in gastric cancer. Overexpression of miR-124-33p.1 can inhibit EMT， cell invasion and migration induced by TGF-β1. And the action mechanism may be related to the downregulated expression of TRAF6.

Objective To investigate the application of MSCT three-dimensional digital navigated biopsy in subcarinal lesions.Methods 82 patients were enrolled.Study subjects were randomly divided into control group and research group.Three-dimensional positioning and three-dimensional navigation needle biopsy were used in research groups, while CT cross-sectional image positioning with conventional puncture needle was used in control group.Puncture accuracy, one-time success rate of puncture, complications, diagnosis accuracy and operation time were compared between the two groups.Results Puncture success rate, definite diagnosis rate were 87.80%(36/41) and 97.56%(40/41) for the research group,and 60.97%(24/41) and 80.49% (33/41) for the control group, respectively,which on the research group were higher than that on the control group(χ2=8.945, 6.116;P<0.05).Complication rate and operating time were 14.63% (6/41) and (11.64±2.76) min for the research group, and 41.45% (17/41) and (22.22±6.31) min for the control group, respectively, which were lower on the research group than that on the control group (χ2=7.31,t=-11.70,P<0.05).Conclusion MSCT three-dimensional digital navigated biopsy technique could promote the efficiency of subcarinal space puncture biopsy significantly,which is a novel, convenient, precise and safe method.

OBJECTIVE:To provide reference for rational drug use in the clinic. METHODS:Irrational medication orders eval-uated by the Affiliated Cancer Hospital of Zhengzhou University during Oct. 2014 to Sep. 2015 were arrangemented,summarized and analyzed. RESULTS:A total of 515 inpatient medical records were reviewed and analyzed,among which there were 165 unrea-sonable medical records and 185 irrational medication orders. Irrational medical records of general surgery department were the most(38 items,accounting for 23.03%). Irrational drug use mainly included irrational usage and dosage(80.00%),drug use with-out indications or not suit indications (7.57%),inappropriate solvent selection (4.86%). Including 66.22% of single overdose, 18.92% of longer medication duration. CONCLUSIONS:There are many irrational medical orders which should be standardized in our hospital,especially overdose and longer medication duration,which increase financial burden of patient. Pharmacists should strengthen communication with clinicians,and hold rational drug use trainings regularly base on the types of the irrationality. These can help to improve rational drug use and guarantee the safety of drug use.

Objective To study the effect of clinical pharmacist interventions on the rational use of antibiot-ics.Methods 1 000 hospitalized patients before the implementation of intervention in April 2012 to April 2013 (control group)and the other 1 000 cases of hospitalized patients in May 2013 to May 2014 after the implementation of the intervention (study group)were selected,the antibiotics use rate,hospitalization time and cost,cost of using antibacterial drugs were compared between the two groups.Results The antibiotics use rate of the study group was 56.0%(560/1 000),significantly lower than 78%(780/1 000)of the control group,with significant differences between the two groups(χ2 =11.089,P=0.032),the hospitalization time,cost of using antibacterial drugs of the study group were (12.6 ±0.8)days,(912.2 ±13.2)yuan,significantly better than (16.9 ±0.7)days,(1 528.1 ± 32.5)yuan of the control group,with significant differences between the two groups (t=9.892,10.142,P=0.028, 0.014);The two groups of hospitalization expenses showed no statistical significance (t =4.984,P =0.072 ). Conclusion Clinical pharmacist intervention has a positive effect on the application of antibacterial drugs,which can significantly reduce the use of antimicrobial drugs and reduce the hospitalization days.

