Objective To investigate the treatment of perinail refracture after surgery of proximal femoral fracture.Methods From January 2010 to January 2015,we treated perinail fractures in 31 patients who had undergone surgery for proximal femoral fracture.They were 11 men and 20 women,with an average age of 75.6 years (range,from 24 to 87 years).On average,their refracture occurred 9.4 months after primary fixation (range,from 3 to 60 months).With reference to the Vancouver classification of peri-prosthestic refractures in the proximal femur and the position and bone quality of perinail refractures,we tried to classify the perinail fractures and chose different treatment protocols accordingly.In our cohort,6 were type A,5 type B,15 type C,and 5 type D.Type A cases were treated conservatively,and types B and C cases with locking compression plate or less invasive stabilization system.In one case of type D,dynamic hip screws were implanted to fixate the femoral neck fracture after removal of the original intramedullary nail,and hip replacement was conducted in the other 4 after removal of the original intramedullary nail.Results The operation time averaged 2.1 hours (range,from 1.6 to 3.0 hours) and intraoperative bleeding 600 mL (range,from 150 to 800 mL) in this cohort.Of them,27 were followed up for an average of 15 months (range,from 12 to 24 months),giving a follow-up rate of 87.1％ (27/31).Six type A fractures obtained bone union after protected weight-bearing walking for 12 weeks.All the 16 fractures of types B and C healed after an average period of 4.2 months (range,from 3 to 6 months).Of the 5 type D fractures,one obtained bone union 12 weeks after change into dynamic hip screwing and 4 had fine functional recovery after hip replacement.No infection,nonunion,or implants failure occurred.Conclusions We have set an exploratory classification system for the perinail refractures at the proximal femur with reference to the Vancouver classification of peri-prosthestic refractures.Our classification can provide effective guidance for the treatment of perinail refracture after surgery of proximal femoral fracture.

ObjectiveThe possibility of the hyperplasi a of prostatic outer gland was studied with transrectal ultrasound (TRUS) guided biopsies. MethodsTwenty-seven prostatic outer glands in patients suspicious for prostatic cancer (PCA) were biopsied by TRUS guided, the total sites were 47. The same site was biopsied in sagittal and longitudinal section respectively. The hypoechoic lesion was biopsied 2 times if it was discovered in the outer gland. The histological results were diagnosed in double blind. Results Twenty prostatic inner glands looked symmetrical hyperplasia; 9 outer glands became thin because of the compression, there was no compressive sign in 18 patients; there was a hypoechoic lesion in outer gland of 3 patients. Benign prostatic hyperplasia was diagnosed in the specimens of 47 sites. ConclusionsThe hyperplasia of prostatic outer gland can occur like inner gland because it is glandular tissue.

Objective To evaluate the clinical value of repeat transrectal ultrasound (TRUS) guided biopsy in prostatic cancer (PCA). Methods Repeat TRUS guided biopsy was conducted on 54 patients of the previous benign TRUS guided biopsy at high risk of PCA. Postatic specific antigen ranged in 0.5- 90.0 ?g/L(mean 16.3 ?g/L). Twenty-nine patients were abnormal in digital rectal examination, 21 patients were abnormal in TRUS. Results Forty-seven patients had 2 consecutive times of the biopsy, 6 patients had 3 consecutive times, 1 patient had 4 consecutive times in 54 patients of repeat TRUS guided biopsy. The pathological finding was confirmed in 14 PCA ( 25.9%), and 31 benign prostatic hyperplasia, 5 prostatic intra-epithelial neoplasmia, 4 chronic prostatitis. Conclusions The detection of PCA will be increased by repeat TRUS guided biopsy at high risk of PCA after the previous benign TRUS guided biopsy.

