Objective To investigate the efficacy of foramen magnum decompression alone and foramen magnum decompression + Syrinx-shunt in the treatment of Chiari anomalies with syringomyelia.Methods Forty-nine Chiari anomalies with syringomyelia patients were selected,28 patients performed foramen magnum decompression alone (surgical method Ⅰ group),21 patients performed foramen magnum decompression + Syrinx-shunt (surgical method Ⅱ group).The treatment efficacy was evaluated by postoperative clinical effect and MRI review.Results In surgical method Ⅰ group,effective in 18 cases,invalid in 10 cases,the effective rate was 64.3％ (18/28).In surgical method Ⅱ group,effective in 19 cases,invalid in 2 cases,the effective rate was 90.5％(19/21).There was statistical difference (x2 =4.45,P =0.034).Conclusion Foramen magnum decompression + Syrinx-shunt is effective in the treatment of Chiari anomalies with syringomyelia,which is applicable for these patients and has a more precise consequence than foramen magnum decompression alone.

Objective To analyze the complications ofventriculoperitoneal shunt in the treatment of pediatric hydrocephalus,and improve operative method,in order to reduce postoperative complications and improve the clinical curative effect.Methods A total of 39 infants with hydrocephalus who underwent adjustable shunt were retrospectively analyzed,including surgical methods,results,and complications,and put forward counter measures.Results Thirty cases of postoperative clinical symptoms obviously improved compared with preoperative,head CT review were clearly seen with ventricle retraction.Nine cases suffered with complications after operation.Obstruction of shunt tube was found in 4 cases,shunt exposed in 3 cases,and postoperative infection in 2 cases.Conclusions Ventriculoperitoneal shunt complications related to surgery itself.Improved surgical techniques,and taking appropriate treatment measures can effectively reduce the incidence of complications.

Objective:To explore the effect of cholesterol on the expression of genes for matrix synthesis and degradation of human meniscal fibrochondrocytes and its mechanism.Methods:Meniscal tissue was taken from patients undergoing arthroscopic surgery to extract fibrochondrocytes. The cells were divided into a control group in which the normal cells were not processed, a positive control group in which interleukin-1 β was used to create a degeneration model, and 2 treatment groups which were subjected to treatment with 15 and 30 μg/mL cholesterol respectively. Safranin O staining, β-galactosidase staining and enzymic kits were used to detect the morphology and total cholesterol (TCH) content of meniscal fibrochondrocytes in the 4 groups. Immunofluorescence and western blot were used to detect the protein expression of type Ⅰcollagen precursor α1 (COL1A1) and type Ⅱ collagen precursor α1 (COL2A1). RT-qPCR was used to detect the mRNA expression of COL1A1, COL2A1, matrix metalloproteinase (MMP) 3, MMP9, MMP13, and genes related to cholesterol efflux pathways [like liver X receptor α (LXR α), ATP binding cassette transporter A1 (ABCA1) and ABCG1]. Results:There was no significant difference between the control and the positive control groups in the TCH content in human meniscal fibrochondrocytes ( P>0.05). The treatments with 15 and 30 μg/mL cholesterol resulted in significantly increased TCH contents in human meniscal fibrochondrocytes in the treatment groups ( P<0.05). Compared with the control group, the mRNA expression of LXR α, ABCA1 and ABCG1 was significantly decreased in the treatment groups ( P<0.05), and the meniscal fibrochondrocytes in the positive group and the treatment groups presented with a lower density, chaotic distribution and obvious signs of degradation. Compared with the control groups, the mRNA expression of matrix synthesis genes (COL1A1 and COL2A1) in the meniscal fibrochondrocytes was significantly inhibited while the mRNA expression of matrix degradation metalloenzymes (MMP3, MMP9 and MMP13) was significantly promoted ( P<0.05). Conclusion:Cholesterol may inhibit the cholesterol efflux pathways of meniscal fibrochondrocytes, and thus cause accumulation of cholesterol in the meniscal fibrochondrocytes, eventually leading to degeneration of meniscus.

