Clinical characteristics, outcomes and risk factors for mortality in hospitalized diabetes and chronic kidney disease patients after COVID-19 infection following widespread vaccination.

BACKGROUND: COVID-19 poses a significant threat to patients with comorbidities, such as diabetes and chronic kidney disease (CKD). China experienced a nationwide COVID-19 endemic from December 2022 to January 2023, which is the first occurrence of such an outbreak following China's widespread administration of COVID-19 vaccinations. METHODS: A total of 338 patients with diabetes and CKD combined with COVID-19 infection between December 7, 2022 and January 31, 2023 were included in this study. The end follow-up date was February 10, 2023. Univariate analysis and multivariate Cox analysis were used to analyze risk factors for death. RESULTS: During the 50-day median follow-up period, 90 patients in the study cohort died, for a mortality rate of 26.63%. The median age of the study cohort was 74 years, with a male predominance of 74%. During hospitalization, 21% of patients had incident AKI, 17% of patients experienced stroke, and 40% of patients experienced respiratory failure. Cox proportional hazard regression showed that older age, a diagnosis of severe or critically severe COVID-19 infection, incident AKI and respiratory failure, higher level of average values of fasting glucose during hospitalization, UA, and total bilirubin were independent risk factors for death in our multivariate model. CONCLUSIONS: These findings highlight the critical importance of identifying and managing comorbid risk factors for COVID-19, especially among the elderly, in order to optimize clinical outcomes, even after COVID-19 vaccination.

[Differentiation between hyperintense hepatocellular carcinoma and focal nodular hyperplasia in hepatobiliary phase with multimodal parameters of magnetic resonance imaging].

Objective: To differentiate hyperintense hepatocellular carcinoma (HCC) with focal nodular hyperplasia (FNH) in the hepatobiliary phase by MRI multimodal parameters. Methods: A retrospective cross-sectional study method was adopted. Clinical data on 15 cases with hyperintense HCC and 15 cases with FNH in the hepatobiliary phase admitted to the First Affiliated Hospital of the Army Medical University from January 2012 to December 2019 were collected. All patients with solitary lesions who underwent Gd-EOB-DTPA-enhanced MRI examinations were included. Surgically resected specimens were verified by pathological and immunohistochemical examination. HCC and FNH imaging features were analyzed by two radiologists. Results: (1) HCC and FNH apparent diffusion coefficient (ADC) values were 1 205.07±239.65×10-3 mm2/s and 1 434.73±217.6×10-3 mm2/s, respectively, and the SIADC difference was statistically significant (P<0.05) between the two groups. (2) In the dynamic contrast-enhanced MRI sequence, 15 cases of HCC were significantly enhanced in the arterial phase, of which 13 cases were characterized by continuous enhancement, and 2 cases were characterized by wash-in and wash-out enhancement. There was no statistically significant difference (P>0.05) between the two groups. SIenhancement rate between HCC and FNH (1.39±0.60 vs. 1.33±0.50, P>0.05) had no significant difference. (3) HCC and FNH morphological features in the hepatobiliary phase included: annular hypointensity: HCC (8 cases) vs. FNH (0 cases); contrast filling defects: HCC (8 cases) vs. FNH (0 cases); linear hyposignal separation: HCC (10 cases) vs. FNH (0 cases); and stellate scars: HCC (0) vs. FNH (5 cases), and there were statistically significant differences (P<0.05) between the two groups . Conclusion: Multimodal MRI have significant value for differentiating hyperintense HCC and FNH in the hepatobiliary phase.

Adoptive transfer of immunomodulatory M2 macrophages suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice via blockading NF-κB pathway.

