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1.
Front Immunol ; 15: 1244392, 2024.
Article En | MEDLINE | ID: mdl-38694506

Objective: Significant advancements have been made in hepatocellular carcinoma (HCC) therapeutics, such as immunotherapy for treating patients with HCC. However, there is a lack of reliable biomarkers for predicting the response of patients to therapy, which continues to be challenging. Cancer stem cells (CSCs) are involved in the oncogenesis, drug resistance, and invasion, as well as metastasis of HCC cells. Therefore, in this study, we aimed to create an mRNA expression-based stemness index (mRNAsi) model to predict the response of patients with HCC to immunotherapy. Methods: We retrieved gene expression and clinical data of patients with HCC from the GSE14520 dataset and the Cancer Genome Atlas (TCGA) database. Next, we used the "one-class logistic regression (OCLR)" algorithm to obtain the mRNAsi of patients with HCC. We performed "unsupervised consensus clustering" to classify patients with HCC based on the mRNAsi scores and stemness subtypes. The relationships between the mRNAsi model, clinicopathological features, and genetic profiles of patients were compared using various bioinformatic methods. We screened for differentially expressed genes to establish a stemness-based classifier for predicting the patient's prognosis. Next, we determined the effect of risk scores on the tumor immune microenvironment (TIME) and the response of patients to immune checkpoint blockade (ICB). Finally, we used qRT-PCR to investigate gene expression in patients with HCC. Results: We screened CSC-related genes using various bioinformatics tools in patients from the TCGA-LIHC cohort. We constructed a stemness classifier based on a nine-gene (PPARGC1A, FTCD, CFHR3, MAGEA6, CXCL8, CABYR, EPO, HMMR, and UCK2) signature for predicting the patient's prognosis and response to ICBs. Further, the model was validated in an independent GSE14520 dataset and performed well. Our model could predict the status of TIME, immunogenomic expressions, congenic pathway, and response to chemotherapy drugs. Furthermore, a significant increase in the proportion of infiltrating macrophages, Treg cells, and immune checkpoints was observed in patients in the high-risk group. In addition, tumor cells in patients with high mRNAsi scores could escape immune surveillance. Finally, we observed that the constructed model had a good expression in the clinical samples. The HCC tumor size and UCK2 genes expression were significantly alleviated and decreased, respectively, by treatments of anti-PD1 antibody. We also found knockdown UCK2 changed expressions of immune genes in HCC cell lines. Conclusion: The novel stemness-related model could predict the prognosis of patients and aid in creating personalized immuno- and targeted therapy for patients in HCC.


Biomarkers, Tumor , Carcinoma, Hepatocellular , Computational Biology , Immunotherapy , Liver Neoplasms , Machine Learning , Neoplastic Stem Cells , Tumor Microenvironment , Humans , Carcinoma, Hepatocellular/immunology , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/therapy , Carcinoma, Hepatocellular/pathology , Liver Neoplasms/immunology , Liver Neoplasms/genetics , Liver Neoplasms/therapy , Liver Neoplasms/pathology , Neoplastic Stem Cells/immunology , Neoplastic Stem Cells/metabolism , Neoplastic Stem Cells/pathology , Computational Biology/methods , Prognosis , Biomarkers, Tumor/genetics , Tumor Microenvironment/immunology , Tumor Microenvironment/genetics , Immunotherapy/methods , Male , Gene Expression Regulation, Neoplastic , Female , Gene Expression Profiling , Middle Aged , Predictive Value of Tests
2.
Radiol Case Rep ; 19(8): 3258-3262, 2024 Aug.
Article En | MEDLINE | ID: mdl-38812594

Clonorchis sinensis infections persist globally among humans. These pathogens mainly inhabit the intrahepatic biliary system. Most individuals with clonorchiasis exhibit mild symptoms. The absence of distinctive symptoms often results in delayed diagnosis and treatment, potentially leading to chronic infection. We herein report a case of a 29-year-old female presented with a year-long history of abdominal distention and dyspepsia. Imaging revealed intrahepatic bile duct dilatation, intrahepatic bile duct cyst, and associated deposits. One month post-cystectomy, the patient developed massive ascites and a significant increase in eosinophil count. After treatment, multiple worms were observed in the drainage tube. Morphological and DNA metagenomic analyses confirmed the presence of C. sinensis. Clinical manifestations of C. sinensis vary widely. Imaging serves as a valuable diagnostic tool in endemic areas, especially in detecting intrahepatic duct dilation where the flukes reside. In addition to intrahepatic bile duct dilation, abnormal echoes within the bile duct and the presence of floating objects in the gallbladder significantly aid in diagnosis. Clinicians may encounter these parasitic diseases unexpectedly, underscoring the importance of understating such cases in routine practice and contributing to our broader understanding of managing similar cases in clinical settings.

