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Objective: To investigate the effects of inhibin subunit beta A antisense RNA 1 (INHBA-AS1) on epithelial-interstitial transformation (EMT) and ornithine metabolic pathway of cervical cancer cells and its mechanism. Methods: Cervical cancer HeLa cells were routinely cultured in vitro and the experiment was divided into 10 groups: control group, negative control (NC) group, sh-INHBA-AS1 group, PluriSIn 1 [stearyl CoA desaturase (SCD) inhibitor] group, NC+PluriSIn 1 group, sh-INHBA-AS1+PluriSIn 1 Group, 10058-F4 (c-Myc inhibitor) group, NC+10058-F4 group, sh-INHBA-AS1+10058-F4 group, sh-INHBA-AS1+OE-c-Myc group. The proliferation ability of cells in each group was detected by plate cloning assay; the apoptosis of cells in each group was detected by flow cytometry; the invasion and migration abilities of cells in each group were detected by Transwell assay; the expressions of INHBA-AS1, c-Myc, SCD and EMT-related genes (N-cadherin, TGF-β and ZEB1) in cells of each group were detected by qPCR; the expressions of c-Myc, SCD, EMT-associated (Ncadherin, TGF-β and ZEB1), S-adenosine-methionine decarboxylase (SAMDC) and spermidine/spermine N1 acetyltransferase (SSAT) proteins in each group were detected by WB method, and the content of ornithine decarboxylase (ODC) in cell supernatant was detected by ELISA. Results: The proliferation, invasion and migration abilities of HeLa cells were significantly decreased after INHBA-AS1 expression was knocked down (all P<0.05). The apoptosis rate was significantly increased (P<0.05). The results of qPCR and WB assay showed that knockdown of INHBA-AS1 could significantly inhibit the expressions of c-Myc, SCD, N-cadherin, TGF-β, ZEB1, and SAMDC in HeLa cells by (all P<0.05), promote the expression of SSAT (P<0.05) and decrease the content of ODC in HeLa cell supernatant (P<0.05). These effects were more significant after further knockdown of INHBA-AS1 compared with c-Myc inhibitor and SCD inhibitor treatments (all P <0.05). Compared with sh-INHBA-AS1 group, further over-expression of c-Myc significantly increased HeLa cell proliferation (P<0.05), SCD and N-cadherin protein expression levels (P<0.05), and the content of ODC in cell supernatant (P<0.05). Conclusion: INHBA-AS1 can regulate the expression of SCD through c-Myc, participate in the ornithine metabolism and EMT process of HeLa cells, and promote the proliferation, invasion, and migration of HeLa cells. [ABSTRACT FROM AUTHOR]

The study was to investigate the structure and function of LPD06283 protein of Rhodococcus opacus PD630. Bioinformatics methods were used to analyze the physicochemical properties, hydrophilicity and hydrophobicity, amphiphilic α helix, homology, signal peptide, transmembrane region, secondary structure, domain, tertiary structure, phosphorylation modification sites and interacting proteins of LPD06283 protein. The results showed that LPD06283 protein was a stable acidic hydrophilic protein, the N-terminal hydrophobic region of which formed an amphiphilic α-helix, closely related to MLDS protein of Rhodococcus jostii RHA1, and contained no signal peptide or transmembrane region. The secondary structure of LPD06283 protein was composed of α-helix (81.88%), β-turn (3.62%) and random coil (14.49%), there was an apolipoprotein domain at N-terminus, the tertiary structure was predicted by comprehensive method and was of high quality; LPD06283 protein contained 19 phosphorylation sites, the strongest interacting protein was XRE family DNA-binding protein. The study indicates that LPD06283 protein may be involved in lipid metabolism of Rhodococcus opacus, which can be used as a potential target for microbial lipid research and development. [ABSTRACT FROM AUTHOR]

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the effect of transcription factor specificity protein 1 (SP1) knockdown on cisplatin (DDP) resistance in small cell lung cancer (SCLC) H466/DDP cells and its molecular mechanism. Methods: SCLC H466/DDP cells with knockdown of SP1 and simultaneous overexpression of ATP binding cassette subfamily C member 1(ABCC1) were constructed, and the expression of SP1 and ABCC1 in non-drug-resistant and drug-resistant SCLC tissues was detected by IHC method. The correlation between SP1 and ABCC1 expression in SCLC tissues was analyzed by the Spearman r method. Western blot was performed to detect the expression of SP1, ABCC1 and CD44 in transfected H446/DDP cells. The proliferation, apoptosis and self-replication ability of H446/DDP cells were detected by CCK-8, flow cytometry and microsphere assay respectively. Chromatin immunoprecipitation (ChIP) assay was performed to detect whether SP1 is a transcription factor of ABCC1. Results: The protein levels of SP1 and ABCC1 in drugresistant H446/DDP cells and drug-resistant SCLC tissues were higher than those in parental H446 cells and non-drug-resistant SCLC tissues (all P<0.05), and the expression of SP1 and ABCC1 protein in SCLC tissues was positively correlated. Knockdown of SP1 inhibited the proliferation ability, reduced CD44 and ABCC1 protein expression levels, decreased the number of cell microsphere formation, and promoted apoptosis (all P<0.05) of H446/DDP cells. SP1 was approved to be the transcription factor of ABCC1. Conclusion: Transcription factor SP1 is involved in drug resistance in SCLC H446/DDP cells by regulating ABBC1 expression, and SP1 is a potential therapeutic target for DDP-resistant SCLC. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect and mechanism of miR-192-5p targeting ZEB2 (zinc finger E-box binding homeobox 2) on the proliferation, migration, invasion and EMT (epithelial-mesenchymal transition) of pancreatic cancer PANC-1 cells. Methods: The TCGA database was used to analyze the expression of miR-192-5p and ZEB2 as well as their correlation in pancreatic cancer tissue. The expression levels of miR-192-5p and ZEB2 were detected by qPCR and WB in human normal pancreatic epithelial HPNE cells and pancreatic cancer PANC-1 cells. PANC-1 cells were transfected with liposome, and divided into miR-192-5p mimic group, Mimic NC group, miR-192-5p inhibitor group, Inhibitor NC group, Mimic NC+pcDNA3.1 group, miR-192-5p mimic+pcDNA3.1 group, and miR-192-5p mimic+pcDNA3.1-ZEB2 group. The proliferation, colony formation, migration and invasion abilities of transfected PANC-1 cells were detected by CCK-8, colony formation, scratch healing and Transwell experiments, respectively. The expression of ZEB2, E-cadherin and vimentin was detected by qPCR, WB method and double immunofluorescence assay. Bioinformatics was used to predict the target gene of miR-192-5p, and the regulatory effect of miR-192-5p on the target gene was verified by dual luciferase report gene experiment. Results: The expression of ZEB2 in pancreatic cancer tissue was significantly higher than that in normal pancreatic tissue (P<0.01), and the expression of miR-192-5p and ZEB2 in pancreatic cancer tissue was inversely correlated (r=-0.419, P<0.01). Compared with normal pancreatic epithelial HPNE cells, the expression level of miR-192-5p was significantly lower while the expression level of ZEB2 protein was higher in pancreatic cancer PANC-1 cells (all P<0.01). Overexpression of miR-192-5p significantly reduced the proliferation, colony formation, migration and invasion ability of PANC-1 cells, upregulated the mRNA and protein expression of E-cadherin, and downregulated the mRNA and protein expression of vimentin and ZEB2, while inhibition of miR-192-5p achieved the opposite results (P<0.05 or P<0.01). miR-192-5p targetedly regulated the expression of ZEB2, and overexpression of ZEB2 could reverse the inhibitory effects of miR-192-5p overexpression on the proliferation, colony formation, migration, invasion and EMT of PANC-1 cells. Conclusion: miR-192-5p regulates the malignant biological behaviors of pancreatic cancer PANC-1 cells by targeting ZEB2. [ABSTRACT FROM AUTHOR]

