m6A-mediated upregulation of lncRNA RMRP boosts the progression of bladder cancer via epigenetically suppressing SCARA5.

Aim: This study aimed to elucidate the relationship between SCARA5 and RMRP in bladder cancer and their underlying mechanism. Methods: Biological functions were evaluated using cell-counting kit 8 assay, 5-ethynyl-2'-deoxyuridine incorporation, wound healing and Transwell assays. RNA immunoprecipitation, RNA pull-down and chromatin immunoprecipitation were employed. A xenograft tumor model in nude mice was also conducted. Results & conclusion: RMRP and SCARA5 exhibited an inverse correlation. Downregulation of RMRP significantly suppressed bladder cancer cell proliferation, migration and invasion, which was reversed by SCARA5 overexpression. RMRP recruited DNA methyltransferases to the promoter region of SCARA5, thereby triggering the methylation of the SCARA5 promoter to epigenetically suppress its expression. Our findings elucidate the machinery by which RMRP, stabilized by METTL3, exerts a promoter role in bladder cancer tumorigenesis by triggering SCARA5 methylation.

SCARA5 as a downstream factor of PCAT29, inhibits proliferation, migration, and invasion of bladder cancer.

Scavenger receptor class A, member 5 (SCARA5) has been identified a novel tumor suppressor in several cancers. However, the functional and underlying mechanism of SCARA5 in bladder cancer (BC) need investigation. Here, we found SCARA5 expression was downregulated in both BC tissues and cell lines. Low SCARA5 in BC tissues was associated with a shorter overall survival. Moreover, SCARA5 overexpression reduced BC cell viability, colony formation, invasion, and migration. Further investigation demonstrated that the expression of SCARA5 was negatively regulated by miR-141. Furthermore, the long non-coding RNA prostate cancer associated transcript 29 (PCAT29) inhibited the proliferation, invasion, and migration of BC cells by sponging miR-141. Luciferase activity assays revealed that PCAT29 targeted miR-141 and miR-141 targeted SCARA5. In conclusion, SCARA5, as a downstream factor of the PCAT29/miR-141 axis, inhibited the proliferation, migration, and invasion of BC cells. These findings provide novel insights into the detailed molecular mechanisms of BC development.

PDCD5 inhibits progression of renal cell carcinoma by promoting T cell immunity: with the involvement of the HDAC3/microRNA-195-5p/SGK1.

BACKGROUND: Epigenetics exerts a vital role in the onset and development of renal cell carcinoma (RCC). Mounting evidence has shed light on the significance of human immune system in response to tumor infiltrating T cells. Hereby, we sought to unmask the immunomodulatory role of histone deacetylase 3 (HDAC3) and its potential upstream molecule, programmed cell death 5 (PDCD5) in RCC. METHODS: RCC and adjacent non-cancerous tissues were clinically resected from 58 patients, in which the expression profile of microRNA-195-5p (miR-195-5p), PDCD5, HDAC3, and serum glucocorticoid-inducible kinase 1 (SGK1) was determined by RT-qPCR and Western blot analysis. Their relations were investigated by a series of luciferase assays in combination with ChIP and co-IP. RCC cells (A498) were intervened using gain- and loss-of-function approaches, followed by cell proliferation evaluation. After co-culture with CD3+ T cells, flow cytometry and interferon-γ (IFN-γ) determination were performed. A xenograft tumor mouse model was developed for in vivo validation. RESULTS: PDCD5 was downregulated in RCC tissues and A498 cells. Upregulation of HDAC3, as well as of SGK1, resulted in suppression of A498 cell proliferation and promotion of T cell activation as evidenced by higher IFN-γ expression. Re-expression of PDCD5 downregulated HDAC3, causing a subsequent upregulation of miR-195-5p, while miR-195-5p could inversely modulate its target gene, SGK1. The regulatory mechanism appeared to be functional in vivo. CONCLUSION: Our results highlight the possible manipulation by PDCD5 on RCC cell proliferation and T cell activation, which provides new clues to better understand the immune balance in RCC progression.

