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| 1 | Bartter's syndrome:clinical findings,genetic causes and therapeutic approach显示文摘Backgound Bartter's syndrome(BS)is a rare group of salt losing tubulopathies due to the impairment of transport mecha-nisms at the thick ascending limb of the Henle's loop.Data sources Literature reviews and original research articles were collected from database,including PubMed and Scopus.Results According to the time of onset and symptoms,BS can be classified into antenatal and classic BS.Molecular studies have identified different subtypes of BS.BS types Ⅰ,Ⅱ and Ⅲ are caused by mutations on genes encoding the luminal Na^(+)-K^(+)-2Cl^(-) co-transporter,the luminal K+ channel ROMK,and the basolateral chloride channel ClC-Kb(CLCNKB),respectively.Loss-of-function mutations of Barttin CLCNK type accessory beta subunit cause BS type Ⅳa.Simultaneous mutations of CLCNKB and CLCNKA cause BS type Ⅳb.BS type Ⅴ consists in a novel transient form characterized by antenatal presentation due to mutations in the MAGE family member D2.Severe gain-of-function mutations of the extracellular calcium sensing receptor gene can result in an autosomal dominant condition of BS.Main clinical and biochemical alterations in BS include polyuria,dehydration,hypokalemia,hypochloremic metabolic alka-losis,hyperreninemia,high levels of prostaglandins,normal or low blood pressure,hypercalciuria and failure to thrive.Treatment focuses mainly at correcting dehydration and electrolyte disturbances and in measures to reduce polyuria,including the use of nonsteroidal anti-inflammatory medications to control excessive renal prostaglandin E2 production.Conclusions Early diagnosis and treatment of BS may prevent long-term consequences such as growth failure,nephrocal-cinosis and end-stage renal disease. | Flavia Cristina Carvalho Mrad Sílvia Bouissou Morais Soares Luiz Alberto Wanderley de Menezes Silva Pedro Versiani dos Anjos Menezes Ana Cristina Simoes-e-Silva | 2021 | World Journal of Pediatrics2021，17，1： | 10 |
| 2 | Toll-like receptor 9 polymorphisms and Helicobacter pylori influence gene expression and risk of gastric carcinogenesis in the Brazilian population显示文摘BACKGROUND Toll-like receptors(TLRs)are the first line of host defense,and are involved in Helicobacter pylori(H.pylori)recognition and activation of both inflammatory and carcinogenic processes.The presence of single nucleotide polymorphisms(SNPs)in genes that activate the immune response may modulate the risk of precancerous lesions and gastric cancer(GC).Among them,Toll-like receptor 9(TLR9)polymorphisms have emerged with a risk factor of infectious diseases and cancer,however the studies are still inconclusive.AIM To evaluate whether TLR9 rs5743836 and rs187084 SNPs contribute to the risk of gastric carcinogenesis,and its influence on mRNA expression.METHODS A case-control study was conducted to evaluate two TLR9 SNPs(TLR9-1237 TCrs5743836 and TLR9-1486 CT-rs187084)in chronic gastritis(CG)and GC patients.A total of 609 DNA samples of peripheral blood[248 CG,161 GC,and 200 samples from healthy individuals(C)]were genotyped by polymerase chain reaction-restriction fragment length polymorphism.All samples were tested for the H.pylori infection using Hpx1 and Hpx2 primers.Quantitative polymerase chain reaction by TaqMan?assay was used to quantify TLR9 mRNA from fresh gastric tissues(48 GC,26 CG,and 14 C).RESULTS For TLR9-1237,the TC+CC or CC genotypes were associated with a higher risk of GC than C[recessive model odds ratio(OR)=5.01,95%confidence interval(CI):2.52-9.94,P<0.0001],and the CG(recessive model OR=4.63;95%CI:2.44-8.79,P<0.0001)groups.For TLR9-1486,an association between the CT+TT genotypes and increased risk of both GC(dominant model OR=2.72,95%CI:1.57-4.72,P<0.0001)and CG(dominant model OR=1.79,95%CI:1.15-2.79,P=0.0094)was observed when compared to the C group.Moreover,the presence of TLR9-1237 TC/CC+TLR9-1486 CC genotypes potentiate the risk for this neoplasm(OR=18.57;95%CI:5.06-68.15,P<0.0001).The TLR9 mRNA level was significantly higher in the GC group(RQ=9.24,P<0.0001)in relation to the CG group(RQ=1.55,P=0.0010)and normal mucosa(RQ=1.0).When the samples were grouped according to the polymorphic genotypes and the presence of H.pylori infection,an influence of TLR9-1237 TC+CC polymorphic genotypes(P=0.0083)and H.pylori infection(P<0.0001)was observed on the upregulation of mRNA expression.CONCLUSION Our findings show that TLR9 rs5743836 and rs187084 polymorphisms are associated with a higher risk of carcinogenesis gastric,and that TLR9 mRNA levels can be modulated by TLR9-1237 TC+CC variant genotypes and H.pylori infection. | Manoela Dias Susi de Matos Lourenco Caroline Lucas Trevizani Rasmussen Spencer Luis Marques Payao Ana Flavia Teixeira Rossi Ana Elizabete Silva Juliana Garcia de Oliveira-Cucolo | 2019 | World Journal of Gastrointestinal Oncology2019，11，11： | 9 |
