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AIM:To evaluate the relationship between dry eye disease(DED)and physical and mental health in teachers, and to explore its mechanism and propose intervention measures.METHODS:Cross-sectional study. A total of 183 teachers from three primary and secondary schools in the urban area of Linyi City, Shandong Province were enrolled in the study. DED symptoms were quantified using the ocular surface disease index(OSDI)questionnaire. A compact version of the depression, anxiety, and stress scale(DASS-21)was used to evaluate psychological state. The relationship between potential influencing factors and DED was evaluated by independent sample t-test of quantitative variables and χ2test of classified variables. Logistic regression analysis was used for multivariate analysis to determine the influencing factors of DED. Pearson correlation coefficient was used to analyze the correlation between OSDI score and depression, anxiety and stress.RESULTS: There were 183 teachers, including 44 males(24.0%)and 139 females(76.0%), aged from 22 to 57 years, with an average age of(34.2±8.6)years. The prevalence of DED was 60.0%(109/183; 95%CI 52.4%-66.7%). The prevalence of depression was 26.2%(48/183; 95%CI 19.8%-32.7%); anxiety prevalence was 39.3%(72/183; 95%CI 32.2%-46.5%); and stress prevalence was 23.0%(42/183; 95%CI 16.8%-29.1%). The univariate analysis showed that increased age, increased working years, increased visual display terminal(VDT)application time, longer written working hours, reduced sleep hours, less alcohol consumption, and high scores of depression, anxiety and stress were all factors affecting DED(all P<0.05). Using depression scores as the psychological index, multivariate Logistic regression analysis showed that years of work, VDT application time, written working hours, sleep time, alcohol consumption and depression score were the influencing factors of DED(all P<0.05); Using anxiety scores as the psychological index, multivariate Logistic regression analysis showed that years of work, VDT application time, written working hours and stress scores were the influencing factors of DED(all P<0.05); Using stress scores as the psychological index, multivariate Logistic regression analysis showed that years of work, VDT application time, written working hours and stress scores were the influencing factors of DED(all P<0.05). OSDI scores were positively correlated with depression, anxiety, and stress scores in the DED group(P<0.05)and across all participants(P<0.05). In the severe DED group, OSDI scores were positively related to depression, anxiety, and stress scores(P<0.05).CONCLUSION: The prevalence of DED is high among the teachers. Alcohol consumption, reduced sleep, longer working years, longer VDT usage and longer written working hours are the influencing factors of DED. In severe DED group, DED is highly correlated with depression, anxiety, and stress. We should pay attention to teachers' DED and related physical and mental health problems, and actively prevent and make early diagnosis and treatment.
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Objective:To summarize the institutional experiences of treating vascular complications caused by donor-derived infection(DDI)after kidney transplantation(KT).Methods:From January 1, 2015 to December 31, 2020, clinical data were retrospectively reviewed for 6 cases of vascular complications caused by DDI.Age, gender, surgical approaches, immunity induction therapy, immune suppression therapy, infection prevention, onset time of complication, type of complications, infection pathogens, therapeutic protocols and prognoses were summarized.Results:Six patients developed vascular complications caused by DDI in 997 KT recipients with an overall morbidity rate of 0.6%.In 3 cases, carbapenem resistant Klebsiella pneumoniae were positive in culture of secretion and blood samples.And Candida albicans was detected by blood cultures and pathological examinations.One case of antibiotic resistant Staphylococcus aureus was detected by blood culture.Among 3 cases of transplant kidney artery pseudoaneurysm on interventional therapy, there were curing(1 case)and immediate recurrent infection(2 cases). The latter two eventually died by cardiac complications.In 2 cases of arterial hemorrhage, graft nephrectomy was followed by hemodialysis.One case of transplanted renal artery stenosis was successfully cured by artery stenting and survived with normal graft function so far.Conclusions:Interventional endovascular therapy and open surgery are indicated for vascular complications caused by DDI post-KT.Interventional therapy may boost the odds of rescuing transplant kidney.However, clinicians should watch out for the risk of recurrent infection.Open surgery is an effective tool of eliminating infected focus.Preserving transplant kidney or nephrectomy may be adopted on the basis of specific conditions.