BackgroundBoth accommodative abnormality and higher order wavefront aberrations associated with near work are interrelated with blurry retinal image.It is very important to investigate the higher order wavefront aberrations in stable and progressive myopic eyes before and after near work. ObjectiveThe present study wasto observe the high order aberration change of myopic eyes before and after computer work upon near work stimulation as well as the relationship of high order aberration changes to types of myopia. MethodsThe case-controlled design was used in this clinical study.Sixty right eyes of 60 subjects were enrolled,including 30 progressive myopias and 30 stable myopias with matched age and gender.Refractive errors of the subjects were completely corrected by the wearing of spectacles.The subjects remained the work for 1 hour in front of a computer monitor with 40 cm distance under the dark environment and nature pupil size,and the height of the eye and monitor center kept the same level.The changes of wavefront aberration in test eyes were measured with Complete Ophthalmic Analysis System before and after 1 hour of continuous computer work.The influences of computer-work and myopia types on wavefront aberration were analyzed in 3,4,5 mm pupil size.Root-mean-square (RMS) of aberrations was calculated as the index of higher order wavefront aberrations.ResultsThere were no significant differences in the higher order wavefront aberrations before and after computer work for the two types of myopic eyes under the 3,4,5 mm pupil.The RMS of higher order wavefront aberrations were similar between progressive myopia and stable myopia under the 3 mm pupil condition.Total higher order RMS,6th-order,5th-order and 3rd-order RMS were significantly higher in progressive myopic group compared with stable myopic group under the 4 mm pupil size ( RMS3:F =5.985,P =0.016 ; RMS5:F =3.975,p=0.049;RMS6:F=8.130,P=0.005:RMST:F=6.493,P=0.012) and 5mm pupil size(RMS3:F=13.132,P=0.000;RMS5:F =4.032,P=0.047 ; RMS6:F =4.393,P=0.038:RMST:F=10.508,P=0.002 ).The spherical aberrations were higher in progressive myopic group under the 3,4,5 mm pupil conditions in comparison with stable myopic group,but these alterations were insignificant between two types of myopias ( P＞0.05 ).Conclusions Higher order wavefront aberrations of progressive myopic eyes is comparable higher than the stable myopic eyes.Computer reading task dose not significantly impact the higher order wavefront aberrations on myopic eyes.

Background Aberrant proliferation of residual lens epithelial cells (LECs) is one of main causes of posterior capsular opacification (PCO).Researches indicated that Wnt3a signaling pathway promote proliferation of epithelial cells,but its effect on LECs is still unclear. Objective The present study was to investigate the effects of Wnt3a on proliferation of human LECs and its mechanism and to provide a new gene target in the prevention and treatment of PCO. Methods Human LECs line (SRA01/04 cells ) was cultured and then incubated to 6-well plate at the density of 4×105/well.A human Wnt3a cDNA expressing vector targeted human LECs was constructed to increase the Wnt3a expression in SRA01/04 cells,and pcDNA3-HA expression vector was used as the control group.The expression of Wnt3a was identified by Western blot assay after transfected.The growth and proliferation of SRA01/04 cells were detected by MTT and flow cytometry (FCM).The expressions of β-catenin,cyclin D1 and c-myc in the cells were detected by Western blot assay.β-Catenin expression was localized using immunofluorescence assay,and the expression and localization of proliferating cell nuclear antigen ( PCNA ) were analyzed by immunocytochemistry for the exploration of the active mechanism of Wnt3a to proliferation of LECs.Results Human Wnt3a cDNA expression vector was designed successfully and transiently transfected to SRA01/04 cells,and Wnt3a/SRA01/04 cells and pcDNA3-HA/SRA01/04 cells were obtained.The expression of Wnt3a was verified in the Wnt3a transfected group compared with the control group.MTT indicated that the cell proliferating rate was significantly different between the Wnt3a transfected group and the control group ( Fgroup =15.235,P =0.005 ;Ftime =369.677,P =0.000),and that in various time points after transfected was significantly different (t =20.843,P=0.001 ;t =26.214,P＜0.001 ;t=25.177,P=0.001 ;t =35.516,P＜0.001 ;t =615.056,P＜0.001 ).The proportion of SRA01/04 cells in G1 phase was 51.74％ in the Wnt3a cDNA transfected group,with a significantly decrease in comparison with 79.44％ of the control group.However,the proportion of SRA01/04 cells in S phase in the Wnt3a cDNA transfected group was higher than that of the control group (36.23％ versus 12.34％ ).The positive expression rate of PCNA protein in SRA01/04 was (47.00％ ±7.58％ ) in the Wnt3a cDNA transfected group and ( 16.00％ ±3.61％ ) in the control group with a significant difference between them (t =8.256,P＜0.01 ).After 48 hours of transfection of the Wnt3a cDNA,the expression amount of β-catenin proteins was higher and the immunofluorescence was stronger in cell nucleus,and the expressions of cyclin D1 and c-myc proteins were elevated in Wnt3a/SRA01/04 cells. Conclusions The overexpression of Wnt3a activates the Wnt/β-catenin signaling pathway and downregulates the expression of a subset of target genes,including cyclin D1 and c-myc,which plays an important role in promoting the proliferation of human LECs.

