Publications by authors named "Xiaoyu Fu"

51 Publications

Elevated Cerebrospinal Fluid Anti-CD4 Autoantibody Levels in HIV Associate with Neuroinflammation.

Microbiol Spectr 2022 Jan 5:e0197521. Epub 2022 Jan 5.

Department of Microbiology and Immunology, Medical University of South Carolinagrid.259828.c, Charleston, South Carolina, USA.

The mechanisms of persistent central nervous system (CNS) inflammation in people with HIV (PWH) despite effective antiretroviral therapy (ART) are not fully understood. We have recently shown that plasma anti-CD4 IgGs contribute to poor CD4 T cell recovery during suppressive ART via antibody-mediated cytotoxicity (ADCC) against CD4 T cells, and that plasma anti-CD4 IgG levels are associated with worse cognitive performance and specific brain area atrophy. However, the role of anti-CD4 IgGs in neuroinflammation remains unclear. In the current study, plasma and cerebrospinal fluid (CSF) samples from 31 ART-naive and 26 treated, virologically suppressed PWH, along with 16 HIV-seronegative controls, were evaluated for CSF levels of anti-CD4 IgG, white blood cell (WBC) counts, soluble biomarkers of neuroinflammation, and neurofilament light chain (NfL). We found that 37% of the PWH exhibited elevated CSF anti-CD4 IgG levels, but few or none of the PWH were observed with elevated CSF anti-CD4 IgM, anti-CD8 IgG, or anti-double-strand DNA IgG. CSF anti-CD4 IgG levels in PWH were directly correlated with neuroinflammation (WBC counts, neopterin, and markers of myeloid cell activation), but not with CSF NfL levels. Using cells from one immune nonresponder to ART, we generated a pathogenic anti-CD4 monoclonal IgG (JF19) presenting with ADCC activity; JF19 induced the production of soluble CD14 (sCD14) and interleukin-8 (IL-8) in human primary monocyte-derived macrophages via CD4 binding . This study demonstrates for the first time that elevated CSF anti-CD4 IgG levels present in a subgroup of PWH which may play a role in neuroinflammation in HIV. This study reports that an autoantibody presents in the CNS of HIV patients and that its levels in the CSF correlate with some markers of neuroinflammation.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1128/spectrum.01975-21DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8729763PMC
January 2022

The immediate and long-term impacts of the COVID-19 pandemic on patients with obsessive-compulsive disorder: A one-year follow-up study.

Psychiatry Res 2021 12 2;306:114268. Epub 2021 Nov 2.

Peking University Sixth Hospital, Peking University Institute of Mental, Health, Key Laboratory of Mental Health, Ministry of Health (Peking University), National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), China. Electronic address:

Several recent publications have revealed that obsessive-compulsive disorder (OCD) patients were adversely affected during coronavirus disease 2019 (COVID-19); however, how long this negative impact will last is unclear. Our study aimed to investigate the impact of the COVID-19 pandemic on OCD patients after one year. Online questionnaires were administered, and clinical interviews were conducted to assess OCD symptoms, depression, anxiety, information about COVID-19 and mental resilience at baseline (1 December 2019-1 January 2020), during early COVID-19 (26 February-25 March 2020) and at the one-year follow-up (26 February-25 March 2021). A total of 110 OCD patients were enrolled. Our findings showed that OCD, depressive and anxiety symptoms worsened during early COVID-19, and the negative impact persisted at the one-year follow-up. Multivariate analysis showed that female gender, concern about COVID-19 and OCD symptom severity at baseline were risk factors for exacerbation of OCD symptoms during early COVID-19, while optimism, as one composite factor of resilience, was a protective factor against exacerbation of OCD symptoms both during early COVID-19 and at follow-up. Our study showed that COVID-19 had immediate and long-term impacts on the exacerbation of OCD symptoms, and interventions targeted at improving resilience are recommended.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.psychres.2021.114268DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8562016PMC
December 2021

Chronic cannabis smoking-enriched oral pathobiont drives behavioral changes, macrophage infiltration, and increases β-amyloid protein production in the brain.

EBioMedicine 2021 Dec 23;74:103701. Epub 2021 Nov 23.

Department of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Ave., Charleston, SC 29425, USA; Department of Medicine, Division of Infectious Diseases, Medical University of South Carolina, Charleston, SC 29425, USA. Electronic address:

Background: Little is known about chronic cannabis smoking-associated oral microbiome and its effects on central nervous system (CNS) functions.

Methods: In the current study, we have analyzed the saliva microbiome in individuals who chronically smoked cannabis with cannabis use disorder (n = 16) and in non-smoking controls (n = 27). The saliva microbiome was analyzed using microbial 16S rRNA sequencing. To investigate the function of cannabis use-associated oral microbiome, mice were orally inoculated with live Actinomyces meyeri, Actinomyces odontolyticus, or Neisseria elongata twice per week for six months, which mimicked human conditions.

Findings: We found that cannabis smoking in humans was associated with oral microbial dysbiosis. The most increased oral bacteria were Streptococcus and Actinomyces genus and the most decreased bacteria were Neisseria genus in chronic cannabis smokers compared to those in non-smokers. Among the distinct species bacteria in cannabis smokers, the enrichment of Actinomyces meyeri was inversely associated with the age of first cannabis smoking. Strikingly, oral exposure of Actinomyces meyeri, an oral pathobiont, but not the other two control bacteria, decreased global activity, increased macrophage infiltration, and increased β-amyloid 42 protein production in the mouse brains.

Interpretation: This is the first study to reveal that long-term oral cannabis exposure is associated oral enrichment of Actinomyces meyeri and its contributions to CNS abnormalities.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ebiom.2021.103701DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8626580PMC
December 2021

The Fecal Microbiota of Dogs Switching to a Raw Diet Only Partially Converges to That of Wolves.

Front Microbiol 2021 29;12:701439. Epub 2021 Sep 29.

Department of Nutrition, Genetics and Ethology, Faculty of Veterinary Medicine, Ghent University, Ghent, Belgium.

