Objective To reduce the feasibility of combining the two fall assessment scales in nursing patients..Methods Two nurses were assigned to conduct the assessments among 60 senile patients using Morse assessment scale and Hendrich Ⅱassessment scale to screen patients with high-risk fall.Result The number of high-risk patients using Morse assessment scale was larger than that using Hendrich II assessment scale(P<0?05) Conclusions The combined use of Morse fall assessment scale and HendrichⅡfall assessment scale may make up the shortcomings of each other,assess the risk factors and predict the high risk factors.

Objective To evaluate the long-term final adult height outcome of combined treatment with gonadotropin-releasing hormone analogue(GnRHa)and recombinant human growth hormone(rhGH)in girls with idiopathic central precocious puberty(ICPP).Methods Out of 49 sirls with ICPP[treated with GnRHa at a dose of 60-80 μg/kg every 4 weeks for at least 6 months,whose height velocity fell below 4 cm/year and showed no improvement of predicted adult height(PAH)in 6 months],26 received(rhGH-combined group),in addition to chronological age,and duration of GnRHa treatment,who showed the same growth pattern but refused rhGH treatment,served to evaluate the efficacy of rhGH in addition.At the conclusion of the smdy,all the girls had been followed up for(3.3±1.9)years,and(3.2±0.9)years in rhGH-combined group and control group,respectively;and had achieved adult heisht.To compare the PAH with the final adult height(FAH)before and after treatment in the two groups.Results During rhGH treatment, height velocity of the rhGH-combined girls increased significantly[(6.7±2.0 vs <4)cm/year baseline],RhGH-combined gids showed an adult height far higher than pretreatment PAH [(157.5±4.5 vs 148.1±4.6)cm,P<0.01],and target height[(154.4±4.6)cm] was,significantly excceded.The control group reached an adult heisht also significandy higher than pretreatment PAH[(154.7±5.5vs 150.3±6.0)cm,P<0.01],while target height[(155.6±4.3)cm]was just reached but not significantlyexcceded.The gain in height obtained,calculated between pretreatment PAH and final heisat,(9.4±4.9)cm in rhGH-combined group was much more than that(4.3±4.2)cm in the control group(P<0.01).Conclusion RhGH may accelerate the linear growth and improve adult height of GnRHa-treated ICPP girls.

Objective To observe the final adult height of 20 boys with idiopathic central precocious puberty (ICPP) treated with slow-releasing gonadotropin-releasing hormone analogue(GnRHa).Methods Twenty boys with ICPP were treated with GnRHa for( 20.0 ± 6.1 ) months.At the beginning of therapy,mean chronological age and bone age was( 11.4 ± 1.0 ) years and ( 13.0 ± 0.4 ) years,respectively,GnRHa was discontinued when the boys reached the chronological age and bone age of( 13.2 ± 1.1 ) years and ( 13.7 ± 0.6 ) years,respectively.After the end of treatment,all the boys had been followed up for( 3.3 ± 1.5 ) years and had achieved adult height.Comparisons were made among their predicted adult height ( PAH ),final adult height ( FAH ),and target height ( THt ).The long-term outcome of final adult height in boys with ICPP was investigated after GnRHa treatment.Results All the boys reached target height range.Final height was similar to the target height [ ( 169.8 ± 5.8 vs 167.8 ± 4.6 ) cm,P＞0.05 ].The height gain,defined as the difference between predicted adult height at the start of treatment using the height SDS for bone age and actual adult height was( 3.62 ± 3.57 ) cm with the residual growth capacity of ( 11.82 ±3.99)cm,PAH significantly improved after GnRHa treatment compared with before treatment [ ( 169.0 ± 5.0 vs166.2 ± 4.2 ) cm,P＜0.01 ].There were no differences among PAH,FAH,and THt.Conclusion GnRHa treatment improves final height within the range of target height in boys with central precocious puberty.

