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Genetic variation is one of the important factors leading to the incidence and development of cancer. Copy number variation is an important source of genetic diversity， which can be expressed as gene amplification or deletion in structure， and is related to the occurrence and development of different tumors. High-throughput sequencing and gene chip technology can be adopted to detect the variation of copy number， and provide relevant information about tumor molecular characteristics， prognosis and treatment， which is conducive to more accurate diagnosis and treatment decisions for patients in clinical practice. Ovarian cancer is one of the female reproductive system diseases with the highest mortality rate. Understanding its pathogenesis is of significance for improving the survival rate of ovarian cancer. At present， the specific role and mechanism of copy number variation in ovarian cancer are still unclear. In this article， relevant copy number variation in ovarian cancer was reviewed based on the existing research results， aiming to provide novel ideas and methods for the prevention， diagnosis and treatment of ovarian cancer.

Study Design. Basic science study using a hemisection spinal cord injury (SCI) model. Objective. We sought to assess the effect of blocking osteopontin (OPN) upregulation on motor function recovery and pain behavior after SCI and to further investigate the possible downstream target of OPN in the injured spinal cord. Summary of Background Data. OPN is a noncollagenous extracellular matrix protein widely expressed across different tissues. Its expression substantially increases following SCI. A previous study suggested that this protein might contribute to locomotor function recovery after SCI. However, its neuroprotective potential was not fully explored, nor were the underlying mechanisms. Materials and Methods. We constructed a SCI mouse model and analyzed the expression of OPN at different time points and the particular cell distribution in the injured spinal cord. Then, we blocked OPN upregulation with lentivirus-delivering siRNA targeting OPN specifically and examined its effect on motor function impairment and neuropathic pain after SCI. The underlying mechanisms were explored in the OPN-knockdown mice model and cultured vascular endothelial cells. Results. The proteome study revealed that OPN was the most dramatically increased protein following SCI. OPN in the spinal cord was significantly increased three weeks after SCI. Suppressing OPN upregulation through siRNA exacerbated motor function impairment and neuropathic pain. In addition, SCI resulted in an increase in vascular endothelial growth factor (VEGF), AKT phosphorylation, and angiogenesis within the spinal cord, all of which were curbed by OPN reduction. Similarly, OPN knockdown suppressed VEGF expression, AKT phosphorylation, cell migration, invasion, and angiogenesis in cultured vascular endothelial cells. Conclusion. OPN demonstrates a protective influence against motor function impairment and neuropathic pain following SCI. This phenomenon may result from the proangiogenetic effect of OPN, possibly due to activation of the VEGF and/or AKT pathways. [ABSTRACT FROM AUTHOR]

Objective To explore the development method of coronavirus gene chip, and to establish a method for rapid qualitative detection of nucleic acids of 7 coronaviruses and 2 influenza viruses in respiratory infection samples such as human throat swabs, sputum, and alveolar lavage fluid. Methods According to the gene sequences of 10 kinds of respiratory infection viruses published on the Internet, the corresponding primers and probe sequences were designed.After screening and verification by agarose gel electrophoresis, the probes were spotted on the aldehyde base modified substrate, completed the detection chip fabrication. Results The PCR amplification product was diluted by 10-fold serial dilution method and then detected by gene chip.The results showed that the lowest detection concentration that could form hybridization spots was 103copies/mL. Conclusion The developed coronavirus gene chip has good specificity and sensitivity, and can be used for simultaneous high-throughput and rapid detection of SARS-CoV-2 and other respiratory viruses.

Presently, onychomycosis is one of the major global public health issues. The diagnosis of onychomycosis relies on typical clinical signs, mycological examination (fungal microscopy, culture) and pathological analysis. The traditional methods are difficult to precisely and rapidly identify fungal species. Emerging technologies, such as PCR-based molecular identification, gene chip, LAMP, MALDI-TOF MS and spectroscopy, exhibit advantages of rapidity, simplicity and accuracy, and overcome the limitations of traditional methods. This paper summarizes the advantages and disadvantages of traditional and modern methods for mycological detection in order to facilitate the development of new detection methods.

To explore a protective tillage method based on planting and land cultivation suitable for sloped farmland, field experiments in combination with gene chip research methods were used to study the effects of straw mulching and fallow cultivation technology (including alternate year straw mulch fallow with rotary tillage (RF) and 2-year rotary tillage with annual straw mulch fallow (RRF) ) in comparison with conventional tillage (CRT, rotary tillage after straw removal) measures on soil carbon, nitrogen, and phosphorus cycling functional genes. The results showed that inputting exogenous C stimulated the organic matter degradation potential of soil microorganisms, whether straw mulching was performed in the previous season or the current season, and that the abundance of degradation functional genes (acsE, xylA and rbcL) involved in the soil C cycle increased to a certain extent. The average relative abundance of the xylA gene increased by 43.12% compared with that of the CRT treatment. Conventional tillage without straw return to the field significantly increased the relative abundance of the genes involved in C assimilation, such as acsA, which increased by 33.03%. After straw mulching and fallow cultivation, the abundance of the gdh gene was increased, indicating promotion of the transformation of soil N from ammonium N to nitrate N. Similarly, accumulation of active P was higher, and the abundance of the alkaline phosphatase gene phoD, which was positively correlated with that of AP and phnk genes, increased by an average of 59.57% compared with the value of CRT. The turnover capacity of soil microorganism C, N, and P was improved under straw return, and the conversion of exogenous organic carbon and accumulation of soil SOC were increased. Although there was little difference between straw mulching in the current season and that in the previous season in the short term, these results provide a scientific basis for the implementation of protective farming techniques on sloped farmland to prevent and control water and soil loss in the black soil region of northeast China. [ABSTRACT FROM AUTHOR]

Presently, onychomycosis is one of the major global public health issues. The diagnosis of onychomycosis relies on typical clinical signs, mycological examination (fungal microscopy, culture) and pathological analysis. The traditional methods are difficult to precisely and rapidly identify fungal species. Emerging technologies, such as PCR-based molecular iientification, gene chip, LAMP, MALDI-TOF MS and spectroscopy, exhibit advantages of rapidity, simplicity and accuracy, and overcome the limitations of traditional methods. This paper summarizes the advantages and disadvantages of traditional and modern methods for mycological detection in order to facilitate the development of new detection methods. [ABSTRACT FROM AUTHOR]

Abstract Background Cadmium (Cd) exposure has been found to have detrimental effects on the development of the central nervous system and cognitive ability in children. However, there is ongoing debate regarding the impact of maternal Cd exposure on the cognitive ability of offspring. In this study, we aimed to investigate the mechanisms underlying the influence of maternal Cd exposure on the cognitive ability of offspring rats. Methods Here, we constructed a model of cadmium poisoning in first-generation rats through gavage. The cognitive and memory abilities of its offspring were evaluated by water maze experiment. Then, we used the gene chip to find out the key genes, and we performed qRT-PCR detection of these genes. Subsequently, enrichment analysis was employed to identify pathways. Finally, we constructed a co-expression network consisting of LncRNAs and mRNAs to elucidate the biological functions and regulatory mechanisms of LncRNAs. Results The results of the water maze trial demonstrated that the offspring of rats exposed to cadmium in the first generation had reduced cognitive and memory abilities. Through an analysis of gene expression in the hippocampus of the cadmium-treated rats' offspring and the control group, we identified a correlation between the islet secretion pathway and the cognitive impairment observed in the offspring. Utilizing various algorithms, we identified Cpa1 and Prss1 as potential key genes associated with the cognitive impairment caused by cadmium. The results of qRT-PCR demonstrated a decrease in the expression levels of these genes in the hippocampus of the cadmium-treated rats’ offspring. In addition, in the co-expression network, we observed that Cpa1 was co-expressed with 11 LncRNAs, while Prss1 was associated with 4 unexplored LncRNAs. Furthermore, we conducted an analysis to examine the relationship between Cpa1, Prss1-related transcription factors, and LncRNAs. Conclusion Overall, this study provides novel insights into the molecular effects of first generation Cd exposure on the cognitive ability of offspring. The target genes and signaling pathways investigated in this study could serve as potential targets for improving neurodevelopment and cognitive ability in children.

