Showing papers by "Fifth Affiliated Hospital of Xinjiang Medical University published in 2020"

Andrographolide Protects Against Adverse Cardiac Remodeling After Myocardial Infarction through Enhancing Nrf2 Signaling Pathway.

Abstract: Adverse cardiac remodeling after myocardial infarction (MI) is associated with extremely high mortality rates worldwide. Although optimized medical therapy, Preservation of lusitropic and inotropic function and protection against adverse remodeling in ventricular structure remain relatively frequent. This study demonstrated that Andrographolide (Andr) significantly ameliorated adverse cardiac remodeling induced by myocardial infarction and improves contractile function in mice with LAD ligation compared with the control group. Briefly, Andr markedly attenuated cardiac fibrosis and relieved inflammation after myocardial infarction. Specifically, Andr significantly blocked oxidative stress and the nuclear translocation of p-P65 following myocardial infarction. At the mechanistic level, antioxidant effect of Andr was achieved through strengthening antioxidative stress capacity and attributed to the activation of Nrf2/HO-1 Signaling. Consistently, H9C2 administrated with Andr showed a decreased oxidative stress caused by hypoxia precondition, but treatment with specific Nrf2 inhibitor (ML385) or the silence of Nrf2 blunted the activation of Nrf2/HO-1 Signaling and removed the protective effects of Andr in vitro. Thus, we suggest that Andr alleviates adverse cardiac remodeling following myocardial infarction through enhancing Nrf2 signaling pathway.

An Eight-Year Follow-Up Study on the Treatment of Single-Level Cervical Spondylosis Through Intervertebral Disc Replacement and Anterior Cervical Decompression and Fusion

Abstract: Objective To compare the efficacy and safety of the postoperative long-term effect of the treatment of single-level cervical spondylosis through anterior cervical discectomy and fusion (ACDF) and artificial cervical disc replacement (ACDR). Methods This is a retrospective contrastive study, which was conducted for the period of January 2007 and January 2009 at the Department of Spine Surgery of the First Affiliated Hospital of Xinjiang Medical University. A total of 113 patients were divided into two groups depending on the operation method: ACDF group (fusion group, n = 66) and ACDR group (replacement group, n = 47). The ACDR group comprised of 23 males and 24 females. The age of these patients ranged from 31-60 years, with an average age of 42.89 ± 6.30 years. The ACDF group comprised of 38 males and 28 females. The age of these patients ranged from 28-73 years old, with an average age of 49.38 ± 9.89 years old. The evaluation index included the visual analogue scale (VAS), neck disability index (NDI), range of motion, dysphagia, adjacent vertebral disease, and related complications (prosthesis displacement, heterotopic ossification, etc.). Results A total of 113 patients met the inclusion criteria, and these patients receive more than 96 months of follow-up. The VAS and NDI of these two groups of patients significantly improved, when compared with those before the operation. In the last follow-up visit, the range of motion in the ACDR group and ACDF group was 43.22 ± 3.58 and 32.54 ± 2.82, respectively, and both are significantly different comparing to the values measured before the operation (P 0.05). Conclusion Overall, the clinical efficacy and related complication rate of single-level cervical spondylosis after an anterior cervical approach operation was superior in the ACDR group when compared to the ACDF group.

Circular RNA circ_ASAP2 promotes cell viability, migration, and invasion of gastric cancer cells by regulating the miR-770-5p/CDK6 axis.

Abstract: Background Gastric cancer (GC) is one of the most common causes of cancer death. GSE83521 microarray analysis suggested that circular RNA circ_ASAP2 (hsa_circ_0008768) expression was increased in GC tissues. However, the molecular mechanism of circ_ASAP2 remains unknown. Methods Expression levels of circ_ASAP2, microRNA-770-5p (miR-770-5p), and the cyclin-dependent kinase 6 (CDK6) were detected by using real time PCR (RT-PCR). 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and transwell assays were applied to explore cell viability, migration, and invasion, respectively. The interactions between miR-770-5p and circ_ASAP2 or CDK6 was predicted by using Starbase software, and then confirmed by luciferase reporter assay. Xenograft tumor model was also used to estimate the effect of circ_ASAP2 on tumor growth in vivo. Results The expression levels of circ_ASAP2 and CDK6 were increased, and miR-770-5p level was decreased in GC tissues and cells. Furthermore, circ_ASAP2 knockdown inhibited cell viability, migration, and invasion of GC cells. Mechanically, circ_ASAP2 functioned as a sponge of miR-770-5p to regulate CDK6 expression, thereby boosting the progression of GC cells. Circ_ASAP2 silencing hindered the tumor growth of GC in vivo. Conclusion Circ_ASAP2 knockdown can repress the development of GC cells partly through regulating the miR-770-5p/CDK6 axis, suggesting an underlying circRNA-targeted therapy for GC treatment.