The genomic signature of dog domestication reveals adaptation to a starch-rich diet compared with their ancestor wolves. Diet is a key element to shape gut microbial populations in a direct way as well as through coevolution with the host. We investigated the dynamics in the gut microbiota of dogs when shifting from a starch-rich, processed kibble diet to a nature-like raw meat diet, using wolves as a wild reference. Six healthy wolves from a local zoo and six healthy American Staffordshire Terriers were included. Dogs were fed the same commercial kibble diet for at least 3 months before sampling at day 0 (DC), and then switched to a raw meat diet (the same diet as the wolves) for 28 days. Samples from the dogs were collected at day 1 (DR1), week 1 (DR7), 2 (DR14), 3 (DR21), and 4 (DR28). The data showed that the microbial population of dogs switched from kibble diet to raw diet shifts the gut microbiota closer to that of wolves, yet still showing distinct differences. At phylum level, raw meat consumption increased the relative abundance of Fusobacteria and Bacteroidetes at DR1, DR7, DR14, and DR21 ( < 0.05) compared with DC, whereas no differences in these two phyla were observed between DC and DR28. At genus level, , , , and were significantly lower in dogs consuming the raw diet from the first week onward and in wolves compared with dogs on the kibble diet. Linear discriminant analysis effect size (LEfSe) showed a higher abundance of , , , and in dogs fed kibble diet compared with dogs fed raw diet for 28 days and wolves. In addition, wolves had greater unidentified Lachnospiraceae compared with dogs irrespective of the diets. These results suggested that carbohydrate-fermenting bacteria give way to protein fermenters when the diet is shifted from kibble to raw diet. In conclusion, some microbial phyla, families, and genera in dogs showed only temporary change upon dietary shift, whereas some microbial groups moved toward the microbial profile of wolves. These findings open the discussion on the extent of coevolution of the core microbiota of dogs throughout domestication.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fmicb.2021.701439DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8511826PMC
September 2021

A novel regQTL-SNP and the risk of lung cancer: a multi-dimensional study.

Arch Toxicol 2021 12 1;95(12):3815-3827. Epub 2021 Oct 1.

Department of Epidemiology, School of Public Health, Nantong University, Nantong, 226019, Jiangsu, China.

RegQTL, a novel concept, indicates that different genotypes of some SNPs have differential effects on the expression patterns of miRNAs and their target mRNAs. We aimed to identify the association between regQTL-SNPs and lung cancer risk and to explore the underlying mechanisms. The two-stage case-control study included the first stage in a Chinese population (626 lung cancer cases and 667 healthy controls) and the second stage in a European population (18,082 lung cancer cases and 13,780 healthy controls). Functional annotations were conducted based on the GTEx and the TCGA databases. Functional experiments were performed to explore the underlying biological mechanisms in vitro and vivo. After strict screening, five candidate regQTL-SNPs (rs7110737, rs273957, rs6593210, rs3768617, and rs6836432) were selected. Among them, the variant T allele of rs3768617 in LAMC1 was found to significantly increase the risk of lung cancer (first stage: P = 0.044; second stage: P = 0.007). The eQTL analysis showed that LAMC1 expression level was significantly higher in subjects with the variant T allele of rs3768617 (P = 1.10 × 10). In TCGA paired database, the regQTL annotation indicated the different expression patterns between LAMC1 and miRNA-548b-3p for the distinct genotypes of rs3768617. Additionally, LAMC1 knockdown significantly inhibited malignant phenotypes in lung cancer cell lines and suppressed tumor growth. A novel regQTL-SNP, rs3768617, might affect lung cancer risk by modulating the expression patterns of miRNA-548b-3p and LAMC1. RegQTL-SNPs could provide a new perspective for evaluating the regulatory function of SNPs in lung cancer development.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00204-021-03170-5DOI Listing
December 2021

Oral Enrichment of Streptococcus and its Role in Systemic Inflammation Related to Monocyte Activation in Humans with Cocaine Use Disorder.

J Neuroimmune Pharmacol 2021 Aug 26. Epub 2021 Aug 26.

Department of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Ave. BSB208D, Charleston, SC, 29425, USA.

Cocaine use is commonly associated with increased chronic systemic inflammation. However, the drivers for cocaine use-mediated systemic inflammation are not fully understood. In the current study, we recruited individuals with cocaine use disorder and healthy individuals who did not use cocaine and collected paired saliva and blood samples. The saliva samples were used to assess the oral microbiome, and the plasma samples were evaluated for 33 cytokines and chemokines. Cocaine users exhibited decreased saliva microbial diversities compared to non-users. Streptococcus was the only increased genus in the saliva from cocaine users, whereas several genera were decreased in cocaine users compared to non-users. Notably, cocaine users exhibited increased plasma levels of several monocyte activation markers, including monocyte chemoattractant protein (MCP)-4, macrophage inflammatory protein (MIP)-3α, macrophage-derived chemokine (MDC), and thymus and activation-regulated chemokine (TARC), all of which were correlated with increased saliva levels of three Streptococcus species. Furthermore, treatment with Streptococcus or its lipoteichoic acid preferentially activated primary human monocytes to produce proinflammatory cytokines and chemokines, such as MIP-3α and TARC, in vitro compared to controls. However, monocytes failed to produce these chemokines after exposure to cocaine or cocaine plus bacteria compared to medium or bacteria alone. This study revealed that chronic cocaine use-associated inflammation in the blood may result from increased oral Streptococcus and its effects on myeloid cell activation, but does not result from cocaine directly.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11481-021-10007-6DOI Listing
August 2021

Exosomal microRNA-25 released from cancer cells targets SIK1 to promote hepatocellular carcinoma tumorigenesis.

Dig Liver Dis 2021 Aug 9. Epub 2021 Aug 9.

Department of Infectious Diseases, Xiangya Hospital, Central South University, No.87, Xiangya Road, Kaifu District, Changsha, Hunan 410008, PR China. Electronic address:

Background: Hepatocellular carcinoma (HCC) is recognized as a leading cause of cancer-associated fatality worldwide. Our study here aimed to probe the mechanism by which exosomes secreted by CSQT-2, an HCC cell line, affected the progression of HCC.