BACKGROUND:Apoptosis of islet cel s is closely related to the long-term hyperglycemia-and hyperlipemia-induced injuries. OBJECTIVE:To observe the effect of Shizidaiping formula on the apoptosis and insulin secretion in MIN6 cel s under the high glucose and lipid environment, and to explore the protective effect of Shizidaiping formula and the related apoptosis mechanism. METHODS:MIN6 cel s were divided into normal, model, melbine, low-, medium-and high-dose Shizidaiping formula groups. The cel activity was examined by cel counting kit-8, the insulin secretion was measured by ELISA, the rate of apoptosis was measured by Annexin V-FITC&PI and the expression levels of MEK1/2, ERK1/2 and p-ERK1/2 were examined by western blot assay. RESULTS AND CONCLUSION:Shizidaiping formula significantly improved MIN6 cel activity under high glucose and lipid condition (P<0.05), decreased early cel apoptosis, increased the level of insulin stimulated by low glucose in cel supernatant (P<0.05), and improved the expression levels of MEK1/2, ERK1/2 and p-ERK1/2 (P<0.05). These results suggest that Shizidaiping formula can protect islet cel s from hyperglycemia and hyperlipemia damage by improving the activity of MIN6 cel s, reducing the insulin secretion and inhibiting the apoptosis of pancreaticβcel s in MIN6 cel s.

Objective: To explore the present perceptions of patient-empowering nurse behaviours, self-efficacy and patient activation among patients with chronic diseases, and analyze the influencing mechanism among these three variables. Methods: Using convenient sampling method, a total of 485 inpatients with chronic diseases were sampled from two tertiary comprehensive hospitals in Guangzhou on the day of discharge between March and October 2017. They were surveyed with the demographic questionnaire, Patient Perceptions of Patient-Empowering Nurse Behaviours Scale , Chronic Disease Self-Efficacy Scale and Patient Activation Measure. Results: Empowerment could positively predict self-efficacy (β=0.402, P<0.01) and patient activation (β=0.169, P<0.01). Self-efficacy could also positively predict patient activation (β=0.887, P<0.01). And self-efficacy, of which the effect accounted for 67.87% of the total effect, played a partial intermediary role between empowerment and patient activation. Conclusions To improve patient activation, empowerment and self-efficacy should be both emphasized and applied by the nurses, so that patients can move smoothly from a care receiver before discharge to one of self-management.

Dermatomyofibroma is a benign and rare proliferation of myofibroblasts and fibroblasts of the skin.Dermatomyofibroma commonly locates at the shoulder and neck of young adults and adolescents.Other frequently affected anatomic sites are upper arms,thigh,chest wall,back,axillary region and abdomen.Herein,we reported a case of dermatomyofibroma occurred in the nasion.The asymptomatic firm nodule and histopathological features were consistent with dermatomyofibroma.Immunohistochemically,the tumor cells expressed vimentin,HHF35 and α-smooth muscle actin (α-SMA).The patient was followed up for 2 years after excision of the tumors and recurrences were not observed.

Tumor cells and tumor microenvironment (TME) are closely related. It is known that many factors will change the TME, then affect tumor development, however the change of TME is also inseparable from tumor cells. More and more studies have confirmed that the regulation of TME is the key to anti-tumor therapy. Therefore, it is critical to understand the effect of tumor cells on TME.

Periprosthetic joint infection (PJI) is one of the destructive complications after artificial joint replacement, which leads to postoperative joint pain, prolonged hospital stays, repeated multiple operations, dysfunction and even mortality. However, there is no specific diagnosis method for PJI. Although some progress has been made in the research of pathogenic microorganisms, diagnostic criteria, prevention strategies and treatment regimens of PJI in recent years, the quick and accurate diagnose and reducing of postoperative PJI is still the hotspot and difficulty in the field of artificial joint replacement. Gram-positive bacteria are the most common pathogenic bacteria, the prevalence of multidrug resistant pathogens, mixed bacterial infections and culture negative bacteria remain increasing. The epidemiological data of pathogen can guide clinical diagnosis and empirical use of antibiotics, which can help reducing of resistant bacteria. The International Consensus Meeting (ICM) proposed new diagnostic criteria, refined secondary criteria and assigned detailed scoring rules. New biochemical markers (such as leucocyte esterase and α-defensin, etc.), sonication of prosthesis combined with gene detection, imaging detection (such as 3-phase bone scanning labeled with technetium-99m, etc.), and next-generation sequencing is helpful to improve the accuracy of PJI diagnosis. Scientific and standardized perioperative management programs and new preventive measures, such as intraoperative application of vancomycin powder and diluted iodophor irrigation, are benefit to prevent and reduce the occurrence of PJI. Two-stage revision is still the standard intervention for chronic PJI, while one-stage revision combined with intra-articular antibiotics injection can effectively eradicate PJI in patients with acute or some chronic PJI with clear pathogenic bacteria.