In humans particularly in children, adenovirus is one of the most common viruses that cause respiratory illnesses. Knowing how to detect adenovirus proficiently and rapidly will help reinforce surveillance of adenovirus infections, detect epidemic situations in real-time, and understand the trend of virus epidemics, which will allow effective actions to be taken quickly. The rapid detection of antiviral antibodies or viral antigens in clinical samples can be achieved by molecular diagnostic techniques like PCR, Real-Time PCR, LAMP, mPCR-RLB, PCR-ELISA, Tem-PCR, Gene Chip, and so on. Some of the molecular diagnostic methods are relatively economical, exceedingly sensitive and explicit. There are several commercially accessible molecular diagnostic techniques that enable their use in clinical laboratories all over the world. In this review, the principles, characteristics, and applications of molecular biology surveillance methods commonly used in labs and clinics for the detection of human adenoviruses are examined and highlighted.

Objective: To screen and analyze the function of specific CircRNAs involved in pathological bone formation in patients with ankylosing spondylitis (AS). Methods: From September 2019 to October 2020, hip capsule tissues obtained from 3 patients with AS developed hip joint fusion and 3 patients with femoral neck fracture (FNF) were obtained. The circular RNA expressions of hip capsule were analyzed by Arraystar CircRNA chip. qRT‐PCR analysis wan performed to identify the expression patterns of differentially expression CircRNAs. Results: Our findings showed that there were 25 up‐regulated and 39 down‐regulated differential CircRNAs. Among these CircRNAs, we screened 10 highest up‐regulatedCircRNAs and 13 lowest down‐regulated CircRNAs (Fold Change≥2,P<0.05). In further verification analysis, hsa_circ_0067103, hsa_circ_0004496, and hsa_circ_0002649, ACTG1 were significantly upregulated, while hsa_circ_0020273, hsa_circ_0005699, and hsa_circ_0048764 were markly downregulated in AS tissue than FNF controls. Conclusion: The expression of CircRNAs involved of pathological bone formation in AS were significantly different from those of control group. These differentially expressed Circular RNAs may be closely related to the occurrence and development of pathological bone formation in AS. [ABSTRACT FROM AUTHOR]

Objective: To investigate the pharmacological action and mechanism of cholic acid derivatives in traditional Chinese medicine (TCM) based on the regulation of gene expression. Methods: Genome-wide gene expression profiles of Michigan Cancer Foundation-7 (MCF-7) cells treated with or without 4 cholic acid derivatives were detected by gene chip technology. Similarities in upregulated and downregulated genes were analyzed using the Connectivity Map (CMap) database. The affinity between cholic acid derivatives and the potential target was confirmed by molecular docking. The cholic acid derivative-regulated pathway enrichment analysis was performed by the STRING database, and the potential pathway was confirmed by in vitro experiments on MD Anderson-Metastatic Breast-231 (MDA-MB-231) cells. Results: Compared with the reference genome in the CMap database, the gene expression profiles of cholic acid derivatives were similar to those of antipsychotic, anticancer, anti-inflammatory, and anti-infective drugs. Among them, 4 derivatives were associated with antianxiety drugs, and molecular docking results showed that these compounds may act by binding to the ligand-binding site of gamma-aminobutyric acid (GABA) receptors. Moreover, the cytoskeletal pathway is one of the pathways enriched in the derivatives. Of them, ursodeoxycholic acid showed significant inhibitory activity on the cytoskeleton formation of MDA-MB-231 cells. Conclusion: The gene expression detection method, combined with CMap and pathway enrichment analysis, could be used to study the mechanism of the active ingredients of TCM. In addition, our research showed that cholic acid derivatives have a potential affinity for membrane receptors, where they can exert anxiolytic activity by modulating opioid receptor, GABA receptor, and dopamine receptor. Moreover, ursodeoxycholic and chenodeoxycholic acid inhibit cytoskeleton formation, probably by acting on membrane proteins to activate the corresponding cytoskeletal pathways.

Abstract Background Classical swine fever (CSF), African swine fever (ASF), and atypical porcine pestivirus (APPV) are acute, virulent, and contagious viral diseases currently hampering the pig industry in China, which result in mummification or stillbirths in piglets and mortality in pigs. Diagnostic assays for the differentiation of infection and vaccination of CSFV, in addition to the detection of ASFV and APPV, are urgently required for better prevention, control, and elimination of these viral diseases in China. Methods A quadruple PCR-based gene microarray assay was developed in this study to simultaneously detect wild-type and vaccine CSFV strains, ASFV and APPV according to their conserved regions. Forty-two laboratory-confirmed samples, including positive samples of 10 other swine viral diseases, were tested using this assay to confirm its high specificity. Results This assay's limit of detections (LODs) for the wild-type and vaccine CSFV were 6.98 and 6.92 copies/µL. LODs for ASFV and APPV were 2.56 × 10 and 1.80 × 10 copies/µL, respectively. When compared with standard RT-PCR or qPCR for CSFV (GB/T 26875–2018), ASFV (MARR issue No.172), or APPV (CN108611442A) using 219 clinical samples, the coincidence was 100%. The results showed that this assay with high sensitivity could specifically distinguish ASFV, APPV, and CSFV, including CSFV infection and immunization. Conclusion This assay provides a practical, simple, economic, and reliable test for the rapid detection and accurate diagnosis of the three viruses and may have good prospects for application in an epidemiological investigation, prevention, and control and elimination of these three diseases.

Abstract Objective To detect differentially expressed genes in patients with neonatal necrotizing enterocolitis (NEC) by bioinformatics methods and to provide new ideas and research directions for the prevention, early diagnosis and treatment of NEC. Methods Gene chip data were downloaded from the Gene Expression Omnibus database. The genes that were differentially expressed in NEC compared with normal intestinal tissues were screened with GEO2R. The functions, pathway enrichment and protein interactions of these genes were analyzed with DAVID and STRING. Then, the core network genes and significant protein interaction modules were detected using Cytoscape software. Results Overall, a total of 236 differentially expressed genes were detected, including 225 upregulated genes and 11 downregulated genes, and GO and KEGG enrichment analyses were performed. The results indicated that the upregulated differentially expressed genes were related to the dimerization activity of proteins, while the downregulated differentially expressed genes were related to the activity of cholesterol transporters. KEGG enrichment analysis revealed that the differentially expressed genes were significantly concentrated in metabolism, fat digestion and absorption pathways. Through STRING analysis, 9 key genes in the protein network interaction map were identified: EPCAM, CDH1, CFTR, IL-6, APOB, APOC3, APOA4, SLC2A and NR1H4. Conclusion Metabolic pathways and biological processes may play important roles in the development of NEC. The screening of possible core targets by bioinformatics is helpful in clarifying the pathogenesis of NEC at the gene level and in providing references for further research.