Objective To observe the detection rate, morphological characteristics and deposition degree of pathological trans-activation response DNA binding protein 43 (TDP-43) in several common neurodegenerative diseases, and to explore its pathological significance. Methods A total of 15 cases with a history of hospitalization in the Second Medical Center, Chinese PLA General Hospital from January 1994 to September 2019 were retrospectively collected, including 5 cases of Alzheimer's disease (AD), 3 cases of Parkinson's disease (PD), 2 cases of progressive supranuclear palsy (PSP), and 5 cases of normal aging brain. HE staining, Lucas fast blue (LFB) staining, Gallyas-Braak silver staining, and immunohistochemical staining of β-amyloid (Aβ), AT8, phosphorylated TDP-43 and α-synuclein (α-Syn) were performed for amygdala tissue sections. The pathological morphological characteristics of pathological TDP-43 protein was observed under a light microscope, and the pathological TDP-43 protein was graded by semi-quantitative method. Results Phosphorylated TDP-43 antibody staining was found in 5/15 of aging brain amygdala tissue, including 2 cases of AD, one case of PD, and 2 cases of normal aging brain. Among them, severe pathological TDP-43 protein deposition and mild short neurodystrophy filaments were found in the amygdala of 2/5 cases of AD, mainly neuronal cytoplasmic inclusion bodies. Cytoplasmic inclusions and short neurodystrophy filaments in rare neurons of amygdala in 1/3 cases of PD. Rare or mild neuronal cytoplasmic inclusions and rare short neurodystrophy filaments were found in the amygdala of 2/5 normal aging brain. Two cases of PSP showed negative staining for phosphorylated TDP-43 antibody in amygdala. No long amygdala neurodystrophy filaments were found in the 15 patients. No glial cytoplasmic inclusions and neuronal intranuclear inclusions were found in PD, PSP and normal aging brain. Conclusions Pathological TDP-43 protein is most severe in the amygdala of AD and may accelerate cognitive decline in AD or lower the threshold of cognitive dysfunction. [ABSTRACT FROM AUTHOR]

Objective: To investigate the diagnostic features of pulmonary sclerosing pneumocytoma (PSP) in needle biopsy specimens so as to improve the preoperative diagnostic accuracy and to prevent misdiagnoses. Methods: A total of 79 needle biopsy cases confirmed as PSP in surgical resection specimens were collected in the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China from January 2015 to January 2023. A retrospective analysis was conducted to investigate the clinical, pathological, and immunohistochemical characteristics of PSP. Results: Among the 79 cases, there were 8 males and 71 females, with an age range of 14 to 67 years (median 47 years). Among the 79 needle biopsy cases of PSP, 5 cases were initially misdiagnosed as adenocarcinoma and 1 as carcinoid preoperatively, while the remaining 73 cases were correctly diagnosed. 84.8% (67/79) of the PSP presented with well-defined, homogeneous, solitary solid tumors on chest imaging. Morphologically, 26.6% (21/79) of the PSP mainly showed a single histological component, 67.1% (53/79) contained two histological components, and 6.3% (5/79) contained three histological components. There were no cases containing all four histological components simultaneously. The tumor was composed of cuboidal cells on the surface and round cells in the stroma and lacked significant cytological atypia and mitotic figures. Some cases exhibited variations in histology and cellular morphology, such as glandular spaces (58.2%, 46/79), sclerotic papillae (46.8%, 37/79), hypercellularity (16.5%, 13/79), and cytological atypia (24.1%, 19/79). Immunophenotyping indicated that both tumor cell types expressed TTF1, EMA and β-catenin, while surface cells expressed pan-cytokeratin and Napsin A, and stromal cells expressed vimentin. In some cases, ER and PR were also expressed. Conclusions: When diagnosing PSP in needle biopsy specimens, the key to avoiding misdiagnosis is recognizing the presence of dual-cell populations within the tumor. The useful clues include presence of cellular papillae, mild cellular atypia, morphological diversity, interstitial foam-like cell aggregates, and prominent background hemorrhage and sclerosis. The characteristic immunophenotype and middle-aged female predilection are also helpful for the diagnosis of PSP.

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objectives: To investigate the effect of osteoblast-derived extracellular vesicles (OB-EVs) on the proliferation and differentiation of osteoclasts, and to explore the possible molecular mechanism of extracellular vesicles involved in the communication between osteoblasts and osteoclasts., Methods: Primary osteoblasts were isolated from newborn mouse calvarial bone and induced by β-glycero phosphate, ascorbic acid and dexamethasone. Osteogenic feature was tested by alkaline phosphatase (ALP) and alizarin red S staining. Extracellular vesicles were isolated by ultracentrifugation from the cell culture supernatant. Vesicle morphology was observed by transmission electron microscopy, and the characteristic markers of tumor susceptibility gene 101 (TSG101), ALG-2 interacting protein X (Alix) and cluster of differentiation 9 (CD9) on the surface of extracellular vesicles were identified by Western blotting. Cell counting kit 8 (CCK-8) assay was used to determine the proliferation effect of OB-EVs on mouse mononuclear macrophage RAW264.7 cells. Furthermore, the expression level of specific markers of osteoclast differentiation in RAW264.7 cells was detected by Western blotting after the combined effect of OB-EVs and receptor activator for nuclear factor κB ligand (RANKL). The number of osteoclasts was observed and compared with OB-EVs-treated mouse bone marrow-derived macrophages (BMMs) by tartrate-resistant acid phosphatase (TRAP) staining, and the effect of OB-EVs on osteoclast differentiation was determined., Results: The extracted OB-EVs showed a double-layer cup-like structure with a diameter of 30-150 nm, and TSG101, Alix and CD9 were expressed. RAW264.7 cells were stimulated with OB-EVs, and the results of CCK-8 assay showed that high concentration of OB-EVs (more than 20 μg/mL) inhibited cell proliferation ( P <0.05). Western blotting analysis showed that the expression of osteoclast differentiation marker proteins such as c-Fos, activated T cell nuclear factor (NFATc1) and c-Jun N-terminal kinase (JNK) in RAW264.7 cells were significantly increased, and the promoting effect was enhanced with increasing of OB-EVs concentration ( P <0.05). In addition, the combination of OB-EVs and RANKL on BMMs showed that the number of TRAP-positive cells was significantly higher than that of the RANKL induction group alone ( P <0.05)., Conclusions: OB-EVs can promote the differentiation of osteoclast precursor cells into osteoclasts, but high concentration of OB-EVs can inhibit proliferation of RAW264.7 cells.

Objective: To explore the gene mutation characteristics and the relationship between gene mutations and long-term prognosis in clinical stage ⅠA lung adenocarcinoma patients. Methods: A retrospective analysis was conducted on 63 clinical stage ⅠA lung adenocarcinoma patients who underwent surgical resection at the Cancer Hospital of the Chinese Academy of Medical Sciences from January 2007 to October 2012, with documented postoperative recurrence or metastasis, as well as those who had a follow-up duration of 10 years or more without recurrence or metastasis. Whole exome sequencing (WES) technology was used to analyze the gene mutation profiles in tumor tissues and univariate and multivariate Cox regression analysis were used to clarify the influencing factors for patient prognosis. Results: After long term follow-up, 13 out of the 63 patients (21%) experienced recurrence or metastasis. WES technology analysis revealed that the most common tumor related gene mutations occurred in epidermal growth factor receptor (EGFR), with a mutation rate of 65.1% (41/63), followed by tumor protein p53 (TP53), fatatypical cadherin 1 (FAT1), low density lipoprotein receptor-related protein 1B (LRP1B), mechanistic target of rapamycin (MTOR), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma (PIK3CG), and SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4 (SMARCA4), with mutation rates of 30.2% (19/63), 20.6% (13/63), 15.9% (10/63), 15.9% (10/63), 15.9% (10/63), and 15.9% (10/63), respectively. Multivariate Cox regression analysis showed that PIK3CG mutations ( HR =21.52, 95% CI: 3.19-145.01),smoothened (SMO) mutations ( HR =35.28, 95% CI : 3.12-398.39), catenin beta 1 (CTNNB1) mutations ( HR =332.86, 95% CI : 15.76-7 029.05), colony stimulating factor 1 receptor (CSF1R) mutations ( HR =8 109.60, 95% CI : 114.19-575 955.17), and v-Raf murine sarcoma viral oncogene homolog B (BRAF) mutations ( HR =23.65, 95% CI : 1.86-300.43) were independent risk factors affecting the prognosis of clinical stage ⅠA lung adenocarcinoma patients. Conclusions: PIK3CG, SMO, CTNNB1, CSF1R, BRAF gene mutations are closely related to long-term recurrence or metastasis in clinical stage ⅠA lung adenocarcinoma. Patients with these gene mutations should be given closer clinical attention.