Levosimendan Protects against Doxorubicin-Induced Cardiotoxicity by Regulating the PTEN/Akt Pathway.

Abstract: Background and aims Myocyte apoptosis plays a critical role in the development of doxorubicin- (DOX-) induced cardiotoxicity. In addition to its cardiotonic effect, laboratory evidence indicates that levosimendan can inhibit apoptosis, but its role in DOX-induced cardiac injury remains unclear. Therefore, the present study is aimed at exploring whether levosimendan could attenuate DOX-induced cardiotoxicity. Methods Levosimendan (1 mg/kg) was administered to mice through oral gavage once daily for 4 weeks, and the mice were also subjected to an intraperitoneal injection of DOX (5 mg/kg) or saline, once a week for 4 weeks, to create a chronic model of DOX-induced cardiotoxicity. A morphological examination and biochemical analysis were used to evaluate the effects of levosimendan. H9C2 cells were used to verify the protective role of levosimendan in vitro. And an Akt inhibitor was utilized to verify the cardioprotection of levosimendan. Results Levosimendan reduced the cardiac dysfunction and attenuated the myocardial apoptosis induced by DOX in vivo and in vitro. Levosimendan also inhibited the activation of phosphatase and tensin homolog (PTEN) and upregulated P-Akt expression both in vivo and in vitro. And inhibition of Akt abolished the cardioprotection of levosimendan in vitro. Conclusion Levosimendan may protect against DOX-induced cardiotoxicity via modulation of the PTEN/Akt signaling pathway.

Atorvastatin improves the proliferation and migration of endothelial progenitor cells via the miR-221/VEGFA axis

Abstract: The present study was aimed at investigating the detailed functions of atorvastatin, a lipid-lowering agent, in the pathogenesis of coronary slow flow (CSF), a clinical disease characterized by delayed angiographic coronary opacity without obstructive coronary disease. In the present study, we successfully identified isolated endothelial progenitor cells (EPCs) from the peripheral blood of patients with CSF. Their VEGFA protein levels were determined using immunoblotting analyses. We determined cell viability using MTT assays, cell migration capacity using Transwell assays, and the angiogenic capacity using a tube formation assay. The target association between miR-221 and VEGFA was validated with a luciferase reporter assay. Atorvastatin treatment increased EPC VEGFA protein levels, proliferation, migration, and angiogenesis. miR-221 expression was downregulated after atorvastatin treatment; miR-221 overexpression exerted an opposing effect to atorvastatin treatment on VEGFA protein, EPC proliferation, migration, and angiogenesis. The protective effects of atorvastatin treatment on VEGFA protein and EPCs could be significantly suppressed by miR-221 overexpression. miR-221 directly bound the VEGFA 3'UTR to inhibit its expression. In conclusion, atorvastatin improves the cell proliferation, migration, and angiogenesis of EPCs via the miR-221/VEGFA axis. Thus, atorvastatin could be a potent agent against CSF, pending further in vivo and clinical investigations.

CXCR7 suppression modulates macrophage phenotype and function to ameliorate post-myocardial infarction injury.

Abstract: Myocardial infarction (MI) is one of the primary causes leading to heart failure in coronary artery disease. However, the mechanisms of macrophage that dominate pathogenesis of MI remain unclear. Mice were induced with MI and pretreated with adenovirus containing indicated shRNA. Post-MI injuries were evaluated by echocardiography. BMDMs and post-MI LV macrophages were used to assess the significance of CXCR7. Macrophages’ migration was examined by chemotaxis assay, Cytokine production, phosphorylation of ERK1/2, p38 MAPK and JNK were measured by ELISA. CXCR7 in macrophages was up-regulated during M1 polarization and following MI in the murine model, with positive correlation with M1 markers but not M2 markers. Besides, CXCR7 down-regulation abolished macrophage M1 polarization. In addition, CXCR7 but not CXCR3 or CXCR4 controlled SDF-1 and I-TAC-mediated chemotaxis and inflammation in M1-like macrophages post-MI, signaling through activating ERK1/2, whereas p38 MAPK and JNK were not involved. Moreover, silencing CXCR7 ameliorated cardiac dysfunction by attenuating infarct area, LVEF and LVFS post-MI along with reduction of CXCR7 expression and ERK1/2 phosphorylation. Our data demonstrate that CXCR7 suppression inhibits macrophages M1 polarization, chemotaxis and inflammation to ameliorate post-MI injury, providing novel insights and promising therapy approaches in post-MI treatment.