Background: Integrin subunit α -v (ITGAV) has been demonstrated to be dysregulated and involved in cancer promotion processes in a variety of cancers, but studies on nasopharyngeal carcinoma (NPC) have been limited. Our study aimed to comprehensively assess the expression level and potential mechanisms of ITGAV in NPC. Results: A total of 13 mRNA expression datasets and internal tissue microarrays were included. ITGAV protein and mRNA were overexpressed in NPC. The pathways of upregulated genes positively related to ITGAV in NPC were analyzed, and the PI3K−Akt signaling pathway, cell cycle, and human papillomavirus infections were most significantly enriched. The protein–protein interaction network was constructed for the genes enriched in these pathways, and the corresponding hub genes were obtained. Among them, breast cancer susceptibility gene 1 (BRCA1) was predicted to be a transcription factor of ITGAV via the Cistrome DB Toolkit, which was also confirmed by ChIP-seq information and correlation calculations. Conclusions: ITGAV is overexpressed in NPC and can regulate BRCA1 to participate in the cancer process. ITGAV serves as a potential therapeutic target in NPC patients.How to cite: Huang S-W, Luo J-Y, Qin L-T, et al. Upregulation of ITGAV and the underlying mechanisms in nasopharyngeal carcinoma. Electron J Biotechnol 2022;60. https://doi.org/10.1016/j.ejbt.2022.09.002.

Background: Leucine zipper protein 2 (LUZP2) is a vital gene encoding leucine zipper protein. It is of great importance in the incidence and progress of several human cancers. However, little is known about the role and clinical effects of LUZP2 in prostate cancer (PCa). Therefore, it is crucial to unravel the clinicopathological value of LUZP2 in PCa. In all, 1467 PCa and 549 non-prostate cancer (non-PCa) prostate samples were collected from mRNA chip and RNA-sequencing datasets. The protein levels of LUZP2 were verified in 91 prostate gland tissues by in-house immunohistochemistry (IHC). The standardized mean difference (SMD) was calculated to analyze LUZP2 expression. Survival analysis was also conducted to explore the prognostic significance of LUZP2 in PCa. R software was employed to identify the upregulated differently expressed genes (up-DEGs) and coexpressed genes (CEGs) of LUZP2. Additionally, we explored the prospective molecular mechanism of CEGs of LUZP2 through GO and KEGG pathway analyses. Results: Compared with non-PCa, LUZP2 showed predominantly higher expression in PCa (SMD = 1.05, AUC = 0.88). IHC indicated the protein expression level of LUZP2 was consistently upregulated in PCa tissues (SMD = 2.23, 95%CI: 1.67–2.79). LUZP2 upregulation had an AUC of 0.88 (95%CI: 0.85–0.90) to distinguish PCa from non-PCa tissues. KEGG pathway analysis showed that the pathways of amino sugar and nucleoside sugar metabolism were chiefly enriched with the LUZP2 CEGs in PCa. Conclusion:: LUZP2 upregulation might play a promoting function in the occurrence of PCa.How to cite: Li S-H, Yang Y-P, He R-Q, et al. Comprehensive expression analysis reveals upregulated LUZP2 in prostate cancer tissues. Electron J Biotechnol 2022;59. https://doi.org/10.1016/j.ejbt.2022.06.001

Objective To explore the expression and clinical significance of CLDN8 in chromophobe renal cell carcinoma (chRCC). Methods The relevant datasets from Gene Expression Omnibus、Sequence Read Archive、ArrayExpress、TCGA、GTEx databases were collected. The expression levels of CLDN8 mRNA in chRCC and non chRCC tissues were analyzed. At the same time, the self purchased tissue microarray (In-house TMA dataset) was used to analyze the expression level of CLDN8 protein in chRCC and non chRCC tissues. The diagnostic efficacy of CLDN8 was analyzed by drawing the sROC curve. Results A total of 5 data sets were included. In TCGA-GTEx dataset, the expression level of CLDN8 mRNA in the chRCC tissues was higher than that in the non chRCC tissues, and the difference was statistically significant (P <0.05). In In-house TMA dataset, the expression level of CLDN8 protein in the chRCC tissues was significantly higher than that in the non chRCC tissues (P <0.000 1). The combined standardized mean difference of five data sets was 1.33 (95%CI:0.39-2.27). The area under sROC curve, sensitivity, specificity, positive likelihood ratio and negative likelihood ratio of CLDN8 in diagnosing chRCC were 0. 93, 0. 86, 0. 87, 6. 78 and 0. 17 respectively. Conclusion The overexpression of CLDN8 may be related to the formation and progression of chRCC. [ABSTRACT FROM AUTHOR]

Foodborne pathogens that enter the human food chain are a significant threat worldwide to human health. Timely and cost-effective detection of them became challenging for many countries that want to improve their detection and control of foodborne illness. We summarize simple, rapid, specific, and highly effective molecular technology that is used to detect and identify foodborne pathogens, including polymerase chain reaction, isothermal amplification, loop-mediated isothermal amplification, nucleic acid sequence-based amplification, as well as gene chip and gene probe technology. The principles of their operation, the research supporting their application, and the advantages and disadvantages of each technology are summarized. [ABSTRACT FROM AUTHOR]

Background: Classical swine fever (CSF), African swine fever (ASF), and atypical porcine pestivirus (APPV) are acute, virulent, and contagious viral diseases currently hampering the pig industry in China, which result in mummification or stillbirths in piglets and mortality in pigs. Diagnostic assays for the differentiation of infection and vaccination of CSFV, in addition to the detection of ASFV and APPV, are urgently required for better prevention, control, and elimination of these viral diseases in China. Methods: A quadruple PCR-based gene microarray assay was developed in this study to simultaneously detect wild-type and vaccine CSFV strains, ASFV and APPV according to their conserved regions. Forty-two laboratory-confirmed samples, including positive samples of 10 other swine viral diseases, were tested using this assay to confirm its high specificity. Results: This assay's limit of detections (LODs) for the wild-type and vaccine CSFV were 6.98 and 6.92 copies/µL. LODs for ASFV and APPV were 2.56 × 10 and 1.80 × 10 copies/µL, respectively. When compared with standard RT-PCR or qPCR for CSFV (GB/T 26875–2018), ASFV (MARR issue No.172), or APPV (CN108611442A) using 219 clinical samples, the coincidence was 100%. The results showed that this assay with high sensitivity could specifically distinguish ASFV, APPV, and CSFV, including CSFV infection and immunization. Conclusion: This assay provides a practical, simple, economic, and reliable test for the rapid detection and accurate diagnosis of the three viruses and may have good prospects for application in an epidemiological investigation, prevention, and control and elimination of these three diseases. [ABSTRACT FROM AUTHOR]

Purpose: To examine the differences in gene expression between ruptured and non-ruptured nucleus pulposus tissues of the intervertebral discs using gene chip technology. Methods: A total of 8 patients with nucleus pulposus from a lumbar disc herniation (LDH) undergoing discectomy in our hospital were selected, including 4 ruptured and 4 non-ruptured herniated nucleus pulposus cases. Total RNA was extracted from cells by using TRIzol reagent. Nucleus pulposus cDNA probes of the two groups were obtained by the single marker method and hybridized with a human gene expression profiling chip (Agilent). The fluorescence signal images were scanned by a laser, and the obtained genes were analyzed by bioinformatics. Results: There were 75 differentially expressed genes with more than 2-foldchanges, of which 56 were up-regulated and 19 were down-regulated. The differential expression of THSD7A, which was up-regulated 18 times, was the most significant, followed by CCL5, AQP3 and SDC4. Conclusion: THSD7A can be used as a characteristic differentially expressed gene in human ruptured nucleus pulposus. Moreover, CCL5, AQP3 and SDC4 may improve the chemotaxis of stem cell migration for self-healing of damaged disc tissue, increase water uptake by nucleus accumbens cells, and inhibit the inflammatory response, thus delaying the process of intervertebral disc degeneration. [ABSTRACT FROM AUTHOR]

