MicroRNA-1269a promotes the occurrence and progression of osteosarcoma by inhibiting TGF-ß1 expression.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "MicroRNA-1269a promotes the occurrence and progression of osteosarcoma by inhibiting TGF-ß1 expression, by S.-N. Yu, Y.-Y. Miao, B.T. Zhang, Y.-M. Dai, L. Liu, Z.-L. Gao, G.-F. Liu, published in Eur Rev Med Pharmacol Sci 2019; 23 (3): 972-981-DOI: 10.26355/eurrev_201902_16984-PMID: 30779063" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/16984.

[Effect of modified double negative-pressure wound therapy combined with debridement and tension-reduced suture in treatment of patients with stage 4 pressure sores and infection in sacrococcygeal region and its surrounding area].

Objective: To investigate the effect of modified double negative-pressure wound therapy combined with debridement and tension-reduced suture in treatment of stage 4 pressure sores and infection in sacrococcygeal region and its surrounding area. Methods: From January 2015 to June 2019, 20 patients with stage 4 pressure sores and infection in sacrococcygeal region and its surrounding area were admitted to Department of Burns and Plastic Surgery and Cosmetology of Linyi People's Hospital. Among them, there were 11 males and 9 females, aged 48 to 88 years. The wounds of 13 patients were located in the sacrococcygeal region, and 8 of them had exposed sacrococcyx. The wounds of 4 patients were located in the greater trochanter area of femur, and the wounds of 3 patients were located in the ischial tuberosity area. All the patients had fever in different degree, bacterial infection, hypoproteinemia, and electrolyte imbalance, etc. at admission. After thorough debridement and dressing change, routine negative-pressure wound therapy with negative pressure value of -16.6 kPa was performed according to the scope of lesions in period Ⅰ. When granulation tissue was fresh with less exudate and without residual necrotic tissue, modified double negative-pressure wound therapy in combination with debridement and tension-reduced suture was performed immediately in period Ⅱ. Modified double negative-pressure wound therapy were persistently performed through negative pressure drainage tube inserted into deep part of wounds and negative pressure drainage tube on surface at the same time, with superficial negative pressure value of -19.9 kPa. Meanwhile, systemic anti-infection and nutritional supports were given. The wounds were monitored for the grade of wound healing and whether skin necrosis, split, or fluid accumulation develop at the suture site. The patients were followed up for 1 to 6 months after discharge to monitor wound healing. Length of hospital stay, infection condition before and after the debridement and tension-reduced suture, and complications during treatment were recorded. Results: All wounds achieved first grade healing, with the skin at the suture site healed without split, fluid accumulation, or necrosis. The patients were followed up for 1 to 6 months after discharge, with good shape of surgical incision, little pigmentation on the skin, no hypertrophic scar or contracture, and no recurrence of pressure sores. Length of hospital stay of patients was 24 to 33 d, with an average of 28.5 d. Before debridement and tension-reduced suture, 2 cases were infected with Pseudomonas aeruginosa, 1 case was infected with Escherichia coli and Staphylococcus aureus, and 1 case was infected with Proteus mirabilis. The results of bacterial culture were all negative after debridement and tension-reduced suture. During the treatment, all patients were not complicated with bone or joint infection, necrotizing fasciitis, septicemia, etc. Conclusions: Modified double negative-pressure wound therapy combined with debridement and tension-reduced suture for treatment of patients with stage 4 pressure sores and infection in sacrococcygeal region and its surrounding area is easy to operate with minimal injury, easy for patients to accept with a very high level of satisfaction, and is suitable to popularize and applicate for primary hospitals.

Long non-coding RNA SNHG5 promotes human hepatocellular carcinoma progression by regulating miR-363-3p/RNF38 axis.