Objective: To evaluate the regulatory effect of Diwu Yanggan (DWYG) Decoction on lysoglycerophospholipids (Lyso-GPLs) in circulating exosomes in a mouse model of nonalcoholic fatty liver disease (NAFLD)., Methods: Circulating exosomes isolated from mouse serum by size exclusion chromatography were morphologically characterized using transmission electron microscope and examined for surface markers CD9, CD63 and TSG101 using Western blotting. Twenty-four male Kunming mice were randomized into 3 groups for normal feeding (control, n =8) or high-fat diet feeding for 1 week to induce NAFLD, after which the latter mice were given DWYG decoction (treatment group, n =8) or normal saline (model group, n =8) by gavage for 4 weeks. After the last treatment, blood samples were collected from the mice for testing serum TC, HDL-C, LDL-C, ALT and AST levels and isolating circulating exosomes. Using multivariate statistical analysis based on targeted metabolomics strategy, the potential biomarkers for Lyso-GPLs in the exosomes were screened., Results: The isolated exosomes about 100 nm in size had a typical saucer-like structure with distinct double-layer membranes and a mean particle size of 137.5 nm and expressed the specific surface marker proteins CD9, CD63 and TSG101. The mouse models of NAFLD had significantly increased serum levels of TC, HDL-C, LDL-C and AST and lowered serum ALT level. A total of 43 Lyso-GPLs with significant reduction after DWYG Decoction treatment were identified in NAFLD mice., Conclusion: DWYG Decoction can regulate Lyso-GPLs in circulating exosomes in NAFLD mice, which provides a new clue for studying the therapeutic mechanism of DWYG Decoction for liver disease.

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Cervical cancer, endometrial cancer and ovarian cancer are the three most common malignant tumors in gynecology, which seriously threaten the life and safety of women. DNA methylation is one of the important epigenetic mechanisms, which can lead to the silencing of tumor suppressor genes and ultimately lead to tumorigenesis. RUNX3 is one of the hot topics in the research of tumor suppressor genes, which plays an important role in cell growth, proliferation, differentiation, apoptosis and signal transduction. RUNX3 promoter methylation will lead to its expression silence, which plays an important role in the occurrence and development of gynecological tumors. Methylation inhibitors can induce the re-expression of RUNX3 to achieve the purpose of tumor treatment. The occurrence, growth and metastasis of tumor are closely related to the internal and external environment of tumor cells, which will form a unique tumor microenvironment. RUNX3 can regulate it through a variety of actions. With the further study of the mechanism of RUNX3 in gynecological tumors, it will lay a foundation for it to become a diagnostic marker and targeted therapy of gynecological tumors. To summarize the research progress of RUNX3 in gynecological tumors, in order to provide new ideas for clinical work. [ABSTRACT FROM AUTHOR]

Background and objective Lung cancer is the most common malignant tumor in clinic. The prognosis of advanced patients is poor, and the 5-year survival rate is low. Therefore, early diagnosis becomes the key to improve the prognosis of patients. In recent years, with the development of molecular biology technology, aberrant modification of some driver genes, such as methylation, has become an important method for early diagnosis of lung cancer. The purpose of the present work was to quantitatively evaluate the diagnostic value of abnormal hypermethylation in short state homeobox 2 (SHOX2) promoter region in lung cancer by evidence-based medicine. Methods We searched MEDLINE, EMBASE, Ovid, Web of Science and CNKI for literatures related to the relationship between SHOX2 gene promoter hypermethylation and lung cancer. The data of SHOX2 promoter hymethylation in the original study were extracted. The diagnostic sensitivity, specificity and area under receiver operating characteristic (ROC) curve of SHOX2 promoter methylation were calculated. Results Finally, 13 publications were included in this meta-analysis, and due to significant statistical heterogeneity among the studies (P<0.05) the data was pooled by random effect model. The diagnostic sensitivity and specificity of SHOX2 promoter hypermethylation in the diagnosis of lung cancer were 0.75 (95%CI: 0.74-0.77) and 0.89 (95%CI: 0.88-0.91), respectively; The positive likelihood ratio value was 6.75 (4.56-9.99), and the negative predictive value was 0.36 (0.25-0.52); The diagnostic odds ratio was 23.16 (11.34-47.31), and the area under the ROC curve was 0.9. Conclusion SHOX2 gene promoter hypermethylation is high in serum, broncholavage fluid and pleural effusion of lung cancer patients, which can be used as a biomarker for auxiliary diagnosis of lung cancer. [ABSTRACT FROM AUTHOR]

Objective This study aims to investigate the effect of the regulator of G-protein signaling 2 (RGS2) on the proliferation and invasion of oral squamous cell carcinoma (OSCC) cells and its potential molecular mechanism. Methods The expression status and clinical significance of RGS2 in head and neck squamous cell carcinomas and matched adjacent normal tissues were evaluated using TCGA database. Three OSCC cell lines (i.e., SCC-9, Cal27, and Fadu) were overexpressed with RGS2, and the effect of RGS2 on cell proliferation and invasion was determined using the Transwell, clone formation, and cell counting kit (CCK)-8 assays. Moreover, the yeast two-hybrid screening and co-immunoprecipitation (Co-IP) assays were conducted to detect the correlation of RGS2, four and a half LIM domains protein 1 (FHL1), and damage DNA-binding protein 1 (DDB1). Results The expression level of RGS2 in OSCC was significantly lower than that in matched adjacent normal tissues (P=0.023). The high RGS2 expression level was negatively correlated with lymphovascular invasion (P<0.001). After transfection with lentiv-RGS2, the expression of RGS2 was increased, and the invasion and proliferation abilities of OSCC cell lines were evidently inhibited. FHL1 could competitively bind with RGS2, which decreased the integration of DDB1 and RGS2, inhibited the ubiquitination process of RGS2, and maintained the stability of the RGS2 protein. Conclusion RGS2 plays an important role in the inhibition of OSCC proliferation and invasion. The structure stability of RGS2 is competitively regulated by FHL1 and DDB1. [ABSTRACT FROM AUTHOR]

Background and objective Lung cancer is one of the leading causes of cancer-related morbidity and mortality. Oncolytic virotherapy is an emerging therapeutic modality that utilizes replication-competent viruses to destroy cancers. As a powerful tool to kill tumor cells with excellent safety profile, attenuated measles virus of the Edmonston strain (MV-Edm) has been widely applied in the development of tumor therapy and preclinical trials. The aim of this study was to investigate the synergistic effect of nuclear factor kappa B (NF-κB) signaling pathway inhibitor and oncolytic measles virus vaccine against lung cancer and the involved mechanisms. Methods Using Western blot to detect MV-Edm infection of A549 and H1299 were infected by MV-Edm alone or used the NF-κB pathway inhibitor PS1145/cell autophagy related siRNA, expression level of p-IκBα, IκBα, PARP and BAX were determined by western blot. Using flow cytometry to analysis the rate of apoptosis, and using MTT [3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide] method to detect the cell survival rate. Results Inhibition of cell autophagy could obviously inhibit the MV-Edm infection induced the NF-κB pathway activation in A549 and H1299. In MV-Edm infected A549 and H1299, p-IκBα level increased and IκBα level decreased over infection time, compared with control group. Inhibition of the NF-κB pathway by PS1145 could promote the apoptosis of MV-Edm infected A549 and H1299 and amplify the tumor killing effect. Conclusion The combination of NF-κB signaling pathway inhibitor pS 1145 and oncolytic measles virus vaccine strains can promote the apoptosis of human lung cancer cells A549 and H1299 and enhance their oncolytic effect. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Henan Agricultural Sciences is the property of Editorial Board of Journal of Henan Agricultural Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the role of RNA m6A methylation in mediating cerebellar dysplasia through analyzing the phenotypes of the mouse cerebella and the expression of several key m6A regulators upon hypobaric hypoxia treatment. Methods: Five-day old C57/BL6 mice were exposed to hypobaric hypoxia for 9 days. The status of mouse cerebellar development was analyzed by comparing the body weights, brain weights and histological features. Immunostaining of cell-type-specific markers was performed to analyze the cerebellar morphology. Real-time PCR, Western blot and immunohistochemical staining were performed to detect the expression of key m6A regulators in the mouse cerebella. Results: Compared with the control, the body weights, brain weights and cerebellar volumes of hypobaric hypoxic mice were significantly reduced ( P< 0.01). The expression of specific markers in different cells, including NeuN (mature neuron), Calbindin-D28K (Purkinje cell) and GFAP (astrocyte), was decreased in hypobaric hypoxic mouse cerebella ( P< 0.01), accompanied with disorganized cellular structure. The expression of methyltransferase METTL3 was significantly down-regulated in the cerebella of hypobaric hypoxic mice ( P< 0.05). Conclusions: Hypobaric hypoxia stimulation causes mouse cerebellar dysplasia, with structural abnormalities in mature granular neurons, Purkinje cells and astrocytes. Expression of METTL3 is decreased in hypobaric hypoxic mice cerebellum compared with that of normobaric normoxic mice, suggesting that its mediated RNA m6A methylation may play an important role in hypobaric hypoxia-induced mouse cerebellar dysplasia.