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Ubiquitin-specific peptidase 10 (USP10) protein is a deubiquitination enzyme involved in many important biological processes. However, the function of USP10 in hepatic ischaemic/reperfusion (I/R) injury remains unknown. The aim of this study was to explore the role of USP10 in hepatic I/R injury. USP10 Heterozygote mice and primary hepatocytes were used to construct hepatic I/R models. The effect of USP10 on hepatic I/R injury was examined via pathological and molecular analyses. Our results indicated that USP10 was significantly downregulated in the livers of mice after hepatic I/R injury and in hepatocytes subjected to hypoxia/reoxygenation stimulation. USP10 Heterozygote mice exhibited exacerbated hepatic I/R injury, as evidenced by enhanced liver inflammation via the NF-κB signalling pathway and increased hepatocyte apoptosis. Additionally, USP10 overexpression inhibited hepatocyte inflammation and apoptosis in hepatic I/R injury in vitro and in vivo. Mechanistically, our study demonstrated that USP10 knockdown exerted its detrimental effects on hepatic I/R injury by inducing activation of the transforming growth factor ß-activated kinase 1 (TAK1)-JNK/p38 signalling pathways. TAK1 was required for USP10 function in hepatic I/R injury as TAK1 inhibition abolished USP10 function in vitro. In conclusion, our study demonstrated that USP10 plays a protective role in hepatic I/R injury by inhibiting the activation of the TAK1-JNK/p38 signalling pathways. Modulation of USP10/TAK1 might be a promising strategy to prevent this pathological process.
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Liver Diseases/immunology , Liver/immunology , MAP Kinase Kinase Kinases/immunology , MAP Kinase Signaling System/immunology , Reperfusion Injury/immunology , Ubiquitin Thiolesterase/immunology , Animals , Liver/pathology , Liver Diseases/genetics , Liver Diseases/pathology , Liver Diseases/prevention & control , MAP Kinase Kinase Kinases/genetics , MAP Kinase Signaling System/genetics , Male , Mice , Reperfusion Injury/genetics , Reperfusion Injury/pathology , Reperfusion Injury/prevention & control , Ubiquitin Thiolesterase/geneticsABSTRACT
Objective:To summarize the clinical experiences of managing patients with novel coronavirus(2019-nCoV) infection after kidney transplantation.Methods:Clinical data were retrospectively analyzed for two patients with 2019-nCoV infection after renal transplantation in January 2020. Case 1 was a 48-year-old male with CMV pneumonia secondary to 2019-nCoV infection at 4 months post-transplantation. CT imaging showed multiple patchy ground-glass opacities of both lungs. Case 2 was a 59-year-old male who screened positive for 2019-nCoV nucleic acid due to fever at 9 days post-transplantation and he showed no clinical manifestations of pneumonia. After a definite diagnosis, case 1 was transferred to a designated hospital for isolation. Treatment regimens: cefoperazone sulbactam sodium plus linezolid for anti-infection, gamma globulin for enhancing immunity, methylprednisolone for controlling inflammatory responses and antiviral regimens of arbidol tablets plus lopina-velitonavir tablets. Case 2 was isolated in a single room. The treatment plan included cefoperazone sulbactam sodium for anti-infection, gamma globulin for enhancing immunity, arbidol for antiviral therapy and other symptomatic measures.Results:During a follow-up period of 3 weeks, case 1 recovered with renal dysfunction, nucleic acid test of nasopharyngeal swab turned negative and pulmonary imaging improved. Case 2 showed no obvious clinical symptoms and nucleic acid test of nasopharyngeal swab turned negative thrice.Conclusions:Renal transplant recipients should take precautions to avoid exposure to high-risk environments. A definite diagnosis should be made on the basis of clinical manifestations and results of nucleic acid test and pulmonary imaging. Currently there is no effective antiviral agent and symptomatic treatment is a major option.