3.
Aging (Albany NY) ; 15(16): 7933-7955, 2023 08 16.
Article En | MEDLINE | ID: mdl-37589508

Tumor oncogenesis, cancer metastasis, and immune evasion were substantially impacted by the mammalian target of the rapamycin complex 1 (mTORC1) pathway. However, in hepatocellular carcinoma (HCC), no mTORC1 signaling-based gene signature has ever been published. mTORC1 scores were computed employing a single sample gene set enrichment analysis based on databases including the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). The PAG1, LHFPL2, and FABP5 expression levels were obtained to construct a mTORC1 pathway-related model. In two databases, the overall survival (OS) rate was shorter for high-mTORC1 score patients compared to those with low scores. The activation of TFs in the group with high risk was enhanced, such as the HIF-1 pathway. Additionally, it was discovered that a high mTORC1 score was linked to an immune exclusion phenotype and enhanced immunosuppressive cell infiltration. Notably, it was discovered that high-mTORC1 scores patients had poorer immunotherapeutic results and might not gain benefit from immunotherapy. When compared to the low HCC metastatic cell lines, the high HCC metastatic cell lines have overexpressed levels of PAG1, LHFPL2, and FABP5 expression. The expression of PAG1, LHFPL2, and FABP5 was inhibited by the MAPK and mTORC1 pathway inhibitors. Our study identified mTORC1 score signature can aid in the development of individualized immunotherapy protocols and predict the HCC patients' prognoses.


Carcinoma, Hepatocellular , Liver Neoplasms , Humans , Prognosis , Carcinogenesis , Immunotherapy , Mechanistic Target of Rapamycin Complex 1 , Fatty Acid-Binding Proteins , Membrane Proteins , Adaptor Proteins, Signal Transducing
4.
BMC Pediatr ; 23(1): 359, 2023 07 13.
Article En | MEDLINE | ID: mdl-37442946

OBJECTIVE: To investigate the feasibility and clinical outcomes of early enteral nutrition (EN) in critically ill neonates supported by extracorporeal membrane oxygenation (ECMO). METHODS: We retrospectively analyzed the clinical data of 16 critically ill neonates who received ECMO support for respiratory and circulatory failure from July 2021 to December 2022 at our center. The patients were divided into two groups: the early EN group (< 24 h) and the late EN group (> 24 h). The related clinical and nutrition-related indicators between the groups were compared. RESULTS: There was a significant difference in the time from ECMO treatment to the start of EN between the early EN group (9 patients, 56.2%) and the late EN group (7 patients, 43.8%) (P < 0.05). However, there were no significant differences in ECMO duration, hospitalization time, vasoactive-inotropic score (VIS), intestinal oxygen saturation, or routine stool occult blood (OB) test between the two groups (all P > 0.05). The incidence of complications such as intestinal obstruction, abdominal distension, diarrhea, and necrotizing enterocolitis (NEC) was slightly lower in the early EN group, but the differences were not statistically significant (all P > 0.05). The early EN group had a shorter time [3.6 (3.5, 5) vs. 7.5 (5.9, 8.5) d] to reach full gastrointestinal nutrition compared to the late EN group (P < 0.05). CONCLUSION: Providing early nutritional support through enteral feeding to critically ill neonates receiving ECMO treatment is both safe and practical, but close monitoring of clinical and nutritional indicators is essential.


Enteral Nutrition , Extracorporeal Membrane Oxygenation , Humans , Infant, Newborn , Critical Illness/therapy , Retrospective Studies , Nutritional Status
5.
Exp Hematol Oncol ; 12(1): 9, 2023 Jan 13.
Article En | MEDLINE | ID: mdl-36639822