In-Hospital Management and Outcomes of Acute Myocardial Infarction Before and During the Coronavirus Disease 2019 Pandemic.

Abstract: The outbreak of coronavirus disease 2019 (COVID-19) has rapidly spread worldwide. This study sought to share our experiences with in-hospital management and outcomes of acute myocardial infarction (AMI) during the COVID-19 pandemic. We retrospectively analyzed consecutive AMI patients, including those with ST-elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI), from February 1, 2020, to April 15, 2020 (during the COVID-19 pandemic), and from January 1, 2019, to December 31, 2019 (before the COVID-19 pandemic), respectively. Fifty-three AMI patients (31 STEMI, 22 NSTEMI) during the COVID-19 pandemic were matched to 53 AMI patients before the pandemic. Baseline characteristics were comparable between the matched patients. STEMI patients during the COVID-19 pandemic had a longer delay time, less primary or remedial PCI and more emergency thrombolysis than those before the pandemic. Less coronary angiography and stenting were performed in AMI patients during the COVID-19 pandemic than before the pandemic. There were no statistically significant differences in the clinical outcomes between the matched patients. However, STEMI patients during the COVID-19 pandemic had a 4-fold (12.9% vs. 3.2%) increase in all-cause mortality rate compared with those before the pandemic. AMI combined with COVID-19 infection was associated with higher rates of mortality than AMI alone. This study demonstrates that the COVID-19 pandemic results in significant reperfusion delays in STEMI patients and has a marked impact on the treatment options selection in AMI patients. The mortality rate of STEMI patients exhibits an increasing trend during the pandemic of COVID-19.

Knockdown of lncRNA ANRIL suppresses the production of inflammatory cytokines and mucin 5AC in nasal epithelial cells via the miR-15a-5p/JAK2 axis

Abstract: The incidence of allergic rhinitis (AR) is increasing worldwide. Human nasal epithelial cells (HNECs) are the key cells in the occurrence of AR. Antisense non-coding RNA in the INK4 locus (ANRIL) was discovered to be involved in the progression of AR. However, the mechanism by which ANRIL mediates the progression of AR remains to be determined. The present study aimed to further explore the mechanism by which ANRIL regulates AR. Thereby, HNECs were treated with IL-13 to mimic AR in vitro. The mRNA expression levels of ANRIL, microRNA (miR)-15a-5p, JAK2, mucin 5AC (MUC5AC), granulocyte-macrophage colony-stimulating factor (GM-CSF) and eotaxin-1, and protein expression levels of JAK2, STAT3 and phosphorylated-STAT3 in HNECs were analyzed using reverse transcription-quantitative PCR and western blotting, respectively. ELISAs were used to detect the secretory levels of inflammatory cytokines and mucin in cell supernatants. In addition, a dual luciferase reporter assay was used to confirm the downstream target of ANRIL and the target gene of miR-15a-5p. The results revealed that the secretory levels of eotaxin-1, GM-CSF and MUC5AC were significantly upregulated by IL-13 in the supernatant of HNECs. The expression levels of ANRIL and JAK2 were also upregulated in IL-13-induced HNECs, while the expression levels of miR-15a-5p were downregulated. In addition, ANRIL was identified to bind to miR-15a-5p. The IL-13-induced upregulation of eotaxin-1, GM-CSF and MUC5AC mRNA expression and secretory levels was significantly inhibited by the genetic knockdown of ANRIL, while the miR-15a-5p inhibitor effectively reversed this effect. JAK2 was also discovered to be directly targeted by miR-15a-5p. The overexpression of JAK2 significantly suppressed the therapeutic effect of miR-15a-5p mimics on IL-13-induced inflammation in vitro. In conclusion, the findings of the present study suggested that the genetic knockdown of ANRIL may suppress the production of inflammatory cytokines and mucin in IL-13-treated HNECs via regulation of the miR-15a-5p/JAK2 axis. Thus, ANRIL may serve as a novel target for AR treatment.

