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Landscape of global urban environmental resistome and its association with local socioeconomic and medical status

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Science China(Life Sciences) 2024年第6期67卷 1292-1301页

作者： Jun Wu Yige Hu Michael H Perlin David Danko Jun Lu Manuela Oliveira Johannes Werner Maria M Zambrano Maria A Sierra Olayinka O Osuolale Paweł Łabaj Nicolás Rascovan Nur Hazlin Hazrin-Chong Soojin Jang Haruo Suzuki Marina Nieto-Caballero Bharath Prithiviraj Patrick K H Lee Agnieszka Chmielarczyk Anna Różańska Yongxiang Zhao Lan Wang Christopher E Mason Tieliu Shi Center for Bioinformatics and Computational Biology and the Institute of Biomedical SciencesSchool of Life SciencesEast China Normal UniversityShanghai 200241China department of Biology Program on Disease EvolutionUniversity of LouisvilleLouisville 40292USA Weill Cornell Medicine New York 10065USA The Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine New York 10065USA department of Pulmonary Medicine Shanghai Chest HospitalShanghai Jiao Tong UniversityShanghai 200025China i3S-Instituto de Investiga玢o e Inova玢o em Saúde Universidade do PortoPorto 4050-290Portugal Ipatimup-Instituto de Patologia e imunologia Molecular da Universidade do Porto Porto 4200-465Portugal departamento de Biologia Faculdade de CiênciasUniversidade do PortoPorto 4050-290Portugal High Performance and Cloud Computing Group Zentrum für Datenverarbeitung(ZDV)Eberhard Karls University of TübingenW鋍hterstra遝7672074TübingenGermany Corporación Corpogen Research Center Bogotá110311Colombia Applied Environmental Metagenomics and Infectious Diseases Research(AEMIDR) Department of Biological SciencesElizade UniversityIlara-Mokin 340271Nigeria Maopolska Centre of Biotechnology Jagiellonian UniversityKraków 30-005Poland Aix-Marseille Université Mediterranean Institute of OceanologyUniversitéde ToulonCNRSIRDUM 110Marseille 83041France department of Biological Sciences and Biotechnology Faculty of Science and TechnologyUniversiti Kebangsaan Malaysia43600 UKM BangiSelangor Institut Pasteur Korea Seoul 13488Republic of Korea Faculty of Environment and Information Studies Keio UniversityFujisawaKanagawa 252-0882Japan University of Colorado at Boulder CivilEnvironmental and Architectural DepartmentBoulder 80303USA Brooklyn College of the City University of New York Brooklyn 11210USA School of Energy and Environment City University of Hong KongHong Kong 999077China department of Microbiology Faculty of MedicineJagiellonian UniversityKraków 30-005Poland Biological Targeting Diagnosis and The

Antimicrobial resistance(AMR)poses a critical threat to global health and development,with environmental factors—particularly in urban areas—contributing significantly to the spread of antibiotic resistance genes(ARGs).However,most research to date has been conducted at a local level,leaving significant gaps in our understanding of the global status of antibiotic resistance in urban *** address this issue,we thoroughly analyzed a total of 86,213 ARGs detected within 4,728 metagenome samples,which were collected by the Meta SUB International Consortium involving diverse urban environments in 60 cities of 27 countries,utilizing a deep-learning based *** findings demonstrated the strong geographical specificity of urban environmental resistome,and their correlation with various local socioeconomic and medical *** also identified distinctive evolutionary patterns of ARG-related biosynthetic gene clusters(BGCs)across different countries,and discovered that the urban environment represents a rich source of novel *** study provides a comprehensive overview of the global urban environmental resistome,and fills a significant gap in our knowledge of large-scale urban antibiotic resistome analysis.

关键词： urban environment metagenome antibiotic resistance resistance diversity biosynthetic gene clusters

The influence of innate and adaptative immune responses on the differential clinical outcomes of leprosy

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Infectious Diseases of Poverty 2017年第1期6卷 34-41页

作者： Adriana Barbosa de Lima Fonseca Marise do Vale Simon Rodrigo Anselmo Cazzaniga Tatiana Rodrigues de Moura Roque Pacheco de Almeida Malcolm S.Duthie Steven G.Reed Amelia Ribeiro de Jesus department of Medicine Molecular Biology LaboratoryUniversity HospitalUniversidade Federal de SergipeSao CristovaoSergipeBrazil Infectious Disease Research Institute SeattleUSA Instituto de Investigacao em imunologia Institutos Nacionais de Ciência e TecnologiaCNPqSao PauloSPBrazil.