Background and Objectives: Myocardial ischemia-reperfusion injury (MIRI) refers to the damage of cardiac function caused by restoration of blood flow perfusion in ischemic myocardium. However, long non-coding RNA prostate androgen regulated transcript 1 (PART1)’s role in MIRI remain unclear. Methods: Immunofluorescence detected LC3 expression. Intermolecular relationships were verified by dual luciferase reporter assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and transferase-mediated dUTP nick-end labeling (TUNEL) assays analyzed cell viability and apoptosis. The release of lactate dehydrogenase was tested via enzyme-linked immunosorbent assay (ELISA). Left anterior descending coronary artery surgery induced a MIRI mouse model. Infarct area was detected by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin and eosin staining examined myocardial injury. ELISA evaluated myocardial marker (creatine kinase MB) level. Results: PART1 was decreased in hypoxia/reoxygenation (H/R) induced AC16 cells and MIRI mice. PART1 upregulation attenuated the increased levels of Bax, beclin-1 and the ratio of LC3II/I, and enhanced the decrease of Bcl-2 and p62 expression in H/R-treated cells.PART1 upregulation alleviated H/R-triggered autophagy and apoptosis via miR-302a-3p. Mechanically, PART1 targeted miR-302a-3p to upregulate transcription factor activating enhancer-binding protein 2C (TFAP2C). TFAP2C silencing reversed the protected effects of miR-302a-3p inhibitor on H/R treated AC16 cells. We further established TFAP2C combined to dual-specificity phosphatase 5 (DUSP5) promoter and activated DUSP5. TFAP2C upregulation suppressed H/R-stimulated autophagy and apoptosis through upregulating DUSP5.Overexpressed PART1 reduced myocardial infarction area and attenuated MIRI in mice. Conclusion PART1 improved the autophagy and apoptosis in H/R-exposed AC16 cells through miR-302a-3p/TFAP2C/DUSP5 axis, which might provide novel targets for MIRI treatment.

Background and Objectives: Myocardial ischemia-reperfusion injury (MIRI) refers to the damage of cardiac function caused by restoration of blood flow perfusion in ischemic myocardium. However, long non-coding RNA prostate androgen regulated transcript 1 (PART1)’s role in MIRI remain unclear. Methods: Immunofluorescence detected LC3 expression. Intermolecular relationships were verified by dual luciferase reporter assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and transferase-mediated dUTP nick-end labeling (TUNEL) assays analyzed cell viability and apoptosis. The release of lactate dehydrogenase was tested via enzyme-linked immunosorbent assay (ELISA). Left anterior descending coronary artery surgery induced a MIRI mouse model. Infarct area was detected by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin and eosin staining examined myocardial injury. ELISA evaluated myocardial marker (creatine kinase MB) level. Results: PART1 was decreased in hypoxia/reoxygenation (H/R) induced AC16 cells and MIRI mice. PART1 upregulation attenuated the increased levels of Bax, beclin-1 and the ratio of LC3II/I, and enhanced the decrease of Bcl-2 and p62 expression in H/R-treated cells.PART1 upregulation alleviated H/R-triggered autophagy and apoptosis via miR-302a-3p. Mechanically, PART1 targeted miR-302a-3p to upregulate transcription factor activating enhancer-binding protein 2C (TFAP2C). TFAP2C silencing reversed the protected effects of miR-302a-3p inhibitor on H/R treated AC16 cells. We further established TFAP2C combined to dual-specificity phosphatase 5 (DUSP5) promoter and activated DUSP5. TFAP2C upregulation suppressed H/R-stimulated autophagy and apoptosis through upregulating DUSP5.Overexpressed PART1 reduced myocardial infarction area and attenuated MIRI in mice. Conclusion PART1 improved the autophagy and apoptosis in H/R-exposed AC16 cells through miR-302a-3p/TFAP2C/DUSP5 axis, which might provide novel targets for MIRI treatment.