[Objective] To study the bacteriological feature of the wound infection of open fracture and supply the reasonable advise to the use of antibacterials. [Methods]One hundred and thirty-six samples were collected from the wound patients with open fracture between January in 2004 and December in 2008. The identification of bacteria and drug sensitive test were carded out by ATP-expression.[Results]One hundred and fifty one isolates were collected from 136 samples. The prevalence of staphylococcus aureus, pseudomonas aeruginosa, staphylococcus haemolyticus,staphylococcus epidermidis, eolon bacillus were most ,accounting for 17.22%, 13.24%, 11.92%, 9.93%and 9.27% respectively. The prevalence of MRSA was higher than 57.7%.Gram positive coccus , gram negative bacilli and candida accounted for 48.34%, 43.05% and 8.61% respectively. The prevalence of ESBLs was 28.6%. None of gram negative bacilli was found resistant to sulbactam and cefopcrazone. The resistance rate of gram negative bacilli to ampicillin , ampicillin -sulbactam and cephazolme were 71.4%. The rate of resistance of staphylococcus to methicillin was higher than 57.7%.Except vancomycin was not drug-fast, some sensitive antibacterials include cotrimoxazole, nitrofurantion, rifampicm tetracycline.[Conclusion]Endogenic normal flora and conditioned pathogen from the surroundings have become the main pathogens of the wound infection of open fracture. So the early debride and reasonable use of antibacterials would play a positive role in preventing postoperative fracture infection.

BACKGROUND:MicroRNAs (miRNAs) play an important role in many diseases. To analyze the miRNA expression profile in degenerative scoliosis patients is helpful for classifying its pathogenesis. OBJECTIVE: To compare miRNAs expression profile in the intervertebral disc tissue between degenerative scoliosis patients and healthy controls, and to investigate its role in the pathogenesis of degenerative scoliosis. METHODS:Degenerative nucleus pulposus tissues from 48 patients with degenerative scoliosis (male 36, female 12; 58-69 years old) and normal nucleus pulposus tissues from 36 patients with lumbar fractures were harvested to isolate, culture and identify nucleus pulposus cels folowed by total RNA extract. Differentialy expressed miRNAs were screened by microRNA microarray analysis and validated by real-Time qPCR. Target genes of highly expressed microRNAs were predicted by analyzing information from MicroCosm v5, TargetScan 5.1 and microRNA.org databases. Biological signal pathways associated with the target genes were analyzed, and qPCR was used to validate the screening results. RESULTS AND CONCLUSION:Nineteen differentialy expressed miRNAs were identified. The miR-98 was highly expressed in degenerative nucleus pulposus tissue, and the fold change was 6.368. Predicted miR-98 target gene was interleukin-10, which was involved in JAK-STAT signaling pathway and located in upstream of this pathway. In degenerative nucleus pulposus cels of degenerative scoliosis patients, miR-98 was highly expressed, and the corresponding target gene was interleukin-10. These results indicate that JAK-STAT signaling pathway may play an important role in the pathogenesis of degenerative scoliosis.