Overexpression of IκBα in cardiomyocytes alleviates hydrogen peroxide-induced apoptosis and autophagy by inhibiting NF-κB activation

Abstract: Inflammation and oxidative stress play predominant roles in the initiation and progression of ischaemia/reperfusion (I/R) injury, with nuclear factor kappa B (NF-κB) serving as a crucial mediator Overexpression of the inhibitor of κB alpha (IκBα) gene is hypothesized to have protective effects against apoptosis and autophagy in cardiomyocytes subjected to hydrogen peroxide (H2O2) by inhibiting the NF-κB pathway The IκBαS32A, S36A gene was transfected via adeno-associated virus serotype 9 (AAV9) delivery into neonatal rat ventricular cardiomyocytes (NRVMs) prior to H2O2 treatment NRVMs were divided into control, H2O2, GFP + H2O2, IκBα+H2O2, and pyrrolidine dithiocarbamate (PDTC) + H2O2 groups Nuclear translocation of the NF-κB p65 subunit was evaluated by immunofluorescence and Western blotting Cell viability was assessed by Cell Counting Kit-8 assay Supernatant lactate dehydrogenase (LDH) and intracellular malondialdehyde (MDA) were measured to identify H2O2-stimulated cytotoxicity Apoptosis was determined by Annexin V-PE/7-AAD staining, and the mitochondrial membrane potential (ΔΨm) was detected by JC-1 staining Western blotting was used to detect apoptosis- and autophagy-related proteins IκBα transfection significantly increased cell viability and ΔΨm but decreased the supernatant LDH and cellular MDA levels in cardiomyocytes exposed to H2O2 Meanwhile, IκBα overexpression decreased H2O2-induced apoptosis by upregulating the Bcl-2/Bax ratio and reduced autophagy by downregulating the expression of Beclin-1 and the LC3-II/LC3-I ratio These effects partly accounted for the ability of IκBα to inhibit the NF-κB signalling pathway, as evidenced by decreases in p65 phosphorylation and nuclear translocation Indeed, the effects of inactivation of NF-κB signalling with the specific inhibitor PDTC resembled the cardioprotective effects of IκBα during H2O2 stimulation IκBα overexpression can ameliorate H2O2-induced apoptosis, autophagy, oxidative injury, and ΔΨm loss through inhibition of the NF-κB signalling pathway These findings suggest that IκBα transfection can result in successful resistance to oxidative stress-induced damage by inhibiting NF-κB activation, which may provide a potential therapeutic target for the prevention of myocardial I/R injury

Changes in Tumor Stem Cell Markers and Epithelial-Mesenchymal Transition Markers in Nonluminal Breast Cancer after Neoadjuvant Chemotherapy and Their Correlation with Contrast-Enhanced Ultrasound.

Abstract: Nonluminal breast cancer has high early metastasis and treatment resistance, and neoadjuvant chemotherapy (NAC) is needed. The presence of cancer stem cells (CSC) and epithelial-mesenchymal transition (EMT) leads to poor prognosis. This study investigated the changes in CSC markers and EMT markers after NAC in nonluminal breast cancer and their correlation with contrast-enhanced ultrasound (CEUS) features and chemotherapy efficacy. Before NAC, the range of nonluminal breast cancer on CEUS was larger than that of two-dimensional ultrasound, but after NAC, it was significantly smaller than that of two-dimensional ultrasound and closer to the postoperative pathological size. After NAC, the enlarged lesions and perfusion defects were significantly less than those before NAC. The time-intensity curve showed the characteristics of slow-in, low enhancement, and low perfusion. Nonluminal breast cancer downregulated the expression of CSC markers and EMT markers after NAC, but the epithelial phenotype of nonluminal breast cancer with good response to chemotherapy was upregulated. In nonluminal breast cancer with poor response to chemotherapy, markers of CSC and EMT were highly expressed before chemotherapy. In conclusion, CEUS is better than conventional ultrasound in estimating NAC efficacy in this mode. CEUS can also predict the prognosis of nonluminal breast cancer before NAC with the characteristics of enhanced enlargement and perfusion defects. The contrast-enhanced time-intensity curve of lesions with relatively poor blood supply may have more CSC and EMT characteristics.