Methods: Exosomes were extracted from CSQT-2 cells. Colony formation, Transwell, sphere formation and flow cytometric analyses were applied to assess cell biological activities. Microarray analysis detected the change of microRNA (miRNA) expression after exosome treatment, followed by RT-qPCR validation. Luciferase reporter was applied to detect the binding between SIK1 and miR-25. Xenograft studies in nude mice manifested tumor growth and metastatic ability of miR-25 and SIK1.

Results: The exosome treatment enhanced cell malignant phenotype in vitro and tumor growth and liver and lung metastases in vivo. The exosomes elevated miR-25 expression in HCC cells. miR-25 targeted SIK1 which was decreased in the exosomes-treated cells. miR-25 inhibitor reduced cell malignant phenotype and attenuated tumorigenesis and metastasis in vivo. SIK1 silencing reversed the effect of miR-25 inhibitor. The exosome treatment potentiated the Wnt/β-catenin pathway in cells, whereas miR-25 inhibitor blunted the pathway activity.

Conclusion: MiR-25 shuttled through CSQT-2-derived exosomes promoted the development of HCC by reducing SIK1 expression and potentiating the Wnt/β-catenin pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.dld.2021.07.017DOI Listing
August 2021

Chalcone Derivatives: Role in Anticancer Therapy.

Biomolecules 2021 06 16;11(6). Epub 2021 Jun 16.

Department of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China.

Chalcones (1,3-diaryl-2-propen-1-ones) are precursors for flavonoids and isoflavonoids, which are common simple chemical scaffolds found in many naturally occurring compounds. Many chalcone derivatives were also prepared due to their convenient synthesis. Chalcones as weandhetic analogues have attracted much interest due to their broad biological activities with clinical potentials against various diseases, particularly for antitumor activity. The chalcone family has demonstrated potential in vitro and in vivo activity against cancers via multiple mechanisms, including cell cycle disruption, autophagy regulation, apoptosis induction, and immunomodulatory and inflammatory mediators. It represents a promising strategy to develop chalcones as novel anticancer agents. In addition, the combination of chalcones and other therapies is expected to be an effective way to improve anticancer therapeutic efficacy. However, despite the encouraging results for their response to cancers observed in clinical studies, a full description of toxicity is required for their clinical use as safe drugs for the treatment of cancer. In this review, we will summarize the recent advances of the chalcone family as potential anticancer agents and the mechanisms of action. Besides, future applications and scope of the chalcone family toward the treatment and prevention of cancer are brought out.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/biom11060894DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8234180PMC
June 2021

Integrated Analysis of Long Noncoding RNA Expression Profiles in Acute-on-Chronic Liver Failure.

Biomed Res Int 2021 18;2021:5387856. Epub 2021 May 18.

Department of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, 410008 Hunan, China.

People infected with chronic hepatitis B virus (HBV) might progress to acute-on-chronic liver failure (ACLF) with a high fatality rate. Long noncoding RNAs (lncRNAs) are involved in human diseases, but it is unknown whether lncRNAs are involved in the progression of chronic HBV infection to ACLF. Hence, this study is aimed at systemically identifying and characterizing the landscape and the molecular mechanism of lncRNAs in the pathogenesis of chronic HBV infection progress to ACLF. RNA sequencing (RNA-Seq) of peripheral blood samples from 5 ACLF and 5 HBV infection patients was performed. We detected 9733 lncRNAs, including 406 annotated lncRNAs and 9327 novel lncRNAs. A total of 407 lncRNAs were found to be significantly dysregulated in the patients with ACLF as compared with those in the chronic HBV infection patients. The flanking protein-coding genes of differentially expressed lncRNAs were enriched with pathways that might contribute to the pathogenesis of ACLF, such as the WNT signaling pathway. Furthermore, 9 selected differentially expressed lncRNAs validated by the qRT-PCR, showing that the expression patterns of these 9 lncRNAs were consistent with the RNA-Seq data. Four selected differentially expressed lncRNAs were also validated in another patient cohort comprising 80 patients with ACLF and 65 patients with chronic HBV infection. Aberrant lncRNAs might be used to develop novel diagnostic biomarkers or drug targets for ACLF.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1155/2021/5387856DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8158414PMC
September 2021

The Cardioprotective Mechanism of Phenylaminoethyl Selenides (PAESe) Against Doxorubicin-Induced Cardiotoxicity Involves Frataxin.

Front Pharmacol 2020 12;11:574656. Epub 2021 Apr 12.

Department of Drug, Discovery and Development, Harrison School of Pharmacy, Auburn University, Alabama, AL, United States.

Doxorubicin (DOX) is an anthracycline cancer chemotherapeutic that exhibits cumulative dose-limiting cardiotoxicity and limits its clinical utility. DOX treatment results in the development of morbid cardiac hypertrophy that progresses to congestive heart failure and death. Recent evidence suggests that during the development of DOX mediated cardiac hypertrophy, mitochondrial energetics are severely compromised, thus priming the cardiomyocyte for failure. To mitigate cumulative dose (5 mg/kg, QIW x 4 weeks with 2 weeks recovery) dependent DOX, mediated cardiac hypertrophy, we applied an orally active selenium based compound termed phenylaminoethyl selenides (PAESe) (QIW 10 mg/kg x 5) to our animal model and observed that PAESe attenuates DOX-mediated cardiac hypertrophy in athymic mice, as observed by MRI analysis. Mechanistically, we demonstrated that DOX impedes the stability of the iron-sulfur cluster biogenesis protein Frataxin (FXN) (0.5 fold), resulting in enhanced mitochondrial free iron accumulation (2.5 fold) and reduced aconitase activity (0.4 fold). Our findings further indicate that PAESe prevented the reduction of FXN levels and the ensuing elevation of mitochondrial free iron levels. PAESe has been shown to have anti-oxidative properties in part, by regeneration of glutathione levels. Therefore, we observed that PAESe can mitigate DOX mediated cardiac hypertrophy by enhancing glutathione activity (0.4 fold) and inhibiting ROS formation (1.8 fold). Lastly, we observed that DOX significantly reduced cellular respiration (basal (5%) and uncoupled (10%)) in H9C2 cardiomyoblasts and that PAESe protects against the DOX-mediated attenuation of cellular respiration. In conclusion, the current study determined the protective mechanism of PAESe against DOX mediated myocardial damage and that FXN is implicitly involved in DOX-mediated cardiotoxicity.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fphar.2020.574656DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8072348PMC
April 2021

The long noncoding RNA lncCIRBIL disrupts the nuclear translocation of Bclaf1 alleviating cardiac ischemia-reperfusion injury.

