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Genomes and Genes
| Michael T HenekaSummaryCountry: Germany Publications
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Publications
Sepsis causes neuroinflammation and concomitant decrease of cerebral metabolismAlexander Semmler
Department of Neurology, University Bonn, Bonn, Germany
J Neuroinflammation 5:38. 2008..Changes in cerebral blood flow, release of inflammatory molecules and metabolic alterations contribute to neuronal dysfunction and cell death...- Focal glial activation coincides with increased BACE1 activation and precedes amyloid plaque deposition in APP[V717I] transgenic miceMichael T Heneka
Department of Neurology, University of Munster, 48149 Munster, Germany
J Neuroinflammation 2:22. 2005..Transgenic mice overexpressing the london mutant of amyloid precursor protein, APP [V717I], robustly recapitulate the amyloid pathology of AD... 
Locus ceruleus degeneration promotes Alzheimer pathogenesis in amyloid precursor protein 23 transgenic miceMichael T Heneka
Department of Neurology, University of Bonn, 53127 Bonn, Germany
J Neurosci 26:1343-54. 2006..Our data demonstrate that the degeneration of LC affects morphology, metabolism, and function of amyloid plaque-containing higher brain regions in APP23 mice. We postulate that LC degeneration substantially contributes to AD development...- Acute treatment with the PPARgamma agonist pioglitazone and ibuprofen reduces glial inflammation and Abeta1-42 levels in APPV717I transgenic miceMichael T Heneka
Department of Neurology, University of Bonn, Bonn, Germany
Brain 128:1442-53. 2005..These findings demonstrate that anti-inflammatory drugs can act rapidly to inhibit inflammatory responses in the brain and negatively modulate amyloidogenesis... - Inflammatory processes in Alzheimer's diseaseMichael T Heneka
Department of Neurology, Molecular Neurology Unit, University of Munster, Mendelstrasse 7, D 48149, Munster, Germany
J Neuroimmunol 184:69-91. 2007.... - Drug insight: effects mediated by peroxisome proliferator-activated receptor-gamma in CNS disordersMichael T Heneka
Department of Neurology, University of Munster, Germany
Nat Clin Pract Neurol 3:496-504. 2007..The verification of these findings in human cells prompted the initiation of clinical studies evaluating PPARgamma activation in patients with multiple sclerosis... - PPARs in the brainMichael T Heneka
Department of Neurology, Molecular Neurology Unit, Mendelstrasse 7, University of Munster, Albert Schweitzer Strasse 33, 48149 Munster, Germany
Biochim Biophys Acta 1771:1031-45. 2007..Less is known about the physiological role of PPARs for brain development, maintenance and function. Lesions from transgenic mouse models, however, provide evidence that PPARs may play pivotal roles for CNS development and function... - Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrineMichael T Heneka
Department of Neurology, Deutsches Zentrum für Neurodegenerative Erkrankungen, University of Bonn, 53105 Bonn, Germany
Proc Natl Acad Sci U S A 107:6058-63. 2010..Consequently, therapies targeting microglial phagocytosis should be tested under NE depletion... - Noradrenergic depletion increases inflammatory responses in brain: effects on IkappaB and HSP70 expressionMichael T Heneka
Department of Neurology, University of Bonn, Germany
J Neurochem 85:387-98. 2003..These findings suggest one mechanism by which PPARgamma agonists could provide benefit in neurological diseases having an inflammatory component... 
