Microvascular Replantation for partial auricle Amputation: Only Arterial anastomoses and Acupuncture Bloodletting.

BACKGROUND: There have been many reports on replantation of complete auricle amputation, but few reports on successful replantation of partial auricle amputation. The main reason is that the diameter of blood vessels at the end of auricle is only 0.3 mm, and it is difficult to find suitable blood vessels, especially venous vessels. The purpose of this study was to investigate the method of revascularization after partial auricle amputation. METHODS: Microvascular repairs were performed in an amputated segment with only identified artery vessels for anastomosis, and vein was unavailable for anastomosis. Postoperative acupuncture bloodletting and heparin compress treatments were planned. RESULTS: Two patients with partial ear amputation were treated at our center between 2019 and 2021. All the amputated ear were replanted successfully. No blood transfusions and no infections were observed. A week later the replanted auricles were seen, blood flow established. CONCLUSION: Microvascular repair should be considered as the best options in cases of auricular avulsion segment replantation. When no vein was available for anastomosis, only one artery repaired was feasible. Acupuncture bloodletting and heparin compress are the effective methods to treat vein congestion. LEVEL OF EVIDENCE V: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Clinical Value Analysis of High-Frequency Ultrasound Combined with Carpal Dorsiflexion Electrophysiological Detection in the Diagnosis of Early Carpal Tunnel Syndrome.

Objective: To investigate the clinical value of ultrasound combined with electrophysiological examination in the diagnosis of early carpal tunnel syndrome, we aimed to provide a new EMG (electromyography) method for detecting early carpal tunnel syndrome by exploring the wrist back stretch position and electrophysiological examination. Methods: For the 82-lateral wrist (case group) of 62 patients with clinical symptoms or confirmed carpal tunnel syndrome and 40 normal healthy patients, neuroelectrophysiological measurements were performed using a Keypoint6.0 EMG evoked potentiometer, measuring each group twice: conventional position (before compression) and dorsal wrist extension position. The measures for each measurement included DSL, DML, and CAMP. Measure sensory conduction first and then measure motor conduction. The measurements were analyzed in a comprehensive comparative analysis. Combined ultrasound examination, the positive rate of combined ultrasound examination and electrophysiological examination was compared, respectively. Results: In the carpal tunnel syndrome (CTS) group, the anterior and posterior median nerve DSL was (4.27 ± 0.73) ms and (4.82 ± 0.65) ms, and SNAP was (13.32 ± 13.68) UV and (12.19 ± 11.04) UV; the median nerve (wrist-bunions) DML was (5.29 ± 1.26) ms and (5.54 ± 1.29) ms, and CMAP was (6.44 ± 2.40) mV and (6.21 ± 2.46) mV. Mid-median DSL and DM in the CTS group L were significantly longer than before compression; median nerve SNAP and CMAP were significantly reduced compared with before compression. Conclusion: Electrophysiological testing at the dorsal carpal extension position has high diagnostic value in the diagnosis of mild carpal tunnel syndrome. It helps to improve the diagnostic rate of early carpal tunnel syndrome, while providing a more accurate and effective EMG detection of early carpal tunnel syndrome, and combination examination of neuroelectrophysiology and ultrasound can improve the diagnosis rate of compression peripheral nerve diseases and clarify the site, nature, and scope of compression lesions, which is worthy of clinical application.

Benzyl butyl phthalate (BBP) triggers the migration and invasion of hemangioma cells via upregulation of Zeb1.

Hemangioma (HA) are tumors formed by hyper-proliferation of vascular endothelial cells. As a potential endocrine disrupting chemical (EDC), benzyl butyl phthalate (BBP) can mimic estrogen to disturb the estrogenic signals. Our present study investigated the potential roles of phthalates on the progression of HA and found that 100 nM BBP can significantly trigger the migration and invasion of HA cells, which was evidenced by the results that BBP can induce the expression of matrix metalloproteinase (MMPs) and vimentin. Further, BBP can increase the expression of Zeb1, one powerful transcription factor for cell migration and invasion. Targeted inhibition of Zeb1 blocked BBP induced cell migration. Mechanistically, BBP can increase the mRNA stability of Zeb1 via suppression of miR-655. Further, BBP can enhance the protein stability of Zeb1 via upregulation of ataxia telangiectasia mutated (ATM). Collectively, our present study revealed that BBP can trigger the migration and invasion of HA cells via upregulation of Zeb1.

