[Risk factors for recurrence after intravitreal anti-vascular endothelial growth factor injection for retinopathy of prematurity]. / çŽ»ç’ƒä½“è ”å† æ³¨å°„æŠ—è¡€ç®¡å† çš®ç”Ÿé•¿å› å­æ²»ç–—æ—©äº§å„¿è§†ç½‘è†œç— å¤å‘çš„å±é™©å› ç´ åˆ†æž.

OBJECTIVES: To investigate the efficacy of intravitreal anti-vascular endothelial growth factor (anti-VEGF) injection in the treatment of retinopathy of prematurity (ROP) and the risk factors for recurrence. METHODS: A retrospective analysis was performed on the medical data of 159 infants with ROP who were born in the First Affiliated Hospital of Zhengzhou University and underwent anti-VEGF treatment from January 2016 to December 2021. According to the presence or absence of recurrence within the follow-up period after initial anti-VEGF treatment, they were divided into a recurrence group with 24 infants and a non-recurrence group with 135 infants. The medical data were compared between the two groups, and a multivariate logistic regression analysis was used to investigate the risk factors for the recurrence of ROP after anti-VEGF treatment. RESULTS: After one-time anti-VEGF treatment, all 159 infants showed regression of plus disease. Recurrence was observed in 24 infants (15.1%) after anti-VEGF treatment, with a mean interval of (8.4±2.6) weeks from treatment to recurrence. The multivariate logistic regression analysis showed that preoperative fundus hemorrhage and prolonged total oxygen supply time were risk factors for the recurrence of ROP (P<0.05), while gestational hypertension was a protective factor (P<0.05). CONCLUSIONS: Intravitreal anti-VEGF injection is effective for ROP. Preoperative fundus hemorrhage and long duration of oxygen therapy may increase the risk of ROP recurrence, and further studies are needed to investigate the influence of gestational hypertension on the recurrence of ROP.

miR-134 inhibits osteosarcoma cell invasion and metastasis through targeting MMP1 and MMP3 in vitro and in vivo.

miR-134 has been shown to be associated with angiogenesis and the progression of osteosarcoma. This study further assessed the effects of miR-134 expression on osteosarcoma cell migration, invasion, and metastasis in vitro and in a nude mouse xenograft model, exploring the underlying molecular events. Luciferase reporter assays revealed that miR-134 directly targets the 3'-UTRs of MMP1 and MMP3 to reduce their expression in osteosarcoma cells. In conclusion, overexpression of miR-134 suppresses osteosarcoma cell invasion and metastasis through the inhibition of MMP1 and MMP3 expression. We propose miR-134 as an attractive novel therapeutic target for the treatment of osteosarcoma.

Clinical efficacy of OrthoPilot navigation system versus conventional manual total hip arthroplasty: A systematic review and meta-analysis.

OBJECTIVE: This study was performed to compare the clinical efficacy between the OrthoPilot navigation system and conventional manual surgery in patients undergoing total hip arthroplasty. METHODS: The Embase, PubMed, CINAHL, and Cochrane databases were searched for clinical trials. The outcome measurements were the anteversion angle, inclination angle, and complications. Review Manager 5.3 statistical software was used for the data analysis. RESULTS: Significant differences were found in the femoral offset and overall complication rate between the conventional and navigation groups. Additionally, the conventional group had significantly less anteversion than the navigation group. However, the navigation group had significantly better inclination. The operation time was significantly shorter in the conventional than navigation group. CONCLUSION: Both the OrthoPilot navigation system and conventional total hip arthroplasty result in significant improvements in patient function with similar overall complication rates and have their own advantages in achieving good cup position. The conventional procedure has a shorter operation time than does use of a navigation system.

[Nasal glioma: report of one case].

Nasal glioma, which is also known as nasal glial heterotopia, is a rare benign congenital lesion. A lot of explanations for the pathogenesis of this disease have already been provided. However, all of them lack theoretical basis. Nowadays, for nasal glioma, complete resection of the tumor is generally used in clinic treatment. CT examination or MRI is necessary for confirming the lesions and the relation between the tumor and intracranial part. This paper reported a neonatal nasal glioma case associated with congenital nasal deformity.

Downregulation of CFTR promotes epithelial-to-mesenchymal transition and is associated with poor prognosis of breast cancer.

