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| 1 | Chevrier's Field Mouse(Apodemus chevrieri) and Père David's Vole(Eothenomys melanogaster) in China Carry Orthohepeviruses that form Two Putative Novel Genotypes Within the Species Orthohepevirus C显示文摘Hepatitis E virus(HEV)is the prototype of the family Hepeviridae and the causative agent of common acute viral hepatitis.Genetically diverse HEV-related viruses have been detected in a variety of mammals and some of them may have zoonotic potential.In this study,we tested 278 specimens collected from seven wild small mammal species in Yunnan province,China,for the presence and prevalence of orthohepevirus by broad-spectrum reverse transcription(RT)-PCR.HEV-related sequences were detected in two rodent species,including Chevrier’s field mouse(Apodemus chevrieri,family Muridae)and Père David’s vole(Eothenomys melanogaster,family Cricetidae),with the infection rates of 29.20%(59/202)and 7.27%(4/55),respectively.Further four representative full-length genomes were generated:two each from Chevrier’s field mouse(named Rd HEVAc14 and Rd HEVAc86)and Père David’s vole(Rd HEVEm40 and Rd HEVEm67).Phylogenetic analyses and pairwise distance comparisons of whole genome sequences and amino acid sequences of the gene coding regions showed that orthohepeviruses identified in Chinese Chevrier’s field mouse and Père David’s vole belonged to the species Orthohepevirus C but were highly divergent from the two assigned genotypes:HEV-C1 derived from rat and shrew,and HEV-C2 derived from ferret and possibly mink.Quantitative real-time RT-PCR demonstrated that these newly discovered orthohepeviruses had hepatic tropism.In summary,our work discovered two putative novel genotypes orthohepeviruses preliminarily named HEVC3 and HEV-C4 within the species Orthohepevirus C,which expands our understanding of orthohepevirus infection in the order Rodentia and gives new insights into the origin,evolution,and host range of orthohepevirus. | Bo Wang Wen Li Ji-Hua Zhou Bei Li Wei Zhang Wei-Hong Yang Hong Pan Li-Xia Wang Thomas Bock Zheng-Li Shi Yun-Zhi Zhang Xing-Lou Yang | 2018 | Virologica Sinica2018，33，1： | 6 |
| 2 | Nucleoporin 88 expression in hepatitis B and C virus-related liver diseases显示文摘AIM: To investigate the expression of nucleoporin 88 (Nup88) in hepatitis B virus (HBV) and C virus (HCV)-related liver diseases. METHODS: We generated a new monoclonal Nup88 antibody to investigate the Nup88 protein expression by immunohistochemistry (IHC) in 294 paraffin-embedded liver specimens comprising all stages of hepatocellular carcinogenesis. In addition, in cell culture experiments HBV-positive (HepG2.2.15 and HB611) and HBV-negative (HepG2) hepatoma cell lines were tested for the Nup88 expression by Western-immunoblotting to test data obtained by IHC.RESULTS: Specific Nup88 expression was found in chronic HCV hepatitis and unspecific chronic hepatitis, whereas no or very weak Nup88 expression was detected in normal liver. The Nup88 expression was markedly reduced or missing in mild chronic HBV infection and inversely correlated with HBcAg expression. Irrespective of the HBV- or HCV-status, increasing Nup88 expression was observed in cirrhosis and dysplastic nodules, and Nup88 was highly expressed in hepatocellular carcinomas. The intensity of Nup88 expression significantly increased during carcinogenesis (P < 0.0001) and correlated with dedifferentiation (P < 0.0001). Interestingly, Nup88 protein expression was significantly downregulated in HBV-positive HepG2.2.15 (P < 0.002) and HB611 (P < 0.001) cell lines as compared to HBV-negative HepG2 cells. CONCLUSION: Based on our immunohistochemical data, HBV and HCV are unlikely to influence the expression of Nup88 in cirrhotic and neoplastic liver tissue, but point to an interaction of HBV with the nuclear pore in chronic hepatitis. The expression of Nup88 in nonneoplastic liver tissue might reflect enhanced metabolic activity of the liver tissue. Our data strongly indicate a dichotomous role for Nup88 in non-neoplastic and neoplastic conditions of the liver. | Martina Knoess Anna Kordelia Kurz Olga Goreva Nuran Bektas Kai Breuhahn Magarethe Odenthal Peter Schirmacher Hans Peter Dienes C Thomas Bock Hanswalter Zentgraf Axel zur Hausen | 2006 | World Journal of Gastroenterology2006，12，36： | 4 |