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most lethal malignant tumors. Cell division cycle associated 8 (CDCA8) is an important multifactorial regulator in cancers. However, its up and downstream targets and effects in HCC are still unclear. METHODS: A comprehensive bioinformatics analysis was performed using The Cancer Genome Atlas dataset (TCGA) to explore novel core oncogenes. We quantified CDCA8 levels in HCC tumors using qRT-PCR. HCC cell's proliferative, migratory, and invasive abilities were detected using a Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, clone formation, and a Transwell assay. An orthotopic tumor model and tail vein model were constructed to determine the effects of CDCA8 inhibition in vivo. The mechanism underlying CDCA8 was investigated using RNA sequencing. The prognostic value of CDCA8 was assessed with immunohistochemical staining of the tissue microarrays. RESULTS: CDCA8 was identified as a novel oncogene during HCC development. The high expression of CDCA8 was an independent predictor for worse HCC outcomes both in publicly available datasets and in our cohort. We found that CDCA8 knockdown inhibited HCC cell proliferation, colony formation, and migration by suppressing the MEK/ERK pathway in vitro. Moreover, CDCA8 deficiency significantly inhibited tumorigenesis and metastasis. Next-generation sequencing and laboratory validation showed that CDCA8 silencing inhibited the expression of TPM3, NECAP2, and USP13. Furthermore, NA-YA overexpression upregulated the expression of CDCA8. CDCA8 knockdown could attenuate NF-YA-mediated cell invasion in vitro. The expression of NF-YA alone or in combined with CDCA8 were validated as significant independent risk factors for patient survival. CONCLUSION: Our findings revealed that the expression of CDCA8 alone or in combined with NF-YA contributed to cancer progression, and could serve as novel potential therapeutic targets for HCC patients.

6.
Mol Med Rep ; 27(2)2023 Feb.
Article En | MEDLINE | ID: mdl-36484391

Following the publication of this article, an interested reader drew to the authors' attention that the primer sequences written for lncRNA DQ786243 and miR­15b­5p on p. 2 in the study were incorrect. Upon requesting an explanation of these errors from the authors, they realized that, regarding the sequence of the reverse primer for lncRNA DQ786243, three nucleotides were omitted from its 3'­end [the sequence of this primer on p. 2, right­hand column, line 25 should have been written as 5'­CTTCTGCTGGGCTGTTGAGTG­3' (with the omitted nucleotides highlighted in bold)]. Regarding the primers of miR­15b­5p, the authors used the mature miR­15b­5p sequence as the forward primer; however, they inadvertently overlooked replacing U with T in the description of the forward primer of miR­15b­5p, and therefore the sequence of the forward primer of miR­15b­5p on line 27 should have been written as 5'­TAGCAGCACATCATGGTTTACA­3'. Moreover, a universal reverse primer was used for the reverse primer of miR­15b­5p, as provided by the kit [specifically, the authors used an Mir­X miRNA qRT­PCR TB Green Kit (Takara Bio USA, Inc.) for detecting the expression of miR­15b­5p, and the reverse primer was supplied in the kit]; however, a different primer sequence used in the authors' lab was erroneously written as the reverse primer of miR­15b­5p in the manuscript. Finally, note that the title was published with a typographical error: "miR­15p­5p" in the title should have been written as "miR­15b­5p", as appeared elsewhere throughout the paper, and the corrected title is presented above.  The authors are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this corrigendum, and all the authors agree with its publication. The authors also regret the inconvenience that these mistakes have caused. [Molecular Medicine Reports 23: 318, 2021; DOI: 10.3892/mmr.2021.11957].

7.
Br J Math Stat Psychol ; 76(1): 192-210, 2023 02.
Article En | MEDLINE | ID: mdl-36250345

Probit models are used extensively for inferential purposes in the social sciences as discrete data are prevalent in a vast body of social studies. Among many accompanying model inference problems, a critical question remains unsettled: how to develop a goodness-of-fit measure that resembles the ordinary least square (OLS) R2 used for linear models. Such a measure has long been sought to achieve 'comparability' of different empirical models across multiple samples addressing similar social questions. To this end, we propose a novel R2 measure for probit models using the notion of surrogacy - simulating a continuous variable S as a surrogate of the original discrete response (Liu & Zhang, Journal of the American Statistical Association, 113, 845 and 2018). The proposed R2 is the proportion of the variance of the surrogate response explained by explanatory variables through a linear model, and we call it a surrogate R2 . This paper shows both theoretically and numerically that the surrogate R2 approximates the OLS R2 based on the latent continuous variable, preserves the interpretation of explained variation, and maintains monotonicity between nested models. As no other pseudo R2 , McKelvey and Zavoina's and McFadden's included, can meet all the three criteria simultaneously, our measure fills this crucial void in probit model inference.


