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  1. Article ; Online: Counteracting Ideology of COVID-19 Total Lockdown of Countries

    Bhakdi, Sucharit

    The Beacon: Journal for Studying Ideologies and Mental Dimensions 3(1) 010840218

    2020  

    Abstract: In view of unprecedented public policy measures aimed at lockdowns of the whole countries across the world, due to the spread of COVID-19 disease, it is becoming obvious that such measures requiring prolonged switching off the economies, are mainly ... ...

    Abstract In view of unprecedented public policy measures aimed at lockdowns of the whole countries across the world, due to the spread of COVID-19 disease, it is becoming obvious that such measures requiring prolonged switching off the economies, are mainly disproportional to the threat, excessive and, therefore, must be reconsidered as soon as possible. Passiveness and laxness of politicians may cause tremendous financial losses to budgets, damage to economies, transition to constant violation of constitutions and human rights. An Open Letter to Federal Chancellor of Germany Angela Merkel disclosing the incorrect interpretation of COVID-19 data by media and politicians, was prepared by the author and is taken as a basis of this communiqué.
    Keywords COVID-19 ; SARS-CoV-2 ; human rights ; democracy ; constitution violation ; lockdowns ; covid19
    Language Russian
    Publishing date 2020-04-16
    Publishing country eu
    Document type Article ; Online
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  2. Article: Scramblases as Regulators of Proteolytic

    Reiss, Karina / Leitzke, Sinje / Seidel, Jana / Sperrhacke, Maria / Bhakdi, Sucharit

    Membranes

    2022  Volume 12, Issue 2

    Abstract: Proteolytic ectodomain release is a key mechanism for regulating the function of many cell surface proteins. The ... ...

    Abstract Proteolytic ectodomain release is a key mechanism for regulating the function of many cell surface proteins. The sheddases
    Language English
    Publishing date 2022-02-04
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2614641-1
    ISSN 2077-0375
    ISSN 2077-0375
    DOI 10.3390/membranes12020185
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  3. Article ; Online: Mechanisms of invasion and persistence of infectious agents.

    Bhakdi, Sucharit

    Medical microbiology and immunology

    2012  Volume 201, Issue 4, Page(s) 407

    MeSH term(s) Animals ; Bacteria/immunology ; Bacteria/pathogenicity ; Communicable Diseases/immunology ; Communicable Diseases/pathology ; Host-Pathogen Interactions ; Humans ; Parasites/immunology ; Parasites/pathogenicity ; Viruses/immunology ; Viruses/pathogenicity
    Language English
    Publishing date 2012-11
    Publishing country Germany
    Document type Editorial
    ZDB-ID 120933-4
    ISSN 1432-1831 ; 0300-8584
    ISSN (online) 1432-1831
    ISSN 0300-8584
    DOI 10.1007/s00430-012-0275-9
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  4. Article: The plasma membrane: Penultimate regulator of ADAM sheddase function.

    Reiss, Karina / Bhakdi, Sucharit

    Biochimica et biophysica acta. Molecular cell research

    2017  Volume 1864, Issue 11 Pt B, Page(s) 2082–2087

    Abstract: Background: ADAM10 and ADAM17 are the best characterized members of the ADAM (A Disintegrin and Metalloproteinase) - family of transmembrane proteases. Both are involved diverse physiological and pathophysiological processes. ADAMs are known to be ... ...