| 3 | Long-term outcomes of autoimmune pancreatitis: a multicentre, international analysis显示文摘 | Phil A Hart Terumi Kamisawa William R Brugge Jae Bock Chung Emma L Culver László Czakó Luca Frulloni Vay Liang W Go Thomas M Gress Myung-Hwan Kim Shigeyuki Kawa Kyu Taek Lee Markus M Lerch Wei-Chih Liao Matthias L?hr Kazuichi Okazaki Ji Kon Ryu Nicolas Sc | 2013 | Gut2013，，12： | 2 |
| 4 | Genetic insights on host and hepatitis B virus in liver diseases显示文摘 | Hoang van Tong C. Thomas Bock Thirumalaisamy P. Velavan | 2014 | Mutation Research-Reviews in Mutation Research2014，，： | 2 |
| 5 | Engineering osteoblastic metastases to delineate the adaptive response of androgen-deprived prostate cancer in the bone metastatic microenvironment显示文摘While stromal interactions are essential in cancer adaptation to hormonal therapies,the effects of bone stroma and androgen deprivation on cancer progression in bone are poorly understood.Here,we tissue-engineered and validated an in vitro microtissue model of osteoblastic bone metastases,and used it to study the effects of androgen deprivation in this microenvironment.The model was established by culturing primary human osteoprogenitor cells on melt electrowritten polymer scaffolds,leading to a mineralized osteoblast-derived microtissue containing,in a 3D setting,viable osteoblastic cells,osteocytic cells,and appropriate expression of osteoblast/osteocyte-derived mRNA and proteins,and mineral content.Direct co-culture of androgen receptordependent/ independent cell lines (LNCaP,C4-2B,and PC3) led cancer cells to display functional and molecular features as observed in vivo.Co-cultured cancer cells showed increased affinity to the microtissues,as a function of their bone metastatic potential.Cocultures led to alkaline phosphatase and collagen-I upregulation and sclerostin downregulation,consistent with the clinical marker profile of osteoblastic bone metastases.LNCaP showed a significant adaptive response under androgen deprivation in the microtissues,with the notable appearance of neuroendocrine transdifferentiation features and increased expression of related markers (dopa decarboxylase,enolase 2).Androgen deprivation affected the biology of the metastatic microenvironment with stronger upregulation of androgen receptor,alkaline phosphatase,and dopa decarboxylase,as seen in the transition towards resistance.The unique microtissues engineered here represent a substantial asset to determine the involvement of the human bone microenvironment in prostate cancer progression and response to a therapeutic context in this microenvironment. | Nathalie Bock Ali Shokoohmand Thomas Kryza Joan Rohl Jonelle Meijer Phong A. Tran Colleen C. Nelson Judith A. Clements Dietmar W. Hutmacher | 2019 | Bone Research2019，7，2： | 2 |
| 6 | High Prevalence of Viral Genomes and Multiple Viral Infections in the Myocardium of Adults With “Idiopathic” Left Ventricular Dysfunction显示文摘 | Uwe Kühl Matthias Pauschinger Michel Noutsias Bettina Seeberg Thomas Bock Dirk Lassner Wolfgang Poller Reinhard Kandolf Heinz-Peter Schultheiss | 2005 | Circulation2005，，7： | 2 |
| 7 | Transactivation of human parvovirus B19 gene expression in endothelial cells by adenoviral helper functions显示文摘 | Tanja Pozzuto Kristina von Kietzell Thomas Bock Caroline Schmidt-Lucke Wolfgang Poller Thomas Zobel Dirk Lassner Heinz Zeichhardt Stefan Weger Henry Fechner | 2010 | Virology2010，，1： | 1 |