BMSC-derived exosomal lncRNA PTENP1 suppresses the malignant phenotypes of bladder cancer by upregulating SCARA5 expression.

LncRNAs can be transported to tumor cells where they exert regulatory effects by bone marrow mesenchymal stem cells (BMSC)-derived exosomes. Here, we aimed to investigate the functional mechanism of BMSC-derived exosomal lncRNA PTENP1 in the progression of bladder cancer (BC). Methods of BMSC were identified by detecting surface markers through flow cytometry. Exosomes from BMSC were identified by transmission electron microscopy, nanoparticle tracking analysis (NTA), and western blot analysis of exosome markers. Cellular internalization of BMSC-derived exosomes (BMSC-Exo) into BC cells was detected by confocal microscopy. CCK-8, colony formation, flow cytometry, wound healing, and transwell assays were adopted to estimate cell proliferation, apoptosis, migration, and invasion abilities, respectively. Interplay between miR-17 and lncRNA PTENP1 or SCARA5 was verified by dual-luciferase reporter, RNA pull down, and/or RNA immunoprecipitation (RIP) assays. Tumor xenograft assay was conducted in nude mice to study the role of exosomal lncRNA PTENP1 in BC progression in vivo. We showed exosomal lncRNA PTENP1 can be delivered into and suppress the malignant phenotypes of BC cells. LncRNA PTENP1 was identified as a sponge of miR-17, and SCARA5 was identified as a target gene of miR-17. The exosomes derived from PTENP1-overexpressing BMSC (BMSCOE-PTENP1-Exo) abolished the promotive effects of miR-17 overexpression or SCARA5 knockdown on the malignant phenotypes of BC cells. Moreover, exosomal lncRNA PTENP1 was demonstrated to inhibit BC tumor growth in nude mice by miR-17/SCARA5 axis. In conclusion, BMSC-derived exosomal PTENP1 suppressed the BC progression by upregulating the expression of SCARA5 via sponging miR-17, offering a potential novel therapeutic target for BC therapy.

Laminin-integrin a6b4 interaction activates notch signaling to facilitate bladder cancer development.

BACKGROUND: Laminins are high-molecular weight (400 ~ 900 kDa) proteins in extracellular matrix, which serve as major component of the basal lamina, and play a crucial role in promoting tumor cell migration. This study aimed at characterizing the role of laminin in promoting cancer development, and elucidating the mechanism of tumor progression driven by laminin-Notch signaling in bladder cancer. METHODS: 2D collagen/laminin culture system was established and CCK-8/transwell assay was conducted to evaluate the proliferation/migration ability of Biu-87 and MB49 cells cultured on 2D gels. Activation of integrins-Notch1 signaling was determined by western blotting. Orthotopic bladder cancer mice model was established to assess the therapeutic effects of Notch inhibitor. RESULTS: Our study demonstrated that extracellular laminin can trigger tumor cell proliferation/migration through integrin α6ß4/Notch1 signaling in bladder cancer. Inhibition of Telomere repeat-binding factor 3 (TRB3)/Jagged Canonical Notch Ligand 1 (JAG1) signaling suppressed Notch signals activation induced by laminin-integrin axis. In MB49 orthotopic bladder cancer mice model, Notch inhibitor SAHM1 efficiently improved tumor suppressive effects of chemotherapy and prolonged survival time of tumor-bearing mice. CONCLUSION: In conclusion, we show that, in bladder cancer, extracellular laminin induced the activation of Notch pathway through integrin α6ß4/TRB3/JAG3, and disclosed a novel role of laminin in bladder cancer cells proliferation or migration.

WITHDRAWN: SCARA5 regulated by MEG3/miR-141 axis attenuates proliferation, migration and invasion of bladder cancer.

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RB1CC1 functions as a tumor-suppressing gene in renal cell carcinoma via suppression of PYK2 activity and disruption of TAZ-mediated PDL1 transcription activation.