BACKGROUND: Chondrocytes degeneration often leads to common orthopedic diseases such as osteoarthritis, intervertebral disc degeneration and meniscus degeneration. SIRT1 gene is closely related to chondrocytes degeneration. When SIRT1 gene is knocked down in ATDC5 mouse chondrocytes, it can affect cell function via signaling pathways related to chondrocyte degeneration, and then affect the process of orthopedic diseases. OBJECTIVE: To investigate the significantly activated signaling pathways related to chondrocyte degeneration and the expression of differential factors in ATDC5 mouse chondrocytes after SIRT1 gene knockdown. METHODS: The lentivirus carrying SIRT1 gene or not was transfected into ATDC cells. The transfected cells were divided into control (transfected with negative control lentivirus) and experiment group (transfected with lentivirus carrying SIRT1 gene). Total RNA was extracted for quality testing. Gene chip was used to detect the expression of coding RNA in the cells. Combined with bioinformatics analysis, we identified significantly activated signaling pathways related to chondrocyte degeneration, and elaborated differentially expressed factors in some signaling pathways. RESULTS AND CONCLUSION: Forty-two signaling pathways were significantly activated in ATDC5 cells after SIRT1 gene knockdown. Among them, we selected five signaling pathways related to chondrocyte degeneration and reported less, including hepatocyte growth factor signaling pathway (ETS1, PIK3CA, NRAS, PIK3C2A, FGFR2, ELF1, FGFR3, CDKN1A, AKT3, FRS2, PRKD3, MAP3K2; Ratio=0.139 0, Z-score=2.673), neuregulin signaling pathway (RPS6KB1, STAT5A, MTOR, BTC, HBEGF, RNF41; Ratio=0.136 0, Z-score=2.309), insulin receptor signaling pathway (TSC1, EIF4EBP1, PRKAR2B, PPP1R12A, TSC2; Ratio=0.106 0, Z-score=2.138), chemokine receptor 4 signaling pathway (PAK4, EGR1, RHOJ, RHOB, PLCB1, GNG5; Ratio=0.097 0, Z-score=2.500), actin cytoskeleton signaling pathway (ABI2, BRK1, PIP4K2B, MYLK, IQGAP1, ARPC1A, ACTA2, EZR, SSH2, ACTG1, IQGAP3; Ratio=0.092 1, Z-score=2.236), so as to provide novel targets for treating chondrocyte degeneration related diseases. [ABSTRACT FROM AUTHOR]

Objective: To analyze the differential gene expression profile of serum exosomes in patients with acute cerebral infarction (ACI) and clarify the changes in gene expression related to cerebral infarction injury and the potential serum markers. Methods: Four patients with ACI and five healthy people were enrolled in the Phase Ⅰ study. After serum isolation from peripheral blood, exosomes were extracted with exosomes kits, high-throughput detection of mRNA was performed with gene chips, and differentially expressed mRNAs were screened. Gene Ontology (GO) functional analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed simultaneously. Furthermore, real-time polymerase chain reaction (qRT-PCR) was used to verify the expression levels of the screened differential mRNAs in the serum exosomes collected in Phase Ⅱ from 32 patients each in the ACI case and normal control groups. Results: In the Phase Ⅰ study, there were 248 differentially expressed mRNAs (fold change ≥ 2.0, P < 0.05) among five patients in the normal control group and four patients in the case group, of which the expression of 242 was upregulated and that of six was downregulated. The results of GO functional enrichment analysis mainly included behavior regulation, cell connection, and antioxidant activity. The results of KEGG pathway enrichment analysis mainly included ribosomes, proteasomes, oxytocin signaling pathways, and oxidative phosphorylation. After researching and screening based on relevant literature, it was found that among the genes with significant differential expression, H3F3B mRNA may be associated with and might play an important role in ACI. The qRT-PCR method was used to detect the H3F3B mRNA expression in serum exosomes of 32 patients each in the normal control and case groups in Phase Ⅱ; the expression was significantly higher in serum exosomes of the case group than in those of the normal control group (P < 0.001). H3F3B mRNA expression in serum exosomes of the case group positively correlated with age, the National Institutes of Health Stroke Scale (NIHSS) score, and the maximum infarct size (P < 0.05). Conclusion: ACI can lead to changes in the serum exosomes mRNA expression profile, which may be closely related to the occurrence, development, and prognosis of this condition. These findings will provide direction for research on the molecular mechanism, diagnostic markers, and therapeutic targets of ACI.

Objective To study the molecular mechanismof miRNA let7. Methods The dataset GSE60848 was downloaded from the GEO database, which contained two pairs of let7 knockdown mouse brain tissue samples and two pairs of normal brain tissue samples. Differential gene expression analysis was carried out by using the GEO2R tool to screen out the differentially expressed candidate genes, and the DAVID online database was used to carry out the GO and KEGG enrichment analysis of candidate genes. The STRING database was used to construct the protein interaction network, and the Cyotoscape software was used to visualize the results to further screen out key genes and construct corresponding regulatory sub-networks. Results A total of 77 genes with significant expression differences were obtained through analysis and screening, of which 68 were significantly up-regulated and 7 were significantly down-regulated. The above differentially expressed genes mainly exerted biological functions such as immune response, antigen presentation, guanosine triphosphate (GTP) enzyme activity, and GTP ligation, and were significantly enriched in the signaling pathway such as glucose metabolism, cell adhesion, antigen processing and presentation, phagosomes, etc. By analyzing the let7-mRNA regulatory network, 10 key genes that played a core regulatory role were finally screened. Conclusion The let7 has a broad-spectrum and effective regulatory effect on biological systems, and its mechanism may be through the targeted regulation of TRIM30A, GBP3, PARP14, IFIT2 and other genes to exert biological functions. [ABSTRACT FROM AUTHOR]

The present study aimed to establish esophageal squamous carcinoma cell (ESCC) sublines with different invasive and metastatic potentials. Gene microarrays were used for differential gene screening with the establishment of ESCC invasive metastatic gene expression profiles. Some differential gene expressions were validated. Parent line Eca109-T0 was screened in a Transwell chamber to establish Eca109-T4 with high invasion and metastasis. The migrative and proliferative capacities of ESCCs were compared. The Eca109-T0 and Eca109-T4 cell lines were taken as the research objects and were hybridized with gene chips to obtain cell sublines for the screening of differential genes of ESCCs with varying invasive and metastatic potentials. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) clustering analyses were conducted. Some differential genes (HSP90AA1, ANXA1, YWHAB, CXCR7, SDC2, and TNFRSF10D messenger ribonucleic acid) were validated by qualitative real-time polymerase chain reaction and Western blot analysis. As a result, some Eca109-T4 ESCC sublines with high invasive and metastatic potential were screened in a Transwell chamber. The gene chip analysis screened out 326 differential genes, of which 123 were upregulated and 203 were downregulated by Eca109-T4. The GO cluster analysis indicated that the genes were in the cytoplasm, nucleus, and cytosol. The molecular functions of these genes involved the binding of proteins and metal ions and participation in biological processes, including cell signal transduction, transcription, and apoptosis. The KEGG clustering showed that these genes were mainly involved in signaling pathways, such as actin cytoskeleton regulation, the mitogen-activated protein kinase pathway, and the cancer pathway. The validation results were basically consistent with the gene microarray screening results. In Eca109-T4 and CE81T-4, HSP90AA1, YWHAB, and CXCR7 were highly expressed, while the expression of ANXA1 was low. In conclusion esophageal squamous carcinoma cell models with different invasive and metastatic potentials were established. The establishment of differential gene expression profiles for invasion and metastasis together with a bioinformatics analysis provided rich information for studies related to ESCC invasion and metastasis. HSP90a, 14-3-3b, and CXCR7 were highly expressed in ESCCs with high invasion and metastasis, while Annexin A1 was highly expressed in ESCCs with low metastasis. [ABSTRACT FROM AUTHOR]