| 3 | Value of a newly sequenced bacterial genome显示文摘Next-generation sequencing(NGS) technologies have made high-throughput sequencing available to medium- and small-size laboratories, culminating in a tidal wave of genomic information. The quantity of sequenced bacterial genomes has not only brought excitement to the field of genomics but also heightened expectations that NGS would boost antibacterial discovery and vaccine development. Although many possible drug and vaccine targets have been discovered, the success rate of genome-based analysis has remained below expectations. Furthermore, NGS has had consequences for genome quality, resulting in an exponential increase in draft(partial data) genome deposits in public databases. If no further interests are expressed for a particular bacterial genome, it is more likely that the sequencing of its genome will be limited to a draft stage, and the painstaking tasks of completing the sequencing of its genome and annotation will not be undertaken. It is important to know what is lost when we settle for a draft genome and to determine the 'scientific value' of a newly sequenced genome. This review addresses the expected impact of newly sequenced genomes on antibacterial discovery and vaccinology. Also, it discusses the factors that could be leading to the increase in the number of draft deposits and the consequent loss of relevant biological information. | Eudes GV Barbosa Flavia F Aburjaile Rommel TJ Ramos Adriana R Carneiro Yves Le Loir Jan Baumbach Anderson Miyoshi Artur Silva Vasco Azevedo | 2014 | World Journal of Biological Chemistry2014，5，2： | 7 |
| 4 | Therapeutic and prophylactic thalidomide in TNBS-induced colitis: Synergistic effects on TNF-α, IL-12 and VEGF production显示文摘AIM: To evaluated the therapeutic and prophylactic effect of thalidomide on 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Thalidomide has been reported to downregulate the expression of tumor necrosis factor a (TNF-α), IL-12, and vascular endothelial growth factor (VEGF), hallmarks of intestinal inflammation in Crohn's disease (CD). METHODS: Male Wistar rats were divided in five groups of ten animals each. Four groups received a rectal infusion of TNBS in ethanol. The first group was sacrificed 7 d after colitis induction. The second and third groups received either thalidomide or placebo by gavage and were sacrificed at 14 d. The fourth group received thalidomide 6 h before TNBS administration, and was sacrificed 7 d after induction. The fifth group acted as the control group and colitis was not induced. Histological inflammatory scores of the colon were performed and lamina propria CD4+ T cells, macrophages, and VEGF+ cells were detected by immunohistochemistry. TNF-a and IL-12 were quantified in the supernatant of organ cultures by ELISA. RESULTS: Significant reduction in the inflammatory score and in the percentage of VEGF+ cells was observed in the group treated with thalidomide compared with animals not treated with thalidomide. Both TNF-αand IL-12 levels were significantly reduced among TNBS induced colitis animals treated with thalidomide compared with animals that did not receive thalidomide. TNF-αlevels were also significantly reduced among the animals receiving thalidomide prophylaxis compared with untreated animals with TNBS-induced colitis. Intestinal levels of TNF-αand IL-12 were significantly correlated with the inflammatory score and the number of VEGF+ cells. CONCLUSION: Thalidomide significantly attenuates TNBS-induced colitis by inhibiting the intestinal production of TNF-α, IL-12, and VEGF. This effect may support the use of thalidomide as an alternate approach in selected patients with CD. | Ana Teresa Carvalho Heitor Souza Antonio Jose Carneiro Morgana Castelo-Branco Kalil Madi Alberto Schanaider Flavia Silva Fernando Antonio Pereira Júnior Márcia G Pereira Cláudio Tortori Ilana Dines Jane Carvalho Eduardo Rocha Celeste Elia | 2007 | World Journal of Gastroenterology2007，13，15： | 6 |