Objective: To investigate the clinical characteristics, coexisting gene mutations and prognosis of acute myeloid leukemia (AML) patients with GATA2 gene mutation., Methods: The clinical data of 370 newly diagnosed AML patients treated in our hospital from January 2008 to January 2021 was analyzed retrospectively, the next-generation sequencing technology was used to detect the mutated genes in those patients. The clinical characteristics of AML patients with GATA2 mutations, the co-mutated genes of GATA2 mutations, and the effect of GATA2 mutation on prognosis were analyzed., Results: A total of 23 patients (6.2%) with GATA2 mutation was detected in 370 AML patients. Compared with GATA2 non-mutation group, patients in GATA2 mutation group were mostly normal karyotypes ( P =0.037) and in low-risk cytogenetic stratification ( P =0.028). The incidence of CEBPAdm and NRAS in GATA2 mutation group was significantly higher than that in GATA2 non-mutation group ( P =0.010, P =0.009). There were no statistically significant differences between the two groups in terms of sex, age, white blood cell count (WBC), platelet count, hemoglobin, bone marrow (BM) blast, induction chemotherapy regimen and CR rate ( P >0.05). Among the 23 patients with GATA2 mutation, the most common co-mutated genes were CEBPAdm , NRAS (both 39.1%), NPM1, FLT3, TET2, WT1 (all 17.4%), ASXL1 and IDH1 (both 13.0%). Survival analysis showed that there was no statistical difference in 5-year overall survival (OS) and leukemia-free survival (LFS) rates between patients with and without GATA2 mutations in whole cohort ( n =370) ( P =0.306, P =0.308). Among 306 patients without CEBPAdm , the 5-year OS and LFS rates in GATA2 mutation group showed an increasing trend compared with GATA2 non-mutation group, but the difference was not statistically significant ( P =0.092, P =0.056). Among 64 patients with CEBPAdm , there was no statistically significant difference in 5-year OS rate between the GATA2 mutation group and the GATA2 non-mutation group ( P =0.104), but the 5-year LFS rate of the GATA2 mutation group was significantly decreased ( P =0.047). Among the 23 patients with GATA2 mutation, 16 cases received the "3+7" induction regimen, of which 12 cases received allogeneic hematopoietic stem cell transplantation (allo-HSCT); 7 cases received the "DCAG" induction regimen, of which 3 cases received allo-HSCT. The CR rate was not statistically different between the "3+7" regimen group and the "DCAG" regimen group ( P =1.000). The 5-year OS rate and LFS rate in the transplantation group were significantly higher than the chemotherapy group ( P =0.021, P =0.020)., Conclusion: GATA2 mutation is more common in AML patients with normal karyotype and low-risk cytogenetic stratification, and it is significantly associated with CEBPAdm and NRAS co-mutations. The prognostic significance of GATA2 is influenced by CEBPAdm . The choice of "3+7" or "DCAG" induction regimen in patients with GATA2 mutation does not affect their CR rate, while the choice of allo-HSCT can significantly improved the prognosis compared with chemotherapy only.

Objective To investigate the effect of Myriocin on high fat diet induced integrated stress response and further explore the mechanism. Methods A total of 18 ApoE-/- mice were fed a high- fat diet and randomly divided into control group (n = 9, phosphate buffer solution) and Myriocin group (n = 9, phosphate buffer solution + Myriocin). The drugs were administered orally for 12 weeks. Serum lipids [total cholesterol (TC), triglyceride (TG), low density lipoprotein-cholesterol (LDL-C), very low density lipoprotein- cholesterol (VLDL-C) and high density lipoprotein-cholesterol (HDL-C)] were measured. Flow-cytometric analysis was used to determine the proportion of lymphocyte antigen 6 complex (Ly - 6c)high phenotype monocytes. HE staining was performed to compare the size and detailed composition of atherosclerotic plaques and immunofluorescence staining was used to observe the expression of monocyte chemotactic protein-1 (MCP-1). Real-time fluorescence quantitative polymerase chain reaction (PCR) was used to detect the mRNA expression levels of inflammation related molecules [including pro - inflammatory factors, interleukin-1β and 6 (IL-1β and IL-6), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), vascular endothelial growth factor (VEGF) and anti- inflammatory factor, IL-10]. In addition, the mRNA expression levels of integrated stress response related molecules [including glucose regulated protein 78 (GRP78), protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic translation initiation factor 2 α (eIF2 α), activating transcription factor 4 and 6 (ATF4 and ATF6), endoplasmic reticulum stress - related apoptosis protein C/EBP homologous protein (CHOP) and Caspase12] were tested. The expression levels of integrated stress response related protein [including eIF2α, ATF4, inositol-requiring enzyme 1α (IRE1α) and phosphorylated IRE1α, p65 nuclear factor (p65 NF) and phosphorylated p65 NF, Caspase12 and cleaved Caspase12] were explored by Western blotting. Results 1) Treatment with Myriocin led to lower level of serum LDLC (t = 2.830, P = 0.012). 2) Myriocin suppressed monocytes differentiating toward a Ly-6chigh phenotype (t = 2.866, P = 0.011). 3) HE staining showed less atherosclerotic lesions at 200 and 300 μm distance away from the aortic valve (t = 2.281, P = 0.045; t = 3.506, P = 0.003) and less necrotic core areas (Z = - 2.870, P = 0.004) in the Myriocin group. 4) Immunofluorescence staining showed the reduction of MCP-1 protein expression in the Myriocin group; real-time fluorescence quantitative PCR showed that IL-1β mRNA (t = 3.968, P = 0.005), TNFα mRNA (t = 7.696, P = 0.000), ICAM mRNA (t = 3.294, P = 0.013), VCAM mRNA (t = 5.449, P = 0.001) and VEGF mRNA (t = 2.574, P = 0.037) were generally decreased in the Myriocin group, while IL-10 mRNA was increased (t = - 3.132, P = 0.017) in the Myriocin group. 5) Myriocin downregulated PERK mRNA (t = 4.174, P = 0.004-, eIF2α mRNA (Z = - 2.692, P = 0.007), ATF4 mRNA (t = 3.342, P = 0.012), ATF6 mRNA (t = 5.841, P = 0.001) and Caspase12 mRNA (t = 7.270, P = 0.000). 6) Western blotting showed that Myriocin suppressed the protein expression of eIF2α (t = 2.175, P = 0.047) and ATF4 (t = 2.923, P = 0.011), and the phosphorylation of p65 NF - B (t = 2.909, P = 0.011). Conclusions Myriocin could alleviate atherosclerosis progression of ApoE-/- mice by reducing integrated stress response and inflammatory response in the arterial walls. [ABSTRACT FROM AUTHOR]