Background: Tuberculosis (TB) is a major global public health issue. Prompt and accurate TB diagnosis is crucial for starting appropriate treatments and preventing the disease's spread. Current diagnostic techniques are either slow or expensive. This study aimed to create and evaluate a new, fast, highly reliable, and cost-effective TB detection method using a gene chip and Restriction Fragment Length Polymorphism (RFLP) analysis on Mycobacteria Growth Indicator Tubes (MGIT) specimens., Methods: We assessed the effectiveness of a novel gene chip and RFLP methods targeting the 16S rRNA gene of Mycobacterium tuberculosis in 2000 MGIT culture-positive specimens. RFLP analysis identified the AfeI restriction site within the M. tuberculosis complex (MTBC) genome. Discrepancies were investigated through extensive sequencing and Cobas TaqMan PCR analysis, along with reviewing patient profiles., Results: Both methods showed high efficacy in detecting MTBC in broth cultures, with the gene chip method achieving a sensitivity of 99.27 %, specificity of 98.35 %, and the RFLP method showing a sensitivity of 98.18 %, specificity of 99.31 %. False negatives in two isolates were due to a mutation in the AfeI site. Additionally, five cases showed MTBC presence when nontuberculous Mycobacterium species grew in cultures., Conclusion: Our novel gene chip and RFLP methods are effective for rapid highly-reliable and cost-effective M. tuberculosis detection in MGIT specimens. Both gene chip and RFLP methods are suitable for resource-limited settings, offering an economical advantage. These methods have significant potential to improve clinical TB diagnosis., Competing Interests: Declaration of Competing interest The authors declared no conflicts of interest., (Copyright © 2024. Published by Elsevier B.V.)

As the eutrophication of natural water bodies becomes more and more serious, the frequency of outbreaks of harmful algal blooms (HABs) mainly formed by harmful algae also increases. HABs have become a global ecological problem that poses a serious threat to human health and food safety. Therefore, it is extremely important to establish methods that can rapidly detect harmful algal species for early warning of HABs. The traditional morphology-based identification method is inefficient and inaccurate. In recent years, the rapid development of molecular biology techniques has provided new ideas for the detection of harmful algae and has become a research hotspot. The current molecular detection methods for harmful algal species mainly include fluorescence in situ hybridization, sandwich hybridization, and quantitative PCR (qPCR), but all of these methods can only detect single harmful algal species at a time. The establishment of methods for the simultaneous detection of multiple harmful algal species has become a new trend in the development of molecular detection technology because various harmful algal species may coexist in the natural water environment. The established molecular techniques for multiple detections of harmful algae mainly include gene chip, multiplex PCR, multiplex qPCR, massively parallel sequencing, antibody chip, and multiple isothermal amplification. This review mainly focuses on the principles, advantages and disadvantages, application progress, and application prospects of these multiple detection technologies, aiming at providing effective references not only for the fisheries but also for economic activities, environment, and human health. [ABSTRACT FROM AUTHOR]

The incidence of obesity has increased significantly on account of the alterations of living habits, especially changes in eating habits. In this study, we investigated the effect of octacosanol on lipid lowering and its molecular mechanism. High-fat diet (HFD)-induced obesity mouse model was used in the study. Thirty C57BL/6J mice were divided into control, HFD, and HFD+Oct groups randomly, and every group included ten mice. The mice of HFD+Oct group were intragastrically administrated 100 mg/kg/day of octacosanol. After 10 weeks for treatment, our results indicated that octacosanol supplementation decreased the body, liver, and adipose tissues weight of HFD mice; levels of TC, TG, and LDL-c were reduced in the plasma of HFD mice; and level of HDL-c were increased. H&E staining indicated that octacosanol supplementation reduces the size of fat droplets of hepatic tissues and adipose cells comparing with the HFD group. Gene chip analysis found that octacosanol regulated 72 genes involved in lipid metabolism in the tissues of liver comparing to the HFD group. IPA pathway network analysis indicated that PPAR and AMPK may play a pivotal role in the lipid-lowering function of octacosanol. Real-time quantitative PCR and Western blot showed that the octacosanol supplementation caused change of expression levels of AMPK, PPARs, FASN, ACC, SREBP-1c, and SIRT1, which were closely related to lipid metabolism. Taken together, our results suggest that octacosanol supplementation exerts a lipid-decreasing effect in the HFD-fed mice through modulating the lipid metabolism-related signal pathway. [ABSTRACT FROM AUTHOR]

Gastrointestinal stromal tumors (GISTs) are common ICC precursor sarcomas, which are considered to be a potential malignant mesenchymal tumor driven by specific KIT or PDGFRA signals in the gastrointestinal tract. The standard treatment for GIST without metastasis is surgical resection. GIST with metastasis is usually treated with tyrosine kinase inhibitors (TKIs) only but cannot be cured. The TKI imatinib is the main drug of GIST drug therapy. In adjuvant therapy, the duration of imatinib adjuvant therapy is 3 years. It has been proved that imatinib can improve the overall survival time (OS). However, many GIST patients develop drug resistance due to the long-term use of imatinib. We were forced to look for new strategies to treat GIST. The purpose of the current academic work is to study the drug-resistant genes of imatinib and their potential mechanisms. A total of 897 differentially expressed genes (DEGs) were found between imatinib-sensitive cell line GIST882 and imatinib-resistant cell line GIST430 by RNA sequencing (RNA-seq). After analyzing the DEGs, 10 top genes were selected (NDN, FABP4, COL4A1, COLEC11, MEG3, EPHA3, EDN3, LMO3, RGS4, and CRISP2). These genes were analyzed by RT-PCR, and it was confirmed that the expression trend of FABP4, COL4A1, and RGS4 in different imatinib-resistant cell lines was in accord with the GEO database. It is suggested that these genes may play a potential role in the clinical diagnosis and treatment of imatinib resistance in GIST. [ABSTRACT FROM AUTHOR]

Gastrointestinal stromal tumors (GISTs) are common ICC precursor sarcomas, which are considered to be a potential malignant mesenchymal tumor driven by specific KIT or PDGFRA signals in the gastrointestinal tract. The standard treatment for GIST without metastasis is surgical resection. GIST with metastasis is usually treated with tyrosine kinase inhibitors (TKIs) only but cannot be cured. The TKI imatinib is the main drug of GIST drug therapy. In adjuvant therapy, the duration of imatinib adjuvant therapy is 3 years. It has been proved that imatinib can improve the overall survival time (OS). However, many GIST patients develop drug resistance due to the long-term use of imatinib. We were forced to look for new strategies to treat GIST. The purpose of the current academic work is to study the drug-resistant genes of imatinib and their potential mechanisms. A total of 897 differentially expressed genes (DEGs) were found between imatinib-sensitive cell line GIST882 and imatinib-resistant cell line GIST430 by RNA sequencing (RNA-seq). After analyzing the DEGs, 10 top genes were selected (NDN, FABP4, COL4A1, COLEC11, MEG3, EPHA3, EDN3, LMO3, RGS4, and CRISP2). These genes were analyzed by RT-PCR, and it was confirmed that the expression trend of FABP4, COL4A1, and RGS4 in different imatinib-resistant cell lines was in accord with the GEO database. It is suggested that these genes may play a potential role in the clinical diagnosis and treatment of imatinib resistance in GIST.