Models, Statistical , Linear Models
8.
BMC Cancer ; 22(1): 1037, 2022 Oct 04.
Article En | MEDLINE | ID: mdl-36195833

BACKGROUND: Fatty acid (FA) metabolism is considered the emerging cause of tumor development and metastasis, driving poor prognosis. Long non-coding RNAs (lncRNAs) are closely related to cancer progression and play important roles in FA metabolism. Thus, the discovery of FA metabolism-related lncRNA signatures to predict outcome and immunotherapy response is critical in improving the survival of patients with hepatocellular carcinoma (HCC). METHODS: FA metabolism scores and a FA metabolism-related lncRNA signature were constructed using a single-sample gene set enrichment analysis based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. "ConsensusClusterPlus" was used to screen molecular subtypes. Chi-squared test and Fisher's exact test were applied to explore the relationship between clinical, genomic mutation characteristics and subtypes. Transcription factor (TF) activity scores, cellular distributions, immune cell infiltration, and immunotherapy response were employed to investigate the functions of FA metabolism-related lncRNA signatures. FA metabolism microarray and western blot were performed to detect the biological function of candidate lncRNAs. RESULTS: A total of 70 lncRNAs that highly correlated with FA metabolism scores in two cohorts were used to construct two distinct clusters. Patients in cluster 2 had lower FA metabolism scores and worse survival than those in cluster 1. Patients in cluster 2 exhibited a high frequency of DNA damage, gene mutations, oncogenic signaling such as epithelial-to-mesenchymal transition, and a high degree of immune cell infiltration. Moreover, the lncRNA signature could predict the effects of immunotherapy in patients with HCC. Furthermore, three lncRNAs (SNHG1, LINC00261, and SNHG7) were identified that were highly correlated with FA metabolism. Additionally, SNHG1 and SNHG7 were found to regulate various FA metabolism-related genes and ferroptosis-related genes in vitro experiments. GSEA analysis revealed that SNHG1 and SNHG7 promote fatty acid beta-oxidation. SNHG1 and SNHG7 silencing dramatically reduced lipid droplets in HCC cells. Many immune-infiltration genes and TFs were overexpressed in HCC tissues with SNHG1 and SNHG7 high expression. CONCLUSIONS: A novel molecular model of FA metabolism-related lncRNAs was developed, which has significantly prognostic potential in HCC diagnosis and aids in clinical decision making.


Carcinoma, Hepatocellular , Liver Neoplasms , RNA, Long Noncoding , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/therapy , Fatty Acids , Gene Expression Regulation, Neoplastic , Humans , Immunotherapy , Liver Neoplasms/genetics , Liver Neoplasms/therapy , Prognosis , RNA, Long Noncoding/metabolism , Transcription Factors/genetics
9.
Article En | MEDLINE | ID: mdl-35795282

Nonalcoholic fatty liver disease (NAFLD) is the most common metabolic liver disease globally, and the incidence of NAFLD has been increasing rapidly year by year. Currently, there is no effective pharmacotherapy for NAFLD. Therefore, studies are urgently needed to explore therapeutic drugs for NAFLD. In this study, we show that isoschaftoside (ISO) dramatically reduces lipid deposition in cells. Meanwhile, ISO treatment reverses the NAFLD and reduces hepatic steatosis in mice. Importantly, we reveal that ISO suppresses the expression of light-chain 3-II (LC3-II) and SQSTM1/p62 in palmitic acid (PA) induced autophagy inhibition in the cell model and the NAFLD mouse model, which suggests that ISO might reverse NAFLD through regulating autophagy flux. We propose that ISO might alleviate hepatic steatosis in NAFLD via regulating autophagy machinery. Consequently, our study suggests that ISO might be of potential clinical value in the field of NAFLD therapy. ISO might have the potential for future therapeutic application.

10.
Microbes Infect ; 24(8): 104999, 2022.
Article En | MEDLINE | ID: mdl-35569749

As a pathogenic microorganism, Listeria monocytogenes is widely used in the research of bacterial pathogenesis and host defense. The phagosomal escape of L. monocytogenes is essential for its replication in the cytoplasm of the host. Here, we reported that the protein abundance of the Six-transmembrane epithelial antigen of the prostate 3 (Steap3) was decreased upon L. monocytogenes infection compared to uninfected cells in macrophages. However, the decreased Steap3 abundance was not regulated by the host but was caused by LLO secreted by L. monocytogenes. Functional experiments showed that deletion of Steap3 facilitated entry of L. monocytogenes from the phagosome into the cytoplasm. Then, the comprehensive proteomic analysis revealed that the deletion of Steap3 could affect the proteins abundance of the lysosomal signaling pathway in macrophages. Among these proteins affected by Steap3, we discovered that only the Ganglioside GM2 activator (Gm2a) inhibited the phagosomal escape of L. monocytogenes as Steap3. In summary, we found that the Steap3-Gm2a axis could restrict the phagosomal escape of L. monocytogenes and serve the potential molecular drug targets for antibacterial treatment.


