OBJECTIVE: Patients with cirrhosis and splenomegaly often have coagulation dysfunction which affects treatment and prognosis. This study explores the status, grading, and treatment strategies of coagulation dysfunction i...OBJECTIVE: Patients with cirrhosis and splenomegaly often have coagulation dysfunction which affects treatment and prognosis. This study explores the status, grading, and treatment strategies of coagulation dysfunction in patients with liver cirrhosis and splenomegaly. METHODS: A retrospective cohort study was conducted on the clinical data on consecutive patients with cirrhosis and splenomegaly treated at Hainan General Hospital, China, from January 2000 to December 2020. Starting research in January 2022. RESULTS: Among 1522 patients included into this study, 297 (19.5%) patients had normal results in all five coagulation tests (prothrombin time, prothrombin activity, activated partial thromboplastin time, thrombin time, and fibrinogen), and 1225 (80.5%) had coagulation dysfunction in at least one of these tests. There were significant differences ( < 0.05) in treatment efficacy on these patients for three of these five coagulation tests, with the exception of prothrombin activity and thrombin time. When coagulation dysfunction was classified into grades I, II, and III based on scores from the three significant coagulation tests, prothrombin time, activated partial thromboplastin time, and fibrinogen, significant differences in surgical outcomes were found among the three grades of coagulation dysfunction and between grades I and III ( < 0.05). The operative mortality rate in patients with grade III in treating liver cancer, portal hypersplenism, and/or splenomegaly was 6.5%. There was no significant difference between patients with grades I and II ( > 0.05). CONCLUSIONS: Approximately, 80% of patients with liver cirrhosis and splenomegaly had coagulation dysfunction. Surgery is feasible for grade I and II patients. For grade III patients, nonsurgical treatment should be given first, and surgery should only be considered when the coagulation function returns to normal or near-normal levels after treatment. This trial is registered with MR-46-22-009299.
PURPOSE: To identify the survival and prognostic factors for cardiac amyloidosis (CA) in Chinese patients. METHODS: This was a prospective cohort study of 72 patients diagnosed with CA and admitted to the PLA General Hos...PURPOSE: To identify the survival and prognostic factors for cardiac amyloidosis (CA) in Chinese patients. METHODS: This was a prospective cohort study of 72 patients diagnosed with CA and admitted to the PLA General Hospital between November 2017 and April 2021. Demographic, clinical, laboratory, electrocardiographic, conventional ultrasound, endocardial LS during LV systole (LV ENDO LSsys), and myocardial strain data were recorded. Survival was assessed. All-cause mortality was the endpoint. Follow-up was censored on September 30, 2021. RESULTS: The mean follow-up was 17.1 ± 12.9 months. Among the 72 patients, 39 died, 23 survived, and 10 were lost to follow-up. Mean survival for all patients was 24.7 ± 2.2 months. Mean survival was 32.7 ± 2.4 months among patients with NYHA class II, 26.6 ± 3.4 months for NYHA class III, and 5.8 ± 1.1 months for NYHA class IV. The multivariate Cox proportional hazard regression model showed that NYHA class (HR = 3.42, 95% CI: 1.36-8.65, = 0.002), log-proBNP level (HR = 1.40, 95% CI: 1.17-5.83, = 0.03), and ENDO LSsys of the LV basal level (HR = 1.25, 95% CI: 1.05-1.95, = 0.004) were independent prognostic factors for CA. CONCLUSION: NYHA class, proBNP level, and ENDO LSsys of the LV basal level were independently associated with the survival of patients with CA.