| 5 | Up-regulation of tumor necrosis factor-a pathway survival genes and of the receptor TNFR2 in gastric cancer显示文摘BACKGROUND Gastric carcinogenesis can be induced by chronic inflammation triggered by Helicobacter pylori(H. pylori) infection. Tumor necrosis factor(TNF)-α and its receptors(TNFR1 and TNFR2) regulate important cellular processes, such as apoptosis and cell survival, and the disruption of which can lead to cancer. This signaling pathway is also modulated by microRNAs(miRNAs), altering gene expression.AIM To evaluate the mRNA and miRNAs expression involved in the TNF-α signaling pathway in gastric cancer(GC) tissues and its relationship.METHODS Quantitative polymerase chain reaction(qPCR) by TaqMan? assay was used to quantify the RNA transcript levels of TNF-α signaling pathway(TNF, TNFR1,TNFR2, TRADD, TRAF2, CFLIP, NFKB1, NFKB2, CASP8, CASP3) and miRNAs that targets genes from this pathway(miR-19 a, miR-34 a, miR-103 a, miR-130 a,miR-181 c) in 30 GC fresh tissue samples. Molecular diagnosis of H. pylori was performed by nested PCR for gene HSP60. A miRNA:mRNA interaction network was construct using Cytoscape v3.1.1 from the in silico analysis performed using public databases.RESULTS Up-regulation of cellular survival genes as TNF, TNFR2, TRADD, TRAF2, CFLIP,and NFKB2, besides CASP8 and miR-34 a was observed in GC tissues, whereas mediators of apoptosis such as TNFR1 and CASP3 were down-regulated. When the samples were stratified by histological type, the expression of miR-103 a and miR-130 a was significantly increased in the diffuse-type of GC compared to the intestinal-type. However, no influence of H. pylori infection was observed on the expression levels of mRNA and miRNAs analyzed. Moreover, the miRNA:mRNA interaction network showed several interrelations between the miRNAs and their target genes, highlighting miR-19 a and miR-103 a, which has as predicted or validated target a large number of genes in the TNF-α pathway,including TNF, TNFR1, TNFR2, CFLIP, TRADD, CASP3 and CASP8.CONCLUSION Our findings show that cell survival genes mediated by TNF/TNFR2 binding is up-regulated in GC favoring its pro-tumoral effect, while pro-apoptotic genes as CASP3 and TNFR1 are down-regulated, indicating disbalance between apoptosis and cell proliferation processes in this neoplasm. This process can also be influenced by an intricate regulatory network of miRNA:mRNA. | Ana Flavia Teixeira Rossi Julia Cocenzo Contiero Fernanda da Silva Manoel-Caetano Fabio Eduardo Severino Ana Elizabete Silva | 2019 | World Journal of Gastrointestinal Oncology2019，11，4： | 5 |
| 6 | Complex interactomes and post-translational modifications of the regulatory proteins HABP4 and SERBP1 suggest pleiotropic cellular functions显示文摘The 57 kDa antigen recognized by the Ki-1 antibody,is also known as intracellular hyaluronic acid binding protein 4 and shares 40.7%identity and 67.4%similarity with serpin mRNA binding protein 1,which is also named CGI-55,or plasminogen activator inhibitor type-1-RNA binding protein-1,indicating that they might be paralog proteins,possibly with similar or redundant functions in human cells.Through the identification of their protein interactomes,both regulatory proteins have been functionally implicated in transcriptional regulation,mRNA metabolism,specifically RNA splicing,the regulation of mRNA stability,especially,in the context of the progesterone hormone response,and the DNA damage response.Both proteins also show a complex pattern of post-translational modifications,involving Ser/Thr phosphorylation,mainly through protein kinase C,arginine methylation and SUMOylation,suggesting that their functions and locations are highly regulated.Furthermore,they show a highly dynamic cellular localization pattern with localizations in both the cytoplasm and nucleus as well as punctuated localizations in both granular cytoplasmic protein bodies,upon stress,and nuclear splicing speckles.Several reports in the literature show altered expressions of both regulatory proteins in a series of cancers as well as mutations in their genes that may contribute to tumorigenesis.This review highlights important aspects of the structure,interactome,post-translational modifications,sub-cellular localization and function of both regulatory proteins and further discusses their possible functions and their potential as tumor markers in different cancer settings. | Carolina Colleti Talita Diniz Melo-Hanchuk Flavia Regina Moraes da Silva Angela Saito Jorg Kobarg | 2019 | World Journal of Biological Chemistry2019，10，3： | 4 |