Objective To study the characteristic of the hyperplasia hypoechoic nodules in outer gland of prostate with transrectal ultrasound (TRUS) guided biopsies. Methods 42 patients were suspected of prostatic cancer (PCa) for the existence of hypoechoic nodules in their outer glands of prostate. Each nodule was TRUS guided biopsied in sagittal and longitudinal section, respectively. The histological examinations were performed in double blind. Results Among the 42 patients, there were 22 cases of benign prostate hyperplasia (52.4%) and 20 cases of prostate cancer (47.6%). Conclusions The sonographic findings of the hypoechoic nodules in outer glands included not only PCa, but also benign hyperplasia nodules. Therefore, the definitive diagnosis must dependent on pathologic examinations.

BACKGROUND:Gelatin-chitosan-hydroxyapatite-minocycline biomimetic nanocomposite materials were developed in our previous studies. OBJECTIVE:To observe the capability of gelatin-chitosan-hydroxyapatite-minocycline biomimetic nanocomposite materials in the repair of rabbit radius defects. METHODS: Thirty healthy adult New Zealand rabbits were selected to make critical-size lacunar bone defects of the upper radius (15 mm×6 mm). Then, the rabbit models were randomized into experimental group (n=15), autogenous bone graft group (n=10) and blank group (n=5). Gelatin-chitosan-hydroxyapatite-minocycline biomimetic nanocomposite materials were implanted into radial bone defects in the experimental group. Bone defect in blank group was implanted without any materials; in the autogenous bone graft group, the contralateral radius with same length was taken and implanted into the defect. General observation, histological observation and X-ray observation were performed respectively at 2, 4, 8, 12 weeks postoperatively. RESULTS AND CONCLUSION:At 12 weeks after operation, the experimental group showed obvious new blood vessels at the defect region, complete bony union and disappearance of the composite implant, but lamelar bone structure appeared, smal blood vessels were visible, the edge of new bone was connected to the original bone edge, exhibiting a continuity of bone, the bone density was slightly lowered, and the defect region became unobvious. In the autogenous bone graft group, bony union and trabecular bone reconstruction were distinct, the lamelar bone became mature, the medulary cavity was recanalized, the fracture line disappeared completely, and the bone density was completely consistent with that of the original bone. In the blank group, there was no obvious bone formation, which led to bone nonunion, and there were a great amount of fiber tissues and inflammatory cel infiltrated. To sum up, the gelatin-chitosan-hydroxyapatite-minocycline biomimetic nanocomposite material can obviously promote the repair of critical-size bone defects, and the repairing effect is basicaly the same with that of autologous bone grafting.

Objective To identity the risk factors for supine hypotension syndrome (SHS) after spinal anesthesia in parturients.Methods A total of 204 parturients,scheduled for elective cesarean section,were divided into either control group or SHS group depending on whether or not SHS (systolic blood pressure [SBP] in the upper extremity decreased by ＞ 30 mmHg or decreased to ＜ 80 mmHg) developed after spinal anesthesia.The baseline patient characteristics such as age,body height and weight,gestational weeks and biparietal diameter were recorded.Supine stress test (SST) was performed.Heart rate,blood pressure in upper and lower extremities,perfusion index,pleth variability index and intravesical pressure were recorded when patients were in supine position and in left lateral position before spinal anesthesia.The risk factors of which P values were less than 0.05 would enter the multi-factor logistic regression analysis to stratify the risk factors for SHS.Results Among the 204 patients,99 cases developed SHS after spinal anesthesia,and the incidence was 48.5％.Logistic regression analysis showed that maternal body weight,biparietal diameter,the difference in SBP between upper and lower extremities in supine position,the difference in SBP in upper extremities caused by changing position and positive SST were risk factors for SHS after spinal anesthesia (P＜0.05 or 0.01).Conclusion Maternal body weight,biparietal diameter,the difference in SBP between the upper and lower extremities in supine position,the difference in SBP in upper extremities caused by changing position and positive SST are risk factors for SHS after spinal anesthesia in parturients.