H1N1 influenza virus is a major factor in seasonal influenza outbreaks. After the body is infected with the influenza virus, the expression of certain mRNAs, including miRNAs, could be affected. However, the association...H1N1 influenza virus is a major factor in seasonal influenza outbreaks. After the body is infected with the influenza virus, the expression of certain mRNAs, including miRNAs, could be affected. However, the association between these mRNAs and miRNAs remains unclear. This study is aimed at identifying differentially expressed genes (DEGs) and miRNAs (DEmiRs) caused by H1N1 influenza virus infection and constructing a miRNA-mRNA regulatory network. Nine GSE datasets were downloaded from the Gene Expression Omnibus database, of which seven were mRNA data and two were miRNA data. The limma package in R language package was used to analyze array data, and edgeR package was used to analyze high-throughput sequencing data. At the same time, the genes related to H1N1 infection were further screened by WGCNA analysis. DEGs were subjected to Gene Ontology and KEGG pathway enrichment analyses by DAVID database, while the STRING database predicted the protein-protein interaction (PPI) network. The correspondence between miRNA and target mRNA was analyzed by the miRWalk database. Cytoscape software was used to output PPI results, identify hub genes, and construct a miRNA-mRNA regulatory network. 114 DEGs and 37 candidate DEmiRs were identified for subsequent analysis. These DEGs were significantly enriched in response to the virus, cytokine activity, and symbiont-containing vacuole membrane. According to KEGG analysis, DEGs were enriched in PD-L1 expression and PD-1 checkpoint pathway. The key point Cd274 (PD-L1) was highly expressed in the H1N1-infected group. Finally, a potential miRNA-mRNA regulatory network (containing 8 candidate DEmiRs and 69 candidate DEGs) and a PPI network were constructed. After that, three hub genes were identified: Ifit3, Stat2, and Irf7. These hub genes and Cd274 were validated by another independent high-throughput dataset and were highly expressed pattern. This study will help researchers gain insights into the intrinsic effects of H1N1 influenza virus infection on the host and suggest a novel association of H1N1 virus with the host immune system.
Recurrence is the major death cause of differentiated thyroid carcinoma (DTC), and a better understanding of recurrence risk at early stage may lead to make the optimal medical decision to improve patients' prognosis. Th...Recurrence is the major death cause of differentiated thyroid carcinoma (DTC), and a better understanding of recurrence risk at early stage may lead to make the optimal medical decision to improve patients' prognosis. The 2015 American Thyroid Association (ATA) risk stratification system primary based on clinic-pathologic features is the most commonly used to describe the initial risk of persistent/recurrent disease. Besides, multiple prognostics models based on multigenes expression profiles have been developed to predict the recurrence risk of DTC patients. Recent evidences indicated that aberrant DNA methylation is involved in the initiation and progression of DTC and can be useful biomarkers for clinical diagnosis and prognosis prediction of DTC. Therefore, there is a need for integrating gene methylation feature to assess the recurrence risk of DTC. Gene methylation profile from The Cancer Genome Atlas (TCGA) was used to construct a recurrence risk model of DTC by successively performed univariate Cox regression, LASSO regression, and multivariate Cox regression. Two Gene Expression Omnibus (GEO) methylation cohorts of DTC were utilized to validate the predictive value of the methylation profiles model as external cohort by receiver operating characteristic (ROC) curve and survival analysis. Besides, CCK-8, colony-formation assay, transwell, and scratch-wound assay were used to investigate the biological significance of critical gene in the model. In our study, we constructed and validated a prognostic signature based on methylation profiles of and and constructed a nomogram based on the methylation-related model, age, and AJCC_T stage that could provide evidence for the long-term treatment and management of DTC patients. Besides, in vitro experiments showed that inhibited proliferation, colony-formation, and migration of BCPAP cells and the gene set enrichment analysis and immune infiltration analysis showed that may promote antitumor immunity in DTC. In conclusion, promoter hypermethylation and loss expression of in DTC may be a biomarker of unfavorable prognosis and poor response to immune therapy.
BACKGROUND: Liver hepatocellular carcinoma (LIHC) is the most frequently seen type of primary liver cancer. Cuproptosis is a novel form of cell death highly associated with mitochondrial metabolism. However, the clinical...BACKGROUND: Liver hepatocellular carcinoma (LIHC) is the most frequently seen type of primary liver cancer. Cuproptosis is a novel form of cell death highly associated with mitochondrial metabolism. However, the clinical impact and pertinent mechanism of cuproptosis genes in LIHC remain largely unknown. METHODS: From public databases, we systematically assessed common genes from LIHC differentially expressed genes (DEGs) and cuproptosis-related genes using bioinformatics analysis. These common genes were then analyzed by enrichment analysis, mutation analysis, risk score model, and others to find candidate hub genes related to LIHC and cuproptosis. Next, hub genes were determined by expression, clinical factors, immunoassay, and prognostic nomogram. RESULTS: Based on 129 cuproptosis-related genes and 3492 LIHC DEGs, we totally identified 21 downregulated and 18 upregulated common genes, and they were enriched in pathways, such as zinc ion homeostasis and oxidative phosphorylation. In the mutation analysis, missense mutation was the most common type in LIHC patients, and the common gene F5 had the highest mutation frequency. After LASSO-Cox regression analysis and prognostic analysis, CDK1, ABCB6, LCAT, and COA6 were identified as prognostic signature genes. Among them, ABCB6 and LCAT were lowly expressed in tumors, and CDK1 and COA6 were highly expressed in tumors. In addition, ABCB6 and LCAT were negatively correlated with 6 kinds of immune cells, while CDK1 and COA6 were positively correlated with them. CDK1 and COA6 were identified as hub genes related to LIHC by Cox regression analysis and prognostic nomogram. CONCLUSION: CDK1 and COA6 are two oncogenes in LIHC, which are involved in the molecular mechanism of cuproptosis and LIHC. Besides, CDK1 and COA6 can positively regulate the expressions of immune cells in LIHC. In clinical practice, they can be used as immunotherapeutic targets and prognostic predictors in LIHC, which sheds new light on the scientific fields of cuproptosis and LIHC.