Objective: To investigate the expression and clinicopathological significances of mitochondrial DNA binding protein 1(SSBP1) and mitochondrial transcription factor A(mtTFA) in the esophageal squamous cell carcinoma(ESCC) tissues. Methods: Immunohistochemical staining was used to detect the expression of SSBP1 and mt-TFA protein in 40 cases of esophageal squamous cell carcinoma and 20 normal esophageal tissue. Their correlation with the clinicopathological features of ESCC were analyzed. Results: The positive rates of SSBP1 and mtTFA in the ESCC were significantly higher than those in the normal esophageal tissues( x²=9.909, P=0.002; x²=23.177, P=0.000). The expression of SSBP1, mtTFA protein were significantly related to the clinical stage of esophageal squamous cell carcinoma( x²=6.506, P=0.039; x²=7.535, P=0.023), lymph node metastasis( x²=7.305, P=0.007; x²=4.815, P=0.028). The expression of mtTFA protein was related to the depth of invasion of esophageal squamous cell carcinoma( x²=8.541, P=0.014). The expression of SSBP1 showed no relationship with the depth of invasion( x²=5.695, P=0.058). There was a positive correlation between SSBP1 and mtTFA expression in esophageal squamous cell carcinoma(r=0.392, P=0.012). Conclusions: SSBP1 and mtTFA proteins are up-regulated in the esophageal squamous cell carcinoma, and they may participate in the development and progression of esophageal squamous cell carcinoma. [ABSTRACT FROM AUTHOR]

[Objectives] The single-stranded DNA binding protein Whirly(WHY), a transcription factor, exists in plants widely and plays an important role in plant leaf senescence. This paper aimed to clone CsWHY1, a single-stranded DNA binding protein gene in cucumber, and to analyze its expression characteristics to provide reference for its functional research on cucumber leaf senescence. [Methods] The full length cDNA of CsWHY1 was cloned with North China cucumber ‘9930’ ‘Changchunmici’ and ‘Xintaimici’ as experimental materials. A series of bioinformatics software were used to speculate nucleotide sequence and protein function of CsWHY1. In addition, the subcellular localization was conducted by onion epidermal cells transient expression system, and gene expression pattern of CsWHY1 was investigated by RT-qPCR in different tissues of 3 cucumber varieties. [Results] The ORF of CsWHY1 gene was 831 bp, encoding 276 amino acids. The relative molecular mass of CsWHY1, a hydrophilic protein, was 30.729×103 with the theoretical isoelectric point(pI) of 9.00. Amino acid sequence analysis revealed that CsWHY1 protein had a conserved Whirly domain, and it was highly homologous in dicotyledonous and monocotyledonous plants and had the closest genetic relationship with melon. Subcellular localization analysis showed that CsWHY1 was located in the plastids of onion epidermal cell. RT-qPCR analysis showed that CsWHY1 expressed in different tissues of three cucumber varieties, with the highest expression level in leaves and the lower expression in roots and stems, and the expression level of CsWHY1 in aged leaves was significantly higher than that in mature leaves. [Conclusions] The expression of CsWHY1 was tissue-specific. CsWHY1 had a high expression level in senescent leaves and participated in the senescence process of leaves in cucumber. [ABSTRACT FROM AUTHOR]

Objective: To observe the effects of auricular thumbtack needle on breast feeding and lactation function in primiparous women with cesarean section, and to explore its mechanism of action from the perspective of lactation-related gene expression., Methods: One hundred cases of primiparous women with cesarean section were randomly divided into an observation group (50 cases, 3 cases dropped off) and a control group (50 cases, 2 cases were eliminated). The patients in the control group were treated with routine obstetric care. Based on the treatment of the control group, the patients in the observation group were treated with auricular thumbtack needle at Neifenmi (CO 18 ), Xiong (AH 10 ), Xiongzhui (AH 11 ), Shenmen (TF 4 ), and Jiaogan (AH 6a ), etc., with one side of auricular point selected, only once for a total of 3 d. The lactation initiation time, lactation adequacy rate at postpartum 72 h, exclusive breastfeeding rate at postpartum 42 d, and breastfeeding score after treatment were compared between the two groups. Real-time quantitative PCR and Western blot method were used to detect the mRNA and protein expression levels of TDP-43, Btn1A1 and XDH., Results: After treatment, the lactation initiation time in the observation group was earlier than that in the control group ( P <0.01), and breastfeeding score in the observation group was higher than that in the control group ( P <0.01). The lactation adequacy rate at postpartum 72 h was 63.8% (30/47) in the observation group, which was higher than 41.7% (20/48) in the control group ( P <0.05). The exclusive breastfeeding rate at postpartum 42 d was 72.3% (34/47) in the observation group, which was higher than 47.9% (23/48) in the control group ( P <0.05). The mRNA and protein expression levels of TDP-43 and Btn1A1 in breast milk in the observation group were higher than those in the control group ( P <0.01), while there was no statistically significant difference in mRNA and protein expression of XDH in breast milk between the two groups ( P >0.05)., Conclusion: The auricular thumbtack needle in addition to routine care could promote lactation initiation, improve lactation adequacy rate and exclusive breastfeeding rate in primiparous women with cesarean section, and the action mechanism may be related to up-regulation of TDP-43 and Btn1A1 expression.

Objective: To explore the genetic basis for a child with congenital heart disease (CHD) and global developmental delay (GDD)., Methods: A child who was hospitalized at the Department of Cardiac Surgery of Fujian Children's Hospital on April 27, 2022 was selected as the study subject. Clinical data of the child was collected. Umbilical cord blood sample of the child and peripheral blood samples of his parents were collected and subjected to whole exome sequencing (WES). Candidate variant was verified by Sanger sequencing and bioinformatic analysis., Results: The child, a 3-year-and-3-month-old boy, had manifested cardiac abnormalities and developmental delay. WES revealed that he had harbored a nonsense variant of c.457C>T (p.Arg153*) in the NONO gene. Sanger sequencing showed that neither of his parents has carried the same variant. The variant has been recorded by the OMIM, ClinVar and HGMD databases, but not in the normal population databases of 1000 Genomes, dbSNP and gnomAD. Based on the guidelines from the American College of Medical Genetics and Genomics (ACMG), it was rated as a pathogenic variant., Conclusion: The c.457C>T (p.Arg153*) variant of the NONO gene probably underlay the CHD and GDD in this child. Above finding has expanded the phenotypic spectrum of the NONO gene and provided a reference for the clinical diagnosis and genetic counseling for this family.

Background It is accepted that cerebral ischemia induces neurogenesis and neural stem cells (NSCs) differentiation in non-neurogenic regions (especially in the basal ganglia). However, the mechanisms possibly involved in modulating the differentiation plasticity of NSCs are still let to known. This study aims to investigate the possible epigenetic mechanisms involved in the differentiation process of NSCs after ischemic stroke. Methods Western blotting analysis was used to detect the protein levels of methyl CpG-binding protien 2 (MeCP2) and phosphorylated MeCP2 (pMeCP2) in the ischemic basal ganglia of rat model at 3 d following middle cerebral artery occlusion (MCAO). Immunohistochemical staining was performed to observe the cellular distribution of MeCP2 and pMeCP2, the cellular colocalization of pMeCP2 with NSCs marker nestin and neuronal marker microtubule-associated protein 2 (MAP-2) in the ischemic basal ganglia of rat brains. Results 1) MeCP2 was phosphorylated in the basal ganglia after ischemic stroke, forming pMeCP2. MeCP2 positive cell number was decreased in the ischemic basal ganglia (t = 12.239, P = 0.000), while pMeCP2 positive cell number was increased in the ischemic basal ganglia (t = 5.808, P = 0.000). 2) Ischemic stroke induced a reduction of MeCP2 levels in the nucleus (t = 14.949, P = 0.000) and an elevation of pMeCP2 levels in the cytoplasm (t = 5.026, P = 0.001). 3) MeCP2 phosphorylation mediated the translocation of MeCP2 from nucleus to cytoplasm. 4) pMeCP2 was colocalized with NSCs marker protein nestin in the ischemic basal ganglia at 3 d after MCAO; pMeCP2 was colocalized with the neuronal marker MAP-2 in the ischemic basal ganglia at 1 week after MCAO. Conclusion Ischemic stroke-induced MeCP2 phosphorylation was able to alter the spatial distribution of MeCP2, transferring it from nucleus to cytoplasm and affecting its biological functions. This study further improved our awareness of brain neurogenesis in adult animals, providing new perspective for making use of neuronal regeneration in the treatment of neurodegenerative diseases and nerve injuries. doi：10.3969/j.issn.1672-6731.2013.11.009