BACKGROUND:Thoracolumbar degenerative kyphosis could experience severe lumbar back pain due to sagittal plane imbalance, thereby affecting quality of life. Thus, it is very important to reconstruct spino-pelvic profile in these patients. OBJECTIVE:To explore the relationships between life quality and spino-pelvic parameters fol owing pedicle subtraction osteotomy for thoracolumbar degenerative kyphosis and the clinical significance. METHODS:Between May 2010 and October 2014, 59 patients with thoracolumbar degenerative kyphosis undergoing L2 pedicle subtraction osteotomy in Cangzhou Hospital of Integrated Traditional and Western Medicine were retrospectively reviewed. Anteroposterior and lateral X-ray films of al patients during standing were photographed before and after surgery. The pre-and post-operative thoracic kyphosis, lumbar lordosis, sagittal imbalance, T1 pelvic angle, pelvic incidence, sacral slope and pelvic tilt were measured in al patients. The patients’ quality of life was evaluated using SF-36 preoperatively and postoperatively. RESULTS AND CONCLUSION:(1) Significant differences were observed in the improvement of thoracic kyphosis, lumbar lordosis, pelvic tilt, sacral slope and sagittal imbalance (P<0.01). With respect to SF-36, postoperative SF-36 score was higher than preoperative postoperative SF-36 score (P<0.01). (2) The alteration of lumbar lordosis showed significant correlation with the change of pelvic tilt, sacral slope and sagittal imbalance. The change of pelvic tilt exhibited cardinal correlation with the change of sacral slope, body pain and general health. The improvement of sagittal imbalance significantly correlated with the improvement of lumbar lordosis, body pain and general health. The improvement of T1 pelvic angle significantly correlated with the improvement of lumbar lordosis, sagittal imbalance, body pain and general health. (3) Pedicle subtraction osteotomy can effectively restore spino-pelvic sagittal profile, improve the life quality and relieve pain for the patients with thoracolumbar degenerative kyphosis.

Objective Even after successful surgical repair,patients with coarctation of the aorta (CoA) are at high risk of long-term morbidity and mortality due to cardiovascular events,which is probably related to persistent arterial disfunction during long-terr follow-up after operation,The aim of the study was to explore the alterations of vascular structure and function in children with successfully repaired CoA in the short-and mid-term follow-up.Methods A cohort of 20 children who underwent CoA repair between January 2010 and October 2010 in Guangzhou women and children's Medical Center was studied.There were 14 males and 6 females in CoA group,which comprised 6 patients with isolated CoA,14 patients with CoA associated with intracardia anomalies,whose median age of operation was 4 months (rang from lmonth to 10.0 years).And 20 patients with isolated ventricular septal defect (VSD) were included as VSD group during the same time,with 12 males and 8 females,whose median age of operation was 5 months (rang from 1 month to 12.0 years).Resting blood pressure,flow-mediated dilation (FMD) of the brachial artery,carotid intima-media thickness (IMT) were compared in CoA group and VSD group,including preoperative media data and follow-up of 1 month,6 months and 1 year.In addition,as comparison to the operation group,20 health children with normal echocardiographic findings,whose median age was 5 months (rang from 3 month to 10.0 years),were selected as health group for the 1-year following up.None of them had obesity,hyperlipidemia,diabetes mellitus,metabolic diseases or systemic inflammatory disease.Results As a result of the datas before operation and those I month,6 months and 1 year after operation,all children were normotensive at rest.In the same period,Carotid IMT in CoA group[(0.47 ± 0.10)mm,(0.49 ±0.10) mm,(0.57 ±0.07)mm,(0.61 ± 0.07) mm]was significantly thicker than that in VSD group[(0.41 ±0.11) mm,(0.43 ±0.11)mm,(0.51 ±0.08) mm,(0.55 ±0.08) mm](P＜0.05) and health group[(0.40 ±0.09) mm,(0.42 ±0.11)mm,(0.50 ±0.08) mm,(0.57 ±0.08) mm](P ＜0.05),Brachial artery FMI in children with CoA[(5.4,6 ±1.51)％,(5.71 ±1.88)％,(5.42±1.69)％,(5.27±1.02)％]was significantly lower than that in the VSD control group[(6.69±1.45) ％,(6.66±1.21)％,(6.81 ±1.03)％,(6.43±1.34)％](P＜0.05) and health group[(6.59 ±1.84)％,(6.84±1.41)％,(6.91 ±1.31)％,(6.56±1.62)％](P＜0.05).Significant difference could not be found in neither the IMT nor the FMI between the VSI control group and health group in 4 period respectively,P ＞ 0.05.Conclusion Children after successful coarctation repair have abnomal structural and functional properties of the aorta above the place of coarctation even their blood pressure at rest is normal.These results confirm that the alterations in mechanical properties of carotid arteries as well as the generalized endothelial dysfunction in children with coarctation of the aorta are persistent,which can not be prevented or reversed by surgical repair,and which may partly explain the high incidence of cardiovascular disease observed in their adulthood and reduced life expectancy,furtherly supporting the claim that coartation of the aorta is a systemic vascular disorder which needs long-term follow-up of vascular function.