EPAS1 plays an important role in the development and progression of multiple tumor types by interacting with a series of other molecules. However, the prognostic and diagnostic values of EPAS1 in acute myeloid leukemia (...EPAS1 plays an important role in the development and progression of multiple tumor types by interacting with a series of other molecules. However, the prognostic and diagnostic values of EPAS1 in acute myeloid leukemia (AML) remain unknown. Here, we systematically explored and clarified the potential functions of EPAS1 in AML using data from Xena Browser and TCGA database. The expression of EPAS1 was significantly lower in AML patients than that in healthy people. The GO, KEGG, GSEA, and GSVA were performed to explore the potential functions and signaling pathways. The survival analysis was conducted using Cox regression analysis and the Kaplan-Meier method. Immune cell infiltration was evaluated via single-sample GSEA (ssGSEA). The results of enrichment analyses suggested that low-EPAS1 expression was related to the initiation, development, and prognosis of AML. The immune microenvironment landscape in AML was described by ssGSEA. ROC analysis of EPAS1 showed high discrimination ability between AML patients and healthy people. Kaplan-Meier method indicated that low-EPAS1 expression correlated significantly with a poor overall survival. Multivariate Cox regression analysis revealed that both age and EPAS1 expression were independent prognostic factors in AML patients. Furthermore, the nomogram based on these two variables performed well in discrimination and calibration. In summary, our study may provide new insights into the molecular mechanisms underlying AML and demonstrate the diagnostic and prognostic value of EPAS1 in AML for the first time.
De Ramón Ortiz C, Justo Sanz R, Beauverd Y
… +9 more, Humala K, López de la Guia A, De Paz R, Gasior M, Gómez Prieto P, Fabra Urdiola M, Canales Albendea M, Butta N, Jiménez Yuste V
BACKGROUND: Sinusoidal obstructive syndrome (SOS) is a potentially fatal complication secondary to hematopoietic stem cell transplant (HSCT) conditioning. Endothelial damage plasma biomarkers such as plasminogen activato...BACKGROUND: Sinusoidal obstructive syndrome (SOS) is a potentially fatal complication secondary to hematopoietic stem cell transplant (HSCT) conditioning. Endothelial damage plasma biomarkers such as plasminogen activator inhibitor-1 (PAI-1), hyaluronic acid (HA), and vascular adhesion molecule-1 (VCAM1) represent potential diagnostic tools for SOS. METHODS: We prospectively collected serial citrated blood samples (baseline, day 0, day 7, and day 14) in all adult patients undergoing HSCT at La Paz Hospital, Madrid. Samples were later analyzed by ELISA (enzyme-linked immunosorbent assay) for HA, VCAM1, and PAI-1 concentrations. RESULTS: During sixteen months, we prospectively recruited 47 patients. Seven patients (14%) were diagnosed with SOS according to the EBMT criteria for SOS/VOD diagnosis and received treatment with defibrotide. Our study showed a statistically significant elevation of HA on day 7 in SOS patients, preceding clinical SOS diagnosis, with a sensitivity of 100%. Furthermore, we observed a significant increase of HA and VCAM1 levels on day 14. Regarding risk factors, we observed a statistically significant association between SOS diagnosis and the fact that patients received 3 or more previous lines of treatment before HSCT. CONCLUSIONS: The early significant increase in HA levels observed opens the door to a noninvasive peripheral blood test which could have the potential to improve diagnosis and facilitate prophylactic and therapeutic management of SOS before clinical/histological damage is established.