OBJECTIVE: The involvement of long non-coding RNA (LncRNAs) in HCC development has been widely recognized in recent decades. LncRNA small nucleolar RNA host gene 5 (SNHG5) has been identified to be implicated in the development of many tumors, and this study aimed to explore the role of SNHG5 in HCC tumorigenesis. PATIENTS AND METHODS: The expression levels of SNHG5, miR-363-3p, and Ring Finger Protein 38 (RNF38) were measured by using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) or Western blot assay, respectively. Cell proliferation was analyzed by MTT assay. Flow cytometry was used to investigate cell apoptosis. Cell migration and invasion abilities were detected by transwell assay. The relationship among SNHG5, miR-363-3p, and RNF38 was confirmed using bioinformatics analysis and Luciferase reporter assay. RESULTS: The expression of SNHG5 and RNF38 was elevated in HCC tissues and cell lines, and highly expressed SNHG5 and RNF38 could induce apoptosis and repress proliferation, migration, as well as invasion in HCC cells. Further investigations showed that SNHG5 might act as a competing endogenous RNA of miR-26a-5p and thereby cause the derepression of the downstream target RNF38. Moreover, rescue experiments indicated that SNHG5 silence inhibited the progression of HCC cells by regulating miR-363-3p, and the facilitated effects of RNF38 in the progression of HCC cells were regulated by miR-363-3p. CONCLUSIONS: LncRNA SNHG5 may promote human HCC progression by regulating the miR-363-3p/RNF38 axis, providing a novel insight into the pathogenesis of HCC and therapeutic strategy for HCC treatment.

MicroRNA-1269a promotes the occurrence and progression of osteosarcoma by inhibit-ing TGF-ß1 expression.

OBJECTIVE: MicroRNAs are endogenous, non-coding small RNAs that are capable of regulating biological and pathological processes. Previous studies have shown that microRNA-1269a serves as an oncogene. However, the role of microRNA-1269a in the pathogenesis of osteosarcoma (OS) has not been reported. The aim of this work was to investigate the expression characteristics of microRNA-1269a in OS and to further study its regulatory effects on the malignant progression of OS. PATIENTS AND METHODS: The expression of microRNA-1269a in 61 pairs of OS tissues and para-cancerous tissues was detected by quantitative Real Time-polymerase Chain Reaction (qRT-PCR). Chi-square test was used to analyze the relationship between microRNA-1269a expression and the characteristics of OS patients, including age, sex, clinical stage and distant metastasis. Subsequently, microRNA-1269a expression in OS cell lines was detected as well. After knockdown of microRNA-1269a by constructing relevant small interference RNA, biological performances of MG63 and U2OS cells were accessed by cell counting kit-8 (CCK-8), colony formation and transwell assay. Meanwhile, the protein expressions of key genes in the EMT/Smad pathway were detected by Western blot. Finally, si-TGF-ß1 (transforming growth factor-ß1) was transfected into OS cells, and cell migration and invasion were detected by transwell assay. RESULTS: MicroRNA-1269a was highly expressed in OS tissues compared with para-cancerous tissues. High expression of microRNA-1269a was positively correlated with young OS patients and high rate of distant metastasis, whereas was not correlated with age, sex and Enneking stage. Kaplan-Meier survival curves showed that high expression of microRNA-1269a was significantly associated with poor prognosis of OS. The knockdown of microRNA-1269a in MG63 and U2OS cells significantly inhibited cell proliferation, migration and invasion. Meanwhile, microRNA-1269a knockdown in OS cells markedly downregulated the expressions of TGF-ß1, p-Smad2, p-Smad3, N-cad, Vimentin and MMP9. Furthermore, TGF-ß1 knockdown remarkably decreased migratory and invasive abilities of OS cells. CONCLUSIONS: MicroRNA-1269a is highly expressed in OS, which is remarkably correlated with tumor stage, distant metastasis and poor prognosis of OS. In addition, microRNA-1269a promotes the malignant progression of OS by regulating TGF-ß1 expression.

Far-field sound radiation of a submerged cylindrical shell at finite depth from the free surface.

The far-field sound radiation behavior of a circular cylindrical shell submerged at finite depth from the free surface is studied. Based on the Flügge shell theory and the Helmholtz equation, the structure-acoustic coupling equation is established. An image method is applied so that the sound boundary condition of the free surface can be satisfied. Analytical expression of the far-field sound pressure is obtained using the stationary phase method and the Graf's addition theorem. In order to evaluate the effect of the submerged depth on sound radiation, the results of the submerged cylindrical shell at finite depth from the free surface are compared with those of the submerged cylindrical shell in the infinite fluid. The characteristics of the far-field sound pressure with the change of the depth are investigated. It is found that the submerged depth has a significant influence on the far-field sound pressure radiated from the submerged cylindrical shell due to the free surface effects. The work provides more understanding on the sound radiation properties of the submerged circular cylindrical shell without assuming infinite fluid field, which was commonly used in previous studies.