Mitochondria are the main site of energy metabolism within cells,generating a substantial amount of ATP to supply energy to the human body.Research has shown that alterations in mitochondrial structure and function exist in individuals with schizophrenia,suggesting their potential impact on the onset of psychiatric disorders and clinical treatment efficacy.Therefore,understanding the research progress on the genetic mechanisms,pathological processes,image manifestations of schizophrenia and mitochondrial quality control,and summarizing the relevant evidence of mitochondrial-related targets as potential therapeutic targets for schizophrenia,can provide references for further research.

Objective:To study the effects of Zuogui Pills on the expressions of miR-133b-3p and RhoA in osteoclasts of postmenopausal osteoporosis rats; To discuss its potential mechanism.Methods:SD female rats were randomly divided into normal group, model group, sham-operation group, and Zuogui Pills group using a random number table method, with 6 rats in each group. The model group and Zuogui Pills group were treated with oophorectomy to construct a rat model of osteoporosis. Zuogui Pills group was orally administered with Zuogui Pills decoction at a concentration of 10 g/kg for 12 consecutive weeks. Colorimetric method was used to measure the serum calcium and phosphorus levels of rats, and ELISA method was used to detect ALP levels. Bone density meter was used to measure the bone density of the femurs of rats in each group. The osteoclast of each group were cultured, and the expressions of RANKL and RUNX2 protein were detected by Western blot. MiRNA sequencing and differential expression analysis were performed on bone tissues of rats. Osteoclasts were treated with miR-133b-3p mimic and its negative control. The cell proliferation activity of osteoclasts was detected by cell counting kit-8 (CCK-8). The osteoclast differentiation activity was detected by the tartrate-resistant acid phosphatase staining. The dual-luciferase reporter assay was used to detect the relationship between miR-133b-3p and RhoA. The "rescue" experiment of miR-133b-3p mimic and RhoA co-expression were used to study the molecular regulatory mechanism of Zuogui Pills on osteoclast activity.Results:Compared with the model group, the bone mineral density of Zuogui Pills group significantly increased ( P<0.05, P<0.01), the levels of calcium and phosphorus in serum increased, the level of alkaline phosphatase ALP decreased ( P<0.05), the expression of RANKL protein decreased, and the expression of RUNX2 protein increased. Sequencing results showed that rno-miR-133b-3p was down-regulated in osteoclasts of postmenopausa osteoporosis rats treated with Zuogui Pills with the maximum difference ( P<0.01). Q-PCR results showed that the expression of miR-133b-3p in osteoclasts of Zuogui Pills group was significantly lower than that of the model group. The upregulation of miR-133b-3p could significantly promote the cell proliferation and differentiation of osteoclasts. RhoA overexpression could reverse the excessive proliferation and differentiation of osteoclasts caused by miR-133b-3p overexpression. Conclusions:RhoA is the target gene regulated by miR-133b-3p. Zuogui Pills can inhibit the activity of osteoclasts by regulating miR-133b-3p/RhoA axis, relieving the symptoms of osteoporosis.