| 7 | Burn Injury Induces Skeletal Muscle Degeneration, Inflammatory Host Response, and Oxidative Stress in Wistar Rats显示文摘 | Nathalia Trasmonte da Silva Hananiah Tardivo Quintana Jeferson André Bortolin Daniel Araki Ribeiro Flavia de Oliveira | 2015 | Journal of Burn Care & Research2015，，3： | 2 |
| 8 | Old game, new players: Linking classical theories to new trends in transplant immunology显示文摘The evolutionary emergence of an efficient immune system has a fundamental role in our survival against pathogenic attacks. Nevertheless, this same protective mechanism may also establish a negative consequence in the setting of disorders such as autoimmunity and transplant rejection. In light of the latter, although research has long uncovered main concepts of allogeneic recognition, immune rejection is still the main obstacle to long-term graft survival. Therefore, in order to define effective therapies that prolong graft viability, it is essential that we understand the underlying mediators and mechanisms that participate in transplant rejection. This multifaceted process is characterized by diverse cellular and humoral participants with innate and adaptive functions that can determine the type of rejection or promote graft acceptance. Although a number of mediators of graft recognition have been described in traditional immunology, recent studies indicate that defining rigid roles for certain immune cells and factors may be more complicated than originally conceived. Current research has also targeted specific cells and drugs that regulate immune activation and induce tolerance. This review will give a broad view of the most recent understanding of the allogeneic inflammatory/tolerogenic response and current insights into cellular and drug therapies that modulate immune activation that may prove to be useful in the induction of tolerance in the clinical setting. | Marina Burgos da Silva Flavia Franco da Cunha Fernanda Fernandes Terra Niels Olsen Saraiva Camara | 2017 | World Journal of Transplantation2017，7，1： | 1 |
| 9 | Donepezil: An Important Prototype to the Design of New Drug Candidates for Alzheimerμs Disease显示文摘 | Maria Cecilia Rodrigues Simoes Flavia Pereira Dias Viegas Marcella Soares Moreira Matheus de Freitas Silva Mariana Maximo Riquiel Patricia Mattos da Rosa Maísa Rosa Castelli Marcelo Henrique dos Santos Marisi Gomes Soares Claudio Viegas | 2014 | Mini-Reviews in Medicinal Chemistry2014，，1： | 1 |
| 10 | Xylo-oligosaccharides from lignocellulosie materials: Chemical structure, health benefits and production by chemical and enzymatic hydrolysis显示文摘 | Ana Flavia Azevedo Carvalho Pedro de Oliva Nero Douglas Fernandes da Silva | 2013 | Food Research International2013，51，： | 1 |
| 11 | Activation of cannabinoid receptors by the pentacyclic triterpene α,β-amyrin inhibits inflammatory and neuropathic persistent pain in mice显示文摘 | Kathryn A.B. Sim?o da Silva Ana F. Paszcuk Giselle F. Passos Eduardo S. Silva Allisson Freire Bento Flavia C. Meotti Jo?o B. Calixto | 2011 | Pain2011，，8： | 1 |
| 12 | Correlation analysis between phenolic levels of Brazilian propolis extracts and their antimicrobial and antioxidant activities显示文摘 | Joaquim Fernando Mendes da Silva Maria Clara de Souza Samara Ramalho Matta Marisol Ribeiro de Andrade Flavia Vila Nova Vidal | 2005 | Food Chemistry2005，，3： | 1 |
| 13 | Metabolomics in chronic hepatitis C:Decoding fibrosis grading and underlying pathways显示文摘BACKGROUND Chronic Hepatitis C(CHC)affects 71 million people globally and leads to liver issues such as fibrosis,cirrhosis,cancer,and death.A better understanding and prognosis of liver involvement are vital to reduce morbidity and mortality.The accurate identification of the fibrosis stage is crucial for making treatment decisions and predicting outcomes.Tests used to grade fibrosis include histological analysis and imaging but have limitations.Blood markers such as molecular biomarkers can offer valuable insights into fibrosis.AIM To identify potential biomarkers that might stratify these lesions and add information about the molecular mechanisms involved in the disease.METHODS Plasma samples were collected from 46 patients with hepatitis C and classified into fibrosis grades F1(n=13),F2(n=12),F3(n=6),and