Trypanosomiasis is a complex of diseases caused by a haemoprotozoan parasite of medical and veterinary importance. One of the leading factors that cause morbidity and death in trypanosomiasis is oxidative stress. The oxi...Trypanosomiasis is a complex of diseases caused by a haemoprotozoan parasite of medical and veterinary importance. One of the leading factors that cause morbidity and death in trypanosomiasis is oxidative stress. The oxidative stress biomarkers in trypanosomiasis at the subacute and chronic stages of infection were investigated in this study. A total of twenty-four Wistar rats were used; the animals were placed in two groups: group A (subacute and chronic) and group B (control). The weight and body temperature of the experimental animals were determined using a digital weighing balance and thermometer. A hematology analyzer was used to determine the erythrocyte indices. Spectrophotometry was used to estimate enzyme (superoxide dismutase, catalase, and glutathione) activities in the serum, kidney, and liver of experimental animals. Liver, kidney, and spleen were harvested and analyzed for histological changes. The mean body weight of the infected decreased compared to the control ( < 0.05). The mean body temperature of infected individuals increased (35-37°C) compared to the control ( < 0.05). The erythrocyte indices of the infected and control groups indicate a significant decrease ( < 0.05). In erythrocyte indices, only MCHC indicated a nonsignificant decrease ( > 0.05). The SOD of serum shows a significant increase ( < 0.05), and no significant increase SOD ( > 0.05) in kidney and the liver SOD indicates a significant decrease ( < 0.05). The serum, kidney, and liver show a significant increase ( < 0.05) in CAT. The serum GSH from the findings indicates a nonsignificant increase ( > 0.05), and the kidney and liver GSH shows a significant increase ( < 0.05). The correlation analysis for SOD shows nonsignificant negative correlation for serum/kidney, and the serum/liver and kidney/liver show significant positive correlation. The result of CAT shows significant correlations for serum and kidney, serum and liver, and kidney/liver with a positive correlation. The GSH result shows no significant negative correlation for serum/kidney and no significant positive correlation for serum/liver and kidney/liver. The histological damage in the kidney, liver, and spleen was much higher in the chronic stage than in the subacute stage and no tissue damage in the control group. In conclusion, subacute and chronic stage trypanosome infection is associated with changes in hematological indices, antioxidants of the liver, spleen and kidney, and histological architecture.
METHODS: In this study, 326 hospitalized patients with acute anterior circulation ischemic stroke (AACIS) were included. A comparison of the clinical characteristics of those with and without AF was conducted. The Spearm...METHODS: In this study, 326 hospitalized patients with acute anterior circulation ischemic stroke (AACIS) were included. A comparison of the clinical characteristics of those with and without AF was conducted. The Spearman rank correlation was used for the correlation analysis of plasma NT-proBNP level, regional leptomeningeal collateral (rLMC) score, and computed tomography perfusion (CTP) status in the AF and non-AF groups. An analysis of multivariate linear regression was used to determine how plasma NT-proBNP level, rLMC score, and CTP status influenced the score on the NIHSS. RESULTS: There was a greater plasma NT-proBNP level in the AF group compared with the non-AF group, an increased CTP volume (including CTP ischemic volume, CTP infarct core volume, and CTP ischemic penumbra volume ( = 0.002)), higher NIHSS score on admission, and lower rLMC score ( < 0.001 for the remaining parameters). A negative correlation exists between plasma NT-proBNP level and rLMC score ( = -0.156, = 0.022), but a positive correlation exists between plasma NT-proBNP level and both CTP ischemic volume and CTP infarct core volume ( = 0.148, = 0.003) in the AF group, but not in the non-AF group. Multivariate linear regression analysis demonstrated that NT-proBNP, CTP ischemic penumbra volume, and rLMC score were associated with NIHSS score, and NT-proBNP was positively associated with NIHSS scores (95% confidence interval (CI), 0.000-0.002; = 0.004) in the AF group, whatever in the unadjusted model or adjusted models, but not in the nonlarge artery atherosclerosis (LAA) group. CONCLUSION: In AACIS patients with AF, NT-proBNP level negatively correlated with collateral status, positively with CTP ischemic volume, and positively with NIHSS score.