Rb1-inducible coiled-coil 1 (RB1CC1) has been demonstrated to function as an inhibitor of proline-rich/Ca-activated tyrosine kinase 2 (PYK2) by binding to the kinase domain of PYK2, which promotes the proliferation, invasion, and migration of renal cell carcinoma (RCC) cells. Additionally, in breast cancer, PYK2 positively regulates the expression of transcriptional co-activator with PDZ-binding motif (TAZ) which in turn can enhance PDL1 levels in breast and lung cancer cells. The current study was performed to decipher the impact of RB1CC1 in the progression of RCC via regulation of the PYK2/TAZ/PDL1 signaling axis. Expression of RB1CC1 and PYK2 was quantified in clinical tissue samples from RCC patients. The relationship between TAZ and PYK2, TAZ and PDL1 was then validated. The cellular processes of doxorubicin (DOX)-induced human RCC cell lines including the abilities of proliferation, colony formation, sphere formation and apoptosis, as well as the tumorigenicity of transfected cells, were evaluated after the alteration of RB1CC1 expression. RB1CC1 exhibited decreased expression in RCC tissues and was positively correlated with patient survival. RB1CC1 could inhibit the activity of PYK2, which in turn stimulated the stability of TAZ protein by phosphorylating TAZ. Meanwhile, TAZ protein activated PDL1 transcription by binding to the promoter region of PDL1. RB1CC1 overexpression or PYK2 knockdown could help everolimus (EVE) to inhibit tumor proliferation and activate immune response. Taken together, RB1CC1 can potentially augment the response of RCC cells to immunotherapy by suppressing the PYK2/TAZ/PDL1 signaling axis.

Core-shell ZnO@C:N hybrids derived from MOFs as long-cycling anodes for lithium ion batteries.

A core-shell hybrid of ZnO and nitrogen-doped carbon (ZnO@C:N) is designed as a long-cycling anode for LIBs. The ZnO@C:N hybrid has a high initial capacity of 1116 mA h g-1 and a reversible capacity of 608 mA h g-1 after 500 cycles at 0.1 A g-1. The unique core-shell structure, high conductivity due to nitrogen doping, and uniform solid electrolyte interphase (SEI) film formed in the electrode are revealed to result in the remarkable electrochemical performances of the ZnO@C:N electrodes.

Two-Dimensional SnSe2 /CNTs Hybrid Nanostructures as Anode Materials for High-Performance Lithium-Ion Batteries.

Tin diselenide (SnSe2 ), as an anode material, has outstanding potential for use in advanced lithium-ion batteries. However, like other tin-based anodes, SnSe2 suffers from poor cycle life and low rate capability due to large volume expansion during the repeated Li+ insertion/de-insertion process. This work reports an effective and easy strategy to combine SnSe2 and carbon nanotubes (CNTs) to form a SnSe2 /CNTs hybrid nanostructure. The synthesized SnSe2 has a regular hexagonal shape with a typical 2D nanostructure and the carbon nanotubes combine well with the SnSe2 nanosheets. The hybrid nanostructure can significantly reduce the serious damage to electrodes that occurs during electrochemical cycling processes. Remarkably, the SnSe2 /CNTs electrode exhibits a high reversible specific capacity of 457.6 mA h g-1 at 0.1 C and 210.3 mA h g-1 after 100 cycles. At a cycling rate of 0.5 C, the SnSe2 /CNTs electrode can still achieve a high value of 176.5 mA h g-1 , whereas a value of 45.8 mA h g-1 is achieved for the pure SnSe2 electrode. The enhanced electrochemical performance of the SnSe2 /CNTs electrode demonstrates its great potential for use in lithium-ion batteries. Thus, this work reports a facile approach to the synthesis of SnSe2 /CNTs as a promising anode material for lithium-ion batteries.

Hepatectomy for spontaneous rupture of hepatocellular carcinoma without portal triad clamping.