The epithelial-to-mesenchymal transition (EMT), a process involving the breakdown of cell-cell junctions and loss of epithelial polarity, is closely related to cancer development and metastatic progression. While the cystic fibrosis transmembrane conductance regulator (CFTR), a Cl(-) and HCO3(-) conducting anion channel expressed in a wide variety of epithelial cells, has been implicated in the regulation of epithelial polarity, the exact role of CFTR in the pathogenesis of cancer and its possible involvement in EMT process have not been elucidated. Here we report that interfering with CFTR function either by its specific inhibitor or lentiviral miRNA-mediated knockdown mimics TGF-ß1-induced EMT and enhances cell migration and invasion in MCF-7. Ectopic overexpression of CFTR in a highly metastatic MDA-231 breast cancer cell line downregulates EMT markers and suppresses cell invasion and migration in vitro, as well as metastasis in vivo. The EMT-suppressing effect of CFTR is found to be associated with its ability to inhibit NFκB targeting urokinase-type plasminogen activator (uPA), known to be involved in the regulation of EMT. More importantly, CFTR expression is found significantly downregulated in primary human breast cancer samples, and is closely associated with poor prognosis in different cohorts of breast cancer patients. Taken together, the present study has demonstrated a previously undefined role of CFTR as an EMT suppressor and its potential as a prognostic indicator in breast cancer.

Engraftment of heavily transfused patients with severe aplastic anemia with a fludarabine-based regimen.

We have developed a practical conditioning regimen without anti-thymocyte globulin (ATG), irradiation, or other myeloablative alkylating agent for low-income countries in which patients with severe aplastic anemia (SAA), who usually have heavily transfused and a prolonged disease history. The application of ATG, Busulphan, and/or irradiation to cyclophosphamide (Cy) to avoid graft rejection has many short- and long-term complications. In this study, we focused on evaluating a fludarabine-based conditioning regimen, among 83 patients with SAA. Patients were treated with fludarabine (40 mg/m(2) /d; day [-5 to -2]) and cyclophosphamide (50 mg/kg/d; day [-5 to -2]). Altogether, 81 patients indicated initial engraftment, whereas two cases showed primary graft failure. And four of the 81 cases indicated graft rejection during follow-up. Regardless of a high cumulative incidence of acute (55/83; 66.2% grade II-IV; 47/83; 56.6% III-IV) and chronic graft-versus-host disease (50/83; 60.2%), in total, 77 patients showed durable engraftment and transfusion independence, and 64 are alive at a median time of 49 months with an overall survival rate of 66%. In conclusion, this conditioning indicated well toleration, mild toxicity, durable engraftment, excellent survival as well as less cost. Its application might shed new light on SAA at high risk of graft rejection in resource-limited countries.

RALY RNA binding protein-like reduced expression is associated with poor prognosis in clear cell renal cell carcinoma.

The molecular mechanisms involved in the progression of clear cell renal cell carcinomas (ccRCCs) are still unclear. The aim of this study was to analyse the relationships between expression of RALYL and clinical characteristics. In 41 paired samples of ccRCCs and adjacent normal tissues, we used real-time qPCR to evaluate the expression of RALYL mRNA. RALYL protein levels were determined in 146 samples of ccRCC and 37 adjacent normal tissues by immunohistochemistry. Statistical analysis was used to explore the relationships between expression of RALYL and the clinical characteristics (gender, age, tumor size, T stage, N stage, M stage, survival times and survival outcome) in ccRCC. In addition, these patients were follow-up period 64 months (range: 4~116 months) to investigate the influence on prognosis. We found significantly differences between ccRCC tissues and normal tissues (p<0.001, paired-sample t test) in mRNA levels of RALYL. Immunohistochemistry analyses in 146 ccRCC samples and 37 adjacent normal tissues showed significantly lower RALYL protein levels in ccRCC samples (χ2-test, p<0.001), inversely correlating with tumour size (p=0.024), T stage (0.005), N stage (p<0.001) as well as M stage (p=0.019), but not age (p=0.357) and gender (p=0.348). Kaplan-Meier survival analysis demonstrated that people with lower level of RALYL expression had a poorer survival rate than those with a higher level of RALYL expression, significantly different by the log-rank test (p=0.011). Cox regression analysis indicated that RALYL expression (p=0.039), N stage (p=0.008) and distant metastasis (p<0.001) were independent prognosis factors for the overall survival of ccRCC patients. We demonstrated that the expression of RALYL was significantly low in ccRCC and correlated with a poor prognosis in a large number of clinical samples. Our findings showed that RALYL may be a potential therapeutic target as well as a poor prognostic factor.

