RESUMO
This novel report presents the first known case, to our knowledge, of a 16-year-old male patient who experienced intraventricular thrombosis and pulmonary embolism after a Nuss procedure for pectus excavatum, attributed to chronic bar displacement. Two years after the operation, the patient experienced post-exercise cough and hemoptysis, which led to his admission. Imaging revealed pulmonary embolism, thrombosis in the right ventricular outflow tract, and lung infiltrative lesions. We hypothesize that the chronic bar displacement led to its embedment in the right ventricle, resulting in thrombus formation, which subsequently contributed to partial pulmonary embolism. Surgery revealed the bars' intrusion into the right ventricle and lung. This case highlights the risk of severe complications from bar displacement in the Nuss procedure, which necessitates long-term follow-up evaluation, caution against strenuous activities after surgery, and use of thoracoscopic guidance during bar implantation and removal. It underscores the importance of vigilant evaluation for late-stage complications in patients with respiratory distress or thrombosis after a Nuss procedure.
Assuntos
Tórax em Funil , Embolia Pulmonar , Trombose , Humanos , Embolia Pulmonar/etiologia , Embolia Pulmonar/diagnóstico , Masculino , Adolescente , Tórax em Funil/cirurgia , Trombose/etiologia , Trombose/diagnóstico por imagem , Trombose/diagnóstico , Ventrículos do Coração/diagnóstico por imagem , Complicações Pós-Operatórias/etiologia , Complicações Pós-Operatórias/diagnóstico , Tomografia Computadorizada por Raios XRESUMO
Estrogen receptor 1 (ESR1) has been recently demonstrated as a potential diagnostic biomarker for thoracic aortic aneurysm (TAA). However, its precise role in the progression of TAA remains unclear. In this study, TAA models were established in ApoE-knockout mice and primary mouse vascular smooth muscle cells (VSMCs) through treatment with angiotensin (Ang) II. Our findings revealed a downregulation of ESR1 in Ang II-induced TAA mice and VSMCs. Upregulation of ESR1 mitigated expansion and cell apoptosis in the mouse aorta, reduced pathogenetic transformation of VSMCs, and reduced inflammatory infiltration and oxidative stress both in vitro and in vivo. Furthermore, we identified macrophage migration inhibitory factor (MIF) as a biological target of ESR1. ESR1 bound to the MIF promoter to suppress its transcription. Artificial MIF restoration negated the mitigating effects of ESR1 on TAA. Additionally, we discovered that murine double minute 2 (MDM2) was highly expressed in TAA models and mediated protein degradation of ESR1 through ubiquitination modification. Silencing of MDM2 reduced VSMC dedifferentiation and suppressed oxidative stress. However, these effects were reversed upon further silencing of ESR1. In conclusion, this study demonstrates that MDM2 activates MIF by mediating ESR1 degradation, thus promoting VSMC dedifferentiation and oxidative stress during TAA progression.
Assuntos
Aneurisma da Aorta Torácica , Fatores Inibidores da Migração de Macrófagos , Animais , Camundongos , Músculo Liso Vascular/metabolismo , Proteínas Proto-Oncogênicas c-mdm2/metabolismo , Fatores Inibidores da Migração de Macrófagos/genética , Fatores Inibidores da Migração de Macrófagos/metabolismo , Desdiferenciação Celular/genética , Receptor alfa de Estrogênio/metabolismo , Aneurisma da Aorta Torácica/metabolismo , Aneurisma da Aorta Torácica/patologia , Estresse OxidativoRESUMO
BACKGROUND: Acute kidney injury (AKI) is a common complication after cardiac surgery. This study aims to develop and validate a risk model for predicting AKI after cardiac valve replacement surgery. METHODS: Data from patients undergoing surgical valve replacement between January 2015 and December 2018 in our hospital were retrospectively analyzed. The subjects were randomly divided into a derivation cohort and a validation cohort at a ratio of 7:3. The primary outcome was defined as AKI within 7 days after surgery. Logistic regression analysis was conducted to select risk predictors for developing the prediction model. Receiver operator characteristic curve (ROC), calibration plot and clinical decision curve analysis (DCA) will be used to evaluate the discrimination, precision and clinical benefit of the prediction model. RESULTS: A total of 1159 patients were involved in this study. The prevalence of AKI following surgery was 37.0% (429/1159). Logistic regression analysis showed that age, hemoglobin, fibrinogen, serum uric acid, cystatin C, bicarbonate, and cardiopulmonary bypass time were independent risk factors associated with AKI after surgical valve replacement (all P < 0.05). The areas under the ROC curves (AUCs) in the derivation cohort and the validation cohort were 0.777 (95% CI 0.744-0.810) and 0.760 (95% CI 0.706-0.813), respectively. The calibration plots indicated excellent consistency between the prediction probability and actual probability. DCA demonstrated great clinical benefit of the prediction model. CONCLUSIONS: We developed a prediction model for predicting AKI after cardiac valve replacement surgery that was internally validated to have good discrimination, calibration, and clinical practicability.