TMEM88 inhibits extracellular matrix expression in keloid fibroblasts.

Keloid is characterized by hyper-proliferation of fibroblasts and excess extracellular matrix (ECM) deposition. Transmembrane protein 88 (TMEM88), belonging to the TMEM family, was involved in the regulation of tumorigenesis and fibrogenesis. However, the role of TMEM88 in keloid formation remains unclear. This study aimed to investigate the effects of TMEM88 on keloid-derived fibroblasts (KFs) proliferation and ECM expression, and explore the underlying mechanism. Our results demonstrated that TMEM88 was lowly expressed in human keloid tissues and TGF-ß1-stimulated KFs. TMEM88 overexpression significantly inhibited the proliferation and migration of KFs, as well as suppressed ECM expression in TGF-ß1-stimulated KFs. Furthermore, TMEM88 overexpression greatly inhibited the protein levels of ß-catenin, cyclin D1 and c-myc in TGF-ß1-stimulated KFs. In conclusion, our data indicate that TMEM88 inhibits the TGF-ß1-stimulated cell proliferation, migration and ECM expression in KFs through the inactivation of Wnt/ß-catenin signaling pathway. Therefore, TMEM88 may be a potential therapeutic target for treating keloids.

Topical versus systemic tranexamic acid after total knee and hip arthroplasty: A meta-analysis of randomized controlled trials.

BACKGROUND: Tranexamic acid (TXA) is an antifibrinolytic drug widely used to reduce blood loss during joint replacements, including total knee arthroplasty (TKA) and total hip arthroplasty (THA). However, there is no final consensus regarding the composition of an optimal administration of TXA regime between topical and systemic (intravenous). The purpose of our study was to compare the efficacy of topical and intravenous (IV) regimen of TXA during TKA and THA. METHODS: Five relevant electronic online databases, PubMed, EMBASE, the Cochrane Central Register of Controlled Trials, Web of Science and Chinese Biomedical Database were systematically searched in November 2015. Randomized controlled trials (RCTs) that compared topical with intravenous TXA in patients with TKA or THA were included. The search terms included "topical," "intravenous," "tranexamic acid," "knee arthroplasty" and "hip arthroplasty." Two reviewers independently extracted data and assessed the risk of bias and study quality. Data were analyzed with Review Manager 5.3 software. Grades of Recommendation Assessment, Development and Evaluation (GRADE) were used to assess the quality of evidence. RESULTS: Sixteen RCTs with 1250 patients undergoing TKA and 4 RCTs involving 550 patients undergoing THA were included. There were no significant differences in total blood loss (mean difference [MD]TKA = -28.72 mL, 95% confidence interval [CI] -195.97 to 138.54 mL, P = 0.74; MDTHA = 14.03 mL, 95% CI -35.53 to 63.59 mL; P = 0.78), total drain out (MDTKA = -3.09 mL, 95% CI -39.05 to 32.88 mL; P = 0.87; MDTHA -31.00 mL, 95% CI -66.56 to 4.66 mL; P = 0.09), and transfusion rates (ORTKA = 0.90, 95% CI 0.58-1.40, P = 0.64; ORTHA = 1.19, 95% CI 0.67-2.09; P = 0.63) between topical and intravenous (IV) TXA. CONCLUSIONS: The current evidence suggested that topical TXA was equally effective and safe compared with intravenous TXA in reducing blood loss and transfusion rate following TKA or THA. We recommended that either topically or systemically could be used in TKA and THA to decrease perioperative blood loss.

Identifying candidate genes involved in osteoarthritis through bioinformatics analysis.