Leprosy is a chronic infectious disease caused by Mycobacterium *** to official reports from 121 countries across five WHO regions,there were 213899 newly diagnosed cases in *** leprosy affects the skin and peripheral nerves,it can present across a spectrum of clinical and histopathological forms that are strongly influenced by the immune response of the infected *** forms comprise the extremes of tuberculoid leprosy(TT),with a ***-specific Th1,but also a Th17,response that limits *** multiplication,through to lepromatous leprosy(LL),with ***-specific Th2 and T regulatory responses that do not control *** replication but rather allow bacterial *** interpolar borderline clinical forms present with similar,but less extreme,immune *** inflammatory episodes,known as leprosy reactions,are complications that may occur before,during or after treatment,and cause further neurological damages that can cause irreversible chronic *** review discusses the innate and adaptive immune responses,and their interactions,that are known to affect pathogenesis and influence the clinical outcome of leprosy.

关键词： Leprosy Clinical presentation Immunology Innate immunity Immune pathogenesis

Therapeutic and prophylactic thalidomide in TNBS-induced colitis: Synergistic effects on TNF-α, IL-12 and VEGF production

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World Journal of Gastroenterology 2007年第15期13卷 2166-2173页

作者： 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 departamento de Clínica Médica Hospital Universitário Clementino Fraga Filho Brazil departamento de Histologia e Embriologia Laboratório de imunologia Celular Instituto de Ci(e|^)ncias BiomédicasUniversidade Federal do Rio de Janeiro21941-590Brazil Laboratório Multidisciplinar de Pesquisa Anatomia Patológica Hospital Universitário Clementino Fraga FilhoBrazil e Cirurgia Experimental Hospital Universitário Clementino Fraga Filho Brazil

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 α （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-α 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-α and IL-12 levels were significantly reduced among TNBS induced colitis animals treated with thalidomide compared with animals that did not receive thalidomide. TNF-α levels were also significantly reduced among the animals receiving thalidomide prophylaxis compared with untreated animals with TNBS-induced colitis. Intestinal levels of TNF-α and 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.

关键词： Thalidomide Experimental colitis Inflammatory bowel disease Tumor necrosis factor α IL-12 Vascular endothelial growth factor

Distinct patterns of mucosal apoptosis in H pylori-associated gastric ulcer are associated with altered FasL and perforin cytotoxic pathways

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World Journal of Gastroenterology 2006年第38期12卷 6133-6141页

作者： Heitor SP Souza Marcelo S Neves Celeste CS Elia Claudio JA Tortori Ilana Dines Cesonia A Martinusso Kalil Madi Leonardo Andrade Morgana TL Castelo-Branco departamento de Clínica Médica Instituto de Ciências Biomédicas Universidade Federal do Rio de Janeiro 21941-590 Brazil Laboratório Multidisciplinar de Pesquisa e Departamento de Anatomia Patologica Instituto de Ciências Biomédicas Universidade Federal do Rio de Janeiro 21941-590 Brazil Hospital Universitário Clementino Fraga Filho departamento de Histologia e Embriologia Instituto de Ciências Biomédicas Universidade Federal do Rio de Janeiro 21941-590 Brazil Laboratório de imunologia Celular Instituto de Ciências Biomédicas Universidade Federal do Rio de Janeiro 21941-590 Brazil

AIM: To analyze the level of apoptosis in different mucosal compartments and the differential expression of Fas/Fas-ligand and perforin in H pylori-associated gastric ulcer. METHODS: Antral specimens from patients with H pylori-related active gastric ulcer (GU), H pylori-related gastritis, and non-infected controls were analysed for densities and distribution of apoptotic cells determined by the TdT-mediated dUDP-biotin nick-end-labelling method. GU patients were submitted to eradication therapy with follow-up biopsy after 60 d. Fas, FasL, and perforin-expressing cells were assessed by immunoper- oxidase, and with anti-CD3, anti-CD20 and anti-CD68 by double immunofluorescence and confocal microscopy. Quantitative analysis was performed using a computer- assisted image analyser. RESULTS: H pylori-infected antrum showed greater surface epithelial apoptosis which decreased after eradi- cation therapy. In the lamina propria, higher rates of mononuclear cell apoptosis were observed in H pylori- gastritis. Co-expression of Fas with T-cell and macro- phage markers was reduced in GU. FasL- and perforin-expressing cells were increased in H pylori-infection and correlated with epithelial apoptosis. Perforin-expressing cells were also increased in GU compared with H pylori- gastritis. CONCLUSION: Epithelial apoptosis is increased in H pylori-infection and correlates to FasL- and perforin- expression by T cells. Expression of perforin is correlated with the tissue damage, and may represent the enhance- ment of a distinct cytotoxic pathway in GU. Increased expression of FasL not paralleled by Fas on T-cells and macrophages may indicate a reduced susceptibility to the Fas/FasL-mediated apoptosis of lymphoid cells in H pylori-infection.