| 8 | Apolipoprotein E Induces Antiinflammatory Phenotype in Macrophages显示文摘 | Daniel Baitsch Hans H. Bock Thomas Engel Ralph Telgmann Carsten Müller-Tidow Georg Varga Martine Bot Joachim Herz Horst Robenek Arnold von Eckardstein Jerzy-Roch Nofer | 2011 | Arteriosclerosis, Thrombosis, and Vascular Biology2011，，5： | 1 |
| 9 | Presentation, Patterns of Myocardial Damage, and Clinical Course of Viral Myocarditis显示文摘 | Heiko Mahrholdt Anja Wagner Claudia C. Deluigi Eva Kispert Stefan Hager Gabriel Meinhardt Holger Vogelsberg Peter Fritz Juergen Dippon C Thomas Bock Karin Klingel Reinhard Kandolf Udo Sechtem | 2006 | Circulation2006，，15： | 1 |
| 10 | Molecular pathology of inflammatory cardiomyopathy显示文摘 | Karin Klingel Martina Sauter C. Thomas Bock Gudrun Szalay Jens-J?rg Schnorr Reinhard Kandolf | 2004 | Medical Microbiology and Immunology (-)2004，，2： | 1 |
| 11 | The next-generation sphingosine-1 receptor modulator BAF312(siponimod) improves cortical network functionality in focal autoimmune encephalomyelitis显示文摘Autoimmune diseases of the central nervous system(CNS) like multiple sclerosis(MS) are characterized by inflammation and demyelinated lesions in white and grey matter regions. While inflammation is present at all stages of MS, it is more pronounced in the relapsing forms of the disease, whereas progressive MS(PMS) shows significant neuroaxonal damage and grey and white matter atrophy. Hence, disease-modifying treatments beneficial in patients with relapsing MS have limited success in PMS. BAF312(siponimod) is a novel sphingosine-1-phosphate receptor modulator shown to delay progression in PMS. Besides reducing inflammation by sequestering lymphocytes in lymphoid tissues, BAF312 crosses the blood-brain barrier and binds its receptors on neurons, astrocytes and oligodendrocytes. To evaluate potential direct neuroprotective effects, BAF312 was systemically or locally administered in the CNS of experimental autoimmune encephalomyelitis mice with distinct grey-and white-matter lesions(focal experimental autoimmune encephalomyelitis using an osmotic mini-pump). Ex-vivo flow cytometry revealed that systemic but not local BAF312 administration lowered immune cell infiltration in animals with both grey and white matter lesions. Ex-vivo voltage-sensitive dye imaging of acute brain slices revealed an altered spatio-temporal pattern of activation in the lesioned cortex compared to controls in response to electrical stimulation of incoming white-matter fiber tracts. Here, BAF312 administration showed partial restore of cortical neuronal circuit function. The data suggest that BAF312 exerts a neuroprotective effect after crossing the blood-brain barrier independently of peripheral effects on immune cells. Experiments were carried out in accordance with German and EU animal protection law and approved by local authorities(Landesamt für Natur, Umwelt und Verbraucherschutz Nordrhein-Westfalen;87-51.04.2010.A331) on December 28, 2010. | Petra Hundehege Manuela Cerina Susann Eichler Christian Thomas Alexander M. Herrmann Kerstin Goel Thomas Müntefering Juncal Fernandez-Orth Stefanie Bock Venu Narayanan Thomas Budde Erwin-Josef Speckmann Heinz Wiendl Anna Schubart Tobias Ruck Sven G. Meuth | 2019 | Neural Regeneration Research2019，14，11： | 1 |
| 12 | Presentation, Patterns of Myocardial Damage, and Clinical Course of Viral Myocarditis显示文摘 | Heiko Mahrholdt Anja Wagner Claudia C. Deluigi Eva Kispert Stefan Hager Gabriel Meinhardt Holger Vogelsberg Peter Fritz Juergen Dippon C Thomas Bock Karin Klingel Reinhard Kandolf Udo Sechtem | 2006 | Circulation2006，，： | 1 |
| 13 | Late HDV RNA relapse after peginterferon alpha‐based therapy of chronic hepatitis delta显示文摘 | Benjamin Heidrich Cihan Yurdayd?n G?khan Kaba?am Boris A. Ratsch Kalliopi Zachou Birgit Bremer George N. Dalekos Andreas Erhardt Fehmi Tabak Kendal Yalcin Selim Gürel Stefan Zeuzem Markus Cornberg C.‐Thomas Bock Michael P. Manns Heiner Wedemeyer | 2014 | Hepatology2014，，1： | 1 |