Objective To explore the effects of Pannexin1 (Px1) channel protein on osteogenic differentiation of mesen?chymal stem cells (MSCs) under mechanical stress stimulation. Methods Bone marrow was extracted from Sprague Dawley (SD) rats (3 weeks, weighing 100-120 g) and cultured following 1st generation cellular technology. The safe dose of CBX (an inhibitor of Px1 channel protein) on MSCs was determined by CCK8 method and 100 μmol/L was used. The MSCs were cultured by the whole marrow culture method. When the cell was passaged to 3-4 generation, high purity of the MSCs were harvested. MSCs were divided into three groups:control group, stress?stimuli group (4 000μstrain) and stress stimuli+CBX group. The duration of stress was 15 min and CBX pre?treatment time point was 3 h, 6 h, 12 h, and 24 h, respectively. The alkaline phosphatase (ALP) activity, type I collagen expression, intracellular calcium ion (Ca2+) concentration, and Px1 channel protein, p?p38MAPK and p?ERK ex?pression were determined. Results ALP activities were highest in the stress group, and it was reduced by pretreatment of CBX. Similarly, stress increased the expression of type I collagen, concentration of Ca2+, and expressions of Px1 channel protein and p?p38MAPK was reduced by CBX. p?ERK was down?regulated by stress but not affected by CBX treatment. Conclusion Mechani?cal stress could promote osteogenic differentiation of MSCs and this promotion was inhibited by pretreatment of CBX, which might result in regulation of p?p38MAPK.

Objective:To investigate how urothelial carcinoma-associated 1 (UCA1) and miR-18a modulates acquired tamoxifen resistance and the relevant mechanisms in estrogen receptor (ER) positive cancer cells.Methods: qRT-PCR was performed to detect UCA1 and miR-18a expression in breast cancer cells.Dual luciferase assay was performed to detect the binding between miR-18a and UCA1 3′UTR.Tamoxifen sensitive MCF-7 cells were transfected with UCA1 expression vector or miR-18a inhi-bitors.Tamoxifen resistant LCC9 and BT474 cells were transfected with UCA1 siRNA or miR-18a mi-mics.CCK-8 assay was performed to detect cell viability.Soft agar assay was performed to assess cell colony formation.Flow cytometric analysis was performed to check cell cycle distribution.Results: UCA1 was significantly upregulated in tamoxifen resistant LCC2,LCC9,and BT474 cells than in tamoxifen sensitive MCF-7 cells.UCA1 expression was significantly upregulated in MCF-7 cells after treatment with 0.1 μmol/L tamoxifen.UCA1 overexpression enhanced cell viability of MCF-7 cells after tamoxifen treatment,while UCA1 siRNA significantly suppressed viability of LCC9 and BT474 cells after tamoxifen treatment.In MCF-7 cells,compared with vector control+tamoxifen group,the average cell colony number and colony size of the UCA1+tamoxifen group was 19.0％ more and 29.0％ larger respectively,while the proportions of the cells in G1 phase and in S phase were 7.3％ lower and 6.7％ higher respectively.In BT474 cells,compared with siRNA control+tamoxifen group,the average cell colony number and colony size of the si-UCA1+tamoxifen group were 54.0％ less and 42.0％ smaller respectively,while the proportions of the cells in G1 phase and in S phase were 9.0％ higher and 6.2％ lower respectively.UCA1 directly interacted with miR-18a and reduced its expression in ER positive breast cancer cells.Knockdown of miR-18a increased viability of MCF-7 cells after tamoxifen treatment,while miR-18a overexpression significantly reduced viability of BT474 cells after tamoxifen treatment.In MCF-7 cells,compared with miRNA inhibitor control+tamoxifen group,the average cell colony number and colony size of the miR-18a inhibitor+tamoxifen group were 15.0％ more and 33.0％ larger respectively,while the proportions of the cells in G1 phase and in S phase were 8.8％ lower and 5.3％ higher respectively.In BT474 cells,compared with miRNA control+tamoxifen group,the average cell colony number and colony size of the miR-18a mimics+tamoxifen group were 47.0％ less and 25.0％ smaller respectively,while the proportions of the cells in G1 phase and in S phase were 13.3％ higher and 7.9％ lower respectively.Conclusion: UCA1 can increase tamoxifen resistance of ER positive breast cancer cells via competitively inhibiting of miR-18a.