Objective To investigate the correlation between asymmetric dimethylarginine (AD-MA) and endothelial dysfunction in patients with uremia.Methods Uremic patients who did not receive hemodialysis were defined as A group (n =40) ; uremic patients who had received hemodialysis were divided into B group (n =45) ;healthy people were defined as C group (n =20) ;and chronic kidney disease (stage 2 ～ 4) patients were defined as D group (n =20).The diameter of intima-media thickness,and endothelium-dependent or independent dilation (EDD or EID) of radial artery in right forearm were detected with diasonography.The levels of ADMA were determined by high-performance liquid chromatography.Results Compared to C group,the levels of ADMA in A,B and D groups were significantly increased [C:(0.78 ±0.19) μmol/L,A:(1.51 ±0.16) μ mol/L,B:(1.13 ±0.14) μmol/L,D:(0.92 ±0.11) μmol/L; P ＜0.05].Compared to A group,the levels of ADMA were significantly decreased in B group (P ＜0.05).EDD and EID were decreased significantly in A,B and D groups compared to C group [EDD:C:(13.52±1.73)％ vs A:(7.32 ±0.54)％,B:(9.02 ±0.86)％,D:(10.13 ±1.25)％,P ＜0.05;EID:C:(14.45±1.85)％ vsA:(10.37 ±1.51)％,B:(9.54±1.39)％,D:(11.17±1.56)％,P ＜0.05].EDD in B group was significantly lower than A group (P ＜0.05).In group A,a negative correlation was found between EDD and the level of ADMA (r =-0.81,P =0.020).Conclusions ADMA level was significantly increased in uremic patients.A close correlation existed between ADMA and endothelial dysfunction of radial artery.

Objective To investigate the role of surfactant protein (SP)-A and SP-D in urinary tract infection mouse model,and evaluate the effects of SP-A and SP-D absence on urinary tract infection.Methods SP-A and SP-D double knockout (SP-A/D KO) mice were made.SP-A/D KO and wild-type (WT) C57BL/6 female mice were used for this study.The expression of SP-A and SP-D in kidney was detected by immunohistochemistry (IHC).The levels of p-p38 and p38 protein in kidneys were measured by Western blotting.Uropathogenic Escherichia coli or buffer was delivered into the bladder of female mice.At 24 and 48 h after inoculation,CFU of Escherichia coli in the kidney and urine of the treated and control mice were measured.Histological,cellular and molecular analysis were performed by several methods of H/E staining,IHC and Western blotting.The effects of SP-A and SP-D on bacterial growth were studied in vitro.Results SP-A and SP-D in kidney were located in the proximal tubules and collecting tubules.Compared with WT mice,infected SP-A/D KO mice with UPEC had higher CFU in kidneys and urine at 24 h and 48 h,increased inflammatory cells infiltration in kidneys (P＜0.05).Compared with WT mice,SP-A/D KO mice had higher p38 MAPK phosphorylation levels in kidneys (P ＜ 0.05).Growth of Escherichia coli was greatly inhibited by both SP-A and SP-D (P＜0.05).Conclusions Both SP-A and SP-D are expressed in kidney.SP-A and SP-D can attenuate UTI induced by UPEC which may be through inhibiting bacterial growth and modulating renal inflammation.

ObjectiveTo evaluate the effects of Ang Ⅱ on apoptosis of podocytes and explore the signaling pathwayof nephrin in preventingAng Ⅱ-inducedpodocyte apoptosis.MethodsDifferentiated mouse podocytes were exposed to Ang Ⅱ at different concentrations for 18 h or at 10-8 mol/L for variable incubation times.Undifferentiated mouse pedocytes were transfected using lipofectamine 2000 with the pcDNA3.1-mNPHS1 plasmid and stably transfected cell lines were generated with G418 selection.In separated experiments,untransfected mouse podocytes (MPC) and stably transfected podocytes with pcDNA3.1-neo and PcDNA3.1-mNPHS1 were exposed toAng Ⅱ(10-8 mol/L) or LY294002(a selective Akt inhibitor,50 μmol/L) for indicated times.Apoptosis was evaluated by flow cytometry.The expression of nephrin was assessed by quantitative real-time PCR,immunofluorescence and Western blotting.The phosphorylation level of Akt was determined by Westem blotting.Results(1) AngⅡ promoted podocyte apoptosis in a dose-and time-dependentmanner. PretreatmentwithlosartansignificantlypreventedAngⅡ -induced apoptosis. (2) Nephfin mRNA and protein were obviously decreased in podocytes exposed to 10-8 mol/L Ang Ⅱ for at least 12 h than those in vehicle-treated cells (P＜0.05).(3) Ang Ⅱ exposure for more than 15 min inhibited the phosphorylation of AKT in MPC,which was dramatically reversed by pcDNA3.1-mNPHS1 transfection,but not by pcDNA3.1-neo transfection. (4) Podocyte apoptosis was promoted byLY294002. Conversely,Ang Ⅱ-induced podocyteapoptosis was significantly alleviated by pcDNA3.1-mNPHS1 transfection.ConclusionAng Ⅱinduces mouse podocyte apoptosis which is suppressed by overexpression of nephrin through PI3K-Akt signaling pathway.