Nat Commun 2021 01 22;12(1):522. Epub 2021 Jan 22.

Department of Pharmacology (The Key Laboratory of Cardiovascular Research, Ministry of Education) at College of Pharmacy, Harbin Medical University, Harbin, 150086, China.

Cardiac ischemia-reperfusion (I/R) injury is a pathological process resulting in cardiomyocyte death. The present study aims to evaluate the role of the long noncoding RNA Cardiac Injury-Related Bclaf1-Inhibiting LncRNA (lncCIRBIL) on cardiac I/R injury and delineate its mechanism of action. The level of lncCIRBIL is reduced in I/R hearts. Cardiomyocyte-specific transgenic overexpression of lncCIRBIL reduces infarct area following I/R injury. Knockout of lncCIRBIL in mice exacerbates cardiac I/R injury. Qualitatively, the same results are observed in vitro. LncCIRBIL directly binds to BCL2-associated transcription factor 1 (Bclaf1), to inhibit its nuclear translocation. Cardiomyocyte-specific transgenic overexpression of Bclaf1 worsens, while partial knockout of Bclaf1 mitigates cardiac I/R injury. Meanwhile, partial knockout of Bclaf1 abrogates the detrimental effects of lncCIRBIL knockout on cardiac I/R injury. Collectively, the protective effect of lncCIRBIL on I/R injury is accomplished by inhibiting the nuclear translocation of Bclaf1. LncCIRBIL and Bclaf1 are potential therapeutic targets for ischemic cardiac disease.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41467-020-20844-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7822959PMC
January 2021

Different polymorphisms in HIF-1α may exhibit different effects on cancer risk in Asians: evidence from nearly forty thousand participants.

Aging (Albany NY) 2020 11 4;12(21):21329-21343. Epub 2020 Nov 4.

Department of Epidemiology, School of Public Health, Nantong University, Nantong, Jiangsu, China.

The effect of different SNPs in and cancer susceptibility remain indistinct. Here, we evaluated the association between all identified SNPs (rs11549465, rs11549467 and rs2057482) in and the overall risk of cancer in all case-control studies published before April 2020. A total of 54 articles including 56 case-control studies were included in this analysis. We found that variant genotypes of rs11549465 and rs11549467 were associated with a significantly increased overall cancer risk. In contrast, the variant T allele of rs2057482 showed a significantly reduced risk of overall cancer. In addition, variant genotypes of the three studied SNPs exhibited a significant association with cancer risk in Asians and specific cancer types. Meanwhile, was significantly highly expressed in head and neck squamous cell carcinoma and pancreatic cancer tissues. More importantly, survival analysis indicated that the high expression of was associated with a poor survival in patients with lung cancer. These findings further provided evidence that different SNPs in may exhibit different effects on overall cancer risk; these effects were ethnicity and type-specific. Further studies with functional evaluations are required to confirm the biological mechanisms underlying the role of SNPs in cancer development and progression.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.18632/aging.103871DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695358PMC
November 2020

A case report of misdiagnosis of Ewing's sarcoma of the duodenum.

Asian J Surg 2021 Jan 15;44(1):394-395. Epub 2020 Oct 15.

Department of General Surgery, 900 Hospital of the Joint Logistics Support Force, (Fuzhou General Hospital of Fujian Medical University), Fuzhou, China. Electronic address:

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.asjsur.2020.10.004DOI Listing
January 2021

Distinct Effects of Social Stress on Working Memory in Obsessive-Compulsive Disorder.

Neurosci Bull 2021 Jan 1;37(1):81-93. Epub 2020 Oct 1.

Peking University Sixth Hospital, Beijing, 100191, China.

Stress might exaggerate the compulsion and impair the working memory of patients with obsessive-compulsive disorder (OCD). This study evaluated the effect of stress on the cognitive neural processing of working memory in OCD and its clinical significance using a "number calculation working memory" task. Thirty-eight patients and 55 gender- and education-matched healthy controls were examined. Stress impaired the performance of the manipulation task in patients. Healthy controls showed less engagement of the medial prefrontal cortex and striatum during the task under stress versus less stress, which was absent in the patients with OCD. The diagnosis × stress interaction effect was significant in the right fusiform, supplementary motor area, precentral cortex and caudate. The failure of suppression of the medial prefrontal cortex and striatum and stress-related hyperactivation in the right fusiform, supplementary motor area, precentral cortex, and caudate might be an OCD-related psychopathological and neural response to stress.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12264-020-00579-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7811969PMC
January 2021

Parabrachial neuron types categorically encode thermoregulation variables during heat defense.

Sci Adv 2020 Sep 2;6(36). Epub 2020 Sep 2.

Shanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, Shanghaitech University, Shanghai 201210, China.

Heat defense is crucial for survival and fitness. Transmission of thermosensory signals into hypothalamic thermoregulation centers represents a key layer of regulation in heat defense. Yet, how these signals are transmitted into the hypothalamus remains poorly understood. Here, we reveal that lateral parabrachial nucleus (LPB) glutamatergic prodynorphin and cholecystokinin neuron populations are progressively recruited to defend elevated body temperature. These two nonoverlapping neuron types form circuits with downstream preoptic hypothalamic neurons to inhibit the thermogenesis of brown adipose tissues (BATs) and activate tail vasodilation, respectively. Both circuits are activated by warmth and can limit fever development. The prodynorphin circuit is further required for regulating energy expenditure and body weight homeostasis. Thus, these findings establish that the genetic and functional specificity of heat defense neurons occurs as early as in the LPB and uncover categorical neuron types for encoding two heat defense variables, inhibition of BAT thermogenesis and activation of vasodilation.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1126/sciadv.abb9414DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7467693PMC
September 2020

Exosomes secreted by chronic hepatitis B patients with PNALT and liver inflammation grade ≥ A2 promoted the progression of liver cancer by transferring miR-25-3p to inhibit the co-expression of TCF21 and HHIP.