PURPOSE: Keloid is a type of benign fibrous proliferative tumor characterized by excessive scarring. C1q/TNF-related protein 3 (CTRP3) has been proven to possess antifibrotic effect. Here, we explored the role of CTRP3 i...PURPOSE: Keloid is a type of benign fibrous proliferative tumor characterized by excessive scarring. C1q/TNF-related protein 3 (CTRP3) has been proven to possess antifibrotic effect. Here, we explored the role of CTRP3 in keloid. In the current research, we examined the influence of CTRP3 on keloid fibroblasts (KFs) and investigated the potential molecular mechanism. METHODS: KF tissue specimens and adjacent normal fibroblast (NF) tissues were collected cultured from 10 keloid participants. For the TGF-1 stimulation group, KFs were processed with human recombinant TGF-1. Cell transfection of pcDNA3.1-CTRP3 or pcDNA3.1 was performed. The siRNA of CTRP3 (si-CTRP3) or negative control siRNA (si-scramble) was transfected into KFs. RESULTS: CTRP3 was downregulated in keloid tissues and KFs. CTRP3 overexpression significantly controlled TGF-1-induced propagation and migration in KFs. Col I, -SMA, and fibronectin mRNA and protein levels were enhanced by TGF-1 stimulation, whereas they were inhibited by CTRP3 overexpression. In contrast, CTRP3 knockdown exhibited the opposite effect. In addition, CTRP3 attenuated TGF- receptors TRI and TRII in TGF-1-induced KFs. Furthermore, CTRP3 prevented TGF-1-stimulated nuclear translocation of smad2 and smad3 and suppressed the expression levels of p-smad2 and p-smad3 in KFs. CONCLUSION: CTRP3 exerted an antifibrotic role through inhibiting proliferation, migration, and ECM accumulation of KFs via regulating TGF-1/Smad signal path.
BACKGROUND: Asthma is one of the most common respiratory diseases and one of the largest burdens of health care resources across the world. This study is aimed at using bioinformatics methods to find effective clinical i...BACKGROUND: Asthma is one of the most common respiratory diseases and one of the largest burdens of health care resources across the world. This study is aimed at using bioinformatics methods to find effective clinical indicators for asthma and conducting experimental validation. METHODS: We downloaded GSE64913 data and performed differentially expressed gene (DEG) screening. Weighted gene coexpression network analysis (WGCNA) on DEGs was applied to identify key module most associated with asthma for protein-protein interaction (PPI) analysis. According to the degree value, ten genes were obtained and subjected to expression analysis and receiver operating characteristic (ROC) analysis. Next, key genes were screened for expression analysis and immunological analysis. Finally, cell counting kit-8 (CCK-8) and qRT-PCR were also conducted to observe the influence of hub gene on cell proliferation and inflammatory cytokines. RESULTS: From the GSE64913 dataset, 711 upregulated and 684 downregulated DEGs were found. In WGCNA, the top 10 genes in the key module were examined by expression analysis in asthma, and CYCS was determined as an asthma-related oncogene with a good predictive ability for the prognosis of asthmatic patients. CYCS is significantly associated with immune cells, such as HHLA2, IDO1, TGFBR1, and CCL18 and promoted the proliferation of asthmatic cells in vitro. CONCLUSION: CYCS plays an oncogenic role in the pathophysiology of asthma, indicating that this gene may become a novel diagnostic biomarker and promising target of asthma treatment.
Diabetes mellitus (DM) is a metabolic disorder that can be categorized mainly into type 1 and type 2. Diabetes type 1 is caused due to -cell destruction, whereas type 2 is caused by the resistance of cell receptors. Many...Diabetes mellitus (DM) is a metabolic disorder that can be categorized mainly into type 1 and type 2. Diabetes type 1 is caused due to -cell destruction, whereas type 2 is caused by the resistance of cell receptors. Many therapies are available for the management of diabetes, but they have some side effects, and as a result of this, people are attracted to natural treatments. mushrooms are well documented for their medicinal attributes and their role in the treatment of diseases like cancer, infectious disease, neurodiseases, and inflammatory disease. The protective mechanism of the () mushroom and its detailed histological study on kidneys and the liver in diabetic conditions were unexplored. The present study evaluated the effects of aqueous extract on histological changes in the diabetic rat model. Male Wistar albino rats were used to create the diabetic model by using streptozotocin (STZ) intraperitoneal (IP) injection. The animals were separated into five different groups, with six animals in each. Only group I, animals that did not receive STZ, was considered a normal control. Group II was a diabetic control and received normal saline, and group III was a drug control and received metformin as a standard drug. Groups IV and V were dosing groups, which received the aqueous extract of in 250 mg/kg and 500 mg/kg of body weight concentrations, labeled as T1 and T2 groups, respectively. The T1 and T2 groups clearly showed their potential to reverse the histopathological changes in the kidney and liver. However, the T2 group was more effective than the T1 group, as results indicate that functions of the glomerulus and its structural deformity were restored to their near-natural form in the T2 group. In the case of the liver, the histological changes like the dilatation of sinusoids, more numbers of the Kupffer cell formation, and necrosis were restored in the T2 group. All these results proved the potential of against the side effects of diabetes. It could protect the organs from developing diabetic nephropathy (DN) and liver-related diseases like cirrhosis and nonalcoholic fatty liver disease (NAFLD).
