ObjectiveTo summarize the clinical application and future application prospects of organoid model in pancreatic cancer. MethodThe domestic and foreign literature related on the application of organoid model in pancreatic cancer was reviewed. ResultsIn recent years, the organoid model of pancreatic cancer was constructed mainly using patient-derived tissues, fine-needle aspiration samples, and human pluripotent stem cells. The biomarkers of pancreatic cancer were screened according to the histological and structural heterogeneities of the primary tumor retained in organoid model, such as microRNA, glypican-1, annexin A6 and protein biomarkers cytokeratin 7 and 20, cell tumor antigen p53, Claudin-4, carbohydrate antigen 19-9, etc.in the extracellular vesicles. The results of organoid model could maintain the original tumor characteristics and the higher correlation between the organoid model drug sensitivity data and the clinical results of pancreatic cancer patients suggested that, the drug sensitivity data of organoid model could be used to avoid ineffective chemotherapy, so as to improve the treatment response rate and reduce the toxicity of chemical drug treatment, and reasonably select individualized treatment plans for pancreatic cancer patients in future. ConclusionsOrganoid model has many research in screening biomarkers of pancreatic cancer, individualized drug screening, and drug sensitivity test. It can simulate the complex pathophysiological characteristics of pancreatic cancer in vitro, and retain the physiological characteristics and gene phenotype of original tumor cells. It is expected to become a new platform for selecting biomarkers of pancreatic cancer, testing drug sensitivity, and formulating individualized treatment methods for pancreatic cancer, which might further accelerate the research progress of pancreatic cancer.
Ferroptosis is a unique way of cell death discovered in recent years, which involves the lethal process of iron ion accumulation and lipid peroxidation, which is obviously different from the traditional cell death pathway such as apoptosis and necrosis. For a long time, tuberculosis has been a major infectious disease in the field of global public health, which brings a serious burden to the society because of its high morbidity and mortality. The emergence of drug resistance aggravates the difficulty of treating tuberculosis, and new treatment strategies and drug targets are urgently needed. Combined with the latest research progress at home and abroad, This article will discuss the molecular mechanism of ferroptosis and pulmonary tuberculosis and the relationship between signal pathways, biomarkers and related genes, in order to provide a new perspective for the diagnosis and treatment of pulmonary tuberculosis.
Non-invasive biomarkers, due to their non-invasive and safe characteristics, hold significant potential for the diagnosis and prognosis of epilepsy. This review summarizes the research progress and future directions of non-invasive biomarkers for epilepsy, encompassing electrophysiological, imaging, biochemical, and genetic markers, and discusses biomarkers for specific types of epilepsy, such as structural lesion-related epilepsy, infection and inflammation-related epilepsy, autoimmune epilepsy, endocrine hormone-related epilepsy, and metabolic epilepsy, to facilitate their clinical application.
Although great progress has been achieved in the techniques and materials of cardiopulmonary bypass (CPB), cardiac surgery under CPB is still one of the surgeries with the highest complication rate. The systemic inflammatory response is an important cause of complications, mainly characterized by activation of innate immune cells and platelets, and up-regulation of inflammatory cytokines. After activation, a variety of molecules on the membrane surface are up-regulated or down-regulated, which can amplify tissue inflammatory damage by releasing cytoplasmic protease and reactive oxygen species, and activate multiple inflammatory signaling pathways in the cell, ultimately leading to organ dysfunction. Therefore, the expression of these cell membrane activation markers is not only a marker of cell activation, but also plays an important role in the process of vital organ injury after surgery. Identification of these specific activation markers is of great significance to elucidate the mechanisms related to organ injury and to find new prevention and treatment methods. This article will review the relationship between these activated biomarkers in the innate immune cells and vital organ injuries under CPB.
ObjectiveTo evaluate the monitoring value of brain injury biomarkers in the patients during extracorporeal membrane oxygenation (ECMO).
MethodsWe searched PubMed, EMbase, the Cochrane Library, CNKI, and CBM from inception of each database to May 2015 to identify randomized controlled trials, or case-control trials, or cohort trials of brain injury biomarkers predict brain injury during ECMO. Data were extracted independently by two reviewers. Meta-analysis was conducted using STATA 12.0 software.
ResultsFour retrospective trials were included. The results showed that compared with patients without brain injury, the patients with brain injury had a higher level of S100B protein (P < 0.05). The incidence of major neurological events was higher for high neuron-specific enolase level patients than mild-to-moderate neuron-specific enolase level patients (85% vs. 29%, P=0.01). The incidence of brain injury was higher for normal glial fibrillary acidic protein level than patients with glial fibrillary acidic protein > 0.436 ng/ml (OR=11.5, 95%CI 1.3-98.3).
ConclusionsBrain injury biomarkers may be used as an indicator for earlier diagnosis of brain injury in patients during ECMO.