Cell Prolif 2020 Jul 11;53(7):e12833. Epub 2020 Jun 11.

Key Laboratory of Viral Hepatitis, Department of Infectious Diseases, Xiangya Hospital, Central South University, Changsha, China.

Objectives: The current study aimed to investigate the mechanism by which exosomes secreted by CHB patients with PNALT and liver inflammation grade (≥A2) affected the development of liver cancer.

Materials And Methods: Gene expression was assessed by RT-PCR, Western blotting and immunohistochemistry. CCK-8, colony formation, transwell, scratch-wound and flow cytometry assays were used to detect cell viability, proliferation, apoptosis and metastasis. The interaction of TCF21 and HHIP was assessed by co-immunoprecipitation assay. Luciferase reporter was used to detect the combination of TCF21/HHIP and miR-25-3p. Xenograft studies in nude mice manifested tumour growth ability of miR-25-3p. Bioinformatics analyses were conducted using TargetScan, EVmiRNA, TCGA, GEO, DAVID, COEXPEDIA, UALCAN, UCSC and the Human Protein Atlas databases.

Results: CHB-PNALT-Exo (≥A2) promoted the proliferation and metastasis of HepG2.2.15 cells. miR-25-3p was upregulated in CHB-PNALT-Exo (≥A2). miR-25-3p overexpression promoted cell proliferation and metastasis and was related to poor survival in patients with CHB-PNALT (≥A2). The cell proliferation- and metastasis-promoting functions of CHB-PNALT-Exo (≥A2) were abolished by miR-25-3p inhibitors. TCF21 directly interacted with HHIP. Inhibition of TCF21 or HHIP promoted cell proliferation and metastasis. Knockdown of TCF21 or HHIP counteracted the effects of CHB-PNALT-Exo (≥A2) containing miR-25-3p inhibitor on cell proliferation, metastasis and the expression of Ki67, E-cadherin and caspase-3/-9.

Conclusions: Transfer of miR-25-3p by CHB-PNALT-Exo promoted the development of liver cancer by inhibiting the co-expression of TCF21 and HHIP.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/cpr.12833DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7377934PMC
July 2020

A Brain Signaling Framework for Stress-Induced Depression and Ketamine Treatment Elucidated by Phosphoproteomics.

Front Cell Neurosci 2020 7;14:48. Epub 2020 Apr 7.

Department of Neurology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Depression is a common affective disorder characterized by significant and persistent low mood. Ketamine, an N-methyl-D-aspartate receptor (NMDAR) antagonist, is reported to have a rapid and durable antidepressant effect, but the mechanisms are unclear. Protein phosphorylation is a post-translational modification that plays a crucial role in cell signaling. Thus, we present a phosphoproteomics approach to investigate the mechanisms underlying stress-induced depression and the rapid antidepressant effect of ketamine in mice. We analyzed the phosphoprotein changes induced by chronic unpredictable mild stress (CUMS) and ketamine treatment in two known mood control centers, the medial prefrontal cortex (mPFC) and the nucleus accumbens (NAc). We initially obtained >8,000 phosphorylation sites. Quantitation revealed 3,988 sites from the mPFC and 3,196 sites from the NAc. Further analysis revealed that changes in synaptic transmission-related signaling are a common feature. Notably, CUMS-induced changes were reversed by ketamine treatment, as shown by the analysis of commonly altered sites. Ketamine also induced specific changes, such as alterations in synapse organization, synaptic transmission, and enzyme binding. Collectively, our findings establish a signaling framework for stress-induced depression and the rapid antidepressant effect of ketamine.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fncel.2020.00048DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156020PMC
April 2020

Upregulation of microRNA-328-3p by hepatitis B virus contributes to THLE-2 cell injury by downregulating FOXO4.

J Transl Med 2020 03 30;18(1):143. Epub 2020 Mar 30.

Department of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, No.87 Xiangya Road, Changsha, 410008, Hunan, China.

Background: Hepatitis B virus (HBV) remains a major cause of chronic hepatitis and hepatocellular carcinoma, and miRNAs play important roles in HBV pathogenesis. Our previous study has shown that miR-328-3p is upregulated in HBV-infected patients and serves as a potent predictor for the prognosis of HBV-related liver failure.

Methods: Here, the role of miR-328-3p in modulating cell injury in HBV-infected liver cells THLE-2 was investigated in detail. MiR-328-3p expression was examined using qRT-PCR. The levels of pro-inflammatory cytokines were measured using ELISA. HBV RNA and HBV DNA levels were quantified. The interactions between STAT3 and miR-328-3p promoter as well as miR-328-3p and FOXO4 were analyzed using chromatin immunoprecipitation (CHIP) assay and luciferase reporter assay, respectively. THLE-2 cell injury was evaluated by examining cell viability and apoptosis.

Results: HBV promoted expression of miR-328-3p through the STAT3 signal pathway and that increasingly expressed miR-328-3p downregulated its target FOXO4, leading to the promotion of cell injury in HBV-infected liver cells THLE-2.

Conclusion: These data demonstrate that HBV-STAT3-miR-328-3p-FOXO4 regulation pathway may play an important role in the pathogenesis of HBV infection.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12967-020-02299-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7106851PMC
March 2020

Plasma miR-146a predicts serological conversion of hepatitis B e-antigen (HBeAg) in chronic hepatitis B patients treated with nucleotide analogs.

Ann Transl Med 2019 Sep;7(18):449

Department of Infectious Diseases, Xiangya Hospital, Central South University, Changsha 410008, China.

Background: To investigate the association of plasma miR-146a with serological conversion of hepatitis B e-antigen (HBeAg) in patients with chronic hepatitis B (CHB) treated with nucleotide analogs (NAs).

Methods: This was a retrospective study of 115 HBeAg-positive patients with CHB treated at Xiangya Hospital, Central South University, Changsha, China, between September 2009 and March 2014. Patients were grouped according to whether they had achieved seroconversion of HBeAg by 104 weeks of NAs treatment. We assessed plasma miR-146a using miScript polymerase chain reaction (PCR). Serum alanine transaminase (ALT), hepatitis B virus (HBV) deoxyribonucleic acid (DNA) load, hepatitis B surface antigen (HBsAg) titer, HBeAg titer, and plasma miR-146a were measured at 0, 24, 48, and 104 weeks of treatment. Finally, we also determined ΔmiR-146a and ΔmiR-146a.