[HLA haploidentical peripheral blood stem cells transplantation for ß thalassemia major].

OBJECTIVE: To evaluate the feasibility of HLA haploidentical peripheral blood hematopoietic stem cell transplantation (PBSCT) for patients with ß thalassemia major. METHODS: Sixteen patients with ß thalassemia major received HLA haploidentical PBSCT from parents. Two conditioning regimens were used. Regimen A was adopted before December 2007, which consisted of fludarabine (total 150 mg/m²), busulfex (total 520 mg/m²), cyclophosphamide (CTX, total 100 mg/kg), antithymocyte globulin (ATG, total 10 mg/kg) and total body irradiation of 3 Gy. Regimen B was adopted after December 2007, which consisted of fludarabine (total 240 mg/m²), busulfex (total 520 mg/m²), CTX (total 100 mg/kg), and ATG (total 10 mg/kg). Combination of cyclosporin (CsA), methotrexate (MTX) and mycophenolate mofetil (MMF) were used for prophylaxis of graft-versus-host disease (GVHD). RESULTS: Of 16 patients, 14 (87.5%) had sustained engraftment. The median days of neutrophil exceeding 0.5 × 109/L and platelet exceeding 20 × 109/L were 13 days (range 10 - 17 days) and 15 days (range 14 - 20 days) after PBSCT, respectively. Complete chimerism was achieved in all the 14 patients at one month after PBSCT. One patient lost his graft with autologous reconstitution 52 days after transplantation. Four patients had grade II-IV acute GVHD and one patient had chronic extensive GVHD. In the 49-month median follow-up duration, 13 of 16 patients were alive in disease-free situation. CONCLUSION: HLA haploidentical PBSCT, which could provide stable and sustained engraftment for thalassemia major patients with no HLA identical donor, is a promising treatment strategy.

No association of EGF 5'UTR variant A61G and hepatocellular carcinoma in Chinese patients with chronic hepatitis B virus infection.

OBJECTIVE: Epidermal growth factor (EGF) has many biological functions, including mitogenesis, tumorigenesis, and proliferation of epidermal tissues. Previous studies have reported that the EGF +61 (A/G) single nucleotide polymorphism in the 5'-untranslated region of the EGF gene is functional, and is associated with development of hepatocellular carcinoma (HCC) in liver cirrhosis and various malignancy. Our aim was to investigate whether EGF gene A61G polymorphism could be implicated in susceptibility to and/or clinicopathological characteristics of HCC in Chinese patients with chronic hepatitis B virus (HBV) infection. METHODS: This polymorphism was studied in 387 patients with chronic HBV infection and in 208 healthy volunteers using restriction fragment-length polymorphism. The patients were divided into two groups: those without (n = 172) and those with HCC (n = 215). These 215 HCC patients with chronic HBV infection were designated as cases, and the remaining 172 patients without HCC served as controls. RESULTS: There were no significant differences in EGF genotype or allelic frequencies between cases and controls nor was EGF genotype or allelic frequencies associated with tumour number, size, growth phase, stage, and invasiveness. We also found ethnic heterogeneity in the functional EGF polymorphism. CONCLUSIONS: The present results show that although EGF gene A61G polymorphism is associated with development of HCC in liver cirrhosis, it is not sufficient for HCC in Chinese patients with chronic HBV infection.

-509C>T polymorphism in the TGF-beta1 gene promoter, impact on the hepatocellular carcinoma risk in Chinese patients with chronic hepatitis B virus infection.