    Abstract Background: ADAM10 and ADAM17 are the best characterized members of the ADAM (A Disintegrin and Metalloproteinase) - family of transmembrane proteases. Both are involved diverse physiological and pathophysiological processes. ADAMs are known to be regulated by posttranslational mechanisms. However, emerging evidence indicates that the plasma membrane with its unique dynamic properties may additionally play an important role in controlling sheddase function.
    Scope of review: Membrane events that could contribute to regulation of ADAM-function are summarized.
    Major conclusions: Surface expression of peptidolytic activity should be differentiated from ADAM-sheddase function since the latter additionally requires that the protease finds its substrate in the lipid bilayer. We propose that this is achieved through horizontal and vertical reorganization of membrane nanoarchitecture coordinately occurring at the sites of sheddase activation. Reshuffling of nanodomains thereby guides traffic of enzyme and substrate to each other. For ADAM17 phosphatidylserine exposure is required to then induce its shedding function.
    General significance: The novel concept that physicochemical properties of the lipid bilayer govern the action of ADAM-proteases may be extendable to other functional proteins that act at the cell surface. This article is part of a Special Issue entitled: Proteolysis as a Regulatory Event in Pathophysiology edited by Stefan Rose-John.
    MeSH term(s) ADAM10 Protein/genetics ; ADAM10 Protein/metabolism ; ADAM17 Protein/genetics ; ADAM17 Protein/metabolism ; Amyloid Precursor Protein Secretases/genetics ; Amyloid Precursor Protein Secretases/metabolism ; Cell Membrane/genetics ; Cell Membrane/metabolism ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Phosphatidylserines/genetics ; Phosphatidylserines/metabolism ; Proteolysis
    Chemical Substances Membrane Proteins ; Phosphatidylserines ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; ADAM10 Protein (EC 3.4.24.81) ; ADAM10 protein, human (EC 3.4.24.81) ; ADAM17 Protein (EC 3.4.24.86) ; ADAM17 protein, human (EC 3.4.24.86)
    Language English
    Publishing date 2017-06-15
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0167-4889 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0167-4889 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbamcr.2017.06.006
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  5. Article ; Online: Role of ADAM10 and ADAM17 in Regulating CD137 Function.

    Seidel, Jana / Leitzke, Sinje / Ahrens, Björn / Sperrhacke, Maria / Bhakdi, Sucharit / Reiss, Karina

    International journal of molecular sciences

    2021  Volume 22, Issue 5

    Abstract: Human CD137 (4-1BB), a member of the TNF receptor family, and its ligand CD137L (4-1BBL), are expressed on immune cells and tumor cells. CD137/CD137L interaction mediates bidirectional cellular responses of potential relevance in inflammatory diseases, ... ...

    Abstract Human CD137 (4-1BB), a member of the TNF receptor family, and its ligand CD137L (4-1BBL), are expressed on immune cells and tumor cells. CD137/CD137L interaction mediates bidirectional cellular responses of potential relevance in inflammatory diseases, autoimmunity and oncology. A soluble form of CD137 exists, elevated levels of which have been reported in patients with rheumatoid arthritis and various malignancies. Soluble CD137 (sCD137) is considered to represent a splice variant of CD137. In this report, however, evidence is presented that A Disintegrin and Metalloproteinase (ADAM)10 and potentially also ADAM17 are centrally involved in its generation. Release of sCD137 by transfected cell lines and primary T cells was uniformly inhibitable by ADAM10 inhibition. The shedding function of ADAM10 can be blocked through inhibition of its interaction with surface exposed phosphatidylserine (PS), and this effectively inhibited sCD137 generation. The phospholipid scramblase Anoctamin-6 (ANO6) traffics PS to the outer membrane and thus modifies ADAM10 function. Overexpression of ANO6 increased stimulated shedding, and hyperactive ANO6 led to maximal constitutive shedding of CD137. sCD137 was functionally active and augmented T cell proliferation. Our findings shed new light on the regulation of CD137/CD137L immune responses with potential impact on immunotherapeutic approaches targeting CD137.
    MeSH term(s) ADAM10 Protein/metabolism ; ADAM17 Protein/metabolism ; Amyloid Precursor Protein Secretases/metabolism ; Anoctamins/metabolism ; Arthritis, Rheumatoid/metabolism ; Arthritis, Rheumatoid/pathology ; Cell Membrane/metabolism ; HEK293 Cells ; HT29 Cells ; Humans ; Membrane Proteins/metabolism ; Neoplasm Proteins/metabolism ; Neoplasms/metabolism ; Neoplasms/pathology ; Phospholipid Transfer Proteins/metabolism ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology ; Tumor Necrosis Factor Receptor Superfamily, Member 9/metabolism
    Chemical Substances ANO6 protein, human ; Anoctamins ; Membrane Proteins ; Neoplasm Proteins ; Phospholipid Transfer Proteins ; Tumor Necrosis Factor Receptor Superfamily, Member 9 ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; ADAM10 Protein (EC 3.4.24.81) ; ADAM10 protein, human (EC 3.4.24.81) ; ADAM17 Protein (EC 3.4.24.86) ; ADAM17 protein, human (EC 3.4.24.86)
    Language English
    Publishing date 2021-03-08
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22052730
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  6. Article: Influence of Anoctamin-4 and -9 on ADAM10 and ADAM17 Sheddase Function.