Results: ΔmiR-146a was independently associated with seroconversion of HBeAg at 104 weeks [odds ratio (OR) =1.302; 95% confidence interval (CI), 1.159-1.962; P=0.029]. We obtained an area under the receiver operating characteristic (ROC) curve (AUC) of ΔmiR-146 of 0.757 for seroconversion of HBeAg (P=0.013). At the optimal cutoff value equivalent to a Youden index of 67.9%, the specificity and sensitivity of ΔmiR-146 were 63.7% and 88.3%, respectively. Positive (PPV) and negative (NPV) predictive values were 70.87% and 84.48%, respectively.

Conclusions: ΔmiR-146a was independently associated with seroconversion of HBeAg in CHB patients treated with NAs.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.21037/atm.2019.08.72DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6803199PMC
September 2019

[Expressions of miR-146a and miR-155 in different samples of chronic hepatitis B patients].

Zhong Nan Da Xue Xue Bao Yi Xue Ban 2019 Aug;44(8):845-849

Department of Infectious Diseases, Xiangya Hospital, Central South University; Hunan Key Laboratory of Viral Hepatitis, Changsha 410008, China.

Objective: To detect the levels of miR-146a and miR-155 in different samples from chronic hepatitis B (CHB), reveal whether there is a correlation between the 2 miRNAs in different samples, and to provide a theoretical basis for sample choice of miRNA research in liver.
 Methods: Real-time PCR was conducted to examine the expression of miR-146a and miR-155 in the plasma, peripheral blood mononuclear cell (PBMC), and liver tissues from 41 CHB patients who underwent nucleoside analogues antiviral therapy for 104 weeks. Correlations between the levels of miR-146a and miR-155 among the 3 samples were analyzed.
 Results: The expressions of miR-146a and miR-155 in the plasma, PBMC and liver tissues were significantly down-regulated at the 104th week than those at the baseline (all P<0.05). There was a correlation in the expression of miR-146a between plasma and liver tissues (r=0.560, P=0.007), PBMC and liver tissues (r=0.428, P=0.047) at baseline. There was a correlation in the expression of miR-155 between plasma and liver tissue (r=0.587, P=0.004), PBMC and liver tissue (r=0.483, P=0.023) at baseline. The expressions of miR-146a and miR-155 between the plasma and PBMC were not correlated (P>0.05).
 Conclusion: Compared with PBMC, miR-146a and miR-155 from plasma can better reflect the expression in the liver tissues, suggesting that plasma can be applied in the mechanism research on miR-146a and miR-155 in the liver diseases instead of liver tissues.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.11817/j.issn.1672-7347.2019.190366DOI Listing
August 2019

LncRNA HOTAIRM1 promotes osteogenesis by controlling JNK/AP-1 signalling-mediated RUNX2 expression.

J Cell Mol Med 2019 11 11;23(11):7517-7524. Epub 2019 Sep 11.

Department of Infectious Diseases, Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, China.

Mesenchymal stem cells (MSCs) have potential ability to differentiate into osteocytes in response to in vitro specific induction. However, the molecular basis underlying this biological process remains largely unclear. In this study, we identify lncRNA HOTAIRM1 as a critical regulator to promote osteogenesis of MSCs. Loss of HOTAIRM1 significantly inhibits the calcium deposition and alkaline phosphatase activity of MSCs. Mechanistically, we find that HOTAIRM1 positively modulates the activity of JNK and c-Jun, both of which are widely accepted as crucial regulators of osteogenic differentiation. More importantly, c-Jun is found to be functionally involved in the regulation of RUNX2 expression, a master transcription factor of osteogenesis. In detail, c-Jun can help recruit the acetyltransferase p300 to RUNX2 promoter, facilitating acetylation of histone 3 at K27 site, therefore epigenetically activating RUNX2 gene transcription. In summary, this study highlights the functional importance of HOTAIRM1 in regulation of osteogenesis, and we characterize HOTAIRM1 as a promising molecular target for bone tissue repair and regeneration.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/jcmm.14620DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6815819PMC
November 2019

miR-146a-5p enhances hepatitis B virus replication through autophagy to promote aggravation of chronic hepatitis B.

IUBMB Life 2019 09 24;71(9):1336-1346. Epub 2019 Apr 24.

Department of Infectious Diseases, Key Laboratory of Hunan Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, Hunan, China.

The objective of this study was to investigate the mechanism by which miR-146a-5p mediated autophagy and hepatitis B virus (HBV) replication. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the mRNA expression levels of miR-146a-5p and X-linked inhibitor of apoptosis (XIAP) and HBV DNA and RNA. The protein expression levels of XIAP, IκB-α, murine double minute 2 oncoprotein (MDM2) and p53, the phosphorylation of p65, and the conversion of light chain 3 (LC3)-I to LC3-II were detected by Western blotting. The expression levels of XIAP, HBV-related pro-inflammatory cytokines, and serum markers were detected by enzyme-linked immunosorbent assay (ELISA). miR-146a-5p was highly expressed in patients with chronic hepatitis B (CHB) and HBV-expressing hepatocytes. HBV core protein (HBc) and HBV X protein (HBx) were responsible for its effects on miR-146a-5p expression through the nuclear factor-κB pathway. Furthermore, the miR-146a-5p inhibitor suppressed autophagic response and HBV replication as well as MDM2/p53 expression. Luciferase reporter assay confirmed that XIAP was a direct target of miR-146a-5p. We therefore demonstrated that miR-146a-5p mediated positive feedback loop by regulating autophagy-induced HBV replication via targeting the XIAP-mediated MDM2/p53 axis. © 2019 IUBMB Life, 71(9):1336-1346, 2019.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/iub.2044DOI Listing
September 2019

Effects of Kudiezi Injection on Serum Inflammatory Biomarkers in Patients with Acute Cerebral Infarction.

Dis Markers 2018 2;2018:7936736. Epub 2018 Sep 2.

Central Laboratory, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China.