BACKGROUND: The incidence of osteoarthritis is increasing as the population ages, and there is still no effective treatment. Gene chip technology has been widely used in the diagnosis and treatment of diseases. OBJECTIVE: To identify the key genes in osteoarthritis by using integrative bioinformatics and weighted gene co-expression network analysis (WGCNA) and to investigate its mechanism. METHODS: Four original data sets of synovial tissue chips in osteoarthritis patients were downloaded from Gene Expression Omnibus database, and the immune infiltration was analyzed by CIBERSORT algorithm. Differentially expressed genes were screened by R-language software. Gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to analyze the selected differentially expressed genes. The text files of these differentially expressed genes were obtained through the online tool STRING (http://string-db.org/) and were imported into the Cytoscape software to edit the visual protein-protein interaction network. R-language software was used to build a bar chart of differentially expressed genes to obtain the top 10 differentially expressed genes in degree values. The four chip data sets were integrated to screen out the genes with the highest correlation of gene co-expression module by WGCNA algorithm, and the intersection genes were screened by Venn analysis method. The synovial tissues of four patients with osteoarthritis and four patients with joint trauma were collected for quantitative real-time PCR verification. RESULTS AND CONCLUSION: (1)A total of 107 differentially expressed genes were screened out, including 46 up-regulated genes and 61 down-regulated genes. (2)The gene ontology enrichment results showed that differentially expressed genes were mainly involved in biological processes such as positive regulation of ossification and cell adhesion. KEGG pathways were mainly enriched in rheumatoid arthritis pathways, nuclear factor-κB signaling pathways, and receptor protein tyrosine kinase B signaling pathways. Immune infiltration results indicated that the contents of M0 macrophages and M2 macrophages were relatively high in the synovial tissue of patients with osteoarthritis. (3)The obtained intersection genes included matrix metalloproteinase 1, tissue inhibitor of metalloproteinase 4, laminin subunit alpha 3, and follistatin 3. The results of quantitative real-time PCR confirmed that there were significant differences in the expression levels of tissue inhibitor of metalloproteinase 4, laminin subunit alpha 3, and follistatin 3 between the synovial tissue samples from patients with osteoarthritis and those with joint trauma. (4)Therefore, tissue inhibitor of metalloproteinase 4, laminin subunit alpha 3, and follistatin 3 may be therapeutic targets for osteoarthritis. [ABSTRACT FROM AUTHOR]

Objective To explore the relationship between gene polymorphism in patients with osteoporosis (OP) and with intervertebral disc degeneration (IDD). Methods The gene expression profile of OP and IDD was obtained from GEO database. The difference genes were analyzed and the intersection was collected. PPI network was then constructed by using Cytoscape software. The key genes were screened out according to the degree value, and the relationship between OP and IDD was analyzed. Finally, the main biological function and signal pathway of the key genes in the process of OP and IDD development were analyzed by using David database. Results The results showed that there were 205 cross genes in the occurrence and development of OP and IDD. UBC, YWHAZ, TP53, CUL3, NTRK1, BRCA1, MCM², and ESR1 were the key genes. The results of GO function analysis and KEGG enrichment analysis showed that the biological process closely related to the occurrence and development of OP and IDD mainly involved protein-DNA complex assembly, protein-DNA complex subunit organization, protein deubiquitination, protein modification by small protein removal, and regulation of chromosome organization. It also involved PI3K/Akt signaling pathway, ubiquitin mediated protein hydrolysis, mitochondrial autophagy, apoptosis pathways, neurotrophin signaling pathway, and thyroid hormone signaling pathway. Conclusion There is highly coincident gene expression between OP and IDD. The involved gene function and signal pathway are helpful to understand the common pathogenesis of the two diseases, and to provide certain reference for the common drug research and treatment of the two diseases. [ABSTRACT FROM AUTHOR]

Background. Immediate early response 3 (IER3) is correlated to the prognosis of several cancers, but the precise mechanisms underlying the regulation by IER3 of the occurrence and development of hepatocellular carcinoma (HCC) remain unknown. Methods. The expression level of IER3 was examined by using in-house immuno-histochemistry (IHC), public gene chip, and public RNA-sequencing (RNA-seq). The standardized mean difference (SMD) was calculated to compare the expression levels of IER3 between HCC patients and controls. The summary receiver operating characteristics (sROC) was plotted to comprehensively understand the discriminatory capability of IER3 between HCC and non-HCC group. The Kaplan-Meier curves and the combined hazard ratios (HRs) were used to determine the prognostic value of IER3 in HCC. Moreover, differentially expressed genes (DEGs) and co-expression genes (CEGs) were used to explored the molecular mechanisms of IER3 underlying HCC. hTFtarget was used to predict the transcription factors (TFs) of IER3. The binding site of TFs and the IER3 promoter region was forecasted using the JASPAR website. The relevant ChIP-seq data were used to determine whether TF peaks were present in the IER3 transcription initiation. Results. A significantly increased expression of IER3 protein was found in HCC tissue relative to non-HCC tissue as detected by IHC (p<0:001). Compared to 1,263 cases of non-HCC tissues, IER3 in 1483 cases of HCC tissues was upregulated (SMD D 0.42, 95% confidence interval [CI] [0.09-0.76]). The sROC showed that IER3 had a certain ability at differentiatingHCCtissues (area under the curve (AUC)D0.65, 95% CI [0.61-0.69]). Comprehensive analysis of the effect of IER3 on the prognosis of patients with HCC demonstrated that higher IER3 expression was associated with poor prognosis in HCC (HRs D 1.30, 95% CI [1.03-1.64]). Pathway enrichment analysis revealed that IER3-related genes were mostly enriched in the PI3K-Akt signaling pathway, cancer-related signaling pathways, the p53 signaling pathway, and other signaling pathways. Regulatory factor X5 (RFX5) was identified as a possible regulator of IER3-related TF. [ABSTRACT FROM AUTHOR]

Background: The systems pharmacology approach is a target prediction model for traditional Chinese medicine and has been used increasingly in recent years. However, the accuracy of this model to other prediction models is yet to be established. Objective : To compare the systems pharmacology modelwithexperimental gene chip technology by using these models to predict targets of a traditional Chinese medicine formulain the treatment of primary liver cancer. Methods: Systems pharmacology and gene chip target predictions were performed for the traditional Chinese medicine formula ZhenzhuXiaojiTang (ZZXJT). A third square alignment was performed with molecular docking. Results: Identification of systems pharmacology accounted for 17% of targets, whilegene chip-predicted outcomes accounted for 19%.Molecular docking showed that the top ten targets (excludingcommon targets) of the system pharmacology model had better binding free energies than the gene chip model using twocommon targets as a benchmark. For both models, the core drugs predictions were more consistent than the core small molecules predictions. Conclusion: In this study, the identified targets of systems pharmacology weredissimilar to those identified by gene chip technology; whereas the core drug and small molecule predictions were similar. [ABSTRACT FROM AUTHOR]

Objective: Network pharmacology was utilized to explore the mechanism of Guanxinning (GXN) tablet for the treatment of stable coronary artery disease (SCAD). Materials and Methods: First, active ingredients and therapeutic targets were predicted by databases and gene chip. Then, we constructed the compound-target (C-T) network and target-disease (T-D) network to screen hub compounds and therapeutic targets based on contribution index (CI), degree, closeness, betweenness, and coreness in the networks. Enrichment analysis was performed on hub therapeutic targets, and finally, the verification of hub ingredients and hub therapeutic targets was performed through molecular docking. Results: With “oral bioavailability ≥30%, druglikeness ≥0.18, and half-life ≥4 h” as screening conditions, 58 active ingredients were obtained. Seven hundred and seventeen compound targets and 636 SCAD targets were retrieved using databases and gene chip, and the intersection of both (139 targets) was defined as therapeutic targets. According to CI, degree, betweenness, closeness, and coreness, 2 hub compounds and 13 hub therapeutic targets were chosen from the C-T network and T-D network, respectively. The Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis indicated that GXN treated SCAD from several aspects including inflammatory reaction, oxidative stress, nutritional metabolism, blood pressure regulation, ventricular remodeling, vascular smooth muscle proliferation, angiogenesis, and platelet aggregation. Tissue enrichment analysis revealed that the therapeutic targets were enriched in multiple organs and tissues. The excellent binding force between the hub compounds and hub therapeutic targets was verified by molecular docking. Conclusions: The treatment of SCAD by GXN has the characteristics of multiple ingredients, multiple targets, and multiple approaches. Consequently, it may theoretically treat SCAD from multiple angles and levels.