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Objective@#To investigate the clinical experience of patients with novel coronavirus (2019-ncov) infection after kidney transplantation.@*Method@#Clinical data of two patients with 2019-nCoV infection after renal transplantationin Jan 2020 Renmin Hospital of Wuhan Universiyt were retrospectively analyzed.Case 1 was a 48-year-old male with CMV pneumonia secondary to 2019-nCoV infection at 4 months after transplantation. CT imaging showed multiple patchy ground-glass images of both lungs. Case 2 was a 59-year-old male, who was screened positive for 2019-nCoV nucleic acid due to fever at 9 days after renal transplantation and showed no clinical manifestations of pneumonia. After diagnosis, case 1 was transferred to a designated hospital for isolation. Treatment regimens: cefoperazone sulbactam sodium + linezolid to resist infection, gamma globulin to enhance immunity function, methylprednisolone to control inflammatory response, antiviral regimens including arbidol tablets + lopina-velitonavir tablets. Case 2 was treated with isolated treatment in a single room. The treatment plan included anti-infection (cefoperazone sulbactam sodium), enhancing immunity function (gamma globulin), antivirus therapy with arbidol and other symptomatic treatment.@*Result@#Follow up with 3 weeks, case 1 recovered with renal dysfunction, nucleic acid test with nasopharyngeal swabs turned negative, and pulmonary imaging improved. Case 2 showed no obvious clinical symptoms, and the nucleic acid test of nasopharyngeal swabs turned negative for 3 times.@*Conclusion@#Renal transplant recipients should receive fine protection to avoid exposure to high-risk environments. Diagnosis should be defined with combination of clinical manifestations, nucleic acid test and pulmonary imaging. At present, there are no antiviral drugs and symptomatic treatment is the main choice.
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Tripartite motif (Trim) 8 is an E3 ubiquitin ligase, interacting with and ubiquitinating diverse substrates, and is closely involved in innate immunity. However, the function of Trim8 in hepatic ischaemia/reperfusion (I/R) injury remains largely unknown. The aim of this study is to explore the role of Trim8 in hepatic I/R injury. Trim8 gene knockout mice and primary hepatocytes were used to construct hepatic I/R models. The effect of Trim8 on hepatic I/R injury was analysed via pathological and molecular analyses. The results indicated that Trim8 was significantly upregulated in liver of mice subjected to hepatic I/R injury. Trim8 knockout relieved hepatocyte injury triggered by I/R. Silencing of Trim8 expression alleviated hepatic inflammation responses and inhibited apoptosis in vitro and in vivo. Mechanistically, our study suggests that Trim8 deficiency may elicit hepatic protective effects by inhibiting the activation of transforming growth factor ß-activated kinase 1 (TAK1)-p38/JNK signalling pathways. TAK1 was required for Trim8 function in hepatic I/R injury as TAK1 activation abolished Trim8 function in vitro. In conclusion, our study demonstrates that Trim8 deficiency plays a protective role in hepatic I/R injury by inhibiting the activation of TAK1-dependent signalling pathways.
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Inflammation/metabolism , Nerve Tissue Proteins/metabolism , Signal Transduction/physiology , Ubiquitin-Protein Ligases/metabolism , Alanine Transaminase/genetics , Alanine Transaminase/metabolism , Animals , Apoptosis/genetics , Apoptosis/physiology , Aspartate Aminotransferases/genetics , Aspartate Aminotransferases/metabolism , Blotting, Western , Cells, Cultured , In Situ Nick-End Labeling , Inflammation/genetics , Male , Mice , Mice, Knockout , Nerve Tissue Proteins/genetics , Polymerase Chain Reaction , Signal Transduction/genetics , Ubiquitin-Protein Ligases/genetics , Ubiquitination/genetics , Ubiquitination/physiologyABSTRACT
PURPOSE: To investigate the long non-coding RNAs (lncRNAs) profile on renal ischemia reperfusion in a mouse model. METHODS: Microarray analysis was used to study the expression of misregulated lncRNA in a mouse model of renal ischemia reperfusion(I/R) with long ischemia time. Quantitative real-time PCR (qPCR) was used to verify the expression of selected lncRNAs and mRNAs.The potential functions of the lncRNA was analyzed by bioinformatics tools and databases. RESULTS: Kidney function was impaired in I/R group compared to the normal group. Analysis showed that a total of 2267 lncRNAs and 2341 messenger RNAs (mRNAs) were significantly expressed in I/R group (≥2.0-fold, p < 0.05).The qPCR result showed that lncRNAs and mRNAs expression were consistent with the microarray analysis. The co-expression network profile analysis based on five validated lncRNAs and 203 interacted mRNAs showed it existed a total of 208 nodes and 333 connections. The GO and KEEG pathway analysis results showed that multiple lncRNAs are involved the mechanism of I/R. CONCLUSION: Multiple lncRNAs are involved in the mechanism of I/R.These analysis results will help us to further understand the mechanism of I/R and promote the new methods targeted at lncRNA to improve I/R injury.