Tragus Nerve Stimulation Suppresses Post-Infarction Ventricular Arrhythmia by Modulating Autonomic Activity and Heterogeneities of Cardiac Receptor Distribution

Abstract: BACKGROUND Imbalanced cardiac autonomic control and cardiac receptors redistribution contribute to the arrhythmogenic substrate under the myocardial infarction (MI) condition. Stimulating the auricular branch of vagus nerve (AB-VNS) has been proven to reduce post-infarction ventricular arrhythmia (VAs), but its potential mechanisms were largely unknown. This study aimed to investigate whether long-term intermittent low-intensity AB-VNS could produce a protective effect on modulating autonomic activities and abnormal redistribution of autonomic nerve efferent receptors in a MI canine model. MATERIAL AND METHODS Twelve healthy beagle dogs underwent ligation of the left anterior descending coronary artery to establish a MI model and were randomized into 2 groups: an AB-VNS group, (AB-VNS for 4 weeks) and a control group (sham stimulation for 4 weeks). Dynamic electrocardiogram recording, neural recording, catecholamine concentration, and histological studies were conducted subsequently. RESULTS Compared to the control group, the AB-VNS group had significantly suppressed post-infarction VAs, reduced low frequency (LF) power and increased high frequency (HF) power. In the AB-VNS group, with the progression of reduced cardiac sympathetic activities and augmented cardiac parasympathetic activities, the catecholamine concentration in heart tissue declined in the peripheral infarction area and right ventricle (RV); tyrosine hydroxylase (TH)-positive neurons decreased in the inferior cardiac sympathetic nerve, and choline acetyltransferase (ChAT)-positive neurons increased in the cervical vagus nerve. Expression of TrkA and P75NGFR were reduced in the peripheral MI (peri-MI) and non-MI area with AB-VNS. The mRNA expression of adrenergic and nicotinic receptors (s₁-AR, s₃-AR, and CHRNA7) significantly declined in the peri-MI and non-MI area of the AB-VNS group. CONCLUSIONS Chronic intermittent low-intensity AB-VNS effectively suppressed post-infarction VAs by potentially rebalancing extracardiac intrathoracic autonomic activities, reducing excessive cardiac sympathetic denervation, and attenuating the heterogeneities of cardiac efferent nerve receptors distribution.

Genome-Scale Expression Pattern of Long Non-Coding RNAs in Chinese Uyghur Patients with Parkinson's Disease

Abstract: BACKGROUND Long non-coding RNAs (lncRNAs) are transcripts thought to regulate gene expression at the post-transcriptional level. Some lncRNAs are associated with Parkinson's disease (PD) and participate in pathological processes of PD. The incidence of PD is relatively high in members of the Uyghur minority living in Xingjiang province of China. This study measured the expression of lncRNAs in the peripheral blood cells of Chinese Uyghur individuals with and without PD and analyzed the possible function of these lncRNAs in the development of PD. MATERIAL AND METHODS Peripheral blood samples were collected from 55 Uyghur patients with PD and 55 healthy volunteers. Total RNA was extracted, and the levels of expression of whole-genome lncRNAs and mRNAs in 10 samples (5 PD and 5 controls) were determined by microarray method. The expression levels of lncRNAs in all 100 subjects were determined by qRT-PCR. The lncRNA expression profiles of PD patients were determined based on lncRNA microarray chip analysis, and differentially expressed lncRNAs were identified. The results of chip analysis were confirmed in a large clinical cohort. RESULTS Comparison of subjects with and without PD identified 32 significantly up-regulated and 18 significantly down-regulated lncRNAs in the PD group. GO analysis showed that mRNAs encoding proteins involved in the regulation of biological processes were differentially expressed, with the inflammatory immune response being the most significantly related pathway. CONCLUSIONS The expression of lncRNAs in peripheral blood differed significantly in PD patients and controls. These differentially expressed lncRNAs may play a role in the development of PD.

Effects of amygdalin on type II collagen-induced arthritis in rats

Abstract: Amygdalin is the active ingredient of Semen Armeniacae Amarum and has anti-inflammatory effects. However, the role of amygdalin in type II collagen-induced arthritis (CIA) is still unknown. In this study, a rat model of CIA was successfully established in female Wistar rats, as demonstrated by severe joint inflammation. The rats were then intragastrically administrated with Tripterygium Glucosides (TG), high dose amygdalin (120 mg kg−1 d−1), low dose amygdalin (60 mg kg−1 d−1) or sterile phosphate-buffered saline (control) for 28 days. Gross morphology and H&E staining showed that treatment with amygdalin significantly alleviated the joint inflammation, similar to the effect of TG. Furthermore, immunohistochemistry, ELISA and qRT-PCR analysis displayed that amygdalin significantly reduced IL-1β and TNF-α levels compared with model group in both synovial tissue and serum. These findings indicate that amygdalin has treatment effect for arthritis probably through inhibiting the expression of inflammatory cytokines of IL-1β and TNF-α.