Bacterial Toxins , Listeria monocytogenes , Listeriosis , Male , Humans , Listeriosis/microbiology , G(M2) Ganglioside/metabolism , Hemolysin Proteins/metabolism , Gangliosides/metabolism , Proteomics , Bacterial Toxins/metabolism , Heat-Shock Proteins/metabolism , Phagosomes/microbiology
11.
Front Oncol ; 12: 812655, 2022.
Article En | MEDLINE | ID: mdl-35223495

NIMA-related kinase 7 (NEK7) is a serine/threonine kinase involved in cell cycle progression via mitotic spindle formation and cytokinesis. It has been related to multiple cancers, including breast cancer, hepatocellular cancer, lung cancer, and colorectal cancer. Moreover, NEK7 regulated the NLRP3 inflammasome to activate Caspase-1, resulting in cell pyroptosis. In the present study, we investigated whether NEK7 is involved in cell pyroptosis of hepatocellular carcinoma (HCC). Interestingly, we found that NEK7 was significantly related to expression of pyroptosis marker GSDMD in HCC. We found that NEK7 expression was significantly correlated with GSDMD expression in bioinformatics analysis, and NEK7 expression was significantly co-expressed with GSDMD in our HCC specimens. Cell viability, migration, and invasion capacity of HCC cell lines were inhibited, and the tumor growth in the xenograft mouse model was also suppressed following knockdown of NEK7 expression. Mechanistic studies revealed that knockdown of NEK7 in HCC cells significantly upregulated the expression of pyroptosis markers such as NLRP3, Caspase-1, and GSDMD. Coculture of HCC cells stimulated hepatic stellate cell activation by increasing p-ERK1/2 and α-SMA. Knockdown of NEK7 impaired the stimulation of HCC cells. Therefore, downregulation of NEK7 inhibited cancer-stromal interaction by triggering cancer cell pyroptosis. Taken together, this study highlights the functional role of NEK7-regulated pyroptosis in tumor progression and cancer-stromal interaction of HCC, suggesting NEK7 as a potential target for a new therapeutic strategy of HCC treatment.

12.
Psychol Health Med ; 27(4): 948-955, 2022 04.
Article En | MEDLINE | ID: mdl-34651528

Many studies have shown that parents of children with congenital heart disease have more stress, anxiety and depression. This study was aimed to explore the effect of implementing WeChat-assisted health education and preoperative care on parents of children with the restrictive ventricular septal defect to improve the psychological state. A prospective randomized controlled study was conducted in a provincial hospital in China. Participants were randomly divided into an intervention group and a control group to explore the psychological state of parents of children with the restricted ventricular septal defect. Before surgery, the state-trait anxiety inventory scale score (STAI) of the WeChat group were 26.8 ± 8.2 and 27.3 ± 7.0, which were significantly higher than those of the leaflet group (37.6 ± 12.9 and 39.3 ± 11.7). Compared with the STAI score at the first visit, the WeChat group preoperative score was significantly lower (P < 0.05). The rate of loss to follow-up in the WeChat group (0%) was significantly lower than that of the leaflet group (14.3%). The complication of the leaflet group was significantly higher than that of the WeChat group. Health education and preoperative care for parents of children with restrictive ventricular septal defect through WeChat can effectively improve the parents' mental state and reduce the incidence of complications and the rate of loss to follow-up.


Heart Septal Defects, Ventricular , Child , Health Education , Heart Septal Defects, Ventricular/surgery , Humans , Parents , Preoperative Care , Prospective Studies
13.
Heart Surg Forum ; 25(5): E778-E783, 2022 11 30.
Article En | MEDLINE | ID: mdl-36602401

OBJECTIVE: Factors leading to an unplanned return to the cardiac intensive care unit (CICU) in children after congenital heart disease and their impact on mortality have not been well characterized. We sought to determine the incidence and outcomes of unplanned return to the CICU. A secondary objective was to identify risk factors. METHODS: Retrospective analysis of the registration data collected by our unit. The study subjects included postoperative patients with congenital heart disease who survived to initial transfer out of the CICU. Patients who unexpectedly returned to the CICU due to an acute change in clinical status were defined as unplanned returns. Demographic, preoperative, intraoperative, and postoperative variables were assessed. Univariate comparisons were performed between the return group and non-return group, and multivariate regression analysis was performed to identify potential risk factors for unplanned return to the CICU. RESULTS: Of the 531 children who met the inclusion criteria, 29 were unplanned returns to the CICU. Respiratory symptoms (41.4%) and cardiac symptoms (44.8%) were the most common reasons for returning to the CICU. Patients with unplanned returns had a higher mortality rate (13.8% vs. 0.56%, P < 0.01). In multivariate analysis, unplanned CICU admission was associated with chromosomal abnormalities (P < 0.01), longer ventilator duration (P < 0.01), and more prolonged cardiopulmonary bypass (P < 0.01) was associated with a return to independence. CONCLUSIONS: Unplanned return to the CICU during the same hospital stay was uncommon but associated with higher mortality. Chromosomal abnormalities, longer ventilator use duration, and prolonged CPB were significant risk factors for the entire cohort. We hope to minimize the impact of unplanned return after congenital heart disease surgery by changing the process of transferring these high-risk postoperative patients out of the CICU and early postoperative care.