Hepatectomy without portal triad clamping may decrease the incidence of liver injury; however, the effects of hepatectomy without portal triad clamping in the treatment of spontaneous rupture of hepatocellular carcinoma (SRHCC) remain unclear. The aims of the present study were to evaluate the therapeutic value of hepatectomy without portal triad clamping in the treatment of patients with SRHCC. The present study retrospectively reviewed patients with SRHCC who received hepatectomy without portal triad clamping (non-clamping group) and the therapeutic efficacy was compared with that of 20 patients with SRHCC undergoing the same surgery in the presence of portal triad clamping (clamping group). Following hepatectomy, the non-clamping group exhibited a significantly lower incidence of acute liver failure compared with the clamping group (P<0.05). No significant differences in operative time, intra-operative blood loss, disease-free or overall survival times between the two groups were identified (all P>0.05). At 1 week and 2 weeks after surgery, the non-clamping group exhibited significantly lower alanine aminotransferase, aspartate aminotransferase and total bilirubin serum levels compared with the clamping group (all P<0.05). Hepatectomy without portal triad clamping may decrease the incidence of liver injury and liver failure in patients with SRHCC, suggesting that it may be a safe and effective therapeutic strategy.

ß-elemene inhibits the proliferation of T24 bladder carcinoma cells through upregulation of the expression of Smad4.

ß-elemene, a non-cytotoxic antitumor reagent, inhibits the growth, proliferation and DNA synthesis of multiple types of malignant cells, resulting in the apoptosis or suppressed vascularization of tumors. ß-elemene is also able to enhance the immunogenicity of the tumor cells and ameliorate systematic cellular immunity in the tumor­bearing body. Moreover, ß-elemene has the advantages of high efficiency, safety and low possibility of drug tolerance over other antitumor agents used in antitumor treatment. Therefore, ß-elemene has great potential in clinical applications. However, the mechanism of ß-elemene antitumor activity is largely unknown. The aim of this study was to investigate whether ß-elemene is able to repress the proliferation of T24 bladder carcinoma cells through regulation of the expression of the tumor suppressor gene, Smad4. Results of a methylthiazolyl tetrazolium (MTT) assay indicated that the proliferation of T24 cells was repressed by ß-elemene in a time- and concentration­dependent manner. The lowest concentration of ß-elemene to inhibit cell survival by >50% was determined using IC50 software. Microscopic observation also demonstrated the potential of ß-elemene to induce the apoptosis of cancer cells. Western blot and RT-PCR analyses revealed that the expression of the Smad4 protein and mRNA was upregulated by treatment with ß-elemene. Our results revealed that ß-elemene was able to upregulate the expression of Smad4 in tumor cells to inhibit the proliferation of these cells.

[Simultaneous inhibition of XIAP and survivin expression on EMT and invasion of human pancreatic cancer cells].

OBJECTIVE: To investigate the simultaneous inhibition of X-linked inhibitor of apoptosis protein (XIAP) and survivin expression on epithelial-mesenchymal transition (EMT) and invasiion of pancreatic cancer cells Panc-1, and its mechanism. METHODS: On the established human pancreatic cancer cells Panc-1-XS, the expression of XIAP and survivin was inhibited simultaneously. Cell invasion and migration were detected by Transwell chamber experiments and scratch test, and the expression of epithelial marker E-cadherin, mesenchymal markers Slug, phosphatase and tensin homolog deleted on chromosome ten (PTEN) and P-Akt protein was determined by Western blot. RESULTS: Cell invasion and migration of Panc-1-XS cells decreased significantly, accompanied by significantly upregulated protein expression of E-cadherin, and significantly declined protein expression of the Slug, indicating increased mesenchymal-epithelial conversion (MET); and increased protein expression of PTEN, and declined protein expression of P-Akt. CONCLUSION: Simultaneously inhibiting the expression of XIAP and survivin can partially reverse EMT phenotype of pancreatic cancer Panc-1 cells, which then significantly reduces the cell invasion and migration of Panc-1 cell lines. This process may be regulated by PTEN/PI3K/Akt signaling pathway.

Protective effect of low-molecular-weight heparin on pancreatic encephalopathy in severe acute pancreatic rats.