关键词： Gastric ulcer H pylori Apoptosis Fas receptor Fas ligand Perforin

Revealing the kinetics of Leishmania chagasi infection in the male genital system of hamsters

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Infectious Diseases of Poverty 2016年第1期5卷 261-265页

作者： Amanda P.N.Quintal Bruna C.Borges Paula C.Brígido Rebecca T.Silva Ana F.Notário Marlus A.Santos Maria A.de Souza Fernanda G.O.Nascimento Antônio V.Mundim Guilherme M.J.Costa André B.Vasconcelos Claudio V.da Silva Instituto de Ciências Biomédicas Universidade Federal de UberlândiaUberlândiaMinas GeraisBrasil Hospital Veterinário Universidade Federal de UberlândiaUberlândiaMinas GeraisBrasil departamento de Ciências Biomédicas Universidade Federal de Minas GeraisBelo HorizonteBrasil Universidade de Uberaba UberabaMinas GeraisBrasil departamento de imunologia–Instituto de Ciências Biomédicas Universidade Federal de UberlândiaCampus UmuaramaUberlândiaMGBrasil

Background:Leishmaniasis causes alterations and lesions in the genital system,which leads to azoospermia and testicular atrophy in animals during the chronic phase of the *** aim of this study was to reveal the kinetics of Leishmania chagasi infection in the genital system of male golden hamsters(Mesocricetus auratus).Methods:Animals were intraperitoneally inoculated with amastigotes from *** different time points animals were euthanized and genital organs processed for histo-pathological,qPCR,cytokines and testosterone detection ***:Our results showed a high parasite load in testis,followed by an increase of pro-inflammatory cytokines IL1-β,TNF-αand IFN-γ,and ***,IL-4 expression was upregulated and basal parasite persistence in testis was observed using the experimental ***:Extracellular amastigotes migrated to the epididymis posing as a potential major factor of parasite persistence and venereal transmission of *** infection in hamsters.

关键词： Leishmania chagasi Extracellular amastigotes Testis Epididymis Immune response Testosterone

Homocysteine as a Biomarker for Predicting Disease-Free Survival in Breast Cancer

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Advances in Breast Cancer Research 2013年第2期2卷 24-31页

作者： Daniela Filippini Ierardi Luis Gustavo Raimundo Gimena Aguiar Patrícia Bandeira Rueda Germano Luiz Henrique Gebrim Nelson Carvas Bruno Frederico Aguilar Calegare Vania D’Almeida Catarina Segreti Porto Miriam Galvonas Jasiulionis Mariangela Correa departamento de Farmacologia Universidade Federal de Sao Paulo Sao Paulo Brazil Instituto do Cancer do Estado de Sao Paulo Sao Paulo Brazil disciplina de imunologia Universidade Federal de Sao Paulo Sao Paulo Brazil Centro de Referência da Saúde da Mulher Hospital Pérola Byington Sao Paulo Brazil disciplina de Mastologia Universidade Federal de Sao Paulo Sao Paulo Brazil departamento de Psicobiologia Universidade Federal de Sao Paulo Sao Paulo Brazil Instituto de Educacao e Ciência Hospital Alemao Oswaldo Cruz Sao Paulo Brazil