Macrophages play important roles in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), and M2 macrophage may have anti-inflammatory effects. In this study, we elucidated the roles of M1 and M2 macrophages in the pathogenesis of EAE and the effects of treatment with M2 macrophages that target certain proinflammatory cytokines and with immunomodulatory preparations that beneficially influence the disease course. We found macrophages increased at the onset of clinical signs in the EAE group, consistent with an increased proportion of M1 macrophages and low numbers of M2 macrophages. As the disease progressed and the symptoms worsened, M1 macrophages decreased and M2 macrophages gradually increased until the peak. In the recovery stage, M2 macrophages gradually decreased. Treatment with M2 macrophages inhibited the nuclear factor kappa B (NF-κB) pathway, alleviated the symptoms of EAE, reduced inflammatory cell infiltration and demyelination in the central nervous system and decreased the numbers of macrophages in the spleens. BAY-11-7082, an NF-κB blocking agent, could reduce the total number of macrophages both in vivo and in vitro, effectively prevented EAE development and significantly inhibited EAE symptoms in mice. Our study demonstrates that macrophages may play a crucial role in the pathogenesis of EAE, while M2 macrophages have anti-inflammatory effects. Transfer of M2 macrophages to EAE mice can block the NF-κB pathway successfully and relieve EAE symptoms. Application of NF-κB blockers is useful in the prevention and treatment of EAE.

High cyclic tensile stress disrupts the extracellular matrix in human chondrocyte by F-actin cytoskeletal polymerization and reactive oxygen species production.

This study aims to explore the mechanism of cyclic tensile stress (CTS) on human chondrocytes (CHs) relating to the reactive oxygen species (ROS) generation and extracellular matrix (ECM) stability in vitro. A well-established CTS model with 5%, 10%, or 20% elongation was performed for CHs stretching. After CTS, the cell viability, total ROS level, main ECM components, matrix metalloproteinase (MMP), tissue inhibitor of metalloproteinase (TIMP), F-actin density, and some anti-oxidative enzymes were analyzed. Additionally, the antioxidant N-acetylcysteine (NAC) and cytochalasin D were used to suppress the ROS production and F-actin polymerization when the CHs underwent CTS, respectively. The treatment of 20% elongation-CST significantly decreased the CH viability and the expressions of collagen II, aggrecan, anti-oxidative enzymes and TIMP3/4, however, it increased the ROS accumulation, F-actin polymerization, and the expression of collagen I and MMP3/13. In contrast, the application of NAC and cytochalasin D could partly rescue the CHs from the injury caused by the high CTS. Therefore, high CTS disrupts the ECM by remodeling the F-actin cytoskeleton and promoting ROS production. Cytochalasin D and NAC are effective in rejecting F-actin cytoskeleton polymerization, and ROS accumulation through a potential synergetic process, which alleviates the ECM injury caused by High CTS.

Diabetes mellitus and risk of hip fractures: a meta-analysis.

UNLABELLED: This meta-analysis revealed that diabetic adults had a twofold greater risk of hip fractures compared with non-diabetic populations, and this association was more pronounced in type 1 diabetes. INTRODUCTION: The relationship between diabetes mellitus and risk of hip fracture yielded conflicting results. We conducted a meta-analysis to investigate the association between diabetes mellitus and the risk of hip fractures based on observational studies. METHODS: We conducted a systematic literature search of PubMed and Embase databases through May 2015. We selected cohort and case-control studies providing at least age-adjusted risk ratio (RR) and corresponding 95 % confidence intervals (CI) of hip fractures among diabetic and non-diabetic subjects. Moreover, we pooled the female-to-male RR of hip fractures from studies that reported gender-specific risk estimate in a single study. RESULTS: Twenty-one studies involving 82,293 hip fracture events among 6,995,272 participants were identified. Diabetes mellitus was associated with an increased risk of hip fractures (RR 2.07; 95 % CI 1.83-2.33) in a random effects model. Subgroup analysis indicated that excess risk of hip fracture was more pronounced in type 1 diabetes (RR 5.76; 95 % CI 3.66-9.07) than that in type 2 diabetes (RR 1.34; 95 % CI 1.19-1.51). The pooled female-to-male RR of hip fractures was 1.09 (95 % CI 0.93-1.28). CONCLUSIONS: Individuals with diabetes mellitus have an excessive risk of hip fractures, and this relationship is more pronounced in type 1 diabetes. The association between diabetes and hip fracture risk is similar in men and women.