OBJECTIVES: This study aims to identify candidate genes and critical pathways involved in osteoarthritis (OA). METHODS: Gene expression data of synovial membrane from OA patients and normal controls (NCs) were downloaded from database. Totally, 15 OA and 14 NC chips were available. Differentially expressed genes (DEGs) were identified through limma package (log2 fold change >0.585, false discovery rate (FDR) < 0.05), and protein-protein interaction (PPI) network was constructed using STRING. Moreover, perturbation and pathway enrichment analyses were performed through PerturbationAnalyzer in Cytoscape (iterative criteria <1×e-10) and clusterProfiler package (FDR <0.05), respectively. RESULTS: Totally, 236 up-regulated and 290 down-regulated DEGs were identified. In PPI network, 10 hub genes were found, including VEGFA, IL6, JUN, IL1B, ICAM1, ATF3, IL8, EGR1, CDKN1A, and JUNB. After perturbation analysis, 32 DEGs were passively and significantly changed, like PISD, RARRES3, EIF4G1, and EPHA3. Furthermore, 526 DEGs were enriched in 176 pathways, and pathway cross-talk network was constructed, involving 12 pathways and 66 cross-talks. CONCLUSIONS: Pathways like rheumatoid arthritis, osteoclast differentiation, and cytokine-cytokine receptor interaction might play critical roles in OA, and previously unreported genes VEGFA, JUN, JUNB, PISD, RARRES3, EIF4G1, and EPHA3 might participate in OA, providing novel directions for drug targeting.

Molecular mechanisms of osteoarthritis using gene microarrays.

This study aimed to investigate the molecular mechanisms of osteoarthritis (OA) by microarray analysis. Three gene expression datasets GSE1919, 19664 and 55235 were downloaded from the Gene Expression Omnibus, and data of OA samples and healthy controls were used. After data preprocessing, differential expression analysis between the OA group and controls was performed using LIMMA (Linear Models for Microarray Data) package and genes with |log2FC (fold change)|>1 and P<0.05 were screened as DEGs (differentially expressed genes). The screened DEGs were then subject to functional annotation and pathway enrichment analysis using DAVID (Database for Annotation Visualization and Integrated Discovery). Next, gene-set enrichment analysis was performed using Enrichment map Cytoscape plug-in, followed by detecting sub-networks using clusterONE. Finally, risk subpathways were screened using iSubpathwayMiner package. A total of 141 DEGs were screened, including 52 up-regulated ones and 89 down-regulated ones. These DEGs were enriched in 48 GO terms that were mainly related to locomotory behavior, taxis, adhesion, and 11 pathways that were related to cytokine-cytokine receptor interaction, ECM-receptor interaction, focal adhesion, as well as several signaling pathways. The enrichment map enriched gene-sets mainly related to cell death and apoptosis, and extracellular components. The risk pathways up-regulated DEGs were exclusively related to arachidonic acid metabolism and glycosphingolipid biosynthesis, and the top two risk pathways were tyrosine metabolism for the down-regulated ones. From this study we conclude that genes involved in cell death and apoptosis, as well as cell-extracellular matrix interaction, may be essential for OA pathogenesis by altering multiple signaling pathways.

TFPI-2 downregulates multidrug resistance protein in 5-FU-resistant human hepatocellular carcinoma BEL-7402/5-FU cells.

Tissue factor pathway inhibitor-2 (TFPI-2) is known to induce apoptosis and to suppress tumor metastasis in several types of cancer cells. However, there is little known about its reversal effect on chemoresistant tumor cells. This study investigated the effect of TFPI-2 in 5-fluorouracil (5-FU)-resistant human hepatocellular cancer BEL-7402/5-FU cells in vitro. We constructed TFPI-2 overexpression BEL-7402/5-FU cell lines and explored resistance index (RI) of 5-FU, function of the P-glycoprotein (P-gp) efflux pump, and the mRNA and protein expression of drug resistance gene, including multidrug resistance gene (MDR1), lung-resistance protein (LRP), multidrug resistance-associated protein (MRP1), glutathione-S-transferase-π (GST-π), excision repair cross-complementing gene 1 (ERCC1), and p38 phosphorylation. We found that TFPI-2 improved the RI of 5-FU and inhibited P-gp function. Western blotting and real-time PCR revealed that TFPI-2 also decreased mRNA and protein expression of MDR1, LRP, MRP1, GST-π, and ERCC1, whereas p38 phosphorylation was increased. We considered that TFPI-2 reduces 5-FU resistance in BEL-7402/5-FU cells, and the mechanism appears to involve p38-mediated downregulation of drug resistance gene expression such as MDR1, LRP, MRP1, GST-π, and ERCC1.