| 14 | Long-term outcomes of autoimmune pancreatitis: a multicentre, international analysis显示文摘 | Phil A Hart Terumi Kamisawa William R Brugge Jae Bock Chung Emma L Culver László Czakó Luca Frulloni Vay Liang W Go Thomas M Gress Myung-Hwan Kim Shigeyuki Kawa Kyu Taek Lee Markus M Lerch Wei-Chih Liao Matthias L?hr Kazuichi Okazaki Ji Kon Ryu Nicolas Sc | 2013 | Gut2013，，12： | 1 |
| 15 | Serum cytokine profiles associated with clinical presentation in Vietnamese infected with hepatitis B virus显示文摘 | Le H. Song Vu Q. Binh Dinh N. Duy Jürgen F.J. Kun Thomas C. Bock Peter G. Kremsner Adrian J.F. Luty | 2002 | Journal of Clinical Virology2002，，1： | 1 |
| 16 | How can the efficiency of the dryer section be increased显示文摘 | Bock Thomas | 2006 | International Paperworld2006，6，： | 1 |
| 17 | Diagnosis and laryngeal complications of Bordatella pertussis infection in the ambulatory aduh population 显示文摘 | Thomas M Leschke Joel H Blumin Jonathan M Bock | 2014 | Otolaryngology-head and neck surgery:official journal of American Academy of Otolaryngology-Head and Neck Surgery2014，151，5： | 1 |
| 18 | In vitro corneal permeability of diclofenac sodium in formulation containing cyclodextrins compared to the commercial product voltan ophtha显示文摘 | Olaf Reer Thomas K Bock Bernd W Muller | 1994 | J Pharm Sci1994，83，9： | 1 |
| 19 | CD83 Expression Influences CD4 + T Cell Development in the Thymus显示文摘 | Yoko Fujimoto LiLi Tu Ann S. Miller Cheryl Bock Manabu Fujimoto Carolyn Doyle Douglas A. Steeber Thomas F. Tedder | 2002 | Cell2002，，6： | 1 |
| 20 | K_(2P)18.1 translates T cell receptor signals into thymic regulatory T cell development显示文摘It remains largely unclear how thymocytes translate relative differences in T cell receptor(TCR)signal strength into distinct developmental programs that drive the cell fate decisions towards conventional(Tconv)or regulatory T cells(Treg).Following TCR activation,intracellular calcium(Ca^(2+))is the most important second messenger,for which the potassium channel K_(2P)18.1 is a relevant regulator.Here,we identify K_(2P)18.1 as a central translator of the TCR signal into the thymus-derived Treg(tTreg)selection process.TCR signal was coupled to NF-κB-mediated K_(2P)18.1 upregulation in tTreg progenitors.K_(2P)18.1 provided the driving force for sustained Ca^(2+) influx that facilitated NF-κB-and NFAT-dependent expression of FoxP3,the master transcription factor for Treg development and function.Loss of K_(2P)18.1 ion-current function induced a mild lymphoproliferative phenotype in mice,with reduced Treg numbers that led to aggravated experimental autoimmune encephalomyelitis,while a gain-of-function mutation in K_(2P)18.1 resulted in increased Treg numbers in mice.Our findings in human thymus,recent thymic emigrants and multiple sclerosis patients with a dominant-negative missense K_(2P)18.1 variant that is associated with poor clinical outcomes indicate that K_(2P)18.1 also plays a role in human Treg development.Pharmacological modulation of K_(2P)18.1 specifically modulated Treg numbers in vitro and in vivo.Finally,we identified nitroxoline as a K_(2P)18.1 activator that led to rapid and reversible Treg increase in patients with urinary tract infections.Conclusively,our findings reveal how K_(2P)18.1 translates TCR signals into thymic T cell fate decisions and Treg development,and provide a basis for the therapeutic utilization of Treg in several human disorders. | Tobias Ruck Stefanie Bock Steffen Pfeuffer Christina B.Schroeter Derya Cengiz Paul Marciniak Maren Lindner Alexander Herrmann Marie Liebmann Stjepana Kovac Lukas Gola Leoni Rolfes Marc Pawlitzki Nils Opel Tim Hahn Udo Dannlowski Thomas Pap Felix Luessi Julian A.Schreiber Bernhard Wunsch Tanja Kuhlmann Guiscard Seebohm Bjorn Tackenberg Patricia Seja Frank Doring Erhard Wischmeyer Achmet Imam Chasan Johannes Roth Luisa Klotz Gerd Meyer zu Hörste Heinz Wiendl Tobias Marschall Stefan Floess Jochen Huehn Thomas Budde Tobias Bopp Stefan Bittner Sven G.Meuth | 2022 | Cell Research2022，32，1： | 1 |
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