Background: Kudiezi injection is a traditional Chinese medicine for acute cerebral infarction, but the exact mechanisms are poorly understood.

Objective: To investigate the mechanisms of Kudiezi injection on the inflammatory response in the treatment of acute cerebral infarction.

Methods: This was a prospective study of patients with acute cerebral infarction within 48 h of onset and treated between July 2012 and July 2016 at three hospitals in China. The patients were randomized to routine treatments (control group) versus routine treatments and Kudiezi injection (Kudiezi group). The National Institutes of Health Stroke Score was assessed on days 1, 3, 5, 7, and 14. The patients were tested for serum levels of pro- and anti-inflammatory cytokines (S100 calcium-binding protein B, neuron-specific enolase, interleukin-6, interleukin-10, interleukin-18, and matrix metaloproteinase-9; by enzyme-linked immunosorbent assay) immediately after admission and on days 3, 5, and 14.

Results: Stroke scores were improved in both groups from days 1 to 14. On days 5 and 7, stroke scores in the Kudiezi group were lower than in the control group ( < 0.05). Compared with controls, the Kudiezi group had lower serum S100 calcium-binding protein B on day 14; higher interleukin-6 and interleukin-10 on day 3; lower interleukin-6 and interleukin-18 on day 5; and lower interleukin-18 and matrix metaloproteinase-9 on day 14.

Conclusion: Kudiezi injection could lead to early reduction of interleukin-6, interleukin-18, matrix metaloproteinase-9, neuron-specific enolase, and S100 calcium-binding protein B levels and increases of interleukin-10 levels in patients with acute ischemic stroke. This trial is registered with ClinicalTrials.gov NCT01636154.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1155/2018/7936736DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6139219PMC
January 2019

[Expression profiles of the exosomal miRNAs in the chronic hepatitis B patients with persistently normal ALT].

Zhong Nan Da Xue Xue Bao Yi Xue Ban 2018 May;43(5):475-480

Department of Infectious Diseases, Xiangya Hospital, Central South University, Hunan Key Laboratory of Viral Hepatitis, 
Changsha 410008, China.

Objective: To investigate expression profiles of the plasma exosomal miRNAs of the chronic hepatitis B (CHB) patients with persistently normal alamine aminotransferase (PNALT) for the first time and try to find exosomal miRNAs which could reflect liver inflammation better. 
 Methods: Five CHB patients with liver tissue inflammation grade ≥A2 of PNALT and 5 CHB patients with liver tissue inflammation grade
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.11817/j.issn.1672-7347.2018.05.003DOI Listing
May 2018

The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1.

Tumour Biol 2017 Jul;39(7):1010428317718135

1 Department of Infectious Disease, Xiangya Hospital, Central South University, Changsha, P.R. China.

Increasing evidence supports the significance of long non-coding RNA in cancer development. Several recent studies suggest the oncogenic activity of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in hepatocellular carcinoma. In this study, we explored the molecular mechanisms by which MALAT1 modulates hepatocellular carcinoma biological behaviors. We found that microRNA-204 was significantly downregulated in sh-MALAT1 HepG2 cell and 15 hepatocellular carcinoma tissues by quantitative real-time polymerase chain reaction analysis. Through bioinformatic screening, luciferase reporter assay, RNA-binding protein immunoprecipitation, and RNA pull-down assay, we identified microRNA-204 as a potential interacting partner for MALAT1. Functionally, wound-healing and transwell assays revealed that microRNA-204 significantly inhibited the migration and invasion of hepatocellular carcinoma cells. Notably, sirtuin 1 was recognized as a direct downstream target of microRNA-204 in HepG2 cells. Moreover, si-SIRT1 significantly inhibited cell invasion and migration process. These data elucidated, by sponging and competitive binding to microRNA-204, MALAT1 releases the suppression on sirtuin 1, which in turn promotes hepatocellular carcinoma migration and invasion. This study reveals a novel mechanism by which MALAT1 stimulates hepatocellular carcinoma progression and justifies targeting metastasis-associated lung adenocarcinoma transcript 1 as a potential therapy for hepatocellular carcinoma.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1177/1010428317718135DOI Listing
July 2017

HBx-related long non-coding RNA MALAT1 promotes cell metastasis via up-regulating LTBP3 in hepatocellular carcinoma.

Am J Cancer Res 2017 1;7(4):845-856. Epub 2017 Apr 1.

Department of Infectious Disease, Xiangya Hospital, Central South UniversityChangsha 410008, P. R. China.

Though it is widely known that hepatitis B virus X protein (HBx) is involved in the progression of hepatocellular carcinoma (HCC), the underlying mechanisms are not entirely clear. In recent years, metastasis associated with lung adenocarcinoma transcript 1 (MALAT1), which is an oncogenic long non-coding RNA (lncRNA), has been proved to be associated with many kinds of tumors, including liver cancer. In this study, we demonstrated that MALAT1 was involved in the HBx-mediated hepatocarcinogenesis. Firstly, we found that expression of MALAT1 was strongly up-regulated in HCC tissues and was directly proportional to the expression of HBx. Moreover, in HBx transfected LO2 and HepG2 cells, MALAT1 was also up-regulated compared with non-transfected cells. Then, we observed up-regulated MALAT1 in HepG2 cells could promote cell invasion and migration, whereas knockdown of MALAT1 in HBx-expressing hepatic cells (HepG2-HBx) resulted in a markedly inhibition of cell invasion and migration both and . To further obtain a deeper understanding of the effect of MALAT1, we took latent transforming growth factor β-binding protein 3 (LTBP3) into account by using several assays such as RNA interference, luciferase, transwell and wound healing. Results showed that MALAT1 could promote tumor growth and metastasis by activating LTBP3, which could also be up-regulated by HBx. Meanwhile, the similar results were detected in nude mice. These findings could demonstrate an important mechanism of hepatocarcinogenesis through the signaling of HBx-MALAT1/LTBP3 axis, and may give a potential target for treatment of HCC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5411792PMC
April 2017

Arabidopsis thaliana FAR-RED ELONGATED HYPOCOTYLS3 (FHY3) and FAR-RED-IMPAIRED RESPONSE1 (FAR1) modulate starch synthesis in response to light and sugar.