OBJECTIVE: This study is to investigate the difference in HIV-1 RNA pol gene expression in AIDS patients before and after antiviral treatment and its effect on the expression level of CD4/CD8 T cells in peripheral blood....OBJECTIVE: This study is to investigate the difference in HIV-1 RNA pol gene expression in AIDS patients before and after antiviral treatment and its effect on the expression level of CD4/CD8 T cells in peripheral blood. METHODS: The participants included 200 AIDS patients who had undergone antiviral medication, and the quantity of HIV-1 RNA pol gene was determined using nested polymerase chain reaction (nPCR). The levels of CD3+, CD4+, and CD8+ T lymphocytes in peripheral blood were measured by flow cytometry before and after therapy. The receiver operating characteristics (ROC) curve was used to assess the impact of HIV-1 RNA pol gene expression and the CD4+/CD8+ ratio on the prognosis of AIDS patients. RESULTS: After three months of therapy, the levels of HIV-1 RNA and viral load in the patients showed a drastic decline, while the levels of CD4+/CD8+ were markedly elevated ( < 0.05). Logistic analysis revealed that patients' viral loads were positively correlated with HIV-1 RNA and negatively correlated with CD4+/CD8+ ( < 0.05). The alanine aminotransferase (ALT), white blood cell (WBC) count, Serum creatinine (Cr), total cholesterol (TC), triglyceride (TG), and platelet (PLT) levels significantly increased following a 24-month therapy, while no significant changes were observed in the level of aspartate aminotransferase (AST), red blood cell (RBC), and neutrophil (NEU) (%). ( > 0.05). CONCLUSION: Antiviral drugs significantly inhibit the HIV-1 RNA POL gene expression and viral load in AIDS patients but upregulate the expression level of CD4/CD8 T cells in peripheral blood.
BACKGROUND: Cystatin C (Cys C) not only regulates the body's immune defenses but also contributes to tissue degradation and destruction by causing an imbalance between protease and antiprotease in infectious diseases. Is...BACKGROUND: Cystatin C (Cys C) not only regulates the body's immune defenses but also contributes to tissue degradation and destruction by causing an imbalance between protease and antiprotease in infectious diseases. Is Cys C involved in pulmonary tuberculosis (PTB) infection and cavitation? We therefore conducted a retrospective study on this question to provide a basis for further studies. METHODS: Cavitary PTB patients, noncavitary PTB patients, and healthy controls were recruited in our study. Serum Cys C, CRP, BUN, UA, and CR were measured in all subjects, and the Kruskal-Wallis test was used to compare medians of these clinical parameters in different groups. The Spearman rank correlation test was used to determine correlations between variables. In addition, a multivariate analysis using binary logistic regression was used to identify factors associated with PTB cavitation. RESULTS: In our study, elevated serum Cys C levels were found in cavitary PTB patients compared to healthy controls and noncavitary patients ( = 0.022). Serum Cys C levels were statistically correlated with serum BUN and CR concentrations ( = 0.278, = 0.005; = 0.281, = 0.004) in PTB patients. The binary logistic regression analysis showed that elevated serum Cys C levels were correlated with pulmonary cavitation in PTB patients (OR = 1.426, 95% CI: 1.071-1.898). CONCLUSION: Elevated serum levels of Cys C are associated with pulmonary cavitation in PTB patients.