Objective To investigate the expressions of MUM1, BCL2 and BCL6 protein in diffuse large B cell lymphoma (DLBCL) tissue and their relation with the DLBCL pathological characteristics and prognosis. Methods The pathological tissue samples in 80 cases of newly diagnosed DLBCL with intact clinical and follow up data in the Weifang Municipal People′s Hospital from February 2010 to February 2014 were collected. The immunohistochemistry technique was used to assess the expressions of MUM1, BCL2 and BCL6 protein in DLBCL tissue, then their mutual relationship and the relation with clinical pathological characteristics and prognosis were analyzed. Results The positive expression rates of BCL2, BCL6, MUM1 protein in 80 cases of DLBCL were 36.3 %(29/80), 65% (52/80) and 77.5% (62/80) respectively. The average survival time in the MUM1 positive group and negative group were 35.4 months and 51.7 months respectively, which in the BCL2 positive group and negative group were 35.7 months and 47.2 months, which in the BCL6 positive group and negative group were 54.5 months and 35.1 months respectively. The BCL6 positive and MUM1 negative groups showed relatively better prognosis,the difference was statistically significant (P<0.05). But the relation between BCL2 and prognosis in the patients with DLBCL was still inexact. Conclusion The expression situation of MUM1, BCL2 and BCL6 protein provides the important information for clinical therapy and prognosis of DLBCL. But it is still a lack of understand on its action mechanism, which is worth deep research. [ABSTRACT FROM AUTHOR]

Streptomyces antibiotic regulatory proteins (SARP) normally play positive regulatory roles during streptomyces antibiotics biosynthesis. sare4854, a gene in Salinispora arenicola CNH643 DSM 44819 was proposed to encode a SARP. Here, sare4854 was expressed in a heterolohous system for functional characterization. However, the antibiotic production in resultant strain was repressed significantly. Bioinfomatic analysis showed that sare4854 has an additional nucleoside triphosphate hydrolases (NTPase) domain at the C-terminus, besides a SARP-like domain (DBD: DNA binding domain and BTA: bacterial transcnptional activation domain) at the N-terminus conserved in all SARPs. The possible mechanism of sare4854 in antibiotic synthesis in this abnormal phenomenon was discussed here. [ABSTRACT FROM AUTHOR]

Objective To construct chromodomain helicase DNA-bingding protein 4 (CHD4/Mi-2β) truncated recombinant plasmids, induce the expression of GST fusion proteins in E.coli, and purify and identify GST fusion proteins of CHD4/Mi-2β. Methods The gene fragments of chromodomains (CHD4-C), SWI2/SNF2-related ATPase/helicase region (CHD4-H) and DNA-binding domain (CHD4-D) were amplified by PCR and cloned into pGEX-5T vector. After the target genes were sequenced, the plasmids were transformed into E.coli BL21 (DE3) respectively, and induced with 0.8mmol/L IPTG to express fusion proteins. The GST-fusioned recombined proteins were purified with glutathione-agarose resin, and identified by SDS-PAGE and Western blotting. Results Three CHD4 truncated recombinant plasmids were constructed. The recombinant fusion proteins of GST-CHD4-C, GST-CHD4-D and GST-CHD4-H were expressed in E.coli BL21 (DE3) and existed mostly in the form of soluble protein with expected relative molecular weight of 130, 110 and 90ku. The purity of the fusion proteins reached 94.5% after purification by high-affinity glutathione-agarose resin. Conclusion GST-CHD4-C, GST-CHD4-D and GST-CHD4-H have been successfully purified, which lays an experimental foundation for further study of CHD4/Mi-2β in chromatin remodeling. [ABSTRACT FROM AUTHOR]

A new polypytdyl nickel complex [Ni (dmbpy)3](H2O) (CIO4)2 ( dmbpy = 4, 4 dmethy-2, 2 bpyidine ) has been synthesized and characterized by single-crystal X-ray diffraction method. It crystallizes in the tricking system, space group P--1, wth a = 11.192(13) Å, 0= 14.444 (18) Å, c = 14. 468 (18) Å, α = 84. 86 (2), β= 76.691 (19)°, γ=68. 24(2)°, V=2114(4) Å3 and Z=2. The molecular structure of the complex consists of a mono nuclear nickel ( II ) complex cation, two perchlorate anons and one water molecule. Each of the three dmbpy molecules chelates to the nìckeK II ) atom in the usual bidentate mode and the nickeK II ) atom ss six-coordinated n a stoned o-tahedral geometry. The bínding stupes of the complex with caf thymus DNA ( CT DNA) have been explored by electron absorption titration and fluorescence quenching experiments. The experimental results suggest that the complex bind to CT-DNA through two models: electrostatic and interrogatively binding. [ABSTRACT FROM AUTHOR]

To assess the dynamics and spectral characteristics of dissolved organic matter of twig litter in continuous increase stage, peak stage, and continuous decrease stage of twig litter production in different types of Castanopsis carlesii forest in middle subtropical China, a field experiment was conducted in C. carlesii natural forest, secondary forest and plantation. The results showed that litter production stage and forest type significantly affected the content and spectral characteristics of dissolved organic matter of twig litter were . Compared with the secondary forest and plantation, natural forest had higher dissolved organic carbon (DOC) content and lower special ultraviolet-visible absorption values at 254, 260 and 280 nm (SUVA 254 , SUVA 260 , SUVA 280 ) at the continuous decrease stage of twig litter production, indicating high twig litter quality of natural forest and high cycling efficiency with dissolved organic matter in the natural forest at this stage. In contrast, the higher contents of total nitrogen (TN), total phosphorus (TP), total dissolved nitrogen (TDN), total dissolved phosphorus (TDP), and lower DOC:TDP and TDN:TDP ratios of twig litter in the plantation were observed at the peak stage of twig litter production, while no differences were detected in dissolved organic matter contents and spectral values in the secondary forest among the stages. In addition, the DOC, TDN, TDP of twig litter were negatively correlated with temperature and precipitation in the natural forests and secondary forests, but TDN and TDP of twig litter were positively correlated with temperature and precipitation in the plantations. These results suggested that the higher nutrient content at the peak stage of twig litter production in the C. carlesii plantation might lead to more efficient material cycling and that there would be a higher efficiency of material cycling for twig litter dissolved organic matter in C. carlesii natural forest at reduction stage of twig litter production.

In order to explore the impact of optimized land use allocation on phosphorus loss in the runoff process of a small watershed in the Three Gorges Reservoir area, a traditional agricultural model catchment area (CG) and a catchment area after optimized land use allocation in the Shipanqiu watershed in Zhong County, Chongqing (EG) were selected as the research object, sampling at the outlets of the two catchment areas, respectively, to monitor the runoff process and different forms of phosphorus in rainfall events and to analyze the influence of land use configuration on the law of phosphorus loss. The results showed that:① in the 10 monitored rainfall and runoff processes, the ρ [total phosphorus (TP)] of EG was lower than that of CG, and the ranges of the two were 0.09-0.75 mg·L -1 and 0.13-2.82 mg·L -1 , respectively. Compared with that of CG, EG significantly reduced the peak value of TP. ② The average EMC of TP, total dissolved phosphorus (TDP), dissolved inorganic phosphorus (DIP), and particulate phosphorus (PP) in the process of rainfall and runoff was lower than that of CG, and EG and CG showed significant differences in EMC of TP, TDP, and DIP ( P <0.05); the main form of phosphorus loss in the two catchment areas in the process of rainfall and runoff was TDP, but the average TDP/TP of EG was larger. ③ The output load of EG was 45%, 43%, 57%, and 47% lower than that of the TP, TDP, DIP, and PP in CG. The output load of EG and CG of various forms of phosphorus was significantly correlated with the total runoff ( P <0.01). In addition, the slope of the linear fitting of various phosphorus forms in the CG catchment area to the total amount of runoff was 1.66 to 1.75 times that of EG. The output load of various phosphorus forms of CG was more sensitive to runoff than that of EG, and the output per unit area in the process of rainfall and runoff was more sensitive than that of EG. The amount of sand could have caused the difference in phosphorus concentration and output load more than the output per unit area. Optimizing land use configuration can effectively reduce the loss of various forms of phosphorus and provide a reference for the prevention and control of phosphorus loss in small watersheds in the Three Gorges Reservoir area.