[A prospective cohort study on the impact of placement timing of LNG-IUS for adenomyosis].

OBJECTIVE: To investigate the impact of placement in the procedures of gynecological laparoscopies or routine placement on the effects of levonorgestrel-releasing intrauterine system (LNG-IUS) for symptomatic adenomyosis in a prospective cohort study. METHODS: From December, 2006 to December, 2014, patients with adenomyosis diagnosed by transvaginal ultrasound in outpatient or inpatient clinics of Peking Union Medical College Hospital received the treatment of LNG-IUS.Before and after placement of LNG-IUS all the parameters were recorded including carrying status of IUS, symptoms and scores of dysmenorrhea, menstruation scores, biochemical indicators, physical parameters, menstruation patterns and adverse effects.Impact of placement timing (in the procedures of laparoscopies vesus routine placement) on the treatment effects, menstruation patterns and adverse effects of LNG-IUS were analyzed. RESULTS: 1 100 patients meet the inclusion criteria, with median age 36 years (20-44 years), median follow-up 35 months (1-108 months), of which 385 cases (35.0%) received LNG-IUS in the procedures of gynecological laparoscopies. Most common indications and pathology outcomes were endometriosis, major of which had deep infiltrating endometriosis. The accumulative carrying ratio of LNG-IUS were 73% and 63% on 60 months for operative patients and non-operative patients respectively (P<0.001), and accumulative take-out ratio were 7.8% and 10.3% (P=0.044). Placement timing of LNG-IUS was the only significant factor related with loss to follow-up (P<0.001) and take-out ratio (P<0.001). Operations and pathological outcome had no significant impact on patients' treatment effects, changes of menstruation patterns, adverse effects in total or in subclass. CONCLUSION: Placement of LNG-IUS in the procedures of gynecological laparoscopies for symptomatic adenomyosis increased carrying ratio and reduce take-out ratio at patients'request, but didn't influence treatment effects or adverse effects.

[Effect and related factors of extracorporeal cardiopulmonary resuscitation combined with emergent percutaneous coronary intervention on cardiac arrest patients due to acute myocardial infarction].

OBJECTIVE: To evaluate the effect of extracorporeal membrane oxygenation (ECMO) combined with primary percutaneous coronary intervention (PPCI) on cardiac arrest in patients with acute myocardial infarction (AMI). METHODS: We retrospectively analyzed the clinical data from twenty cardiac arrest patients due to AMI from January 2010 to January 2015, who received both ECMO and PPCI after failed conventional cardiopulmonary resuscitation (CCPR) procedure in our center. The mean age was (58.8±13.9) years old and seventeen cases were male. The patients were divided into weaned (8 cases) and non-weaned group (12 cases) according to the outcome of ECMO removal, or survivor (6 cases) and non-survivor group (14 cases) according to the in-hospital outcome. The risk factors that affected weaning from ECMO and survival to discharge were analyzed via Spearman rank correlation test. RESULTS: (1) The mean duration of CCPR and ECMO support was (46.7±22.2)min and (102.3±66.6)h, respectively. The rate of return of simultaneous beating was 100%(20/20). (2) CCPR duration was significantly shorter ((35.1±11.8)min vs. (54.4± 24.5) min, P<0.05) and cardiac care unit(CCU) stay time was significantly longer ((20.5±12.3)d vs. (4.3±4.0)d, P<0.05) in weaned group than in non-weaned group. Moreover, a significant difference was identified in culprit vessel distribution between the two groups (P<0.05). Culprit vessel distribution (left anterior descending artery r=-0.612, P<0.01; right coronary artery r=0.612, P<0.01) and length of cardiac care unit stay (r=0.784, P<0.01) were associated with weaned patients. (3) CCPR duration was significantly shorter ((29.2±4.9)min vs. (51.0±24.5)min, P<0.01). CCU stay time was significantly longer(16.0(9.5, 37.8)d vs. 3.0(2.0, 11.0) d, P<0.01). Weaning rate (6/6 vs. 2/14, P<0.01) and mean blood pressure ((87.9±19.4)mmHg(1 mmHg=0.133 kPa) vs. (63.7±18.6)mmHg, P<0.05) were significantly higher, while lactic acid level in arterial blood((1.74±0.85)mmol/L vs. (6.41±5.65) mmol/L, P<0.05) 48 hours after ECMO support was significantly lower in survivor group compared with non-survivor group. Culprit vessel of right coronary artery (r=0.491, P<0.05), length of CCU stay (r=0.609, P<0.01), successful weaning rate (r=0.802, P<0.01), and mean blood pressure at 48 hours after ECMO establishment (r=0.558, P<0.05) were positively associated with survival. CONCLUSION: ECMO combined with PPCI is an effective therapeutic option to rescue AMI patients complicating with cardiac arrest.