Assuntos
Injúria Renal Aguda , Procedimentos Cirúrgicos Cardíacos , Humanos , Estudos Retrospectivos , Ácido Úrico , Injúria Renal Aguda/diagnóstico , Injúria Renal Aguda/epidemiologia , Injúria Renal Aguda/etiologia , Procedimentos Cirúrgicos Cardíacos/efeitos adversos , Fatores de Risco , Valvas Cardíacas , Medição de Risco , Complicações Pós-Operatórias/diagnóstico , Complicações Pós-Operatórias/epidemiologia , Complicações Pós-Operatórias/etiologia , Curva ROCRESUMO
BACKGROUNDS: Hyperlactatemia is a common metabolic disorder after cardiac surgery with cardiopulmonary bypass. Epinephrine use has been identified as a potential cause of increased lactate levels after cardiac surgery. Stress can lead to an increase in catecholamines, mainly epinephrine, in the body. Exogenous epinephrine causes hyperlactatemia, whereas endogenous epinephrine released by stress may have the same effect. Opioids are the most effective anesthetics to suppress the stress response in the body. The authors sought to provide evidence through a retrospective data analysis that helps investigate the relationship between intraoperative opioid dosage and postoperative lactic acidosis after cardiac surgery. METHODS: The clinical data of 215 patients who underwent valvular heart surgery with cardiopulmonary bypass from July 2016 to July 2019 were analyzed retrospectively. Blood lactate levels were measured at 0.1 h, 2 h, 4 h, and 8 h after surgery. Patients with continuous increases in lactate levels and lactate levels exceeding 5 mmol/L at two or more time points were included in the lactic acidosis group, whereas the other patients were included in the control group. First, univariate correlation analysis was used to identify parameters that were significantly different between the two groups, and then multivariate regression analysis was conducted to elucidate the independent risk factors for lactic acidosis. Fifty-one pairs of patients were screened by propensity score matching analysis (PSM). Then, lactic acid levels at four time points in both groups were analyzed by repeated measures ANOVA. RESULTS: he EF (heart ejection fraction) (OR = 0.94, P = 0.003), aortic occlusion time (OR = 10.17, P < 0.001) and relative infusion rate (OR = 2.23, P = 0.01) of sufentanil was an independent risk factor for lactic acidosis after valvular heart surgery. The patients were further divided into two groups with the mean sufentanil infusion rate as the reference point. The data were filtered with PSM (Propensity Score Matching). Lactic acid values in both groups peaked at 4 h after surgery and then declined. The rate of lactic acid decline was significantly faster in the group with a higher sufentanil dosage than in the lower group. The difference was statistically significant (P < 0.05). There was also a significant difference in lactic acid levels at the four time points (0.1 h, 2 h, 4 h and 8 h after surgery) in both groups (P < 0.001). CONCLUSION: The inadequate intraoperative infusion rate of sufentanil is an independent risk factor for lactic acidosis after heart valve surgery. The possibility of lactic acidosis caused by this factor after cardiac surgery should be considered, which is helpful for postoperative patient management.