Subject(s)
Kidney/blood supply , RNA, Long Noncoding/analysis , RNA, Messenger/analysis , Reperfusion Injury/genetics , Animals , Down-Regulation , Gene Expression , Gene Expression Profiling , Gene Regulatory Networks , Mice , Mice, Inbred C57BL , Real-Time Polymerase Chain Reaction , Reference Values , Tissue Array Analysis/methods , Up-RegulationABSTRACT
Clear cell renal cell carcinoma (ccRCC) is one of the most common malignancies. Anti-silencing function 1B histone chaperone (ASF1B) has been reported to be involved in various diseases. However, its role in ccRCC is largely unknown. In the present study, using genetic data and clinical information obtained from the TCGA data portal and GEO database, we found that ASF1B was highly expressed in ccRCC cancer tissue compared with normal tissue, and ASF1B expression was positively correlated with tumor stage, tumor grade and patient survival. The function of ASF1B in cell proliferation and migration was assessed by pathological and molecular analyses. The results showed that ASF1B overexpression significantly enhanced the proliferation and migration of 786-O cells and Caki-1â¯cells, while silencing ASF1B expression significantly inhibited the proliferation and migration. In addition, ASF1B overexpression enhanced cell proliferation by upregulating PCNA and downregulating P27 expression and promoted cell migration by upregulating MMP2 and MMP9. Furthermore, the phosphorylation levels of protein kinase B (AKT) and P-P70 S6K1 were significantly upregulated in the ASF1B overexpression group. More importantly, AKT inhibitor blocked the promotional effect of ASF1B on proliferation and migration. In summary, the present study demonstrated that ASF1B overexpression promoted tumor cell proliferation and migration, which was dependent on the AKT/P70 S6K1 pathway.
Subject(s)
Carcinoma, Renal Cell/metabolism , Cell Cycle Proteins/metabolism , Kidney Neoplasms/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Signal Transduction , Carcinoma, Renal Cell/pathology , Cell Line, Tumor , Cell Movement , Cell Proliferation , Humans , Kidney Neoplasms/pathologyABSTRACT
Objective To explore the diagnosis and treatment of BKV nephropathy after renal transplantation .Methods A total of 62 patients with progressive creatinine elevation were routinely examined by blood and urine BKV-DNA . And 21 patients with positive results underwent graft biopsies for confirming a diagnosis .Results Among 21 cases of BKV infection ,20 cases received leflunomide in replacing mycophenolate mofetil (MMF) and a lower dose of tacrolimus .One case with urine (-) & blood (+ ) received sirolimus in replacing tacrolimus and a lower dose of MMF .Among 11 cases with urine (+ ) and blood (-) ,urinary BKV-DNA turned negative & creatinine decreased markedly (n= 4) ,urinary BKV-DNA load decreased & creatinine stablized (n= 4) ,death from pulmonary infection with hepatic & renal failure (n=1) ,urine BKV-DNA load decreased & creatine increased ( n = 1 ) , BKV – DNA load was not re-examined in 1 case of acute rejection and hydronephrosis with elevated creatine ;Among 9 cases with urine (+ ) & blood (+ ) ,blood BKV-DNA turned negative with urinary BKV-DNA load & creatine decreased (n= 6) ,blood BKV-DNA load decreased & creatine stablized (n=2) and no re-examination with a stable level of creatine (n=1);One case with urine (-) & blood (+ ) was not timely treated and ultimately leading to graft loss after an onset of acute rejection .Conclusions BKV nephropathy may be effectively treated by decreasing immunosuppressive intensity . However ,clinicians should stay on a high alert for acute rejection due to an excessive reduction of immunosuppressive agents .