COVID-19 susceptibility, hospitalization and severity and the risk of brain cortical structure: a Mendelian randomization study.

BACKGROUND: Observational studies have reported structural changes in the brains of patients with coronavirus disease 2019 (COVID-19); it remains unclear whether these associations are causal. AIM: We evaluated the causal effects of COVID-19 susceptibility, hospitalization and severity on cortical structures. DESIGN: Mendelian randomization (MR) study. METHODS: Data on the different COVID-19 phenotypes were obtained from the latest large-scale genome-wide association study (R7) of the COVID-19 Host Genetics Initiative. Brain structure data, including cortical thickness (TH) and surface area (SA), were obtained from the ENIGMA Consortium. Additionally, we employed the round 5 dataset released in January 2021 as the validation cohort. The inverse-variance weighted (IVW) method was used as the primary analysis in MR. Sensitivity analyses were conducted to evaluate heterogeneity and pleiotropy. We performed enrichment analysis on the MR analyses that passed the sensitivity analysis filtering. RESULTS: After IVW and sensitivity analyses, we observed causal associations between COVID-19 susceptibility and rostral middle frontal SAw (P = 0.0308, ß = -39.1236), cuneus THw (P = 0.0170, ß = -0.0121), medial orbitofrontal THw (P = 0.0002, ß = 0.0225), postcentral THw (P = 0.0217, ß = -0.0106), temporal pole THw (P = 0.0077, ß = 0.0359), medial orbitofrontal SAnw (P = 0.0106, ß = -24.0397), medial orbitofrontal THnw (P = 0.0007, ß = 0.0232), paracentral SAnw (P = 0.0483, ß = -20.1442), rostral middle frontal SAnw (P = 0.0368, ß = -81.9719) and temporal pole THnw (P = 0.0429, ß = 0.0353). COVID-19 hospitalization had causal effects on medial orbitofrontal THw (P = 0.0053, ß = 0.0063), postcentral THw (P = 0.0143, ß = -0.0042), entorhinal THnw (P = 0.0142, ß = 0.0142), medial orbitofrontal THnw (P = 0.0147, ß = 0.0065) and paracentral SAnw (P = 0.0119, ß = -7.9970). COVID-19 severity had causal effects on rostral middle frontal SAw (P = 0.0122, ß = -11.8296), medial orbitofrontal THw (P = 0.0155, ß = 0.0038), superior parietal THw (P = 0.0291, ß = -0.0021), lingual SAnw (P = 0.0202, ß = -11.5270), medial orbitofrontal THnw (P = 0.0290, ß = 0.0039), paracentral SAnw (P = 0.0180, ß = -5.7744) and pars triangularis SAnw (P = 0.0151, ß = -5.4520). CONCLUSION: Our MR results demonstrate a causal relationship between different COVID-19 phenotypes and cortical structures.