BACKGROUND AND AIMS: Pancreatic encephalopathy (PE) is a severe complication and significant cause of death in patients with severe acute pancreatitis (SAP). We have reported previously that low-molecular-weight heparin (LMWH) treatment could reduce incidence of PE in SAP patients. Our objective here was to investigate the protective effect of LMWH and its mechanism on PE in SAP rats. METHODS: SD rats were randomly divided into three groups: (1) Sham-operation (S) group, (2) SAP group, and (3) LMWH treatment (LMWH) group. LMWH was administrated 4 h after the SAP model conducted. The levels of serum amylase, myelin basic protein (MBP), tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), brain water content, occurrence of apoptosis, and pathological changes of pancreas and brain were measured at 1 day after models were set up in the SAP and S groups, and 1 day after LMWH treatment was administrated in the LMWH group. RESULTS: (1) The levels of serum amylase, TNF-α, and IL-6 in the SAP group were increased significantly more than those in the S and LMWH groups (all P < 0.001), as were the levels of serum MBP in the SAP group compared to those in the S and LMWH groups (P < 0.01, <0.05 respectively). However, while the level of serum amylase and IL-6 in the LMWH group were significantly increased compared to those in the S group (P < 0.05, <0.001 respectively), the levels of TNF-α and MBP showed no significant difference between the LMWH and S groups (all P > 0.05). (2) The brain water content in the SAP group was significantly increased compared to the S group and LMWH group (P < 0.01, <0.05 respectively). (3) Neuronal apoptosis, demyelination, and mitochondrial vacuolation in neuronal cells were observed in the SAP group; in contrast, in the LMWH group, significantly lower rates of neuronal apoptosis, demyelination and mitochondrial edema were observed in neuronal cells. CONCLUSIONS: The protective effect of LMWH on PE progression in SAP rats might result from inhibition of inflammatory activation and reduction of the occurrence of neuronal apoptosis.

Non-recurrent laryngeal nerve related to thyroid surgery: a report of 5 cases and literature review.

BACKGROUND: Non-recurrent laryngeal nerve, a rare anomaly, passes transversely into larynx with or without its recurrent branches directly arising from the vagus nerve. The paper investigates clinical significance of non-recurrent laryngeal nerve during thyroid surgery. Clinical data from 5 cases of non-recurrent laryngeal nerve and related literature reviews were made to acknowledge its incidence, variant types and matters concerned during thyroid operations. CASE REPORT: 821 recurrent laryngeal nerves were anatomized during 2496 thyroid operations, from which 5 were confirmed to hold non-recurrent laryngeal nerves (0.61%). 3 patients were found to have non-recurrent laryngeal nerves during re-operation because of voice horse after the first operation which improved much after re-operation. The other two patients were recognized during the first operation. All 5 cases were not diagnosed preoperatively. CONCLUSIONS: Non-recurrent laryngeal nerve, a rare anomaly, is very vulnerable during thyroid surgery. It is helpful to avoid injuring non-recurrent laryngeal nerve that identification of the non-recurrent laryngeal nerve and its types.

Effect of lower-molecular weight heparin in the prevention of pancreatic encephalopathy in the patient with severe acute pancreatitis.

OBJECTIVE: To study the effect of lower-molecular weight heparin in the prevention of pancreatic encephalopathy (PE) in the patient with severe acute pancreatitis (SAP). METHODS: Two hundred sixty-five SAP patients were randomly divided into 2 groups: (1) conventional treatment group (C group, n = 130) and (2) conventional treatment plus lower-molecular weight heparin treatment group (LT group, n = 135). The clinical parameters, laboratory parameters and computed tomographic (CT) score of pancreatic necrosis (CTSPN), incidence of PE, and mortality in the 2 groups were compared. RESULTS: On admission, all the clinical parameters, laboratory parameters, and CTSPN in the 2 groups were not significantly different (P > 0.05). However, 1 to 2 weeks after treatment, the symptoms and signs improvement rate, the levels of blood and urine amylase, the CT score, and the Acute Physiology and Chronic Health Evaluation II score in the LT group were obviously lower than those in the C group (P < 0.05-0.01), and PE occurrence rate, mortality, and mean hospital stay in LT group were obviously lower than those in the C group (P < 0.05-0.01). CONCLUSIONS: Lower-molecular weight heparin can enhance the effect of conventional treatment of SAP and can markedly decrease the PE incidence and improve the survival rate of SAP. Lower-molecular weight heparin is a simple, safe, less expensive, and effective method for treatment of SAP. It can be used in every hospital.