Assuntos
Acidose Láctica , Procedimentos Cirúrgicos Cardíacos , Hiperlactatemia , Acidose Láctica/induzido quimicamente , Analgésicos Opioides/efeitos adversos , Procedimentos Cirúrgicos Cardíacos/efeitos adversos , Epinefrina , Valvas Cardíacas/cirurgia , Humanos , Hiperlactatemia/induzido quimicamente , Ácido Láctico , Masculino , Estudos Retrospectivos , Fatores de Risco , Sufentanil/efeitos adversosRESUMO
Cardiopulmonary bypass (CPB), though indispensable in many cardiac surgery procedures, has several undesirable consequences. The aim of this study was to identify potential genes that may reduce the inflammatory response and complications after CPB. The GSE132176 dataset was selected from the Gene Expression Omnibus (GEO) database and included 10 patients with tetralogy of Fallot and 10 patients with an atrial septal defect who underwent CPB surgery. TSV files were downloaded after GEO2R processing. Protein-protein interaction analysis of common differentially expressed genes (DEGs) was performed using the Search Tool for the Retrieval of Interacting Genes. Gene modules and hub genes were visualized in the protein-protein interaction network using Cytoscape. Enrichment analysis was performed for all important DEGs, modular genes, and hub genes. A total of 72 DEGs were screened, including two functional and one hub gene module. FOS modular genes were primarily enriched in NGF-stimulated transcription, spinal cord injury, and PID AP1 pathway. The ATF3 modular gene was mainly enriched in cytomegalovirus infection and transcriptional misregulation in cancer. Hub gene modules were primarily enriched in the PID AP1 pathway, positive regulation of pri-miRNA transcription by RNA polymerase II, and the PID ATF2 pathway. FOS, JUN, ATF3, and EGR1 were the four most important hub genes; the top three hub genes were involved in the formation of AP-1 and enriched in the AP-1 pathway. Finally, we measured the expression levels of these four genes in patients undergoing CPB via qRT-PCR, and the results were consistent with those obtained in bioinformatic analysis. FOS, JUN, ATF3, and EGR1 and the AP-1 pathway may play key roles in inflammation and complications caused by CPB.
Assuntos
Biologia Computacional , Perfilação da Expressão Gênica , Ponte Cardiopulmonar/efeitos adversos , Biologia Computacional/métodos , Perfilação da Expressão Gênica/métodos , Humanos , Inflamação/genética , Inflamação/prevenção & controle , Fator de Transcrição AP-1RESUMO
BACKGROUND: Nonsmall cell lung cancer (NSCLC) is one of the leading incidence and mortality of malignant tumors worldwide. While aberrant DNA methylation is a frequent event occurred during NSCLC carcinogenesis and development, therefore holding the potential to predict the process of tumor development. This study aims to explore the feasibility of gene nidogen 2 (NID2) as the diagnostic biomarker for NSCLC. MATERIALS AND METHODS: Quantitative methylation specific polymerase chain reaction of NID2 has been done among the following sample panels: For tissue methylation evaluation, we collected 96 cases of NSCLC versus 18 cases of noncancerous lung lesions (NCLLs); 46 from the 96 NSCLC patients also provided DNA of bronchoalveolar lavage (BAL) and plasma sample, the methylation status of which are assessed against 12 cases of NCLL for BAL and 30 cases of NCLL for plasma samples, respectively. RESULTS: The methylation rate of NID2 in NSCLC versus NCLL is evaluated as: In tissue 59.40% versus 16.67%, (P = 0.0001); in BAL 30.43% versus 16.67% (P = 0.1640); in plasma 45.65% versus 20.00% (P = 0.0191). CONCLUSIONS: Our study revealed the frequent occurrence of aberrant NID2 methylation in NSCLC and peripheral blood, which might be useful as a biomarker to predict NSCLC or to screen the high-risk population for NSCLC.