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Objective@#To explore the diagnosis and treatment of BKV nephropathy after renal transplantation.@*Methods@#A total of 62 patients with progressive creatinine elevation were routinely examined by blood and urine BKV-DNA. And 21 patients with positive results underwent graft biopsies for confirming a diagnosis.@*Results@#Among 21 cases of BKV infection, 20 cases received leflunomide in replacing mycophenolate mofetil (MMF) and a lower dose of tacrolimus. One case with urine (-) & blood (+ ) received sirolimus in replacing tacrolimus and a lower dose of MMF. Among 11 cases with urine (+ ) and blood (-), urinary BKV-DNA turned negative & creatinine decreased markedly (n=4), urinary BKV-DNA load decreased & creatinine stablized (n=4), death from pulmonary infection with hepatic & renal failure (n=1), urine BKV-DNA load decreased & creatine increased (n=1), BKV–DNA load was not re-examined in 1 case of acute rejection and hydronephrosis with elevated creatine; Among 9 cases with urine (+ ) & blood (+ ), blood BKV-DNA turned negative with urinary BKV-DNA load & creatine decreased (n=6), blood BKV-DNA load decreased & creatine stablized (n=2) and no re-examination with a stable level of creatine (n=1); One case with urine (-) & blood (+ ) was not timely treated and ultimately leading to graft loss after an onset of acute rejection.@*Conclusions@#BKV nephropathy may be effectively treated by decreasing immunosuppressive intensity. However, clinicians should stay on a high alert for acute rejection due to an excessive reduction of immunosuppressive agents.
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Abstract Purpose: To investigate the long non-coding RNAs (lncRNAs) profile on renal ischemia reperfusion in a mouse model. Methods: Microarray analysis was used to study the expression of misregulated lncRNA in a mouse model of renal ischemia reperfusion(I/R) with long ischemia time. Quantitative real-time PCR (qPCR) was used to verify the expression of selected lncRNAs and mRNAs.The potential functions of the lncRNA was analyzed by bioinformatics tools and databases. Results: Kidney function was impaired in I/R group compared to the normal group. Analysis showed that a total of 2267 lncRNAs and 2341 messenger RNAs (mRNAs) were significantly expressed in I/R group (≥2.0-fold, p < 0.05).The qPCR result showed that lncRNAs and mRNAs expression were consistent with the microarray analysis. The co-expression network profile analysis based on five validated lncRNAs and 203 interacted mRNAs showed it existed a total of 208 nodes and 333 connections. The GO and KEEG pathway analysis results showed that multiple lncRNAs are involved the mechanism of I/R. Conclusion: Multiple lncRNAs are involved in the mechanism of I/R.These analysis results will help us to further understand the mechanism of I/R and promote the new methods targeted at lncRNA to improve I/R injury.
Subject(s)
Animals , Rats , RNA, Messenger/analysis , Reperfusion Injury/genetics , RNA, Long Noncoding/analysis , Kidney/blood supply , Reference Values , Down-Regulation , Gene Expression , Up-Regulation , Gene Expression Profiling , Tissue Array Analysis/methods , Gene Regulatory Networks , Real-Time Polymerase Chain Reaction , Mice, Inbred C57BLABSTRACT
Objective To analyze the reasons and outcomes of the unplanned re-operation in renal transplant recipients during perioperative period,and to summarize the corresponding strategies.Methods From January 2014 to September 2017,the clinical data of 20 cases of kidney transplantation which had a total of 22 unplanned re-operations were retrospectively analyzed.All patients were given quadruple immunosuppression with antibody induction and tacrolimus (TAC) and mycophenolate mofetil (MMF) plus prednisone (Pred).We analyzed the reasons,occurrence time,effect of re-operation and the renal function,as well as survival rate of all graft and recipient.The delayed graft function (DGF),acute rejection (AR) and incidence of pulmonary infection were monitored as well.Results Up to September 2017,during the follow-up of 1-36 months,the overall rate of unplanned re-operation was 4.6%,and 2 patients underwent 3 operations.For the reasons of re-operation,there were 18 cases of bleeding (13 cases of blood oozing from the wound surface,3 cases of renal parenchyma rupture because of rejection,and 2 cases of rupture of renal artery infection),2 cases of renal artery thrombosis and 2 cases of the repair of leakage of urine.Two operations were performed within 1 days for 9 cases,2-5 days for 5 cases,6-10 days for 3 cases,above 10 days for 45 cases.There was no deaths during the perioperative period.One patient died of rupture of exiliac aneurysm 3 months after the operation.One patient died of cerebral hemorrhage 6 months postoperation.The death censored graft survival rate was 72.2% (13/18) and the incidence of DGF was 55 %.Conclusion The major reason of unplanned re-operation for renal transplantation is associated with bleeding of various causes.And the incidence of DGF is high.If the secondary operation was performed with the correct decision,the kidney allograft recovers well.