New Phytol 2017 Mar 15;213(4):1682-1696. Epub 2016 Nov 15.

State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai'an, 271018, China.

In living organisms, daily light/dark cycles profoundly affect cellular processes. In plants, optimal growth and development, and adaptation to daily light-dark cycles, require starch synthesis and turnover. However, the underlying molecular mechanisms coordinating daily starch metabolism remain poorly understood. To explore the roles of Arabidopsis thaliana light signal transduction proteins FAR-RED ELONGATED HYPOCOTYLS3 (FHY3) and FAR-RED-IMPAIRED RESPONSE1 (FAR1) in starch metabolism, the contents of starch and water-soluble polysaccharides, and the structure of starch granules were investigated in fhy3, far1 and fhy3 far1 mutant plants. Disruption of FHY3 or FAR1 reduced starch accumulation and altered starch granule structure in the fhy3-4, far1-2, and fhy3-4 far1-2 mutant plants. Furthermore, molecular and genetic evidence revealed that the gene encoding the starch-debranching enzyme ISOAMYLASE2 (ISA2) is a direct target of FHY3 and FAR1, and functions in light-induced starch synthesis. Our data establish the first molecular link between light signal transduction and starch synthesis, suggesting that the light-signaling proteins FHY3 and FAR1 influence starch synthesis and starch granule formation through transcriptional activation of ISA2.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/nph.14300DOI Listing
March 2017

[MicroRNA-33b inhibits cell proliferation in hepatocellular carcinoma via targeting SALL4].

Zhong Nan Da Xue Xue Bao Yi Xue Ban 2016 Sep;41(9):905-10

Department of Infectious Diseases; Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha 410008, China.

Objective: To investigate the expression of miR-33b in hepatocellular carcinoma (HCC) and to explore regulatory mechanism of miR-33b for cell proliferation of HCC.


Methods: HCC tissues and adjacent non-tumor tissues were collected for this study (n=32 for each). Real-time PCR and Western blot were conducted to examine the mRNA and protein expression, respectively. MTT assay was used to detect the cell proliferation. Luciferase reporter gene assay was performed to verify the target relationship between miR-33b and Sal-like 4 (SALL4).


Results: MiR-33b was significantly downregulated in HCC tissues compared with adjacent non-tumor tissues. Overexpression of miR-33b decreased the proliferation of HCC LH86 cells. SALL4 was identified as a target gene of miR-33b, and its protein expression was negatively regulated by miR-33b. Overexpression of SALL4 reversed the suppressive effect of miR-33b on LH86 cell proliferation. SALL4 was significantly upregulated in HCC tissues compared with adjacent non-tumor tissues.


Conclusion: The miR-33b suppresses HCC cell proliferation through down-regulation of SALL4.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.11817/j.issn.1672-7347.2016.09.004DOI Listing
September 2016

[Feasibility analysis of quantitative detection on serum HBeAg/HBeAb by time-resolved immunofluorescence assay].

Zhong Nan Da Xue Xue Bao Yi Xue Ban 2016 Aug;41(8):852-5

Department of Infectious Disease, Xiangya Hospital; Hunan Key Laboratory of Viral Hepatitis, Central South University, Changsha 410008, China.

Objective: To determine whether time-resolved immunofluorescence assay (TRIFA) shares the similar accuracy and specificity with automatic chemiluminescence immunoassay (CMIA) in analyzing HBeAg levels in hepatitis B.


Methods: A total of 157 serum samples were collected from outpatients with infection of HBV in Xiangya Hospital, Central South University. CMIA and TRIFA were used to analyze HBeAg quantitation and HBeAg/HBeAb qualitative detection, respectively.


Results: The linear regression equation for the two methods was Y=0.72779X-4.0551 (r=0.712, P<0.001). Compared with the CMIA, the sensitivity and specificity in detection of HBeAg by TRIFA were 89.89% and 100%, respectively, and the coincidence rate of HBeAg was 94.27% by two assays. Similarly, the sensitivity and specificity in detection of HBeAb by TRIFA were 100% and 95.45%, respectively. The coincidence rate was 97.45% by two assays.


Conclusion: TRIFA has similar accuracy, sensitivity, and specificity with CMIA in quantitative detection of HBeAg, and their coincidence rate in detection of HBeAg/HBeAb is high.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.11817/j.issn.1672-7347.2016.08.013DOI Listing
August 2016

A multi-center clinical study comparing Sansure Magb and CAP/CTM HBV tests in the quantitative detection of HBV DNA.

J Infect Dev Ctries 2016 Aug 2;10(7):755-61. Epub 2016 Aug 2.

Xiangya Hospital, Central South University, Changsha, China.

Introduction: As the most reliable means of diagnosing hepatitis (HBV) infection and predicting the prognosis of HBV-related chronic liver disease, the COBAS AmpliPrep/COBAS TaqMan real-time polymerase chain reaction (PCR) (CAP/CTM) assay provides a highly sensitive and accurate method for quantifying HBV DNA. However, the high cost of the COBAS reagents is prohibitive in many developing countries. Thus, we compared the Sansure magnetic bead (Magb) assay, a novel technology developed by a Chinese company, with the CAP/CTM assay.

Methodology: The reproducibility and sensitivity of the Sansure Magb assay were first validated using HBV DNA reference samples. Next, the quantitative results for the two assays using 635 blood samples collected from chronic hepatitis B patients and 10 healthy controls were compared.

Results: The Sansure Magb assay showed high reproducibility and was at least as sensitive and specific as the CAP/CTM assay. Among the patient samples, 407 tested positive by both methods, with 386 (94.84%) showing quantitative differences of less than 1 log unit and 21 (5.16%) showing quantitative differences of between 1 and 2 log units. The results from the assays were closely correlated. Bland-Altman plot analysis showed that only 6.6% of the data points fell outside the 95% limits of agreement, which suggests that the differences between methods are clinically acceptable.

Conclusions: This study demonstrates that the Sansure Magb assay is highly sensitive and reproducible. Based on its reduced cost, the Sansure Magb assay may be more applicable than the CAP/CTM assay for HBV diagnosis in developing countries such as China.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3855/jidc.7112DOI Listing
August 2016
-->