ATP13A2 Gene Variants in Patients with Parkinson's Disease in Xinjiang.

Abstract: Objective To analyze the ATP13A2 gene variants in the Han and Uyghur populations residing in Xinjiang and to determine their correlation with the risk of Parkinson's disease (PD). Methods Four ATP13A2 SNVs-rs56367069 (Arg294Gln), rs151117874 (Thr12Met), rs147277743 (Ala746Thr), and rs2076603-were analyzed in 218 patients (75 Uyghurs and 143 Hans) with sporadic PD and 234 healthy controls (90 Uyghurs and 144 Hans) by Sanger DNA sequencing. Results Only one Han patient harbored the AG genotype of the rs147277743 SNV, indicating a frequency of 0.46% in the Han population. In addition, this SNV was not associated with PD risk. The rs2076603 SNV was correlated with PD development, and the A allele in particular was significantly different across ethnicity and age. The rs56367069 and rs151117874 SNVs were not detected in the entire cohort. Conclusion ATP13A2 rs2076603 SNV is associated with PD susceptibility, and the A allele is a PD protective factor in the Han population.

Silencing of miR-23a attenuates hydrogen peroxide (H2O2) induced oxidative damages in ARPE-19 cells by upregulating GLS1: an in vitro study

Abstract: Oxidative damages contributes to age-related macular degeneration (AMD) caused vision blindness, but the molecular mechanisms are still largely unknown. This study managed to investigate this issue by conducting in vitro experiments. Oxidative stress were evaluated by L-012 dye, DHE staining and MDA assay. CCK-8 and colony formation assay were conducted to examine cell proliferation. Cell death was evaluated by trypan blue staining and Annexin V-FITC/PI double staining method through flow cytometry (FCM). The binding sites of miR-23a and GLS1 mRNA were predicted by online miRDB database and validated by dual-luciferase reporter gene system. Real-Time qPCR for miR-23a levels and Western Blot for protein expressions. The retinal pigment epithelial (RPE) cells (ARPE-19) were subjected to hydrogen peroxide (H2O2) stimulation to simulate AMD progression in vitro, and we identified a novel miR-23a/glutaminase-1 (GLS1) pathway that regulated H2O2 induced oxidative damages in ARPE-19 cells. Mechanistically, H2O2 induced oxidative stress, inhibited cell proliferation and induced cell death in ARPE-19 cells in a dose- and time-dependent manner. Also, H2O2 stimulation hindered cell invasion, migration and glutamine uptake in ARPE-19 cells. Interestingly, we proved that H2O2 increased miR-23a levels, while downregulated glutaminase-1 (GLS1) in ARPE-19 cells, and miR-23a targeted 3′ untranslated region (3′UTR) of GLS1 mRNA for GLS1 degradation. Finally, our data suggested that silencing miR-23a upregulated GLS1 to reverse the detrimental effects of H2O2 treatment on ARPE-19 cells. In general, analysis of the data suggested that miR-23a ablation upregulated GLS1 to attenuate H2O2 stimulation induced oxidative damages in ARPE-19 cells in vitro, and this study broadened our knowledge in this field, which might help to provide novel theranostic signatures for AMD.

Application of Self-Made Connection Device in Intractable Intramedullary Device.

Abstract: Background Intramedullary fixation a standard surgical technique for long bone meta/diaphyseal fractures. There were many difficulties in removal of the intractable intramedullary device. The authors reported a new technique to remove the intractable intramedullary nail by using a self-made connecting device. Methods The subject underwent removal of the intramedullary nail using a self-made connecting device, the core components of which were a caudal connecting rod and a sliding hammer in the common intramedullary nail removal device, and the auxiliary device was mainly a clinically commonly used Kirschner wire (K-wire; diameter 1.5-2.5 mm). In technical procedure, the key point was the connection between the k-wire and the intramedullary device, according to the specific conditions of the intramedullary device. Results From 2012 to 2017, a total of 10 cases of intractable intramedullary devices were taken out using this self-made connection device, including 7 cases of tibial intramedullary nails, 1 case of femoral nail, and 1 case of tibial elastic nail. The technique provided satisfactory results, no infection or re-fracture occurred after the. Conclusion The self-made connecting device may provide new technique for more surgeons in the face of intractable intramedullary device.