Objective To evaluate the efficiency of second trimester screenings for Down syndrome using alpha-fetoprotein and β-human chorionic gonadotropin duplex.MethodsPregnant women of south Zhejiang were screened for Down syndrome fetuses by maternal alpha-fetoprotein and β-human chorionic gonadotropin duplex during second trimester.The high-risk women underwent prenatal diagnosis by amniocentesis,cell culture and chromosome analysis.The newborns followed up by the maternal and child tertiary health care network and suspected to have Down syndrome were diagnosed by peripheral blood chromosome analysis.Statistical analysis was performed using two-sample t test and x2 test.Risk probability of Down Syndrome was calculated by random screening software. Results From Oct.2007 to May 2009,1130 of 32 188 singleton pregnant women in second trimester received prenatal screening were discovered with high risk(≥1 ∶ 270).Prenatal diagnosis was performed in 90.79％ cases (1026/1130) of high risk women and seven fetuses were diagnosed as Down syndrome by amniotic fluid chromosome analysis,and the pregnancies were terminated.Among the other 104 cases without prenatal diagnosis one Down syndrome baby was delivered.Six of 31 058 pregnancy women with low risk delivered Down syndrome babies with the incidence of Down syndrome of 0.19‰ (6/31 058).Detection rate of second trimester screenings for Down syndrome using alpha-fetoprotein and β-human chorionic gonadotropin duplex was 57.14％(8/14).False positive rate was 3.48％ (1122/32 188).Positive predictive value was 7.08‰(8/1130).During the same period,there were 23 813 pregnant women who didn't receive screening and 15 fetuses with Down syndrome were diagnosed after birth.There was no statistical difference in the prevalence rate of Down syndrome between those pregnant women who received prenatal screening or not [0.43‰ (14/32 188) vs 0.63‰ (15/23 813),x2 =1.004,P＞0.05].The prevalence of Down syndrome was 0.52‰ (29/56 001) in this area. ConclusionsThe prenatal screening and diagnosis could reduce the birth rate of Down syndrome patients.However,detection rate,false positive rate and positive predictive value of which were lower than reports in other studies.It's possible that the reference data might be not suitable for Chinese.

OBJECTIVE: To investigate the feasibility of a drill template for the placement of guided template of middle and upper thoracic percutaneous vertebroplasty in thoracic pedicle approach on digital design and 3D printing technology. METHODS: The preoperative CT images of 20 patients with thoracic fracture were collected retrospectively. With the 3D soft tissue printing technology, the data was reconstructed by 3D imaging reconstruction software to produce 1∶1 three dimensional soft tissue model. The pedicle screw channel and the digital template were designed by the 3-matic module of Mimics15.0 software. After guide template was printed by 3D printer and three dimensional template was fixed on the model, 2.0 mm Kirschner was placed and the accuracy of a drill template was observed by CT scans, bone cement was injected through the puncture tube and verified with images. The time of nail guide design, guide template production and cost were recorded. RESULTS: The effectiveness of three dimensional thoracic model and digital guided template of middle and upper thoracic percutaneous vertebroplasty of thoracic fractures in thoracic pedicle approach was confirmed. Kirschner was placed and the accuracy of screw placement was confirmed with CT scanning. Template and the corresponding anatomical landmark fitted well, bone cement had showed good filling. The average printing time of upper thoracic spine model with soft tissue, the mean time of nail guide design, guide template production and cost were (719.00±3.03) min, (12.30±1.01) min, (55.50±10.30) min and RMB 3 150 yuan on average respectively. CONCLUSION By means of individual design and 3D soft tissue printingtechnology, accurate placement of guided template of middle and upper thoracic percutaneous vertebroplasty could be realized.
Humans ; Pedicle Screws ; Printing, Three-Dimensional ; Retrospective Studies ; Surgery, Computer-Assisted ; Vertebroplasty