F4(n=15).To ensure that the identified biomarkers were exclusive to liver lesions(CHC fibrosis),healthy volunteer participants(n=50)were also included.An untargeted metabolomic technique was used to analyze the plasma metabolites using mass spectrometry and database verification.Statistical analyses were performed to identify differential biomarkers among groups.RESULTS Six differential metabolites were identified in each grade of fibrosis.This six-metabolite profile was able to establish a clustering tendency in patients with the same grade of fibrosis;thus,they showed greater efficiency in discriminating grades.CONCLUSION This study suggests that some of the observed biomarkers,once validated,have the potential to be applied as prognostic biomarkers.Furthermore,it suggests that liquid biopsy analyses of plasma metabolites are a good source of molecular biomarkers capable of stratifying patients with CHC according to fibrosis grade. | Adriana Camargo Ferrasi Samara Vitória Granja Lima Aline Faria Galvani Jeany Delafiori Flavia Luísa Dias-Audibert Rodrigo Ramos Catharino Giovanni Faria Silva Roberta Rodrigues Praxedes Driele Bretones Santos Dayane Trevisan de Macedo Almeida Estela Oliveira Lima | 2023 | World Journal of Hepatology2023，15，11： | 1 |
| 14 | The effect of a minor constituent of essential oil from Citrus aurantium : The role of β-myrcene in preventing peptic ulcer disease显示文摘 | Flavia Bonamin Thiago M. Moraes Raquel C. dos Santos Hélio Kushima Felipe M. Faria Marcos A. Silva Ivan V. Junior Leonardo Nogueira Tais M. Bauab Alba R.M. Souza Brito Lucia R.M. da Rocha Clélia A. Hiruma-Lima | 2014 | Chemico-Biological Interactions2014，，： | 1 |
| 15 | Prevalence of congenital cytomegalovirus infection in preterm,small for gestational age and low birth weight newborns:characteristics and cytokines profile显示文摘Cytomegalovirus is the most frequent agent of congenital viral infections,affecting approximately 0.2%-2.4%of live births in different countries[1-7].Universal screening for congenital cytomegalovirus infection in newborns is not a standard practice considering cost-benefit issues and viabil-ity of diagnostic tests.Besides,most newborns are asympto-matic and there is no effective treatment for this population[2-5]. | Janaina Fortes Lino Llian Martins Oliveira Diniz Debora Marques de Miranda Daniela Valadao Freitas Rosa Nathalia Gualberto Souza e Silva Eduardo de Souza Nicolau Larissa Goncalves Rezende Lais Silva Carvalho Marianna Fischer de Paula Lopes Luisa Petri Correa Gabriela Mafra de Oliveira Flavia Miranda da Silva Alves Lorena Batista Pascoal Erika Lima Dolabella Teixeira da Costal Leni Marcia Anchieta Roberta Maia de Castro Romaneli | 2022 | World Journal of Pediatrics2022，18，7： | 1 |
| 16 | Cytotoxicity and inhibition of platelet aggregation caused by an l -amino acid oxidase from Bothrops leucurus venom显示文摘 | Gustavo B. Naumann Liliana F. Silva Luciana Silva Gilson Faria Michael Richardson Karla Evangelista Markus Kohlhoff Celia M.F. Gontijo Alexei Navdaev Flavia F. de Rezende Johannes A. Eble Eladio F. Sanchez | 2011 | BBA - General Subjects2011，，7： | 1 |
| 17 | Long-term effects of aerobic plus resistance training on the adipokines and neuropeptides in nonalcoholic fatty liver disease obese adolescents显示文摘 | Aline de Piano Marco T. de Mello Priscila de L. Sanches Patrícia L. da Silva Raquel M.S. Campos June Carnier Flavia Corgosinho Denis Foschini Deborah L. Masquio Lian Tock Lila M. Oyama Claudia Maria da Penha Oller do Nascimento Sérgio Tufik Ana R. Damaso | 2012 | European Journal of Gastroenterology & Hepatology2012，，11： | 1 |
| 18 | Influence of partial sub- stitution of dietary fish meal on the activity of digestive enzymes inthe intestinal brush border membrane of gilthead sea bream, Sparus aurata and goldfish, Carassius auratus 显示文摘 | Flavia C P Silva J R Nicoli J L | 2010 | Aquaculture2010，30，6： | 1 |
| 19 | Antimutagenicity of ursolic acid and oleanolicacid against doxorubicin-induced clastogenesis in Balb/c mice显示文摘 | FLAVIA A R DE ANDRADE BARCALA C A M DA SILVA FARIA M C | 2006 | Life Sci2006，79，13： | 1 |
| 20 | Xylo-oligosaccharides from lignocellulosic materials: Chemical structure, health benefits and production by chemical and enzymatic hydrolysis显示文摘 | ANA FLAVIA AZEVEDO CARVALHO PEDRO DE OLIVA NETO DOUGLAS FERNANDES DA SILVA | 2013 | Food Research International2013，，51： | 1 |
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