Abstract Background Hepatocellular carcinoma (HCC) remains one of the most common cancers worldwide and tends to be detected at an advanced stage. More effective biomarkers for HCC screening and prognosis assessment are needed and the mechanisms of HCC require further exploration. The role of MAOA in HCC has not been intensively investigated. Methods In‐house tissue microarrays, genechips, and RNAsequencing datasets were integrated to explore the expression status and the clinical value of MAOA in HCC. Immunohistochemical staining was utilized to determine MAOA protein expression. Intersection genes of MAOA related co‐expressed genes and differentially expressed genes were obtained to perform functional enrichment analyses. In vivo experiment was conducted to study the impact of traditional Chinese medicine nitidine chloride (NC) on MAOA in HCC. Results MAOA was downregulated and possessed an excellent discriminatory capability in HCC patients. Decreased MAOA correlated with poor prognosis in HCC patients. Downregulated MAOA protein was relevant to an advanced TNM stage in HCC patients. Co‐expressed genes that positively related to MAOA were clustered in chemical carcinogenesis, where CYP2E1 was identified as the hub gene. In vivo experiment showed that nitidine chloride significantly upregulated MAOA in a nude mouse HCC model. Conclusions A decreased MAOA level is not only correlated with aggressive behaviors in males but also serves as a promising biomarker for the diagnosis and prognosis of HCC patients. Moreover, MAOA may play a role in AFB1 toxic transformation through its synergistic action with co‐expressed genes, especially CYP3A4. MAOA also serves as a potential therapy target of NC in HCC patients.

Background: The systems pharmacology approach is a target prediction model for traditional Chinese medicine and has been used increasingly in recent years. However, the accuracy of this model to other prediction models is yet to be established.Objective: To compare the systems pharmacology modelwithexperimental gene chip technology by using these models to predict targets of a traditional Chinese medicine formulain the treatment of primary liver cancer.Methods: Systems pharmacology and gene chip target predictions were performed for the traditional Chinese medicine formula ZhenzhuXiaojiTang (ZZXJT). A third square alignment was performed with molecular docking.Results: Identification of systems pharmacology accounted for 17% of targets, whilegene chip-predicted outcomes accounted for 19%.Molecular docking showed that the top ten targets (excludingcommon targets) of the system pharmacology model had better binding free energies than the gene chip model using twocommon targets as a benchmark. For both models, the core drugs predictions were more consistent than the core small molecules predictions.Conclusion:In this study, the identified targets of systems pharmacology weredissimilar to those identified by gene chip technology; whereas the core drug and small molecule predictions were similar.

Psoriasis is chronic skin disease and an important health concern. Traditional Chinese Medicine (TCM) has shown great promise in the treatment of psoriasis. However, the correlation between TCM Syndromes and genomics of psoriasis has not been evaluated. Here, we analyzed gene expression profiling of monocytes from psoriasis vulgaris patients with different TCM syndrome types to reveal the molecular basis of different psoriasis syndromes. Of the 62 cases of psoriasis vulgaris recruited, 16, 23, and 23 cases were of blood-heat syndrome, blood stasis syndrome, and blood-dryness syndrome, respectively; 10 healthy controls were recruited as controls. Affymertix's Gene Chip ®clariom D gene chip was used to detect the gene expression profile of peripheral blood monocytes collected from recruited individuals. Compared with the healthy control group, 1570 genes were up-regulated and 977 genes were down-regulated in the psoriasis vulgaris patients group; 798 genes and 108 genes were up- and down-regulated in the blood-heat syndrome group respectively; 319 and 433 genes were up- and down-regulated in the blood-dryness syndrome group, respectively; and 502 and 179 genes were up-and down-regulated in the blood-stasis syndrome group. Our analyses indicated not only common differential genes and pathways between psoriasis syndrome groups and healthy controls, but also syndrome-specific genes and pathways. The results of this study link the three syndromes at the gene level and will be useful for clarifying the molecular basis of TCM syndromes of psoriasis. Clinical Trial Registration: (http://www.chictr.org.cn/showproj.aspx?proj=4390), identifier (ChiCTR-TRC-14005185). [ABSTRACT FROM AUTHOR]

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.)

Clinical studies have shown similarities in the genetic background and biological functional characteristics between Hashimoto's thyroiditis (HT) and papillary thyroid carcinoma (PTC), and that HT may increase risks of PTC. Here, we set to determine the gene expression specificity of HT and PTC by screening related genes or co-expressed genes and exploring their genetic correlation. Referencing the Oncomine database, HT-related genes were discovered to be expressed in many different types of thyroid cancer, such as TSHR that is highly expressed in thyroid cancer. An in-depth genetic analysis and verification of 35 cancer and paracancerous tissue pairs from patients with thyroid cancer, and 35 tissues and blood cells pairs from patients with Hashimoto's thyroiditis was conducted. Gene chip technology research showed that TSHR, BACH2, FOXE1, RNASET2, CTLA4, PTPN22, IL2RA and other HT-related genes were all expressed in PTC, in which TSHR was significantly over-expressed in PTC patients sensitive to radioactive iodine therapy, while BACH2 was significantly under-expressed in these patients. The biologically significant candidate Tag SNP highlighted from HT-related genes was screened by the high-throughput detection method. Somatic mutations in patients with HT and PTC were detected by target region capture technique, and 75 mutations were found in patients with HT and PTC. The upstream regulatory factors of the different genes shared by HT and PTC were analyzed based on Ingenuity Pathway Analysis (IPA), and it was found that HIF-1α and PD-L1 could be used as important upstream regulatory signal molecules. These results provide a basis for screening key diagnostic genes of PTC by highlighting the relationship between some HT-related genes and their polymorphisms in the pathogenesis of PTC. [ABSTRACT FROM AUTHOR]

Abstract Background To investigate the species distribution of non-tuberculous mycobacteria (NTM) among tuberculosis (TB) specimens collected from January 2013 to December 2018 at Peking Union Medical Hospital (Beijing), China. NTM species identification was carried out by DNA microarray chip. Results Mycobacterial species were detected in 1514 specimens from 1508 patients, among which NTM accounted for 37.3% (565/1514), increasing from a proportion of 15.6% in 2013 to 46.1% in 2018 (P

Psoriasis is chronic skin disease and an important health concern. Traditional Chinese Medicine (TCM) has shown great promise in the treatment of psoriasis. However, the correlation between TCM Syndromes and genomics of psoriasis has not been evaluated. Here, we analyzed gene expression profiling of monocytes from psoriasis vulgaris patients with different TCM syndrome types to reveal the molecular basis of different psoriasis syndromes. Of the 62 cases of psoriasis vulgaris recruited, 16, 23, and 23 cases were of blood-heat syndrome, blood stasis syndrome, and blood-dryness syndrome, respectively; 10 healthy controls were recruited as controls. Affymertix’s Gene Chip ®clariom D gene chip was used to detect the gene expression profile of peripheral blood monocytes collected from recruited individuals. Compared with the healthy control group, 1570 genes were up-regulated and 977 genes were down-regulated in the psoriasis vulgaris patients group; 798 genes and 108 genes were up- and down-regulated in the blood-heat syndrome group respectively; 319 and 433 genes were up- and down-regulated in the blood-dryness syndrome group, respectively; and 502 and 179 genes were up-and down-regulated in the blood-stasis syndrome group. Our analyses indicated not only common differential genes and pathways between psoriasis syndrome groups and healthy controls, but also syndrome-specific genes and pathways. The results of this study link the three syndromes at the gene level and will be useful for clarifying the molecular basis of TCM syndromes of psoriasis.Clinical Trial Registration: (http://www.chictr.org.cn/showproj.aspx?proj=4390), identifier (ChiCTR-TRC-14005185).