Objective:To identify the pathogenic gene of a pedigree with symphalangism and to prove the pathogenicity of this locus in vitro.Methods:The clinical data of patients’families were collected at Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, peripheral blood was collected and genomic DNA was extracted and NOG, FGF9, GDF5 exon regions were amplified by PCR, and the exon gene mutations were detected by first-generation sequencing technique. The structure of noggin-GDF5 protein complex was simulated in silicon. COS-7 cells were transfected with 5 μg empty plasmid, wild type plasmid and V202G mutant plasmid in vitro. Each group of plasmids was transfected into 3 well cells. The experiment was repeated for 3 times, and the expression of noggin protein was detected by Western blotting. C2C12 cells were also transfected with the above plasmids in vitro for osteogenic differentiation. By applying alkaline phosphatase staining and quantitative assay. Relative expression level of osteoblast-related genes Col1α1, ALP and Runx2 were detected by qRT-PCR. Each group of plasmids was transfected into 3 well cells, and the experiment was repeated for 3 times. All statistical analysis were performed by Prism 6 software. The result were shown as mean±standard deviation, and the comparison between groups was done by unpaired t-test. Data were considered statistically significant when P value is less than 0.05. Results:Both the proband and his mother suffered from symphalangism. The result of Sanger sequencing showed that there was a heterozygous missense mutation of NOG gene (p.V202G) in all patients in this pedigree. No disease-related mutations were detected in FGF9 and GDF5. Computer three-dimensional mechanism simulation showed that the site was located at the α helix. The result of Western blotting showed that the expression of mutant protein was significantly lower than that of wild type. Osteogenic differentiation in vitro showed that the inhibitory effect of V202G mutant protein on osteogenic differentiation decreased. The quantitative result of alkaline phosphatase staining showed that the alkaline phosphatase activity in the vector group was (12.3±0.8) U/L, and the alkaline phosphatase activity in the wild type plasmid group was (2.6±0.3) U/L, which was significantly lower than that in the vector group ( t=11.550, P<0.001). The alkaline phosphatase activity in the mutant plasmid group was (10.8±0.3) U/L. There was no significant difference between the mutant group and the vector group ( t=1.830, P=0.141). The mRNA expression level of osteogenesis-related genes was consistent with the above result . Compared with vector group, the expression of osteogenesis-related genes in wild-type noggin group decreased significantly ALP、 Col1α1 and Runx2 ( t=5.987, 4.498, 4.170; P=0.004, 0.011, 0.014). There was no significant difference between mutant plasmid group and blank vector group in ALP、 Col1α1 and Runx2 ( t=0.433, 0.177, 1.159; P=0.688, 0.868, 0.311). Conclusions:NOG gene c. 605T < G p. V202G is a novel mutation in symphalangism, which is located in the α helix of noggin protein, leading to the decrease of the expression of noggin protein and the manifestation of ankylosis.

Objective:To identify the pathogenic gene of a pedigree with symphalangism and to prove the pathogenicity of this locus in vitro.Methods:The clinical data of patients’families were collected at Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, peripheral blood was collected and genomic DNA was extracted and NOG, FGF9, GDF5 exon regions were amplified by PCR, and the exon gene mutations were detected by first-generation sequencing technique. The structure of noggin-GDF5 protein complex was simulated in silicon. COS-7 cells were transfected with 5 μg empty plasmid, wild type plasmid and V202G mutant plasmid in vitro. Each group of plasmids was transfected into 3 well cells. The experiment was repeated for 3 times, and the expression of noggin protein was detected by Western blotting. C2C12 cells were also transfected with the above plasmids in vitro for osteogenic differentiation. By applying alkaline phosphatase staining and quantitative assay. Relative expression level of osteoblast-related genes Col1α1, ALP and Runx2 were detected by qRT-PCR. Each group of plasmids was transfected into 3 well cells, and the experiment was repeated for 3 times. All statistical analysis were performed by Prism 6 software. The result were shown as mean±standard deviation, and the comparison between groups was done by unpaired t-test. Data were considered statistically significant when P value is less than 0.05. Results:Both the proband and his mother suffered from symphalangism. The result of Sanger sequencing showed that there was a heterozygous missense mutation of NOG gene (p.V202G) in all patients in this pedigree. No disease-related mutations were detected in FGF9 and GDF5. Computer three-dimensional mechanism simulation showed that the site was located at the α helix. The result of Western blotting showed that the expression of mutant protein was significantly lower than that of wild type. Osteogenic differentiation in vitro showed that the inhibitory effect of V202G mutant protein on osteogenic differentiation decreased. The quantitative result of alkaline phosphatase staining showed that the alkaline phosphatase activity in the vector group was (12.3±0.8) U/L, and the alkaline phosphatase activity in the wild type plasmid group was (2.6±0.3) U/L, which was significantly lower than that in the vector group ( t=11.550, P<0.001). The alkaline phosphatase activity in the mutant plasmid group was (10.8±0.3) U/L. There was no significant difference between the mutant group and the vector group ( t=1.830, P=0.141). The mRNA expression level of osteogenesis-related genes was consistent with the above result . Compared with vector group, the expression of osteogenesis-related genes in wild-type noggin group decreased significantly ALP、 Col1α1 and Runx2 ( t=5.987, 4.498, 4.170; P=0.004, 0.011, 0.014). There was no significant difference between mutant plasmid group and blank vector group in ALP、 Col1α1 and Runx2 ( t=0.433, 0.177, 1.159; P=0.688, 0.868, 0.311). Conclusions:NOG gene c. 605T < G p. V202G is a novel mutation in symphalangism, which is located in the α helix of noggin protein, leading to the decrease of the expression of noggin protein and the manifestation of ankylosis.