Objective To investigate the transcription factors GATA-3 expression in breast cancer tissue and its clinical value. Methods A total of 382 cases of breast cancer in our hospital from May 1, 2013 to November 1, 2015 were selected as the research subjects and divided into the breast malignant tumor tissue group (254 cases), breast benign tumor tissue group (58 cases) and breast paracancerous tissue group (70 cases). The GATA-3 expression levels were comparatively observed in various groups. The relationship between GATA-3 expression with breast cancer morphological classification and between GATA-3 expression with the clinicopathological features of breast cancer were analyzed. Results The GATA-3 expression positive rates in breast malignant tumor tissue was 79.53% (202/254). The GATA-3 positive rate in the 3-negative type breast cancer cells was lower than that in the glandular lumen type A and B, HER-2 overexpression type, and the differences were statistically significant (P<0.05). GATA-3 was expressed in invasive ductal cancer tissue, invasive lobular cancer tissue and neuroendocrine cancer tissue, while not expressed in diffuse large B cell lymphoma and malignant spindle cells tumor tissues. Conclusion The pathological classification and pathological type of breast tumor in breast cancer cells is closely related with GATA-3 expression. There-fore, GATA-3 has an important role in the diagnosis and prognosis of breast cancer. [ABSTRACT FROM AUTHOR]

Objective: To investigate the diagnostic value of long noncoding RNA (lncRNA) extracted from serum exosomes in epithelial ovarian cancer (EOC). Methods: (1) Patients with ovarian tumors who were hospitalized in the Affiliated Tumor Hospital of Guangxi Medical University from August 2018 to December 2019, including 35 cases of EOC patients (malignant group) and 20 cases of benign ovarian tumor patients (benign group) were collected; during the same period, 15 healthy women (normal group) who underwent physical examination in the Affiliated Tumor Hospital of Guangxi Medical University were used as controls. Fasting venous blood serum was collected from the above three groups of women, and serum exosomes were isolated and purified using commercial kits. The morphology of exosomal particles was observed with transmission electron microscope, and the particle size distribution of the exosomes was detected by NanoSight technology. The expression of specific proteins cluster of differentiation (CD) 63 , CD 81 , and tumor susceptibility gene 101 (TSG101) of exosomes were analyzed by western blot. (2) Four cases of EOC patients and three cases of healthy women were randomly selected. High-throughput sequencing technology was used to analyze the differentially expressed lncRNA in serum exosomes of these four EOC patients and three healthy women, and screen out the significantly differentially expressed lncRNA. The screened lncRNA with different expression levels was verified by quantitative reverse transcription-polymerase chain reaction (QRT-PCR) in these seven original clinical samples, furtherly confirmed and tested with QRT-PCR in larger clinical samples (a total of 70 serum samples). (3) The receiver operating characteristic (ROC) curve of the target lncRNA was drawn and its diagnostic indicators such as sensitivity and specificity were evaluated. By using logistic binary regression model, multi-factor joint diagnostic models were constructed and evaluated. Results: (1) Under transmission electron microscope, clear lipid bilayer structure was observed in serum exosomes, and one side presented a concave hemispheric or cup like structure; the peak diameter of the exosomal particles detected with NanoSight technology was 127.6 nm, and the particles between 30 and 150 nm accounted for 58.9%; western blot confirmed that the obtained (exosomal) particles could detect the expression of the marker proteins CD 63 , CD 81 , and TSG101. (2) Analysis of high-throughput sequencing technology showed that compared with the women in the normal sequencing group (3 cases), 425 differentially expressed lncRNAs (including 23 up-regulated and 402 down-regulated) were screened in the serum exosomes of the malignant sequencing group (4 cases). Six types of lncRNA with significantly abnormal expression levels (including FER1L6-AS2, LINC00470, LINC01811, CXXC4-AS1, LINC02343, and LINC02428) were randomly selected for original sample verification, and the results were consistent with the sequencing results. Subsequently, these six lncRNAs were used for larger samples QRT-PCR verification. Compared with the benign and normal groups, the expression of FER1L6-AS2, LINC00470 and LINC01811 in malignant group increased by 1.66 and 1.84-fold, 2.05 and 2.46-fold, 2.94 and 2.35-fold, respectively; the expressions of CXXC4-AS1, LINC02343 and LINC02428 were down-regulated to 29% and 34%, 40% and 46%, 42% and 42%, respectively. For the same lncRNA, there were statistical differences between the malignant group and the benign group, between the malignant group and the normal group (all P <0.05), and there were no statistical differences between the benign group and the normal group (all P >0.05). (3) The results showed that the area under curve (AUC) of these six lncRNAs ranged from 0.722 to 0.805, which had moderate diagnostic efficiency. To use logistic binary regression model to establish multi-indicator joint diagnostic models and establish different joint factor ROC curves. The results showed that the AUC of the joint factor prediction model 1 (composed of FER1L6-AS2 and LINC01811), the joint factor prediction model 2 (composed of CXXC4-AS1, LINC02343, and LINC02428), and the joint factor prediction model 3 (composed of FER1L6-AS2, CXXC4-AS1, LINC02343, and LINC02428) were 0.865, 0.934, and 0.962, respectively. The diagnostic efficacy of the combined factor prediction models was higher than that of the single lncRNA (all P <0.05). Conclusions: High-throughput sequencing technology is an effective method for screening out the different expression levels of lncRNA extracted from serum exosomes. The combined detection of multiple serum exosomal lncRNA indicators has a certain diagnostic efficacy for patients with EOC. Detection of serum exosomal lncRNA indicators will provide new ideas for the diagnosis of EOC.

Objective: To investigate the role and regulatory mechanism of ring finger protein 11 (RNF11) on Akt signaling pathway in the process of osteogenesis of bone marrow mesenchymal stem cells (BMSCs) to provide ideas for further clarifying its osteogenesis mechanism and its use in clinical treatment in the future., Methods: BMSCs were isolated and cultured from fresh bone marrow of healthy donors and subcultured. The 4th generation cells were used in experiments after identification by flow cytometry, and osteogenic, chondrogenic, and adipogenic induction. BMSCs were cultured in osteogenic differentiation medium for 0-14 days. The degree of osteogenic differentiation was detected by Alizarin red staining and alkaline phosphatase (ALP) staining, and the protein expression of RNF11 was detected by Western blot. The 4th generation BMSCs were divided into blank control group (group A), empty lentivirus (Lv-NC) group (group B), and knockdown RNF11 (Lv-ShRNF11) group (group C). Osteogenesis was induced and cultured for 0-14 days. The expression of RNF11 protein was detected by Western blot, the degree of osteogenic differentiation was detected by Alizarin red staining and ALP staining, and the relative mRNA expressions of Runx2, osteocalcin (OCN), and osteopontin (OPN) were detected by real-time fluorescence quantitative PCR (qRT-PCR). The protein relative expressions of Akt, Smad1/5/8, and β-catenin signaling pathway were detected by Western blot, expressed as the ratio before and after phosphorylation. In order to study the effect mechanism of RNF11 on Akt signaling pathway, the 4th generation BMSCs were divided into Lv-NC transfection group (group A1), Lv-ShRNF11 transfection group (group B1), and Lv-ShRNF11 transfection supplemented with Akt signaling pathway activator SC79 group (group C1). The protein relative expressions of RNF11 and Akt signaling pathway were detected by Western blot, the related osteogenesis indexes were detected by Alizarin red staining, ALP staining, and qRT-PCR., Results: The flow cytometry, and osteogenic, chondrogenic, adipogenic induction culture identification showed that the isolated and cultured cells were BMSCs. The protein relative expression of RNF11 increased gradually with the extension of osteogenic differentiation time ( P <0.05); after knockdown RNF11, Alizarin red and ALP stainings showed that the degree of osteogenic differentiation of BMSCs in group C were significantly lower than those in groups A and B, and qRT-PCR detection showed that the relative expression of Runx2, OCN, and OPN mRNA significantly decreased ( P <0.05). The protein relative expressions of RNF11 and Akt signaling pathway significantly increased with the extensions of osteogenic differentiation time ( P <0.05). After knockdown RNF11, the protein relative expression of Akt signaling pathway in group C was significantly lower than that in groups A and B ( P <0.05), while Smad1/5/8 and β-catenin signaling pathway had no significant effect ( P >0.05). Compared with group A1, the protein relative expression of RNF11 in groups B1 and C1 significantly decreased ( P <0.05). Compared with groups A1 and C1, the protein relative expression of Akt signaling pathway in group B1 was significantly lower ( P <0.05); Alizarin red and ALP stainings showed that the degree of osteogenic differentiation of BMSCs in group C1 were slightly lower than that of group A1 ( P> 0.05), but significantly higher than that of group B1 ( P <0.05); qRT-PCR detection showed that the relative expressions of Runx2, OCN, and OPN mRNA in group C1 were slightly lower than those of group A1 ( P> 0.05), but were significantly higher than those of group B1 ( P <0.05)., Conclusion: RNF11 promotes the differentiation of BMSCs into osteoblasts by positively regulating the activation level of Akt signaling pathway. RNF11 can be used as a potential target to improve the bone repair efficacy of BMSCs and treat bone metabolic diseases.