Pharmacological activity of ibuprofen released from mesoporous silica.

Novel drug delivery systems (DDS) to improve the pharmacokinetic profile of hydrophobic drugs following oral administration are an area of keen interest in drug research. An ideal DDS should not adversely affect drug activity, be capable of delivering a therapeutic dose of drug, and allow homogenous drug loading and drug release. Mesoporous silica has been proposed for this application, with ibuprofen employed as the model drug. It was hypothesised that mesoporous silica MCM-41 is capable of delivering a pharmacologically therapeutic dose of ibuprofen. Ibuprofen-loaded MCM-41 can be prepared reproducibly at a drug to carrier ratio of 30% (wt/wt). The release profile was seen to be 90% within 2 h. Initial assessment of COX-1 inhibitory activity suggests the absence of adverse effects attributable to drug-carrier interaction. The results of this study provide further evidence in support of the proposed use of mesoporous silica in drug delivery.

Erratum: Avalanches triggered by Kelvin-Helmholtz instability in a cylindrical plasma device [Phys. Rev. E 100, 033212 (2019)].

This corrects the article DOI: 10.1103/PhysRevE.100.033212.

Circular RNA circ-SMAD7 promoted ovarian cancer cell proliferation and metastasis by suppressing KLF6.

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, "Circular RNA circ-SMAD7 promoted ovarian cancer cell proliferation and metastasis by suppressing KLF6, by Y. Zhao, X.-P. Qin, Y.-P. Lang, D. Kou, Z.-W. Shao, published in Eur Rev Med Pharmacol Sci 2019; 23 (13): 5603-5610-DOI: 10.26355/eurrev_201907_18294-PMID: 31298312" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18294.

Circ_CHFR expedites cell growth, migration and inflammation in ox-LDL-treated human vascular smooth muscle cells via the miR-214-3p/Wnt3/ß-catenin pathway.

OBJECTIVE: Atherosclerosis (AS) is a representative inflammatory vascular disease. This study explored the molecular pathogenesis of AS based on circular RNA (circRNA), the checkpoint with forkhead-associated and ring-finger domains (circ_CHFR). PATIENTS AND METHODS: The cell model of AS in vitro was established by stimulating human vascular smooth muscle cells (VSMCs) with oxidized low-density lipoprotein (ox-LDL). The RNA expression was measured by quantitative Real-time polymerase chain reaction (qRT-PCR). Cell viability and colony formation ability were separately evaluated using 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) and colony formation assay. Cell migration was assessed via the transwell assay. The inflammation injury was analyzed by enzyme-linked immunosorbent assay (ELISA). Associated proteins were determined through Western blot. The combination of hypothetic targets was ascertained using Dual-Luciferase reporter assay. RESULTS: Circ_CHFR was up-regulated in AS serums and ox-LDL-stimulated VSMCs. Circ_CHFR depletion weakened the ox-LDL-induced promotion of cell growth, migration and inflammation in VSMCs. Circ_CHFR positively regulated Wnt3 expression and the downregulation of Wnt3 abrogated the ox-LDL-triggered injuries in VSMCs. Circ_CHFR functioned as the sponge of microRNA-214-3p (miR-214-3p) and miR-214-3p targeted Wnt3. Circ_CHFR regulated cell growth, migration and inflammation via regulating the expression of Wnt3 as a competitive endogenous RNA (ceRNA) of miR-214 in ox-LDL-treated VSMCs. Circ_CHFR/miR-214-3p axis mediated the Wnt3/ß-catenin signal pathway. CONCLUSIONS: Circ_CHFR contributed to the progression of AS through the miR-214-3p/Wnt3/ß-catenin signals, which illuminated the molecular mechanism of AS and suggested circ_CHFR might be an index for AS treatment.

Avalanches triggered by Kelvin-Helmholtz instability in a cylindrical plasma device.