OBJECTIVE: To investigate the relationship between changes in blood glucose and blood lipid levels and the risk of thyroid cancer in patients with type 2 diabetes mellitus. METHODS: A total of 159 patients with type 2 di...OBJECTIVE: To investigate the relationship between changes in blood glucose and blood lipid levels and the risk of thyroid cancer in patients with type 2 diabetes mellitus. METHODS: A total of 159 patients with type 2 diabetes who were treated in our hospital between June 2018 and February 2021 were recruited and assigned into the observation group, including 136 patients with type 2 diabetes without thyroid cancer (nonthyroid cancer group) and 23 patients with type 2 diabetes complicated with thyroid cancer (thyroid cancer group), and 120 healthy subjects during the same period were selected as the control group. Glycated hemoglobin (HbAlc), total cholesterol (TC), triacylglycerol (TG), high density lipoprotein cholesterol (HDL-C), and low density lipoprotein cholesterol (LDL-C) were detected and compared. Pearson's method was conducted to analyze the correlation between serum HbAlc level and TC, TG, HDL-C, and LDL-C levels in patients with type 2 diabetes mellitus; multivariate logistic regression analysis was performed to analyze the influencing factors of thyroid cancer in patients with type 2 diabetes mellitus. RESULTS: The serum HbAlc level and the incidence of thyroid cancer in patients with type 2 diabetes mellitus in the observation group were significantly higher than those in the control group ( < 0.05). The levels of TC, TG, and LDL-C in patients with type 2 diabetes mellitus in the observation group were significantly higher than those in the control group, and the level of HDL-C was significantly lower than that in the control group ( < 0.05). The correlation analysis showed that serum HbAlc levels in patients with type 2 diabetes were positively correlated with TC and TG levels and negatively correlated with HDL-C levels ( < 0.05) and not correlated with LDL-C levels ( > 0.05). Compared with the type 2 diabetes patients without thyroid cancer, the serum HbAlc, TC, and TG levels of the patients with type 2 diabetes mellitus in the thyroid cancer group were significantly higher, and the levels of HDL-C were significantly lower ( < 0.05). There was no significant change in the level of LDL-C ( > 0.05). Multivariate logistic regression analysis showed that serum HbAlc, TC, and TC levels were all risk factors for thyroid cancer in patients with type 2 diabetes mellitus ( < 0.05), while serum HDL-C level was a protective factor for thyroid cancer in patients with type 2 diabetes mellitus ( < 0.05). CONCLUSION: Thyroid cancer in type 2 diabetes patients may be linked to elevated levels of blood HbAlc, TC, and TG. HbAlc may raise the risk of thyroid cancer in type 2 diabetes patients by modulating blood lipid levels, which might serve as a marker to assess the risk of thyroid cancer in type 2 diabetes mellitus patients. However, since this study did not conduct in vitro and in vivo experiments, how HbAlc affects the pathogenesis of thyroid cancer has not been described in this study, which is also our future research direction. It is expected to provide new ideas for the prevention and treatment of thyroid cancer.
OBJECTIVE: To investigate the efficacy of butylphthalide combined with edaravone in the treatment of acute ischemic stroke and the effect on serum inflammatory factors. METHODS: One hundred and sixty patients with acute...OBJECTIVE: To investigate the efficacy of butylphthalide combined with edaravone in the treatment of acute ischemic stroke and the effect on serum inflammatory factors. METHODS: One hundred and sixty patients with acute ischemic stroke who attended the neurovascular intervention department of our hospital from May 2020 to June 2022 were enrolled as study subjects for prospective analysis and were equally divided into a control group and an experimental group using the random number table method, with 80 cases in each group. The control group was treated with edaravone injection, while the experimental group was treated with butylphthalide combined with edaravone. The disease was recorded to compare the efficacy, erythrocyte sedimentation rate, homocysteine, serum inflammatory factors including tumor necrosis factor-, C-reactive protein and interleukin-6 levels, and the incidence of adverse reactions between the two groups. RESULTS: The total effective rate of treatment in the experimental group was 90.0% (72/80), while that of the control group was 62.5% (50/80), the total effective rate of the experimental group was significantly higher than that of the control group, and the difference was statistically significant ( < 0.05). After treatment, the erythrocyte sedimentation rate, homocysteine level, and serum TNF-, CRP, and IL-6 levels of patients in the experimental group improved compared with those before treatment, and the degree of improvement was better than that of the control group, and the difference was statistically significant ( < 0.05). After 3 months of treatment, a comparison of the incidence of adverse reactions in the two groups showed no statistically significant difference between the two groups ( > 0.05). CONCLUSION: The treatment of acute ischemic stroke with butylphthalide combined with edaravone has positive significance in improving blood circulation regulation and serum inflammatory factor levels and is reliable and worthy of clinical promotion.