This experimental study was aimed to construct the recombinant bisbicistronic eukaryotic expression vector containing endocrine and exocrine protein (EECP) gene associated with breast cancer and enhanced green fluorescent protein (EGFP) gene. And then we transfected it into breast cancer cells MCF-7 to detect the expression of EECP protein and study preliminary biological function of EECP gene. The EECP sequence was cloned to pBluescript II SK (+) plasmid. After restriction endonuclease reaction of pBluescript II SK(+) plasmid, the EECP fragment was cloned to pIRES2-EGFP vector forming a recombinant eukaryotic expression vector named pEECP-IRES2-EGFP. The potential vector was identified by restriction endonuclease digestion and sequencing. Correct plasmid was extracted and transfected into breast cancer cells MCF-7. The expression of EECP protein was detected by western blot analysis. Its biological function was studied by MTT and Flow-cytometry. It turns out that the recombinant eukaryotic expression vector containing EECP gene and EGFP gene was constructed successfully, and it could transfect MCF-7 cells efficiently. It can get higher expression of EECP protein and higher cell proliferation, thus providing an important and convenient tool for studying the function of EECP gene in vitro and in vivo.
Base Sequence ; Breast Neoplasms ; genetics ; pathology ; Female ; Genetic Vectors ; genetics ; Green Fluorescent Proteins ; biosynthesis ; genetics ; Humans ; MCF-7 Cells ; Molecular Sequence Data ; Proteins ; analysis ; genetics ; metabolism ; Recombinant Fusion Proteins ; biosynthesis ; genetics ; Ribosomes ; chemistry ; metabolism

OBJECTIVETo investigate the effect of estrogen on cell proliferation and expression of proteins of C-type natriuretic peptide (CNP), natriuretic peptides B receptor (NPR-B) and natriuretic peptides C receptor (NPR-C) in ATDC5 cells during chondrogenesis.

METHODATDC5 cells were induced for differentiation with insulin 10 µg/ml (day 0), and were started to be investigated on day 6. They were incubated with: (1) Estradiol (E2) at different concentrations (10(-11)-10(-5) mol/L) for 24 hours (for studying cell proliferation), or for 48 hours (for studying CNP, NPR-B and NPR-C protein expression); (2) E2 (10(-8) mol/L) for 24, 48, 72, 96 and 120 h (for studying cell proliferation), or for 24, 48, 72 and 96 hours (for studying CNP, NPR-B and NPR-C protein expression); (3) E2 (10(-8) mol/L) , and/or ICI 182782 (estrogen receptor antagonist ) (10(-7) mol/L) for 24 hours (for studying cell proliferation). ATDC5 cells proliferation were determined by MTT (OD value). Western-blotting was performed to identify the protein levels of CNP, NPR-B and NPR-C.

RESULT(1) After incubation with E2 (10(-11)-10(-5) mol/L) for 24 h, ATD5 cell number increased with the increasing E2 concentration, peak in E2 concentrations of 10(-9) and 10(-8) mol/L (0.56 ± 0.06 and 0.52 ± 0.02, P < 0.05 and <0.01, respectively) , while significantly decreased in E2 (10(-5) mol/L) (0.30 ± 0.02) compared with DMSO-control (0.38 ± 0.02) (P < 0.05). After incubation with E2 (10(-11)-10(-5) mol/L) for 48 h, the protein level of CNP, NPR-B and NPR-C increased significantly, with the greatest effect seen at a concentration of 10(-10) mol/L E2 for CNP and NPR-B, 10(-9) mol/L E2 for NPR-C (P < 0.05). (2) After incubation with E2 (10(-8) mol/L) for 24 to 96 hours: (1) The cell number in each of the four time points was significantly increased compared with DMSO-control, with the greatest effect in 48 h (0.030 ± 0.003) (P < 0.05 or <0.01, respectively). While the cell number at 120 h was similar to that in DMSO-control. (2) The protein level of CNP increased significantly at 24 h (P < 0.05), seemed to be increased at 48 h and 72 h and decreased at 96 h. Both NPR-B and NPR-C level seemed to be increased at 24 h (P = 0.060 and 0.055, respectively) and seemed to decrease at 48 h, with decreasing significantly at both 72 h and 96 h (P < 0.05). (3) After incubation for 24 h, there was significant difference among the cell number of the four groups (P < 0.05). Cell number of group E2 (0.470 ± 0.032) was increased compared with group (E2+ICI) (0.410 ± 0.018), both being increased compared with group DMSO-control (0.370 ± 0.011, P < 0.05, respectively). There was no difference in cell number between group ICI 182782(0.360 ± 0.035) and group DMSO-control.

