Scientific publications on orthopedic surgery from three major East Asian countries (2012-2021).

BACKGROUND: East Asia is the most dynamic region in the world and includes three major countries: Japan, South Korea and China. Due to rapid economic growth, orthopedics research in East Asia has achieved great advances during the past 10 years. However, the current status of orthopedic research in Japan, South Korea and China is still unclear. AIM: To understand the current status of orthopedic research in Japan, South Korea, and China. METHODS: Journals listed in the ''Orthopedics'' category of Science Citation Index Expanded subject categories were included. The PubMed and Web of Knowledge electronic databases were searched to identify scientific publications from the selected journals written by researchers from Japan, South Korea and China. A systematic analysis was conducted to analyze orthopedic research articles published in the three countries based on the number of articles, study design, impact factors (IFs) and citations. Furthermore, we also ranked the top 10 countries worldwide with the highest publications in the past 10 years. Additionally, we ranked the top 10 countries with the highest number of publications in the world in the past 10 years. Statistical analyses were performed using SPSS 20.0 software (SPSS Inc., Chicago, IL, United States), and statistical results are given in Tables and Figures. The Kruskal-Wallis test and the Mann-Whitney test were used to detect differences between countries. The tendency regarding the number of articles was analyzed by curvilinear regression. A two-tailed P < 0.05 was considered significant. RESULTS: From 2012-2021, a total of 144518 articles were published in the 86 selected orthopedic journals. During this period, the number of worldwide published orthopedic articles has shown an annual increasing trend. A total of 27164 orthopedic research articles were published by Japan, South Korea and China during the past 10 years; 44.32% were from China, 32.98% were from Japan, and 22.70% were from South Korea. From 2012 to 2021, the annual number of articles markedly increased in each of the three countries. Over time, the worldwide share of articles increased substantially in South Korea (3.37% to 6.53%, P < 0.001) and China (5.29% to 9.61%, P < 0.001). However, the worldwide share of articles significantly decreased in Japan (5.22% to 3.80%, P < 0.001). The annual total IFs of articles from China were well above those of articles from Japan and South Korea (36597.69 vs 27244.48 vs 20657.83, P < 0.05). There was no significant difference among the articles in the top 10 high-IF orthopedics journals published from those three countries [South Korea (800) > China (787) > Japan (646), P > 0.05]. CONCLUSION: Over the past 10 years, China's scientific publications in orthopedic journals have shown an increasing trend. Considering the relative scale of the populations, Japan and South Korea have outpaced China with respect to quality.

Surgical resection of intradural extramedullary tumors in the atlantoaxial spine via a posterior approach.

BACKGROUND: The anatomical features of the atlantoaxial spine increase the difficulty of complete and safe removal of atlantoaxial intradural extramedullary (IDEM) tumors. Studies concerning surgical interventions via a posterior approach are limited. AIM: To investigate the safety and efficacy of atlantoaxial IDEM tumor resection using a one-stage posterior approach. METHODS: We retrospectively analyzed clinical databases for one-stage atlantoaxial IDEM tumor resection via a posterior approach between January 2008 and January 2018. The analyzed data included tumor position, histopathological type, pre- and post-operative Japanese Orthopedic Association (JOA) scores and Nurick grades, postoperative complication and recurrence status. RESULTS: A total of 13 patients who underwent C1-C2 Laminectomy and/or unilateral facetectomy via the posterior approach were enrolled in the study. In all cases reviewed, total tumor resection and concomitant C1-C2 fusion were achieved. The average follow-up was 35.3 ± 6.9 mo (range, 26-49 mo). A statistically significant difference was noted between the preoperative JOA score (11.2 ± 1.1) and the score at the last final follow-up (15.6 ± 1.0) (P < 0.05). A statistically significant difference was noted between the preoperative Nurick grade (2.3 ± 0.9) and that at the last follow-up (1.2 ± 0.4) (P < 0.05). However, no statistically significant difference was noted between the preoperative and last follow-up C1-2 Cobb angle and C2-7 Cobb angle (P > 0.05). No mortalities, severe complications or tumor recurrence were observed during the follow-up period. CONCLUSION: Total resection of atlantoaxial IDEM tumors is feasible and effective via a posterior approach. Surgical reconstruction should be considered to avoid iatrogenic kyphosis and improve spinal stability and overall clinical outcomes.

Upregulation of Wnt signaling under hypoxia promotes lung cancer progression.

The hypoxic tumor microenvironment induces epithelial-mesenchymal transition (EMT) in tumor cells and increases tumor cell malignancy. Previous studies indicated that malfunction of Wnt signaling is observed in some lung cancer patients. Athough crosstalk between hypoxia and Wnt signaling in tumor cells has recently been revealed, the detailed underlying mechanisms have not been well defined. In the present study, we demonstrated that hypoxia in lung adenocarcinoma cells can enhance Wnt signaling activity by stabilizing ß-catenin and altering its localization into the nucleus. Overexpression of HIF-2α increased ß-catenin expression, promoted cell mobility, and induced morphological changes to a greater degree than HIF-1α overexpression. Knockdown of HIF-2α decreased ß-catenin expression and inhibited hypoxia-induced cell mobility. Moreover, we identified that phosphorylational activation of AKT1 by hypoxia and HIF-2α was required for Wnt activation upon hypoxia treatment. Downregulation of HIF-2α and ß-catenin reduced colony formation when cells were exposed to long-term hypoxia treatment. Taken together, our data support that hypoxia activates PI3K/AKT as well as Wnt signaling in a HIF-2α-dependent manner, thus elevating the resistance of lung cancer cells to chronic hypoxia-induced stress.

Glibenclamide, a diabetic drug, prevents acute radiation induced liver injury of mice via up-regulating intracellular ROS and subsequently activating Akt-NF-κB pathway.

BACKGROUND: Acute radiation-induced liver injury is a limitation for hepatoma radiotherapy. Come so far the clinical treatments are insufficient. The effective, specific, low toxicity and novel drugs are in powerful need. Glibenclamide is a common hypoglycemic. Some studies have revealed its relation with intracellular reactive oxygen species, the crucial mediator to radiation injury. This study is aimed to investigate if glibenclamide could act on the acute radiation-induced liver injury. RESULTS: Glibenclamide mitigated acute radiation-induced liver injury of mice, indicating as regression of hepatocellular edema, reduction of hepatic sinusoid, decline in serum ALP level and reduction of hepatocellular apoptosis. Pretreatment of glibenclamide reduced the radiosensitivity of NCTC-1469 cells. In mechanism, glibenclamide elevated cells membrane potential to up-regulate intracellular reactive oxygen species. The increased reactive oxygen species subsequently activated Akt-NF-κB pathway to promote survival of irradiated cells. METHODS: BALB/C male mice were intraperitoneal injected with glibenclamide 1 hour before hepatic irradiation. At designed time points the livers were taken to make histological study and bloods were collected to measure serum transaminase. With/without glibenclamide pretreatment the irradiated NCTC-1469 cells were tested apoptosis, viability and proliferation. By western blotting the involved molecules were detected. CONCLUSIONS: Glibenclamide, prevents acute radiation-induced liver injury of mice via up-regulating intracellular reactive oxygen species and subsequently activating Akt-NF-κB pathway.