Low molecular weight heparin in the treatment of severe acute pancreatitis: a multiple centre prospective clinical study.

OBJECTIVE: To study the effect of low molecular weight heparin (LMWH) in the treatment of severe acute pancreatitis (SAP). METHODS: A total of 265 SAP patients were randomly divided into two groups: firstly, the conventional treatment group (C group, n = 130; and secondly the conventional treatment plus the LMWH treatment group (LT group, n = 135). The clinical parameters, laboratory parameters and computed tomography (CT) score of pancreatic necrosis (CTSPN) in the two groups were compared. RESULTS: On admission, all the clinical parameters, laboratory parameters and CTSPN in the two groups were not significantly different (p > 0.05). However, after treatment, in LT group, the clinical presentation improvement rate and laboratory parameters improvement were significantly higher than those in C group (p < 0.05-0.01), and the acute physiology and chronic health evaluation (APACHE) II score, complication rate, mortality and mean hospital stay in LT group were obviously lower than those in C group (p < 0.05-0.01). The CT score in LT group was much lower than that in C group (p < 0.05). Two weeks after treatment FBI decreased obviously in C group, but not in LT group, and no haemorrhagic complications occurred. CONCLUSIONS: LMWH can enhance the effect of conventional treatment for SAP, and can markedly decrease the mortality of SAP. LMWH is a simple, safe, economic and effective method for treatment of SAP. It is can be used in every hospital.

Effect of low molecular weight heparin on pancreatic micro-circulation in severe acute pancreatitis in a rodent model.

BACKGROUND: Alleviation of microcirculation disorders in severe acute pancreatitis (SAP) can improve survival rates, and low molecular weight heparin (LMWH) is well known to have potent ameliorative effect on microcirculation disorders caused by anti-coagulant activity. The aim of this study was to investigate the effects of LMWH on pancreatic microcirculation in SAP in rats. METHODS: SD rats were randomly divided into 3 groups: sham operation (S) group, SAP group, and LMWH treatment (LT) group. The concentrations of serum amylase, tumor necrosis factor-alpha (TNF-alpha), endothelin-1 (ET-1), pancreatic ultrastructure were examined at 24 hours after the models were set up in each group. RESULTS: Compared with S group, the concentration of serum amylase, ET-1, and TNF-alpha in SAP group were significantly increased (P < 0.001); After LMWH treatment, the concentration of serum amylase, ET-1, TNF-alpha were decreased significantly compared with SAP group (P < 0.001, 0.01, 0.001, respectively). On electron microscopy, the microthrombosis in LT group was significantly less than that in SAP group. The 3-day survival rate in SAP group (25.0%) was significantly lower than that in S group (100.0%, P < 0.05) and in LT group (87.5%, P < 0.05). CONCLUSIONS: The disorder of pancreatic microcirculation may be involved in the inflammatory response of rats with SAP. LMWH can effectively improve the survival rate of SAP, and alleviate the severity of microcirculation disorders through its antithrombin effects and down-regulate the levels of serum ET-1 and TNF-alpha.

Effect of normothermic liver ischemic preconditioning on the expression of apoptosis-regulating genes C-jun and Bcl-XL in rats.