    Leitzke, Sinje / Seidel, Jana / Ahrens, Björn / Schreiber, Rainer / Kunzelmann, Karl / Sperrhacke, Maria / Bhakdi, Sucharit / Reiss, Karina

    Membranes

    2022  Volume 12, Issue 2

    Abstract: ... ...

    Abstract Ca
    Language English
    Publishing date 2022-01-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2614641-1
    ISSN 2077-0375
    ISSN 2077-0375
    DOI 10.3390/membranes12020123
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  7. Article ; Online: Covid-19 Outbreak Role in the Development of Societies

    VanMeter, Karin / Bhakdi, Sucharit / Gerilovych, Antony

    The Beacon: Journal for Studying Ideologies and Mental Dimensions 3(1) 011040018

    Questions and Inconsistencies

    2020  

    Abstract: This Letter is composed from answers to the certain questions on COVID-19 role in the development of societies, posed by an Editor. Three scientists pay attention to the epidemiological dimension of the development of global society that came into ... ...

    Abstract This Letter is composed from answers to the certain questions on COVID-19 role in the development of societies, posed by an Editor. Three scientists pay attention to the epidemiological dimension of the development of global society that came into closest contact with what we call “nature,” as well as to the role of “natural” factors in reconsidering the societies by the political elites.
    Keywords COVID-19 ; social policy ; epidemiology ; development of society ; role of viruses ; covid19
    Language English
    Publishing date 2020-04-25
    Publishing country eu
    Document type Article ; Online
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  8. Article: Pathogenese der Atherosklerose. Das Mainzer Konzept.

    Bhakdi, Sucharit

    Medizinische Monatsschrift fur Pharmazeuten

    2006  Volume 29, Issue 10, Page(s) 356–359

    Abstract: Atherosclerosis is widely regarded as a chronic inflammatory disease that develops as a consequence of entrapment of low density lipoprotein (LDL) in the arterial intima. Native LDL lacks inflammatory properties, so the lipoprotein must undergo ... ...

    Title translation Immunopathogenesis of atherosclerosis: the Mainz hypothesis.
    Abstract Atherosclerosis is widely regarded as a chronic inflammatory disease that develops as a consequence of entrapment of low density lipoprotein (LDL) in the arterial intima. Native LDL lacks inflammatory properties, so the lipoprotein must undergo biochemical alterations in order to become atherogenic. Modification is commonly regarded as being dangerous because it bestows inflammatory properties onto the lipoprotein. Most current models regard oxidation to be the decisive modifying event. However, we have obtained experimental evidence in support of a different concept. We propose that modification of tissue-entrapped LDL is required because it enables the lipoprotein to signal to the immune system and effect its own removal. Oxidation would be too haphazard to fulfill this function. The evidence indicates that modification occurs through the action of ubiquitous hydrolytic enzymes. Enzymatically remodeled LDL binds C-reactive protein. C-reactive protein bound to remodeled LDL not only activates complement but also regulates it by inhibiting activation of the terminal complement cascade. Simultaneously, epitopes are exposed to enable the lipoprotein to be recognized and taken up by macrophages. The high density lipoprotein-dependent reverse transport pathway concludes the sequence of events that clear tissues of cholesterol in a non-inflammatory manner very similar to what has been described for the removal of apoptotic cells. It is proposed that these physiological processes occur throughout life without harm, pathology evolving only when the machinery suffers overload. Detrimental effects are then evoked primarily by the unreigned activation of complement, macrophages, and other effectors of the immune system in the lesions.
    MeSH term(s) Animals ; Anti-Bacterial Agents/therapeutic use ; Antioxidants/therapeutic use ; Atherosclerosis/etiology ; Atherosclerosis/immunology ; Atherosclerosis/pathology ; Humans ; Infection/complications ; Infection/immunology
    Chemical Substances Anti-Bacterial Agents ; Antioxidants
    Language German
    Publishing date 2006-10
    Publishing country Germany
    Document type English Abstract ; Journal Article ; Review
    ZDB-ID 132805-0
    ISSN 0342-9601
    ISSN 0342-9601
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  9. Article: Atherosklerose: "Die Atherosklerose ist eine besiegte Krankheit!" - DAZ-Interview