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide. The risk for developing HCC increases with severity of inflammation and fibrosis. Transforming growth factor-beta1 (TGF-beta1) is most frequently upregulated in tumor cells. The most studied -509C>T polymorphism of TGF-beta1 gene has been associated with colorectal, gynecologic, and lung cancers. To assess whether this polymorphism in TGF-beta1 gene is associated with susceptibility to and/or clinicopathologic characteristics of HBV-related HCC, a total of 575 patients with chronic HBV infection and 299 healthy volunteers with no evidence of recent or remote HBV infection were prospectively enrolled. The patients were divided into two groups: those without (n = 196) and those with HCC (n = 379). These 379 HCC patients with chronic HBV infection were designated as cases, the remaining 196 patients without HCC and 299 healthy volunteers served as disease and healthy controls, respectively. -509C>T polymorphism in the TGF-beta1 gene promoter was studied using restriction fragment-length polymorphism. In addition, tumor tissues of liver (n = 60) were obtained from the studied HCC patients for measurement of TGF-beta1 mRNA expression levels. We also assessed the plasma TGF-beta1 levels of HBV patients without (n = 94) or with HCC (n = 136) and healthy subjects (n = 120). In our study group, the risk of HCC in Chinese patients with HBV infection was significantly lower with the TT genotypes than in those with the CC genotypes at position -509 of TGF-beta1 gene (P = 0.01). In addition, in the case group, patients with the CC genotype had a statistically significant higher median plasma TGF-beta1 or liver tumor tissue TGF-beta1 mRNA level compared with the individuals with the TT genotype. However, in a subsequent analysis of the association between this polymorphism and clinicopathological characteristics including tumor number, size, grade, stage, and invasiveness, there was no significant difference in both the distribution of genotype or allelic frequency within HCC patients, indicating that -509C>T exchange in TGF-beta1 gene may play an important role in the occurrence, not the progression of HBV-related HCC through influencing plasma concentrations of TGF-beta1 or TGF-beta1 mRNA expression of liver tumor tissue.

1-Bromo-3,5-diphenyl-benzene.

The title compound, C(18)H(13)Br, crystallizes with two crystallographically independent mol-ecules in the asymmetric unit. The C-Br bond lengths and the C-C bond lengths between the benzene rings are slightly different in the two mol-ecules. The dihedral angles between adjacent benzene rings are 26.85 (2) and 39.99 (2)° in one mol-ecule, and 29.90 (2) and 38.01 (2)° in the other. There are three types of inter-molecular C-H⋯π inter-actions in the crystal structure.

[Transduction efficiency of recombinant adeno-associated virus 2 in human bone marrow CD34+ hematopoietic stem/progenitor cells and mesenchyme stem cells].

OBJECTIVE: To investigate the transduction efficiency of recombinant adeno-associated virus 2 ( rAAV2) in human bone marrow CD34+ hematopoietic stem/progenitor cells and mesenchyme stem cells. METHODS: The rAAV2 containing green fluorescent protein genes (rAAV2/GFP) were constructed, packaged and purified. CD34+ hematopoietic stem/progenitor cells and mesenchyme stem cells were infected with the rAAV2/GFP. After transduction for 48 hours, the expression of GFP was detected under fluorescence microscope. Furthermore, the transduction efficiency of AAV transduced CD34+ with hydroxyurea (HU) pretreatment and that of untreated were compared. RESULTS: GFP genes were expressed in 5.3% +/- 1.7% CD34+ cells. After pretreatment with HU, the expression of the GFP gene in CD34+ cells increased to 13.2% +/- 2.8%, and 23% +/- 3.6% mesenchyme stem cells expressed the GFP gene. Conclusion The transduction efficiency of mesenchyme stem cells is higher than that of CD34+ hematopoietic stem/progenitor cells. HU pretreatment can obviously increase the transduction efficiency of CD34+ hematopoietic stem/progenitor cells.

CD95-induced osteoarthritic chondrocyte apoptosis and necrosis: dependency on p38 mitogen-activated protein kinase.

One of the hallmarks of osteoarthritic cartilage is the loss of chondrocyte cellularity due to cell death. However, considerable controversy has recently arisen surrounding the extent of apoptotic cell death involved in development of osteoarthritis (OA). To shed light on this issue, we characterized cell death in primary OA chondrocytes mediated by the CD95 (Fas) pathway. Treatment of chondrocytes with anti-CD95 not only increased the rate of cell death but also increased the production of CD95 ligand by chondrocytes. This reveals a novel autocrine regulatory loop whereby activated chondrocytes may amplify CD95 signals by inducing synthesis of CD95 ligand. Multiple morphologic detection analyses indicated that apoptosis accounted for only a portion of chondrocyte death, whereas the other chondrocytes died by necrosis. Both chondrocyte apoptosis and necrosis depended on the activity of p38 mitogen-activated protein kinase (MAPK) within chondrocytes. Treatment of chondrocytes with the p38 MAPK inhibitor SB203580 abolished anti-CD95 induced cell death by inhibiting the activities of activating transcription factor-2 and caspase-3. In addition, inhibition of p38 MAPK activity in chondrocytes stimulated chondrocyte proliferation, as indicated by 5-bromo-2-deoxyuridine (BrdU) index. Thus, p38 MAPK is a potential therapeutic target, inhibition of which may maintain the cellularity of articular chondrocytes by inhibiting cell death and its amplification signal and by increasing cell proliferation.