【Abstract】 Objective To evaluate the relationship between multiple tumor biomarkers and idiopathic pulmonary fibrosis ( IPF) , and analyze the prognostic value of these biomarkers in IPF. Methods Clinical data of 43 confirmed IPF patients with no evidence of malignant disaeses, admitted in Peking Union Medical College Hospital between January 2000 and June 2010, were retrospectively analyzed. All IPF patients had detected serum alpha fetoprotein ( AFP) , cancer antigen 50 ( CA50) , cancer antigen 24-2( CA24-2) , carcinoembryonic antigen ( CEA) , carbohydrate antigen 19-9 ( CA19-9) , cancer antigen 125( CA125) , cancer antigen 15-3 ( CA15-3) , tissue polypeptide antigen ( TPA) , neuron specific enolase( NSE) , and cytokeratin-19-fragment ( Cyfra211) . Results The serum levels of CEA, CA19-9, CA125,CA15-3, and TPA were obviously higher than normal range, while the serum levels of AFP, CA50, CA24-2,NSE, and Cyfra211 were within normal range. Neither tumor biomarkers had correlation with 6-minute walk distance, FVC% pred, TLC% pred, DLCO/VA, PaO2 , PaO2 /FiO2 , P( A-a) O2 , BALF cell differentiation counting,or CD4 /CD8. The patients with increased CA19-9 level had shorter survival time than those with normal CA19-9 level ( P lt; 0. 05) . There was no significant difference in survival time between the patients with increased CEA/TPA levels and those with normal CEA/TPA levels( P gt;0. 05) , neither between the patients with glucocorticoid treatment and those with non-glucocorticoid treatment ( P gt; 0. 05) . Conclusions Multiple tumor biomarkers, especially CA19-9, increase in IPF patients. The degrees of those increases arenot associated with the severity of disease, but closely relate to prognosis, and may also indicate the progression. The increases of multiple tumor biomarkers may be a sign of poor prognosis of IPF with no evidence of malignant disaeses.
Metaiodobenzylguanidine (MIBG) is an analog of norepinephrine that accumulates in sympathetic nerve endings soon after intravenous administration. The degree of accumulation reflects the uptake, storage and release of transmitters by noradrenergic neurons. Myocardial imaging with 123I labeled MIBG (123I-MIBG) can be used to estimate the extent of local myocardial sympathetic nerve damage, which has been widely used in the diagnosis and treatment of various heart diseases. In recent years, numerous studies have been carried out on the application of 123I-MIBG in the diagnosis of degenerative diseases of the nervous system (such as Parkinson's disease and dementia of Lewy body), and have made some achievements. The purpose of this review is to summarize the current clinical application of 123I-MIBG myocardial imaging in the diagnosis of dementia with Lewy bodies, the problems in imaging technology and the possible research directions in the future, so as to provide valuable reference information for clinicians to reasonably and accurately apply this technology in the early diagnosis and discrimination of dementia.
Objective To explore the change of serum levels of neutrophil gelatinase-associated lipocalin (NGAL), tissue inhibitor of metalloproteinases-2 (TIMP-2), and insulin-like growth factor-binding protein 7 (IGFBP-7) in the early stage of multiple trauma, and their predictive efficacy for acute kidney injury (AKI). Methods The multiple trauma patients admitted between February 2020 and July 2021 were prospectively selected, and they were divided into AKI group and non-AKI group according to whether they developed AKI within 72 h after injury. The serum levels of NGAL, TIMP-2, and IGFBP-7 measured at admission and 12, 24, and 48 h after injury, the Acute Pathophysiology and Chronic Health Evaluation Ⅱ(APACHE Ⅱ) score, intensive care unit duration, rate of renal replacement therapy, and 28-day mortality rate were compared between the two groups. Results A total of 51 patients were included, including 20 in the AKI group and 31 in the non-AKI group. The APACHE Ⅱ at admission (20.60±3.57 vs. 11.61±3.44), intensive care unit duration [(16.75±2.71) vs. (11.13±3.41) d], rate of renal replacement therapy (35.0% vs. 0.0%), and 28-day mortality rate (25.0% vs. 3.2%) in the AKI group were higher than those in the non-AKI group (P<0.05). The serum levels of NGAL and IGFBP-7 at admission and 12, 24, and 48 h after injury in the AKI group were all higher than those in the non-AKI group (P<0.05). For the prediction of AKI, the areas under receiver operating characteristic curves and 95% confidence intervals of serum NGAL, TIMP-2 and IGFBP-7 12 h after injury were 0.98 (0.96, 1.00), 0.92 (0.83, 1.00), and 0.87 (0.78, 0.97), respectively. Conclusion Serum NGAL, TIMP-2, and IGFBP-7 have high predictive efficacy for AKI secondary to multiple trauma, and continuous monitoring of serum NGAL can be used for early prediction of AKI secondary to multiple trauma.
Objective To explore key genes and mechanisms of depression aggravating Crohn disease. Methods In March 2023, the Public Health Genomics and Precision Health Knowledge Base and Gene Expression Omnibus database were used to identify the overlapping differentially expressed genes between Crohn disease and depression and the key genes were screened by Metascape, STRING, Cytoscape, and protein interaction network analysis. The Gene Expression Omnibus database was used to analyze the correlations between key genes and clinical pathologies such as Crohn Disease Endoscopic Index of Severity and intestinal microvilli length. Results There were 137 overlapping differentially expressed genes between Crohn disease and depression, and 25 key genes were further screened out. Among them, CREB1, FKBP5, MAPT, NTSR1, OXTR, PROK2, POMC, HTR2B, and PPARGC1A genes were significantly correlated with multiple clinical parameters. The functions of PROK2 and PROK2-related genes were mainly enriched in neutrophil and granulocyte migration, neutrophil and granulocyte chemotaxis, etc. Conclusions There are 25 key genes, especially CREB1, FKBP5, MAPT, NTSR1, OXTR, PROK2, POMC, HTR2B, and PPARGC1A, that possibly contribute to the establishment and deterioration of Crohn disease caused by depressive disorder. Among these genes, PROK2 showes the possibility of regulating immune cell (neutrophils and CD8+ T cells) infiltration.
Unhealthy diet, habits and drug abuse cause a variety of liver diseases, including steatohepatitis, liver fibrosis, liver cirrhosis and liver cancer, which seriously affect human health. The fabrication of highly simulated cell models in vitro is important in the treatment of liver diseases and drug development. This article summarized the common strategies for the construction of liver pathology models in vitro. It introduced four typical cell models in vitro related to liver disease and provided a reference for the study of liver disease models.