Assuntos
Biomarcadores Tumorais/genética , Líquido da Lavagem Broncoalveolar/química , Carcinoma Pulmonar de Células não Pequenas/diagnóstico , Moléculas de Adesão Celular/genética , Metilação de DNA , DNA/genética , Neoplasias Pulmonares/diagnóstico , Adenocarcinoma/diagnóstico , Adenocarcinoma/genética , Proteínas de Ligação ao Cálcio , Carcinoma Pulmonar de Células não Pequenas/genética , Carcinoma de Células Escamosas/diagnóstico , Carcinoma de Células Escamosas/genética , Estudos de Casos e Controles , DNA/análise , Feminino , Seguimentos , Humanos , Neoplasias Pulmonares/genética , Masculino , Pessoa de Meia-Idade , Prognóstico , Regiões Promotoras GenéticasRESUMO
Effector memory T cells (TEM) are a subset of memory T cells which play an important role in stimulation of adaptive immunity. Although they are associated with multiple immune responses, the antitumor effect of TEM is not clearly understood. In this research, generation of anti-tumor TEM was induced through skin allografts in C57BL/6 mice with B16 melanoma. We observed that the growth of tumor tissues in C57BL/6 mice treated with allografts was interrupted. Furthermore, the survival time for the treated mice was prolonged along with increased serum levels for CXCL9, CXCL10 and INF-γ. Additionally, the concentrations of TEM in the spleens, lymph nodes and tumor tissues were markedly elevated in allografts treated mice. The tumor cell proliferation and tissue growth were suppressed in C57BL/6 mice with B16 melanoma induced by allografts, upon tail vein injection of purified TEM. These results demonstrate that skin allografts promote the generation of anti-tumor TEM in C57BL/6 mice with B16 melanoma, which emphasize the strong promise of TEM stimulation using allografts transplants in effective tumor immunotherapy.
Assuntos
Aloenxertos , Melanoma Experimental , Animais , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Linfócitos T , Transplante HomólogoRESUMO
BACKGROUND: Anti-CD105 mAb-conjugated immunoliposomes, loaded with secreted mouse endostatin gene, were developed for targeted tumor imaging and antiangiogenic gene therapy. METHODS: The liposomes were investigated for size, zeta-potential, lipid content, antibody binding ability, and pcDNA loading capacity. The ability of immunoliposomes to target tumor-derived endothelial cells and perform gene transfer in vitro was measured and their basic biocompatibility was evaluated. A nude mouse/breast cancer xenograft model was used to examine the tumor internalization of fluorescent-labeled liposomes and the clinical potential of immnuoliposomes loaded with pcDNA3.1-CSF1-endostatin. RESULTS: Loaded immunoliposomes were homogenously distributed with a well-defined spherical shape and bilayer, diameter of 122 ± 11 nm, and zeta potential + 1.40 mV. No significant differences were observed in body weight, liver index, oxidative stress, or liver and kidney function in mice after liposomes exposure. The addition of CD105 mAb to liposomes conferred the ability to target tumor-derived endothelial cells in vitro and in vivo. Systemic intravenous administration of fluorescent immunoliposomes in the xenograft model resulted in selective and efficient internalization in tumor vasculature. Treatment of mice with pcDNA3.1-CSF1-endostatin-loaded immunoliposomes suppressed tumor growth by 71%. CONCLUSIONS: These data demonstrate the advantages of using anti-CD105 mAb-conjugated immunoliposomes to enhance tumor targeting, imaging, and gene transfer applications.
Assuntos
Anticorpos Monoclonais/administração & dosagem , Endoglina/antagonistas & inibidores , Endostatinas/genética , Lipossomos , Imagem Molecular , Neoplasias/diagnóstico , Neoplasias/genética , Animais , Linhagem Celular Tumoral , Cromatografia Líquida de Alta Pressão , Modelos Animais de Doenças , Endostatinas/biossíntese , Feminino , Técnicas de Transferência de Genes , Terapia Genética , Glutationa/metabolismo , Humanos , Lipossomos/química , Lipossomos/ultraestrutura , Camundongos , Neoplasias/terapia , Imagem Óptica/métodos , Plasmídeos/química , Plasmídeos/genética , Superóxido Dismutase/metabolismo , Espectrometria de Massas em Tandem , TransgenesRESUMO
OBJECTIVE: To report a rare type of aortic arch aneurysm. METHODS: Three cases of aortic arch aneurysm derived from the fourth aortic arch were retrospectively analyzed. The pathogenesis and treatment of this type of aortic arch aneurysm were investigated. RESULTS: Most of the aneurysm body was located in the Z2 zone, which was the stem from the fourth aortic arch in the embryonic development period. All of the 3 cases could not be explained by common etiology. We speculated that the cause might be developmental anomaly of the fourth aortic arch. All the 3 aortic arch aneurysms were totally excluded with a covered stent. The technical success rate was 100%. Endoleak of type I was seen in one case, which was resolved in a later open surgery. During the follow-up, no type of complications was found. CONCLUSION: To the best of our knowledge, this is the first report of this type of aortic arch aneurysm. The cause may be developmental anomaly of the fourth aortic arch. Endovascular treatment of this type of aortic arch aneurysm is feasible.