Heart Defects, Congenital , Intensive Care Units , Humans , Child , Retrospective Studies , Incidence , Heart Defects, Congenital/epidemiology , Heart Defects, Congenital/surgery , Heart Defects, Congenital/diagnosis , Risk Factors , Length of Stay
14.
Front Oncol ; 11: 705797, 2021.
Article En | MEDLINE | ID: mdl-34295827

The prognosis for pancreatic ductal adenocarcinoma (PDAC) patients is still dismal. Elucidation of associated genomic alteration may provide effective therapeutic strategies for PDAC treatment. NIMA-related protein kinase 7 is widely expressed in various tumors, including breast cancer, colorectal cancer and lung cancer, and promotes the proliferation of liver cancer cells in vitro and in vivo. We investigated the protein expression level of NEK7 in tumor tissues and adjacent normal tissues using immunohistochemistry of 90 patients with PADC. Meanwhile, the RNA expression level of NEK7 was examined using database-based bioinformatic analysis. Correlation and significance of NEK7 expression with patient clinicopathological features and prognosis were examined. Cell proliferation, cell adhesion, migration and invasion capabilities were measured following downregulation of NEK7 expression. 3D tumor organoids of pancreatic cancer were established and splenic xenografted into nude mice, then liver metastatic ability of NEK7 was evaluated in following 4 weeks. We observed NEK7 expression was upregulated in tumor tissues compared to normal tissues at both RNA and protein levels using bioinformatic analysis and immunohistochemistry analysis in PDAC. NEK7 expression was undetectable in normal pancreatic ducts; NEK7 was overexpressed in primary tumor of PDAC; NEK7 expression was highly correlated with advanced T stage, poorly differentiated histological grade invasive ductal carcinoma, and lymphatic invasion. Meanwhile, patients with higher NEK7 expression accompanied by worse survival outcome. Moreover, NEK7 promoted migration, invasion, adhesion, proliferation and liver metastatic ability of pancreatic cancer cells. Taken together, our data indicate that NEK7 promotes pancreatic cancer progression and it may be a potential marker for PDAC prognosis.

15.
Angew Chem Int Ed Engl ; 60(38): 20906-20914, 2021 Sep 13.
Article En | MEDLINE | ID: mdl-34255409

A universal strategy is developed to construct a cascade Z-Scheme system, in which an effective energy platform is the core to direct charge transfer and separation, blocking the unexpected type-II charge transfer pathway. The dimension-matched (001)TiO2 -g-C3 N4 /BiVO4 nanosheet heterojunction (T-CN/BVNS) is the first such model. The optimized cascade Z-Scheme exhibits ≈19-fold photoactivity improvement for CO2 reduction to CO in the absence of cocatalysts and costly sacrificial agents under visible-light irradiation, compared with BVNS, which is also superior to other reported Z-Scheme systems even with noble metals as mediators. The experimental results and DFT calculations based on van der Waals structural models on the ultrafast timescale reveal that the introduced T as the platform prolongs the lifetimes of spatially separated electrons and holes and does not compromise their reduction and oxidation potentials.

16.
J Paediatr Child Health ; 57(10): 1666-1671, 2021 Oct.
Article En | MEDLINE | ID: mdl-34057253

AIM: This study aimed to explore the effect of performing remote health education via WeChat to improve the pre-operative nutritional status of non-restrictive ventricular septal defects (VSD). METHODS: A prospective randomised controlled study was conducted in a provincial maternity and child hospital in China. Participants were randomised regarding education to the intervention group (WeChat) and the control group (leaflets). The nutritional status and complications of the patients were compared after intervening for 1 month. RESULTS: Nutrient status comparison at 1 month after intervention showed that the body weight, head circumference, haemoglobin, albumin and pre-albumin of the WeChat group were significantly higher than those of the leaflet group (P < 0.05). The STRONGkids score of the WeChat group was significantly lower than that of the leaflet group (P < 0.05). The incidence of feeding intolerance and respiratory tract infection in the WeChat group was significantly lower than that found in the leaflet group (P < 0.05). There was no significant difference in the incidence of liver insufficiency and jaundice between the two groups (P > 0.05). CONCLUSION: Providing pre-operative feeding and care guidance for parents of infants with non-restrictive VSD, via remote health education through WeChat, can effectively improve nutritional status and reduce the risk of malnutrition and feeding complications.