OBJECTIVE: To assess the use of cytotoxic drugs as first-line chemotherapy for nonsquamous non-small-cell lung cancer (NSCLC) with EGFR mutation. METHOD: This study uses the network meta-analysis (NMA) method, with the i...OBJECTIVE: To assess the use of cytotoxic drugs as first-line chemotherapy for nonsquamous non-small-cell lung cancer (NSCLC) with EGFR mutation. METHOD: This study uses the network meta-analysis (NMA) method, with the inclusion of prospective randomized control studies related to the treatment of EGFR-positive nonsquamous NSCLC, to compare the efficacy of various EGFR-TKIs. As of September 4, 2022, 16 studies on a total of 4180 patients were included. The retrieved literature was comprehensively evaluated as per the established inclusion and exclusion criteria, and valid data were extracted and included for analysis. RESULTS: The 6 treatment regimens included cetuximab, CTX (cyclophosphamide), icotinib, gefitinib, afatinib, and erlotinib. All of the 16 studies reported their findings about overall survival (OS), and 15 of them also reported findings about progression-free survival (PFS). The NMA results showed that there was no significant difference in OS among the 6 treatment regimens. It was observed that erlotinib had the highest likelihood of obtaining the best OS, followed by afatinib, gefitinib, icotinib, CTX, and cetuximab, in descending order. This indicates that the highest possibility of achieving the best OS was with erlotinib, while the lowest was with cetuximab. The NMA results also showed that the PFS achieved with treatment using afatinib, erlotinib, and gefitinib were all higher than that with treatment using CTX, with statistically significant differences. The results showed that there was no significant difference in PFS among erlotinib, gefitinib, afatinib, cetuximab, and icotinib. CTX, cetuximab, icotinib, gefitinib, afatinib, and erlotinib were ranked in descending order based on the PFS indicator SUCRA values, which implied that erlotinib had the highest possibility in achieving the best PFS, while CTX had the lowest. . EGFR-TKIs must be carefully selected for the treatment of different histologic subtypes of NSCLC. For EGFR mutation (+) nonsquamous NSCLC, erlotinib is most likely to achieve the best OS and PFS, which makes it the first choice in the formulation of a treatment plan.
Performing cardiopulmonary bypass (CPB) to reduce ischemic injury during surgery is a common approach to cardiac surgery. However, this procedure can lead to systemic inflammation and multiorgan dysfunction. Therefore, e...Performing cardiopulmonary bypass (CPB) to reduce ischemic injury during surgery is a common approach to cardiac surgery. However, this procedure can lead to systemic inflammation and multiorgan dysfunction. Therefore, elucidating the molecular mechanisms of CPB-induced inflammatory cytokine release is essential as a critical first step in identifying new targets for therapeutic intervention. The GSE143780 dataset which is mRNA sequencing from total circulating leukocytes of the neonatorum was downloaded from the Gene Expression Omnibus (GEO) database. A total of 21 key module genes were obtained by analyzing the intersection of differentially expressed gene (DEG) and gene coexpression network analysis (WGCNA), and then, 4 genes (TRAF3IP2-AS1, PPARGC1B, CD4, and PDLIM5) were further confirmed after the least absolute shrinkage and selection operator (LASSO) and support vector machine recursive feature elimination (SVM-RFE) screening and were used as hub genes for CPB-induced inflammatory cytokine release in patients with congenital heart defects. The enrichment analysis revealed 21 key module genes mainly related to the functions of developmental cell growth, regulation of monocyte differentiation, regulation of myeloid leukocyte differentiation, ERK1 and ERK2 cascade, volume-sensitive anion channel activity, and estrogen receptor binding. The result of gene set enrichment analysis (GSEA) showed that the hub genes were related to different physiological functions of cells. The ceRNA network established for hub genes includes 3 hub genes (PPARGC1B, CD4, and PDLIM5), 55 lncRNAs, and 34 miRNAs. In addition, 4 hub genes have 215 potential therapeutic agents. Finally, expression validation of the four hub genes revealed that they were all significantly low expressed in the surgical samples than before.