Assuntos
Aneurisma da Aorta Torácica , Implante de Prótese Vascular , Humanos , Estudos Retrospectivos , Stents , Resultado do TratamentoRESUMO
Epidermal growth factor receptor (EGFR) is a member of the tyrosine kinase receptor family, which is thought to be involved in the development of cancer, as the EGFR gene is often amplified, and/or mutated in cancer cells. Lung cancer remains one of the most major causes of morbidity and mortality worldwide, accounting for more deaths than any other cancer cause. Gene polymorphism factor has been reported to be an important factor which increases the susceptibility of lung cancer. There lacks a well-documented diagnostic approach for the lung cancer risk, and the etiology of lung cancer is not clear. The current systematic review was performed to explore the association of EGFR gene polymorphism with lung cancer risk. In this review, association of EGFR 181946C > T, 8227G > A gene polymorphism with lung cancer was found, and EGFR Short genotype of cytosine adenine repeat number polymorphism was significantly associated with an increased risk of lung cancer.
Assuntos
Receptores ErbB/genética , Predisposição Genética para Doença/epidemiologia , Predisposição Genética para Doença/genética , Neoplasias Pulmonares/epidemiologia , Neoplasias Pulmonares/genética , Polimorfismo de Nucleotídeo Único/genética , Estudos de Associação Genética , Marcadores Genéticos/genética , Humanos , Prevalência , Reprodutibilidade dos Testes , Medição de Risco , Sensibilidade e EspecificidadeRESUMO
The relationship between glutathione S-transferase T1 (GSTT1) null/presence gene polymorphism and the risk of lung cancer from the published reports are still conflicting. This study was conducted to evaluate the relationship between GSTT1 null/presence gene polymorphism and the risk of lung cancer using meta-analysis method. The association studies were identified from PubMed, and Cochrane Library on July 1, 2012, and eligible investigations were included and synthesized using meta-analysis method. 51 reports were recruited into this meta-analysis for the association of null genotype of GSTT1 with lung cancer susceptibility, consisting of 15,140 patients with lung cancer and 16,662 controls. There was a marked association between GSTT1 null genotype and lung cancer risk in overall populations (OR = 1.15, 95 % CI 1.04-1.27, P = 0.007). Furthermore, GSTT1 null genotype was associated with the lung cancer risk in Asians (OR = 1.47, 95 % CI 1.23-1.76, P < 0.0001). However, GSTT1 null genotype was not associated with the risk of lung cancer in Caucasians, Brazilian population and Africans. In conclusion, GSTT1 null genotype is associated with the lung cancer in overall populations and in Asians.
Assuntos
Predisposição Genética para Doença , Glutationa Transferase/genética , Neoplasias Pulmonares/genética , Polimorfismo Genético , Povo Asiático/genética , População Negra/genética , Brasil , Estudos de Associação Genética , Humanos , Viés de Publicação , Fatores de Risco , População Branca/genéticaRESUMO
BACKGROUND: Results of the published reports on the relationship between glutathione S-transferase P1 (GSTP1) gene polymorphism and the adenocarcinomas of lung cancer are still debated. OBJECTIVE: This meta-analysis was performed to evaluate the association between GSTP1 A/G gene polymorphism and the risk of adenocarcinomas of lung cancer. METHODS: The association investigations were identified from PubMed and Cochrane Library, and eligible studies were included and synthesized using meta-analysis method. RESULTS: 16 reports were included into this meta-analysis for the association of GSTP1 A/G gene polymorphism and the risk of adenocarcinomas of lung cancer. The G allele and GG genotype were not associated with the susceptibility of risk of adenocarcinomas. Furthermore, in the sensitivity analysis, the results were similar with those from the non-sensitivity analysis. CONCLUSIONS: GSTP1 G allele or GG genotype is not a biomarker to be associated with the susceptibility of adenocarcinomas of lung cancer.