Heart Septal Defects, Ventricular , Nutritional Status , Child , Female , Health Education , Heart Septal Defects, Ventricular/surgery , Humans , Infant , Infant, Newborn , Pregnancy , Prospective Studies , Research Design
17.
Heart Surg Forum ; 24(2): E305-E310, 2021 03 26.
Article En | MEDLINE | ID: mdl-33798055

OBJECTIVE: To investigate the effect of music therapy on chronic pain, quality of life, and quality of sleep in adolescent patients after transthoracic occlusion of ventricular septal defects. METHODS: Patients were divided into 2 groups based on whether they received music therapy: a control group and a music group. The music group received 30 minutes of music therapy every day for 6 months after surgery. Patients in the control group received standard treatment and had 30 minutes of quiet time every day for 6 months after surgery. The short-form McGill pain questionnaire (SF-MPQ), the SF-36 scale and the Karolinska Sleep Questionnaire (KSQ) was used as the evaluation tool for chronic pain, quality of life, and quality of sleep, respectively. RESULTS: In terms of the degree of postoperative chronic pain, the Pain Rating Index (PRI) emotion item score in the SF-MPQ evaluation of the music group was significantly lower than that of the control group (1.6 ± 1.1 versus 2.2 ± 0.9). The role emotional (RE) scores of the SF-36 in the music group were significantly higher than that in the control group (77.35 ± 18.55 versus 42.66 ± 22.63). KSQ scores were significantly higher in the music group than in the control group for sleep status (4.1 ± 1.0 versus 3.3 ± 0.9), falling asleep (3.9 ± 1.1 versus 3.1 ± 1.0), and not feeling refreshed by sleep (3.6 ± 1.3 versus 2.7 ± 0.9) (P < .05). CONCLUSION: This study preliminarily showed that music therapy could effectively reduce patients' chronic pain and improve quality of life and sleep after surgery. These results suggest that music therapy may be an essential therapy worth considering in managing patients' postoperative recovery after cardiovascular surgery.


Heart Septal Defects, Ventricular/surgery , Music Therapy/methods , Pain, Postoperative/rehabilitation , Quality of Life , Sleep/physiology , Child , Female , Follow-Up Studies , Humans , Male , Pain Measurement , Pain, Postoperative/diagnosis , Pain, Postoperative/psychology , Retrospective Studies , Severity of Illness Index , Surveys and Questionnaires
18.
Mol Med Rep ; 23(5)2021 05.
Article En | MEDLINE | ID: mdl-33760109

Increasing evidence suggests that long noncoding RNAs (lncRNAs) influence the pathogenesis and progression of hepatocellular carcinoma (HCC). The authors of the present study previously reported that abnormal upregulation of lncRNA DQ786243 (lncDQ) was associated with poor prognoses for patients with HCC. However, the elucidation of underlying mechanisms which influenced these results was not completed. Thus, the current study aimed to characterize the mechanisms and functions of lncDQ that facilitate its promotion of HCC progression. lncDQ, miR­15b­5p and Wnt3A expression levels were characterized in HCC and portal vein tumor thrombus tissue samples and for liver cancer and liver cancer cell lines using reverse transcription­quantitative PCR. Bioinformatics software was used for the analysis of interactions between lncDQ and miR­15b­5p, miR­15b­5p and Wnt3A. Luciferase assays confirmed the binding relationships between miR­15b­5p and the 3' untranslated region (UTR) of Wnt3A. Using online databases, prognostic values of miR­15b­5p and Wnt3A were also assessed. Proliferation and invasion assays were used to assess liver cancer and HCC cell functions after individually silencing lncDQ and miR­15b­5p expression in the cells. Western blotting was used for the investigation of alterations of the expression of Wnt3A/ß­catenin and epithelial­mesenchymal transition (EMT) signal pathways. lncDQ and Wnt3A expression were significantly increased in HCC tissues, whereas miR­15b­5p was downregulated in HCC tissues. Low expression of miR­15b­5p was also associated with poor prognoses for patients with HCC. lncDQ was able to bind with miR­15b­5p and served as a competing endogenous RNA. As the target gene of miR­15b­5p, Wnt3A was correlated with poor prognoses for patients with HCC. Silencing of lncDQ expression significantly attenuated proliferation and invasion of liver cancer and HCC cells, however the inhibition of miR­15b­5p was able to reverse this effect. However, silencing of lncDQ and miR­15b­5p expression simultaneously resulted in the partial rescue of the inhibitory effect in the liver cancer and HCC cells. lncDQ inhibited miR­15b­5p so as to promote HCC cell invasion and proliferation through activation of the Wnt3A/ß­catenin/EMT pathway. Taken together, the results of the present study suggested that the lncDQ/miR­15b­5p axis modulates the progression of HCC.