CONCLUSIONE2 promotes the proliferation of ATDC5 cells i.e. chondrogenesis via estrogen receptor mediated mechanism, in both concentration-dependent and time-dependent manner. E2 (10(-11)-10(-8) mol/L) up-regulates protein expression of CNP, NPR-B and NPR-C of ATDC5 cells during chondrogenesis, and regulate the expression of the three proteins mentioned above positively or negatively at different time point, which implied that estrogen is one of the regulators of CNP signaling pathway.

Animals ; Blotting, Western ; Cell Differentiation ; drug effects ; Cell Line ; Cell Proliferation ; drug effects ; Chondrogenesis ; Dose-Response Relationship, Drug ; Estradiol ; pharmacology ; Gene Expression Regulation ; drug effects ; Mice ; Natriuretic Peptide, C-Type ; metabolism ; Receptors, Atrial Natriuretic Factor ; metabolism ; Signal Transduction ; drug effects ; Time Factors

Objective: To investigate the use of conventional MR imaging to guide treatment in patients with cholecystolithiasis and diffuse inflammatory thickening of gallbladder wall. Methods: The clinical data of patients who were treated in the Ningbo Huamei Hospital, University of the Chinese Academy of Sciences between January 2017 and January 2018 were analyzed. These patients were divided into two groups: patients with acute cholecystitis (n=139) and patients with viral hepatitis combined with cholecystolithiasis (n=67). Differences in the imaging signs in standardized upper abdominal contrast enhanced MRI examinations were retrospectively analyzed. Results: The imaging signs, including stone location, continuity of gallbladder mucosa, exudation in peri-gallbladder space, edema of intrahepatic portal area showed significant differences between the two groups (all P<0.05). On stratification analysis, the type of thickened gallbladder wall, background of liver parenchyma and extent of edema in intrahepatic catchment area also showed significant differences (all P<0.05). The imaging signs, including non-gallbladder neck ductal stones, concentric thickening of gallbladder wall, continuous mucous membrane in gallbladder and no peri-gallbladder space exudation but diffuse edema of intrahepatic catchment area supported the diagnosis of viral hepatitis combined with gallstones. The imaging signs, including discontinuity of gallbladder mucosa, exudation of peri-gallbladder space, diffuse edema of gallbladder wall without a cirrhotic background and edema in intrahepatic portal area supported the diagnosis of acute calculous cholecystitis of gallbladder. Conclusions Routine upper abdominal contrast enhanced MRI plays an important role in demonstrating the underlying cause of gallbladder wall diffuse edema thickening in patients with gallstones. It provides an important reference for the choice of clinical treatment pathway.

Objective To investigate the effect of piR-9994 on the biological behavior of gastric cancer cells and its possible mechanism. Methods The expression of piR-9994 in gastric cancer cell lines (MGC803 and AGS) and normal gastric epithelial cells (GES-1) were detected by qRT-PCR. MGC803 cell line with piR-9994 overexpression and knockdown were constructed. The effects of piR-9994 expression changes on cell proliferation were detected by MTT and clone formation assay. The scratch wound healing assay and Transwell invasion assay were used to detect cell migration and invasion abilities. qRT-PCR and Western blot were used to detect cell proliferation and EMT-related genes expression. Results The expression level of piR-9994 in MGC803 cells was significantly higher than that in normal gastric epithelial cell line GES-1 (P < 0.05). The overexpression of piR-9994 promoted the proliferation, invasion and metastasis of gastric cancer cells, while piR-9994 knockdown had the opposite effect. piR-9994 expression was closely related to cell cycle, especially in S phase. The overexpression of piR-9994 promoted the expression of proliferation-related genes PCNA, CCND1 and Bcl-2, inhibited the expression of apoptosis gene C-PARP, and promoted the expression of EMT-related genes N-cadherin, MMP7, Twist and Vimentin; while piR-9994 knockdown had the opposite effect. Conclusion Abnormal expression of piR-9994 affects the proliferation, invasion, metastasis and EMT process of gastric cancer cells. piR-9994 may be a new biomarker and therapeutic target for gastric cancer.