Runx2 is a transcription factor belongs to RUNXX family, and it is one of the important factors involved in expression and participation in regulation of mammary specific genes in the mammary gland. The overexpression is also associated with certain characteristics of breast cancer. This article aims to summarize the recent progress of the role that Runx2 plays in breast cancer. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of overexpression of the oncogenic transcription factor ELF4 on proliferation and apoptosis in human insulinoma cells and explore the underlying mechanism., Methods: A human insulinoma BON cell line with stable overexpression of ELF4 (BON-ELF4 cells) was constructed using a recombinant retrovirus vector and the expression of ELF4 protein was verified using Western blotting. MTT assay was used to assess the proliferation of BON-ELF4 cells and BON-Vector cells, and the cell apoptosis induced by treatment with epirubicin (0.1 μmol/L for 24 h) was analyzed by detecting the expressions of cleaved caspase-8, caspase-9, and PARP using Western blotting. Flow cytometry with Annexin VFITC/PI staining was performed to analyze the numbers of apoptotic BON-Vector or BON-ELF4 cells. The expressions of phosphorylated Akt and total Akt in the cells were detected using Western blotting., Results: BON-ELF4 cell line with stable overexpression of ELF4 was successfully established. ELF4 overexpression significantly promoted the proliferation ( P < 0.05) and obviously suppressed epirubicin- induced apoptosis in BON cells, resulting also in significantly reduced expressions of cleaved caspase-8, caspase-9 and PARP ( P < 0.05). The results of flow cytometry showed a significantly lower apoptotic rate in BON-ELF4 cells than in BON-Vector cells following epirubicin treatment (6.03% vs 22.90%). The phosphorylation levels of Akt (Thr308 and Ser473) were significantly increased ( P < 0.05) while the level of total Akt remained unchanged ( P >0.05) in ELF4- overexpressing cells., Conclusion: ELF4 overexpression enhances the proliferation and suppresses apoptosis of insulinomas cells by activating Akt signaling.

Objective: To analyze the association between low-frequency variants of ARID1A gene and primary liver cancer using latent category model. Methods: The low-frequency variants of ARID1A gene was combined according to different functional areas, and the combined variables were analyzed by using the latent class model to obtain the latent variables. Then the logistic regression was used to analyze the association between low-frequency variants of ARID1A gene and primary liver cancer. Results: The low-frequency variants of ARID1A gene were divided into three categories by the latent class model. The class 1 was mainly unmutated population, the proportion was 94.2% (2 454/2 603). The class 2 was mainly transcriptional regulatory domain mutation, take 4.8% (124/2 603). The class 3 was dominantly exon mutation, about 1.0% (27/2 603). Using class 1 as a reference, it was found that mutations in the transcriptional regulatory domain could reduce the risk of liver cancer ( OR =0.601, 95% CI =0.364-0.992, P =0.046). Conclusion: The latent class model can identify low-frequency variants of gene associated with liver cancer and can be extended to more genetic association studies of low-frequency variants related to complex diseases.

FAM60A,a cell cycle protein,is a subunit of the SIN3 transcription regulator family member A/histone deacetylase(SIN3-HDAC)complex and plays an important role in cell cycle regulation,cell morphology change,cell proliferation,differentiation and migration,early embryogenesis and so on.Studies in recent years have shown that FAM60A plays a role in the occurrence and development of tumors including human osteosarcoma,esophageal cancer,gastric cancer,lung cancer and liver cancer,providing a new research direction for tumor diagnosis and treatment.Based on the research results in recent years at home and abroad,this paper discussed the effects of FAM60A on cellular functions.

Objective: To investigate the expression of SET-NUP214 fusion gene in hematological malignancies and to analyze its related clinical biological characteristics. Methods: The clinical data of 24 patients with SET-NUP214 fusion gene-positive hematological malignancies were retrospectively analyzed, and the Kaplan-Meier method was used for survival analysis. Results: Among the 24 patients with SET-NUP214 fusion gene, 15 cases of acute lymphoblastic leukemia (ALL) (13 cases of T-ALL and 2 cases of B-ALL) , 7 cases of acute myeloid leukemia (AML) , and 2 cases of T/myeloid mixed acute leukemia have been identified. The immunophenotype of 13 cases of T-ALL was mainly characterized by CD3(+)CD2(-), 73.3% of ALL was characterized by myeloid marker expression, and 85.7% of AML was characterized by CD7 expression. Complete remission (CR) was achieved in 22 patients (91.7%) after induction chemotherapy. All 24 patients received allogeneic hematopoietic stem cell transplantation (HSCT) . With a median follow-up of 24 months, the 3-year relapse free survival (RFS) of AML and ALL was 85.7% and 33.3%, respectively ( P =0.128) . Comparing 13 cases of SET-NUP214-positive and 62 cases of SET-NUP214-negative T-ALL, the CR rates of induction chemotherapy were 92.3% and 93.5% ( P =0.445) , and the 4-week CR rates of induction chemotherapy were 69.2% and 72.6%, respectively ( P =0.187) ; the differences were not statistically significant. After HSCT, the 3-year RFS of SET-NUP214(+)T-ALL and SET-NUP214(-)T-ALL was 38.5% and 66.4%, respectively ( P =0.028) , and the difference was statistically significant. Conclusion: The SET-NUP214 fusion gene is mainly detected in T cell-derived hematological malignancies, and the prognosis of SET-NUP214 positive T-ALL is relatively poor.

Objective: To analyze the dynamic molecular expression characteristics of single cell RNA binding proteins (RBPs) in the development of mouse embryonic hematopoitic stem cells (HSCs), and obtain the functional research target RNA splicing factor--Mbnl1, to clarify the function of Mbnl1 involved in regulating mouse embryonic HSC development., Methods: Bioinformatics was used to analyze the single-cell transcriptome data of mouse embryos during HSC development, and the single-cell RBP dynamic molecular expression maps in HSC development was obtained. Mbnl1 was obtained by combining differential analysis and literature research screening. The Mbnl1-knockout mouse model was constructed by the CRISPER/Cas9 technology. Aorta-gonad-mesonephros (AGM) and yolk sac (YS) tissue in two genotype embryos of Mbnl1 +/+ and Mbnl1 -/- at E11.5 were digested into single cells, and then a methylcellulose semi-solid culture system was used to perform an in vitro CFU-C of hematopoietic cells. The number and type of hematopoietic cell colonies in the two hematopoietic tissues in Mbnl1-knockout mice after 7 days were calculated. Furthermore, the whole AGM tissue cells of E11.5 Mbnl1 +/+ and Mbnl1 -/- donor mice were transplanted via tail vein injection respectively, and the function of HSC in AGM region of mice after Mbnl1 knockout was evaluated through the chimerism rate of peripheral blood in recipient mice at 4w and 8w and the kinetic experiment of hematopoietic system reconstruction., Results: The in vitro CFU-C experiment of hematopoietic cells preliminarily indicated that there was no significant difference in the number of cell colonies in AGM region and YS transformed by the two genotypes of Mbnl1 +/+ and Mbnl1 -/- at E11.5, which suggested that HPC function in AGM and YS tissues had no abnormality after Mbnl1 knockout. Single cell transplantation in AGM region vin tail vein showed no significant difference in the hematopoietic reconstruction chimeric rate between Mbnl1 +/+ and Mbnl1 -/- mice, suggesting that there was no abnormality in HSC function in AGM tissues after Mbnl1 knockout., Conclusion: Through functional experiments in vivo and in vitro, it has been confirmed that knockout of the RNA splicing factor--Mbnl1 does not affect the development of HSPC in AGM region of mouse embryo.