Assuntos
Adenocarcinoma/enzimologia , Adenocarcinoma/genética , Glutationa S-Transferase pi/genética , Neoplasias Pulmonares/enzimologia , Neoplasias Pulmonares/genética , Adenocarcinoma de Pulmão , Predisposição Genética para Doença , Humanos , Polimorfismo Genético , Fatores de RiscoRESUMO
The conclusions of the published reports on the relationship between glutathione S-transferase P1 (GSTP1) A/G gene polymorphism and the histological types of lung cancer are still debated. GSTP1 is one of the important mutant sites reported at present. This meta-analysis was performed to evaluate the association between GSTP1 and histological types of lung cancer. The association investigations were identified from PubMed and Cochrane Library, and eligible studies were included and synthesized using meta-analysis method. Seventeen reports were included into this meta-analysis for the association of GSTP1 A/G gene polymorphism and histological types of lung cancer. The G allele and GG genotype were not associated with the susceptibility of risk of squamous cell carcinomas, adenocarcinomas, small cell carcinoma, non-small cell carcinoma or large cell carcinoma. However, in the sub-group analysis, there was an association between G allele/GG genotype with the risk of squamous cell carcinomas in East-Asians and GG genotype was associated with the risk of small cell carcinoma in Caucasians. In conclusion, GSTP1 A/G gene polymorphism is not associated with the susceptibility of squamous cell carcinomas, adenocarcinomas, small cell carcinoma, non-small cell carcinoma or large cell carcinoma.
Assuntos
Predisposição Genética para Doença , Glutationa S-Transferase pi/genética , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patologia , Polimorfismo Genético , Adenocarcinoma/genética , Carcinoma de Células Grandes/genética , Carcinoma de Células Escamosas/genética , Humanos , Razão de Chances , Viés de Publicação , Risco , Carcinoma de Pequenas Células do Pulmão/genéticaRESUMO
OBJECTIVE: The conclusions of published reports on the relationship between the glutathione S-transferase M3 (GSTM3) A/B gene polymorphism and the risk of lung cancer are still debated. This meta-analysis was performed to evaluate the association between GSTM3 and the risk of lung cancer. METHODS: Association investigations were identified from PubMed, Embase, and Cochrane Library, and eligible studies were included and synthesized using a meta-analysis method. RESULTS: Eight reports were included into this meta-analysis for the association of GSTM3 A/B gene polymorphism and lung cancer susceptibility, covering 1,854 patients with lung cancer and 1,926 controls. No association between the GSTM3 A/B gene polymorphism and lung cancer was found in this meta-analysis (B allele: OR = 1.25, 95% CI: 0.89-1.76, P = 0.20; BB genotype: OR = 1.53, 95% CI: 0.71-3.32, P = 0.28; AA genotype: OR = 0.85, 95% CI: 0.59-1.23, P = 0.39). CONCLUSIONS: The GSTM3 A/B gene polymorphism is not associated with lung cancer susceptibility. However, more studies on the relationship between GSTM3 A/B gene polymorphism and the risk of lung cancer should be performed in the future.
Assuntos
Glutationa Transferase/genética , Neoplasias Pulmonares/genética , Alelos , Estudos de Casos e Controles , Intervalos de Confiança , Predisposição Genética para Doença , Genótipo , Proteínas de Homeodomínio , Humanos , Isoenzimas/genética , Polimorfismo GenéticoRESUMO
The conclusions of the published reports on the relationship between glutathione S-transferase P1 (GSTP1) gene polymorphism and the risk of lung cancer are still debated. GSTP1 is one of the important mutant sites reported at present. This meta-analysis was performed to evaluate the association between GSTP1 and the risk of lung cancer. The association investigations were identified from PubMed and Cochrane Library, and eligible studies were included and synthesized using meta-analysis method. Forty-four reports were included into this meta-analysis for the association of GSTP1 A/G gene polymorphism and lung cancer susceptibility, consisting of 12,363 patients with lung cancer and 13,948 controls. The association between GSTPI G allele and lung cancer risk was found in this meta-analysis (OR 1.08, 95 % CI 1.02-1.15, P = 0.01). However, the GG genotype and AA genotype were not associated with the susceptibility of lung cancer. Furthermore, there was no association between GSTP1 A/G gene polymorphism and the risk of lung cancer in Caucasians, and East-Asians. In conclusion, GSTP1 G allele is associated with the lung cancer susceptibility. However, more studies on the relationship between GSTP1 A/G gene polymorphism and the risk of lung cancer should be performed in the future.