Objective·To measure the parameters of the uterine artery,umbilical artery and middle cerebral artery in a rat model of preeclampsia(PE)by Doppler ultrasound,and compare the pathological changes in placental blood vessels and pregnancy outcomes,in order to provide an effective method and reference for evaluating placental function in PE animal models.Methods·PE(n=8)and normal pregnancy(NP,n=8)groups in Sprague-Dawley(SD)rat models were established by intraperitoneal injections of N'-nitro-L-arginine methylesterhydrochloride(L-NAME)and 0.9%sodium chloride solution.Blood pressure and proteinuria indexes were detected to evaluate whether the model was successfully established.On gestational day 19(GD19),Doppler ultrasound was utilized to measure the parameters of the uterine artery,umbilical artery and the fetal middle cerebral artery in both the PE and NP groups.After termination of the pregnancies,placental function was evaluated through the pathology of placental blood vessels and the quality of the fetuses and placentas.Results·In the PE group,both blood pressure(GD15:P=0.001;GD19:P=0.001)and proteinuria(GD15:P=0.001;GD19:P=0.001)were significantly higher than those in the NP group.The pulsatility index(PI)of the umbilical artery and uterine artery was notably elevated in the PE group compared to the NP group(both P=0.000).Furthermore,the resistance index(RI)of the fetal middle cerebral artery was significantly lower than that in the PE group(P=0.000).While the number of fetal rats did not differ significantly,the quality of placental and fetal rats was notably lower in the PE group(P=0.006 and P=0.000,respectively).Immunohistochemical staining of placental tissue revealed that the number of placental micro vessel densities in the PE group was less than that in the NP group(P=0.001).Correlation analysis revealed that placental micro vessel density,fetal quality and placental quality were inversely related with the RI of the umbilical artery and the PI and RI of the uterine artery,and positively correlated with the S/D,PI and RI of the fetal middle cerebral artery(all P<0.05).Conculsion·Doppler ultrasound assessment of the uterine artery,umbilical artery and middle cerebral artery indices in L-NAME-induced PE rat models effectively reflects pregnancy outcomes and placental vascular pathology.This method is valuable for evaluating placental vascular perfusion in PE rat models,offering practicality and convenience for research involving animal models.

Schizophrenia is a common chronic mental disorder.Cognitive dysfunction is one of its core symptoms,which severely affects the social functioning of patients.Currently,antipsychotic medication treatments have poor efficacy in improving cognitive functions.Recent studies have found that metformin can improve cognitive dysfunction in patients with schizophrenia.However,the mechanism of action remains unclear.This review summarizes the therapeutic effects of metformin on cognitive dysfunction in schizophrenia patients such as improving insulin resistance,repairing neuronal damage,regulating neuroimmunity,and combating oxidative stress,thereby providing new insights for the treatment of cognitive dysfunction in schizophrenia.