Objective To evaluate the effect of aldosterone (Ald) on glomerular mesangial cells apoptosis and to explore the possible mechanisms.Methods Twenty-four Sprngue-Dawley rats were subcutaneously embedded with osmotic mini-pumps and randomly divided into 3 groups.Aldosterone (1.5 μg/h) was administrated subcutaneouly by osmotic mini-pumps in Ald group,eplerenone (Epl,100 mg·kg-1·d-1) and Ald (1.5 μg/h) was given to Epl group.And normal saline was used in control group (Con group).Systolic blood pressure and urinary albumin excretion rate (UAER) were detected on day 0,7,14,21,28.Blood and kidney samples were harvested on day 28.Plasma creatinine,potassium and aldosterone were measured.Renal paraffin sections were stained by PAS and the morphological changes were evaluated by light microscopy.Apoptosis index of mesangial cells were detected by TUNEL assay.The glomerular mesangial cells (MCs) were cultured in a DMEM-F12 media.MCs apoptosis was evaluated by staining cells with Annexin V and propidium iodide (PI) using flow cytometer.Expression of Bcl-2 and Bax mRNA was examined by RT-PCR.The protein level of Bad or phospho-Bad was measured by Western blotting.Results Ald-infused rats developed hyperaldosteronemia and hypokalemia.Rats in Ald group exhibited significant hypertension and marked albuminuria.Ald group rats showed increased number of TUNEL-positive mesangial cells when compared with control rats (P＜0.05).Aldosterone induced mesangial cells apoptosis in a time-dependent manner.Expression of Bcl-2 mRNA was decreased but Bax mRNA was increased in aldosterone treated MCs compared to that in Con group (P＜0.05).Aldosterone promoted dephosphorylation of cytosolic phospho-Bad compared with vehicle treated cells (P＜ 0.05).However,eplerenone attenuated these effects of aldosterone.Conclusion Aldosterone directly promotes mesangial cells apoptosis,and eplerenone can attenuate this effect of aldosterone.Dephosphorylation of cytosolic phospho-Bad may be the key role in the progression of mesangial cells apoptosis induced by aldosterone.

Objective To investigate the effect of angiotensin 1-7(Ang 1-7) on renal proximal tubular epithelial cell(HK-2) transdifferentiation induced by high glucose.Methods All the raised HK-2 cells were divided into 5 groups: normal control group,high glucose group,high glucose with Ang1-7 group,high glucose with Ang1-7 and A779 group,high glucose with pioglitazone group.Expression of peroxisome proliferator activated receptor-γ(PPAR-γ) and α-smooth muscle actin(α-SMA) was detected by Western blotting,real-time PCR and immunofluorescence.Results The levels of PPAR-γ protein and mRNA in HK-2 cells were significantly increased after treatment with high glucose and Ang 1-7.Expression of α-SMA protein and mRNA was inhibited remarkably after treatment with high glucose and Ang 1-7.These effects of Ang 1-7 on HK-2 cells could be reversed by Mas receptor antagonist A779.Conclusion Ang 1-7 inhibits high glucose-induced expression of o-SMA in HK-2 cells,which is in part through the Mas.