Introduction: Breast cancer is the leading cause of cancer mortality among women. Some biomarkers and clinical features are used for the diagnosis and prognosis of this tumor, but no prognostic or predictive marker is routinely available specifically for hormone receptor positive tumors. Homocysteine is well known as a risk factor in atherosclerotic vascular diseases, but its participation in cancer biology is still unclear. The aim of this study was to evaluate serum Homocysteine and Cysteine as biomarkers of disease progression in breast tumor. As a secondary objective, the effect of a short course (one month) of hormonal treatment on Homocysteine, Cysteine and DNA methylation levels was also evaluated. Methods: Blood samples, tumor samples and normal adjacent tissue were collected during the initial biopsy (pre-treatment) and after one month of hormonal therapy (post-treatment). Serum Homocysteine and Cysteine were analyzed by HPLC and tissue global DNA methylation was determined by the Methylation-Sensitive Restriction Enzyme (MSRE) technique. Results: Variations in Homocysteine levels were significantly correlated with Disease-Free Survival. Cox proportional risk model demonstrated that nodal status and Homocysteine levels were independent prognostic factors for disease-free survival (DFS). A significant difference was observed between pre-and post-treatment levels of Homocysteine and Cysteine in advanced tumors, suggesting a prognostic role in patients with poor clinical characteristics. Conclusion: Although more studies are needed to confirm these results, our research suggests that Hcy might be used as a prognostic biomarker for breast cancer.

关键词： Homocysteine Cysteine Breast Cancer Estrogen Receptor Prognostic and Predictive Biomarker Tamoxifen Anastrozol

Sympathetic activity in breast cancer and metastasis:partners in crime

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Bone Research 2021年第1期9卷 26-36页

作者： Francisco Conceição Daniela M.Sousa Joana Paredes Meriem Lamghari I 3S-Instituto de Investigação e Inovação em Saúde Universidade do Porto4200-135 PortoPortugal INEB-Instituto Nacional de Engenharia Biomédica Universidade do Porto4200-135 PortoPortugal ICBAS-Instituto de Ciências Biomédicas Abel Salazar Universidade do Porto4050-313 PortoPortugal IPATIMUP-Instituto de Patologia e imunologia Molecular da Universidade do Porto 4200-135 PortoPortugal FMUP-Faculdade de Medicina da Universidade do Porto 4200-319 PortoPortugal

The vast majority of patients with advanced breast cancer present skeletal complications that severely compromise their quality of *** cancer cells are characterized by a strong tropism to the bone *** engraftment and colonization of bone,breast cancer cells interact with native bone cells to hinder the normal bone remodeling process and establish an osteolytic“metastatic vicious cycle”.The sympathetic nervous system has emerged in recent years as an important modulator of breast cancer progression and metastasis,potentiating and accelerating the onset of the vicious cycle and leading to extensive bone ***,sympathetic neurotransmitters and their cognate receptors have been shown to promote several hallmarks of breast cancer,such as proliferation,angiogenesis,immune escape,and invasion of the extracellular *** this review,we assembled the current knowledge concerning the complex interactions that take place in the tumor microenvironment,with a special emphasis on sympathetic modulation of breast cancer cells and stromal ***,the differential action of epinephrine and norepinephrine,through eitherα-orβ-adrenergic receptors,on breast cancer progression prompts careful consideration when designing new therapeutic *** addition,the contribution of sympathetic innervation to the formation of bone metastatic foci is *** particular,we address the remarkable ability of adrenergic signaling to condition the native bone remodeling process and modulate the bone vasculature,driving breast cancer cell engraftment in the bone ***,clinical perspectives and developments on the use ofβ-adrenergic receptor inhibitors for breast cancer management and treatment are discussed.

关键词： breast metastasis invasion

The full length <i>PtSRP</i>(<i>Pisolithus tinctorius</i>symbiosis related protein) fungal mRNA encodes a potential marker of ectomycorrhiza formation

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American Journal of Molecular Biology 2012年第3期2卷 258-264页

作者： Helder Elísio E. Vieira Cláudia E. P. Lima Carlos E. Calzavara-Silva Bartolomeu Acioli-Santos Elaine Malosso departamento de Micologia Universidade Federal de Pernambuco Recife Brazil Laboratório de imunologia Celular e Molecular Centro de Pesquisas René Rachou Belo Horizonte Brazil