Carcinoma, Hepatocellular/genetics , Liver Neoplasms/genetics , RNA, Long Noncoding/genetics , Wnt3A Protein/genetics , Animals , Apoptosis , Carcinoma, Hepatocellular/pathology , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Epithelial-Mesenchymal Transition/genetics , Female , Gene Expression Regulation, Neoplastic/genetics , Hep G2 Cells , Humans , Liver Neoplasms/pathology , Male , Mice , Neoplasm Invasiveness/genetics , Neoplasm Invasiveness/pathology
19.
Proteomics ; 21(10): e2000262, 2021 05.
Article En | MEDLINE | ID: mdl-33763969

Macrophages are sentinels in the organism which can resist and destroy various bacteria through direct phagocytosis. Here, we reported that expression level of mitochondrial ribosomal protein S35 (Mrps35) continued to decrease over infection time after Listeria monocytogenes (L. monocytogenes) infected macrophages. Our results indicated that knockdown Mrps35 increased the load of L. monocytogenes in macrophages. This result supported that Mrps35 played the crucial roles in L. monocytogenes infection. Moreover, we performed the comprehensive proteomics to analyze the differentially expressed protein of wild type and Mrps35 Knockdown Raw264.7 cells by L. monocytogenes infection over 6 h. Based on the results of mass spectrometry, we presented a wide variety of hypotheses about the mechanism of Mrps35 controlling the L. monocytogenes intracellular proliferation. Among them, experiments confirmed that Mrps35 and 60S ribosomal protein L22-like 1 (Rpl22l1) were a functional correlation or potentially a compensatory mechanism during L. monocytogenes infection. This study provided new insights into understanding that L. monocytogenes infection changed the basic synthesis or metabolism-related proteins of host cells.


Listeria monocytogenes , Cell Proliferation , Macrophages , Phagocytosis , Proteomics
20.
Heart Surg Forum ; 23(6): E845-E849, 2020 Nov 18.
Article En | MEDLINE | ID: mdl-33234196

OBJECTIVE: To explore the effects of breast milk feeding and formula milk feeding on infants after cardiac surgery in the cardiac intensive care unit (ICU). METHODS: Infants who underwent cardiac surgery in our ICU were divided into two groups, according to feeding type. Breast milk feeding and formula milk feeding were separately implemented in the two groups, and the remaining treatment regimens were the same. The related clinical data and feeding effects were recorded and compared. RESULTS: The prealbumin (147.3 ± 15.2 versus 121.5 ± 18.3mg/L) and albumin (46.4 ± 4.2 versus 40.5 ± 5.1 g/L) levels in the breast milk feeding group were better than those in the formula milk feeding group (P < .05). Infants in the breast milk feeding group achieved a better total enteral nutrition time (3.0 ± 1.2 versus 5.2 ± 2.1 d), average daily weight gain (19.0 ± 3.4 versus 14.4 ± 2.3 g/kg·d), length of ICU stay (6.0 ± 2.2 versus 8.1 ± 2.9 d) and length of hospital stay (13.9 ± 4.2 versus 17.8 ± 5.6 d) than those in the formula milk feeding group (P < .05). The incidence of complications such as feeding intolerance, anemia, dyspeptic diarrhea, and nosocomial infection was lower in the breast milk feeding group than in the formula milk feeding group (P < 0.05). CONCLUSION: Breast milk feeding has a definite nutritional effect on infants after cardiac surgery. It is better than formula milk feeding, making it worthy of popularization and application.


Breast Feeding/methods , Cardiac Surgical Procedures/methods , Enteral Nutrition/methods , Heart Defects, Congenital/surgery , Milk, Human , Postoperative Care/methods , Weight Gain/physiology , Female , Follow-Up Studies , Heart Defects, Congenital/rehabilitation , Humans , Infant , Male , Retrospective Studies
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