    Bhakdi, Sucharit

    Deutsche Apotheker-Zeitung

    2010  Volume 150, Issue 5, Page(s) 98

    Language German
    Document type Article
    ZDB-ID 399-2
    ISSN 0011-9857
    Database Current Contents Medicine

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  10. Article ; Online: Complement and atherosclerosis-united to the point of no return?

    Torzewski, Michael / Bhakdi, Sucharit

    Clinical biochemistry

    2013  Volume 46, Issue 1-2, Page(s) 20–25

    Abstract: Atherosclerosis is widely regarded as a chronic inflammatory disease that develops as a consequence of entrapment of oxidized low-density lipoprotein (LDL) in the arterial intima and its interaction with components of both innate and adaptive immunity. ... ...

    Abstract Atherosclerosis is widely regarded as a chronic inflammatory disease that develops as a consequence of entrapment of oxidized low-density lipoprotein (LDL) in the arterial intima and its interaction with components of both innate and adaptive immunity. This article reviews the role of the complement system in the context of a different concept on atherogenesis. Arguments are forwarded in support of the contention that enzymatic and not oxidative modification of LDL is the prerequisite for transforming the lipoprotein into a moiety that is recognized by the innate immune system. In a departure from general wisdom, it is proposed that these processes are initially not pathological. To the contrary, they are physiological and meaningful because only thus can the stranded lipoprotein with its insoluble cargo, cholesterol, be removed from tissues. It is contended that histopathologically defined initial foam cell formation develops without inflammation and is reversible. Atherosclerosis as a disease evolves only when the cholesterol removal machinery is overloaded and it then represents a special type of immunopathological process primarily involving immune effectors of the innate rather than the adaptive immune system. This sets it apart from classical immunopathological reactions that are all based on dysfunctional adaptive immunity. But as with all other diseases of known origin, a defined molecular trigger, enzymatically modified-LDL (eLDL), exists whose intimal accumulation is required to initiate the pathologic process. And as with other diseases, the course of atherosclerosis will then be influenced by myriad genetic, endogenous, and environmental factors that by themselves, however, will not cause the disease. This simple concept is completely in line with general clinical experience and with the results of major clinical trials that have been conducted during the past decades.
    MeSH term(s) Atherosclerosis/etiology ; Atherosclerosis/immunology ; C-Reactive Protein/metabolism ; Cholesterol/metabolism ; Complement Activation ; Complement System Proteins/metabolism ; Foam Cells/metabolism ; Foam Cells/pathology ; Humans ; Inflammation/metabolism ; Lipoproteins, LDL/immunology ; Lipoproteins, LDL/metabolism
    Chemical Substances Lipoproteins, LDL ; oxidized low density lipoprotein ; Complement System Proteins (9007-36-7) ; C-Reactive Protein (9007-41-4) ; Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2013-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 390372-2
    ISSN 1873-2933 ; 0009-9120
    ISSN (online) 1873-2933
    ISSN 0009-9120
    DOI 10.1016/j.clinbiochem.2012.09.012
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