Clinical studies have shown similarities in the genetic background and biological functional characteristics between Hashimoto’s thyroiditis (HT) and papillary thyroid carcinoma (PTC), and that HT may increase risks of PTC. Here, we set to determine the gene expression specificity of HT and PTC by screening related genes or co-expressed genes and exploring their genetic correlation. Referencing the Oncomine database, HT-related genes were discovered to be expressed in many different types of thyroid cancer, such as TSHR that is highly expressed in thyroid cancer. An in-depth genetic analysis and verification of 35 cancer and paracancerous tissue pairs from patients with thyroid cancer, and 35 tissues and blood cells pairs from patients with Hashimoto’s thyroiditis was conducted. Gene chip technology research showed that TSHR, BACH2, FOXE1, RNASET2, CTLA4, PTPN22, IL2RA and other HT-related genes were all expressed in PTC, in which TSHR was significantly over-expressed in PTC patients sensitive to radioactive iodine therapy, while BACH2 was significantly under-expressed in these patients. The biologically significant candidate Tag SNP highlighted from HT-related genes was screened by the high-throughput detection method. Somatic mutations in patients with HT and PTC were detected by target region capture technique, and 75 mutations were found in patients with HT and PTC. The upstream regulatory factors of the different genes shared by HT and PTC were analyzed based on Ingenuity Pathway Analysis (IPA), and it was found that HIF-1α and PD-L1 could be used as important upstream regulatory signal molecules. These results provide a basis for screening key diagnostic genes of PTC by highlighting the relationship between some HT-related genes and their polymorphisms in the pathogenesis of PTC.

Foodborne pathogens that enter the human food chain are a significant threat worldwide to human health. Timely and cost-effective detection of them became challenging for many countries that want to improve their detection and control of foodborne illness. We summarize simple, rapid, specific, and highly effective molecular technology that is used to detect and identify foodborne pathogens, including polymerase chain reaction, isothermal amplification, loop-mediated isothermal amplification, nucleic acid sequence-based amplification, as well as gene chip and gene probe technology. The principles of their operation, the research supporting their application, and the advantages and disadvantages of each technology are summarized.

Purpose: To investigate the effect of miR-486 on rats with acute myocardial infarction (AMI), and its mechanism of action. Methods: A rat model of AMI was established. They were randomly divided into 4 groups, namely, sham, model, agomiR-486 and antagomiR-486 groups, respectively. Rats in these different groups were treated with agomiR-21 (5 μL, 40 nmol/mL), antagomiR-21 (5 μL, 40 nmol/mL) or agomiR-NC (5 μL, 40 nmol/mL), respectively. Then, key miRNAs were sorted out using gene-chip assay and verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay. Luciferase reporter gene assay was conducted to determine the interaction between miR-486 and gene of PTEN. After intraperitoneal injection of agomiR-486 and antagomiR-486, hemodynamics was measured to determine the effect of miR-486 on myocardial function of the rats. The effect of miR-486 expression level on the expression of myocardial enzymes in serum, the morphology of myocardial tissues, and the apoptosis of myocardial tissues in rats, were investigated. Additionally, the effect of miR-486 expression level on PTEN/AKT signaling pathway in the rats was determined by Western blotting. Results: The results of gene-chip and qRT-PCR assays revealed that there were 8 differentially expressed genes in rat myocardial tissues in the model group when compared with the sham group. MiR-486 improved the cardiac function of rats and the morphology of myocardial tissues, but reduced AMI-induced apoptosis of myocardial cells and the expression of myocardial enzymes (markers of myocardial injury) in a dose-dependent manner (p < 0.05). The results of luciferase reporter gene assay showed that PTEN was a direct target of miR-486. In rat models of AMI, a raised expression of miR-486 remarkably suppressed the protein expression level of PTEN and up-regulated that of p-AKT/AKT (p < 0.05). Conclusion: MiR-486 protects against AMI in rats probably by targeting PTEN and activating the AKT signaling pathway. The results of the current study may provide new insights for the treatment of AMI. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Shenzhen University Science & Engineering is the property of Editorial Department of Journal of Shenzhen University Science & Engineering 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 Journal of Food Safety & Quality is the property of Journal of Food Safety & Quality 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 Journal of Harbin University of Science & Technology is the property of Journal of Harbin University of Science & Technology 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.)

β-Casomorphin is an opioid-like bioactive peptide derived from β-casein of milk that plays a crucial role in modulating animal’s feed intake, growth, nutrient utilization and immunity. However, the effect of β-casomorphin on lipid metabolism in chickens and its mechanism remain unclear. The aim of this study was to investigate the effects of β-casomorphin on fat deposition in broiler chickens and explore its mechanism of action. A total of 120 21-day-old Arbor Acres male broilers (747.94±8.85 g) was chosen and randomly divided into four groups with six replicates of five birds per replicate. Three groups of broilers were injected with 0.1, 0.5 or 1.0 mg/kg BW of β-casomorphin in 1 ml saline for 7 days, whereas the control group received 1 ml saline only. The results showed that subcutaneous administration of β-casomorphin to broiler chickens increased average daily gain, average daily feed intake and fat deposition, and decreased feed : gain ratio (P

This study explored the possible bioactive ingredients and target protein of Rostellularia procumbens (L.) Nees. The results of optical turbidimetry revealed that the ethyl acetate extraction obtained from R. procumbens (L.) Nees could inhibit platelet aggregation. Gene chip was used to investigate differentially expressed genes. According to the results of the gene chip, the targets of compounds isolated from the ethyl acetate extraction were predicted by network pharmacology. Computational studies revealed that chinensinaphthol methyl ether and neojusticin B may target the integrin αIIbβ3 protein. The results of Prometheus NT.48 and microscale thermophoresis suggested that the molecular interactions between the two compounds with purified integrin αIIbβ3 protein in the optimal test conditions were coherent with the docking results. To our best knowledge, this is the first report to state that chinensinaphthol methyl ether and neojusticin B target the integrin αIIbβ3 protein.

The incidence of obesity has increased significantly on account of the alterations of living habits, especially changes in eating habits. In this study, we investigated the effect of octacosanol on lipid lowering and its molecular mechanism. High-fat diet (HFD)-induced obesity mouse model was used in the study. Thirty C57BL/6J mice were divided into control, HFD, and HFD+Oct groups randomly, and every group included ten mice. The mice of HFD+Oct group were intragastrically administrated 100 mg/kg/day of octacosanol. After 10 weeks for treatment, our results indicated that octacosanol supplementation decreased the body, liver, and adipose tissues weight of HFD mice; levels of TC, TG, and LDL-c were reduced in the plasma of HFD mice; and level of HDL-c were increased. H&E staining indicated that octacosanol supplementation reduces the size of fat droplets of hepatic tissues and adipose cells comparing with the HFD group. Gene chip analysis found that octacosanol regulated 72 genes involved in lipid metabolism in the tissues of liver comparing to the HFD group. IPA pathway network analysis indicated that PPAR and AMPK may play a pivotal role in the lipid-lowering function of octacosanol. Real-time quantitative PCR and Western blot showed that the octacosanol supplementation caused change of expression levels of AMPK, PPARs, FASN, ACC, SREBP-1c, and SIRT1, which were closely related to lipid metabolism. Taken together, our results suggest that octacosanol supplementation exerts a lipid-decreasing effect in the HFD-fed mice through modulating the lipid metabolism-related signal pathway.