The Pisolithus tinctorius symbiosis related protein expressed sequence tag (EST PtSRP) was previously identified in the first hours of the interaction between the fungus Pisolithus tinctorius and sweet chestnut Castanea sativa, and partially characterized as a fungal marker gene of ectomycorrhizal symbiosis formation. We used the 5’ rapid amplification of cDNA ends (RACE) to obtain the PtSRP mRNA 5’ region, and together with our previously reported 3’ mRNA region, the full mRNA sequence was assembled by use of bioinformatics tools and deposited to GenBank (Accession: GU733439). The full-length mRNA sequence (636 bp) revealed the locations of the 5’ and 3’ untranslated regions (UTRs) and contained the Kozak sequence (ccc aag ATG A) in the 5’ UTR. The in silico translated PtSRP open reading frame (ORF) codes for a 127 amino acid protein and contained four putative post-translational modification sites (two N-glycosylation and two phosphorylation). The protein secondary structure is postulated to be composed of one N-terminal hydrophobic transmembrane alpha helix and at least six hydrophilic beta-strands spread across the protein. Sub-cellular localization prediction suggests that the protein is involved in cellular secretory pathway, supported by the presence of a cleavage site motif close to the membrane anchor. The data presented herein indicate the role of PtSRP as a fungal membrane secreted protein involved in early stages of ectomycorrhizal formation, with application as a possible marker for nascent ectomy-corrhiza fungal development.

关键词： Ectomycorrhiza Symbiosis Related Genes/Proteins RACE EST

Changes in cellular proliferation and plasma products are associated with liver failure

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World Journal of Hepatology 2016年第32期8卷 1370-1383页

作者： Juliana Gil Melgaco Frederico Marianetti Soriani Pedro Henrique Ferreira Sucupira Leonardo Assaf Pinheiro Yasmine Rangel Vieira Jaqueline Mendes de Oliveira Lia Laura Lewis-Ximenez Cristina Carvalho Vianna Araújo Lúcio Filgueiras Pacheco-Moreira Gustavo Batista Menezes Oswaldo Goncalves Cruz Claudia Lamarca Vitral Marcelo Alves Pinto departamento de Microbiologia e Parasitologia Universidade Federal Fluminense Instituto Oswaldo Cruz/Fiocruz Laboratório de Desenvolvimento Tecnológico em Virologia departamento de Biologia Geral Instituto de Ciencias BiologicasUniversidade Federal de Minas Gerais Instituto Oswaldo Cruz/Fiocruz Ambulatório de Hepatites Virais Hospital Federal de Bonsucesso Laboratório de Imunofarmacologia Departamento de Bioquímica e ImunologiaInstituto de Ciencias BiológicasUniversidade Federal de Minas Gerais Fundacao Oswaldo Cruz Programa de Computacao Científica

AIM To study the differences in immune response and cytokine profile between acute liver failure and selflimited acute *** Forty-six patients with self-limited acute hepatitis(AH), sixteen patients with acute liver failure(ALF), and twenty-two healthy subjects were involved in this study. The inflammatory and anti-inflammatory products in plasma samples were quantified using commercial enzyme-linked immunoassays and quantitative real-time PCR. The cellular immune responses were measured by proliferation assay using flow cytometry. The groups were divided into viral- and non-viral-induced selflimited AH and ALF. Thus, we worked with five groups: Hepatitis A virus(HAV)-induced self-limited acute hepatitis(HAV-AH), HAV-induced ALF(HAV-ALF), nonviral-induced self-limited acute hepatitis(non-viral AH), non-viral-induced acute liver failure(non-viral ALF), and healthy subjects(HC). Comparisons among HAV and non-viral-induced AH and ALF were *** The levels of mitochondrial DNA(mt DNA) and the cytokines investigated [interleukin(IL)-6, IL-8, IL-10, interferon gamma, and tumor necrosis factor] were significantly increased in ALF patients, independently of etiology(P death [mt DNA: OR = 12.1(95%CI: 2.57-57.07), P = 0.002; and IL-10: OR = 8.01(95%CI: 1.26-50.97), P = 0.027]. In the cellular proliferation assay, NK^(bright), NKT and regulatory T cells(TReg) predominated in virusspecific stimulation in HAV-induced ALF patients with an anergic behavior in the cellular response to mitotic stimulation. Therefore, in non-viral-induced ALF, anergic behavior of activated T cells was not observed after mitotic stimulation, as expected and as described by the literature. CONCLUSION mt DNA and IL-10 may be predictors of ALF and death. TReg cells are involved in immunologi

关键词： Acute liver failure Cytokines Mitochondrial DNA Cellular immune response Hepatitis A virus