A profile-evolving simulation of the Controlled Shear Decorrelation Experiment (CSDX) linear device is performed with our newly developed code. The simulation result shows an excellent agreement with the experimental observations of profiles and fluctuations of plasma density and electric potential in the B=1000 G standard discharges, suggesting the mechanism of their evolutions. According to our simulation, an avalanche of plasma density, featuring a rapid destruction of particle profile, is triggered every time the dominant instability transits from near adiabatic collisional drift wave to non-adiabatic Kelvin-Helmholtz instability. The avalanches always start at the point where the local vorticity is the maximum among the whole device. A critical vorticity is found for any avalanche to happen. The avalanches always lead to intermittent particle and heat convective structures outside the main plasma column, and these structures are ejected out as avaloids when zonal flow intensity at birth time is weak.

LncRNA NR027113 promotes malignant progression of gastric carcinoma via EMT signaling pathway.

OBJECTIVE: The aim of this study was to explore the characteristics of long noncoding RNA (lncRNA) NR027113 in gastric carcinoma, and to further investigate whether it could promote the development of gastric carcinoma via epithelial mesenchymal transition (EMT) signaling pathway. PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction (qRT-PCR) was performed to analyze the expression of NR027113 in 68 paired of gastric carcinoma and para-carcinoma tissues. Subsequently, the relationship between NR027113 expression and clinical indexes of gastric carcinoma as well as the prognosis of patients was analyzed. NR027113 expression in gastric carcinoma cells was detected by qRT-PCR as well. NR027113 knockdown model was constructed by lentivirus transfection in gastric carcinoma cells (including AGS and SGC-7901). Meanwhile, the effects of NR027113 on the biological functions of gastric carcinoma cells were analyzed by cell counting kit-8 (CCK-8), wound healing, transwell invasion and migration assay, respectively. Furthermore, the correlation between NR027113 and EMT signaling pathways was studied. RESULTS: QRT-PCR results showed that the expression level of NR027113 in gastric carcinoma tissues was significantly higher than that of para-carcinoma tissues. Compared with patients with low expression of NR027113, the incidence of lymph node metastasis and distant metastasis was significantly higher in patients with high NR027113 expression. Meanwhile, the survival rate of patients with low NR027113 expression was significantly lower. Compared with control group, the invasion and migration abilities of cells in NR027113 knockdown group were significantly decreased. Subsequent qRT-PCR results demonstrated that the expression of EMT signaling pathway-related proteins was significantly changed after transfection of sh-NR027113. The above finding indicated that NR027113 could inhibit the malignant progression of gastric carcinoma. Moreover, the addition of transforming growth factor-ß (TGF-ß) cytokines synergistically promoted the malignant progression of gastric carcinoma with NR027113. CONCLUSIONS: NR027113 expression was significantly increased in gastric carcinoma. Meanwhile, it was positively correlated with lymph node metastasis, distant metastasis and poor prognosis of gastric carcinoma patients. Furthermore, NR027113 could accelerate the invasion and migration abilities of gastric carcinoma cells via EMT signaling pathway.

Circular RNA circ-SMAD7 promoted ovarian cancer cell proliferation and metastasis by suppressing KLF6.