AIM: To explore the expression of apoptosis-regulating genes C-jun and Bcl-XL after normothermic liver ischemic preconditioning and its protective effect on hepatocytes in the rat. METHODS: Wistar rats are randomly divided into sham operation group (S group, n = 10), ischemic reperfusion group (IR group, n = 10) and ischemic preconditioning group (IP group, n = 10). After dissection of the hepatoduodenal ligament in S group, and after 30-min reperfusion in IR group and in IP group, the samples of liver tissue were taken for studying the hepatocellular apoptosis, the expressions of C-jun mRNA, Bcl-XL mRNA and their proteins, and morphologic changes at 0, 3, 6, 20 h. Meanwhile the venous blood samples were drawn at 3, 6 and 20 h for testing ALT, AST and LDH. RESULTS: The levels of ALT, AST and LDH in IR group and IP group were significantly higher than those in S group. Hepatocellular apoptosis was significantly increased in both IR group and IP group, especially in IR group. Expressions of C-jun mRNA and protein were significantly increased in IR group compared with those in both IP group and S group, but no significant difference between IP group and S group (P>0.05). Expressions of Bcl-XL mRNA and protein in IR group and S group were not significant (P>0.05), but were significantly increased in IP group compared with those in both S group and IR group. Patch necrosis of hepatocytes because of severe injury could be seen in IR group microscopically, and the ultrastructural changes were irreversible. Meanwhile in IP group, no hepatocellular necrosis occurred, and the ultrastructural changes were reversible because of mild injury. CONCLUSION: (1) IP can protect the rat liver from normothermic IR injury by modulation of the expression of apoptosis-regulating genes C-jun and Bcl-XL; (2) IR injury may activate the apoptosis of hepatocytes by increasing the expression of apoptosis-inducing gene C-jun; (3) IP may prohibit the apoptosis of hepatocytes by increasing the expression of apoptosis-inhibitory gene Bcl-XL.

[Surgical treatment of recurrent laryngeal nerve injury caused by thyroid operation].

OBJECTIVE: To study the surgical treatment of recurrent laryngeal nerve (RLN) injury caused by thyroid operation. METHODS: From 1970 to 2001, 50 patients with RLN injury were caused by thyroid operation. The causes, location, type, operative procedures and follow-up were retrospectively analyzed. RESULTS: Unilateral RLN injury occurred in 46 cases and bilateral nerve injury in 4 cases. The RLN injuries were located within 2cm below the point of RLN entering to throat in 45 nerves (83.3%), other places in 6 nerves (11.3%), and unknown location in 3 nerves (5.4%). Transection of the nerve was found in 19 nerves (36.5%), suture or scare pressing the nerve in 35 nerves (64.8%). All the injured nerves were repaired surgically. Meanwhile all 4 patients with bilateral RLN injuries underwent tracheotomy. Of the 50 cases, 44 cases (88.0%) were followed up for more than 1.5 years. Among the 44 followed-up patients, phonation was restored to normal or obvious improvement in 42 cases (95.5%), and improvement in 2 (4.5%). Of the 35 patients with 39 nerves underwent indirect or direct laryngoscopy, the affected vocal cord movement entirely recovered in 21 cords (53.8%), partially recovered in 7 cords (17.9%), uncovered in 11 cords (28.3%). There was no relation between the recovery of phonation or vocal cord movement with the timing or the procedure of repairing operation. CONCLUSIONS: The location of most RLN injuries caused by thyroid surgery are just below the point of RLN entering to throat, and most are mechanical injury, and need operation to resolve the cause. Once the RLN injury is made, an operation should be performed as early as possible.

[Non-recurrent laryngeal nerve during thyroid surgery: a report of 4 cases and literature review].

OBJECTIVE: To investigate clinical significance of non-recurrent laryngeal nerve. METHODS: Clinical data from 4 cases of non-recurrent laryngeal nerve and related literature review was made to acknowledge its incidence, variant types and matters concerned during thyroid surgery. RESULTS: Seven hundred and nineteen recurrent laryngeal nerves were exposed during 2156 thyroid operations in Xiangya Hospital, from which 4 were confirmed to hold non-recurrent laryngeal nerves (0.56%). Two cases were found on the right side and the other 2 on the left. Among the 4 cases, 3 (patients) were found to have non-recurrent laryngeal nerves during reoperation because of voice horse after the first operation. The other one was recognized during the first operation. CONCLUSIONS: Non-recurrent laryngeal nerve, a rare anomaly, is very vulnerable during thyroid surgery. Knowing the related knowledge of the non-recurrent laryngeal nerve and its types is helpful to avoid its damage during thyroid surgery.