OBJECTIVE: Recently, the roles of circular RNAs (circRNAs) in tumor progression have attracted much attention. Currently, circ-SMAD7 has been identified as an oncogene in cancers. The aim of this study was to investigate the function of circ-SMAD7 in the progression of ovarian cancer. PATIENTS AND METHODS: Circ-SMAD7 expression in both ovarian cancer cells and tissue samples was detected by quantitative Real Time-Polymerase Chain reaction (qRT-PCR). Circ-SMAD7 shRNA was constructed and transfected into the ovarian cancer cells. To identify the function of circ-SMAD7 in ovarian cancer, cell proliferation assay, colony formation assay, transwell assay, and Matrigel assay were conducted, respectively. In addition, qRT-PCR and Western blot assays were performed to elucidate the underlying mechanism and, then, it was analyzed. RESULTS: Circ-SMAD7 expression was remarkably higher in ovarian cancer tissue samples than in corresponding normal tissues. The proliferation of the ovarian cancer cells was significantly inhibited after circ-SMAD7 downregulation. Meanwhile, the migration and invasion of ovarian cancer cells were significantly inhibited after circ-SMAD7 downregulation in vitro. Both the mRNA and the protein expressions of the Krüppel-like factor 6 (KLF6) were remarkably promoted after circ-SMAD7 was knocked down in ovarian cancer cells. Furthermore, the KLF6 expression level was negatively correlated with circ-SMAD7 expression level in ovarian cancer samples. CONCLUSIONS: Our study suggests that circ-SMAD7 promotes the progression of ovarian cancer and enhances cell metastasis and proliferation via suppressing KLF6. In addition, circ-SMAD7 may be a novel therapeutic strategy in ovarian cancer.

MiR-25 overexpression promotes fracture healing by activating the Wnt signaling pathway.

OBJECTIVE: To study the mechanism of micro-ribonucleic acid (miR)-25 in regulating the fracture healing in rats. MATERIALS AND METHODS: A total of 45 male Sprague-Dawley (SD) rats were selected and randomly divided into group A [Phosphate Buffered Saline (PBS), n=15], group B (mimics NC, n=15) and group C (miR-25 mimics, n=15). The fracture model in rats was established via operation in all groups. From 1 d after the successful modeling, 50 µL (2 nmoL) of PBS was intraperitoneally injected into rats in group A, an equal amount of mimics NC was injected into rats in group B, and an equal amount of miR-25 mimics was injected into rats in group C. The above agents were injected once a week for consecutive 6 weeks. Fracture healing in rats was evaluated via X-ray imaging. At the same time, miR-25 expression in the three groups was detected via Reverse Transcription-Polymerase Chain Reaction (RT-PCR). Protein expressions of ß-catenin, proliferating cell nuclear antigen (PCNA) and bone morphogenetic protein-2 (BMP-2) in the three groups were detected via Western blotting. The OCN-, PCNA- and BMP-2-positive osteoblasts in the three groups were detected via immunohistochemical staining and were further quantified. Moreover, the biomechanical properties of femoral fracture healing in the three groups were analyzed via the 4-point bending flexural test. RESULTS: The X-ray examination of the femoral fracture healing at postoperative 1 and 7 weeks revealed that the fracture line disappeared, and both callus formation and fracture healing were good in miR-25 mimics group. In PBS group and mimics NC group, a few fracture lines could be observed, and both callus formation and fracture healing were poor. RT-PCR data showed that the expression level of miR-25 significantly increased in the miR-25 mimics group compared with that in the other two groups, and the differences were statistically significant (p<0.01). Western blotting analyses showed upregulated levels of ß-catenin, PCNA and BMP-2 in the miR-25 mimics group compared with those in the control group, and the differences were statistically significant (p<0.01). Immunohistochemical staining manifested that the numbers of OCN-, PCNA- and BMP-2-positive osteoblasts in miR-25 mimics group markedly increased compared with that in the other two groups (p<0.01), suggesting that osteoblast differentiation in miR-25 mimics group was affected. The above immunohistochemical results indicated that the osteoblast differentiation at the fracture end in miR-25 mimics group was markedly enhanced compared with that in control groups. The results of the biomechanical test of femur specimens at 7 weeks after operation showed that in miR-25 mimics group, the maximum load, fracture energy and stiffness increased by 188%, 333% and 90%, respectively, compared with those in the PBS group (p<0.01). It is indicated that miR-25 promoted the mechanical properties of fracture healing. CONCLUSIONS: The overexpression of miR-25 in the fracture in rats promotes fracture healing by activating the Wnt signaling pathway.