NOS2 gene deficiency protects from sepsis-induced long-term cognitive deficitsMarc Weberpals
Department of Neurology, University of Bonn, 53127 Bonn, Germany
J Neurosci 29:14177-84. 2009..Together, this data set outlines the importance of the NOS2 activation for long-term cerebral changes after severe sepsis...- Nitration of tyrosine 10 critically enhances amyloid β aggregation and plaque formationMarkus P Kummer
Clinical Neuroscience Unit, Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
Neuron 71:833-44. 2011..Further, injection of 3NTyr(10)-Aβ into the brain of young APP/PS1 mice induced β-amyloidosis. This suggests a disease modifying role for NOS2 in AD and therefore represents a potential therapeutic target... - Nonsteroidal anti-inflammatory drugs repress beta-secretase gene promoter activity by the activation of PPARgammaMagdalena Sastre
Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
Proc Natl Acad Sci U S A 103:443-8. 2006.... - Nonsteroidal anti-inflammatory drugs and peroxisome proliferator-activated receptor-gamma agonists modulate immunostimulated processing of amyloid precursor protein through regulation of beta-secretaseMagdalena Sastre
Department of Neurology, University of Bonn, 53127 Bonn, Germany
J Neurosci 23:9796-804. 2003..In conclusion, proinflammatory cytokines activate beta-secretase, and NSAIDs inhibit this effect through PPARgamma... - Anti-inflammatory and antiproliferative actions of PPAR-gamma agonists on T lymphocytes derived from MS patientsStephan Schmidt
Department of Neurology, University of Bonn, Germany
J Leukoc Biol 75:478-85. 2004..In summary, the data support the potential use of PPAR-gamma agonists as immunomodulatory, therapeutic agents for autoimmune diseases... - Noradrenaline induces expression of peroxisome proliferator activated receptor gamma (PPARgamma) in murine primary astrocytes and neuronsLuisa Klotz
Department of Neurology, University of Bonn, Bonn, Germany
J Neurochem 86:907-16. 2003..Conversely, decreased NA due to LC cell death in AD may reduce endogenous PPARgamma expression and therefore potentiate neuroinflammatory processes... - Contribution of inflammatory processes to Alzheimer's disease: molecular mechanismsMagdalena Sastre
Department of Neurology, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
Int J Dev Neurosci 24:167-76. 2006..The implication of PPAR-gamma in the control of Abeta-induced inflammation suggests a new target for AD therapy and emphasize the contribution of neuroinflammatory mechanisms to the pathogenesis of AD... - Systemic inflammation induces apoptosis with variable vulnerability of different brain regionsAlexander Semmler
Department of Neurology, University of Bonn, Germany
J Chem Neuroanat 30:144-57. 2005..We therefore conclude, that peripheral inflammation leads to a profound glial activation, the generation of nitric oxide and changes of Bax and Bcl-2 protein regulation critical for apoptosis... - Persistent cognitive impairment, hippocampal atrophy and EEG changes in sepsis survivorsAlexander Semmler
Department of Neurology, University of Bonn, Bonn, Germany
J Neurol Neurosurg Psychiatry 84:62-9. 2013.... - PPARγ/RXRα-induced and CD36-mediated microglial amyloid-β phagocytosis results in cognitive improvement in amyloid precursor protein/presenilin 1 miceMitsugu Yamanaka
Clinical Neuroscience Unit, Department of Neurology, University of Bonn Medical Center, 53127 Bonn, Germany
J Neurosci 32:17321-31. 2012..Furthermore, DSP-8658-treated mice showed improved spatial memory performance. Therefore, stimulation of microglial clearance by simultaneous activation of the PPARγ/RXRα heterodimer may prove beneficial in prevention of AD... - Noradrenergic depletion potentiates beta -amyloid-induced cortical inflammation: implications for Alzheimer's diseaseMichael T Heneka
Department of Neurology, University of Bonn, Germany 53127
J Neurosci 22:2434-42. 2002..These data demonstrate that LC loss and NE depletion augment inflammatory responses to Abeta and suggest that LC loss in AD is permissive for increased inflammation and neuronal cell death... - Proinflammatory stimulation and pioglitazone treatment regulate peroxisome proliferator-activated receptor gamma levels in peripheral blood mononuclear cells from healthy controls and multiple sclerosis patientsLuisa Klotz
Department of Neurology, University of Bonn, Germany
J Immunol 175:4948-55. 2005.... - Long-term cognitive impairment, neuronal loss and reduced cortical cholinergic innervation after recovery from sepsis in a rodent modelAlexander Semmler
Department of Neurology, Sigmund Freud Strasse 25, University Hospital Bonn, 53105 Bonn, Germany
Exp Neurol 204:733-40. 2007..Together these results suggest that sepsis can induce persistent behavioral and neuroanatomical changes and warrant studies of the neurological long-term consequences of sepsis in humans... - GGA1 is expressed in the human brain and affects the generation of amyloid beta-peptideTina Wahle
Department of Neurology, University of Bonn, 53127 Bonn, Germany
J Neurosci 26:12838-46. 2006..Thus, GGA proteins might be involved in the pathogenesis of AD... - Locus coeruleus degeneration exacerbates olfactory deficits in APP/PS1 transgenic miceNolwen L Rey
Laboratoire Neurosciences Sensorielles, Comportement, Cognition, UMR5020 CNRS, University Lyon1, University of Lyon, Lyon, France
Neurobiol Aging 33:426.e1-11. 2012..Importantly, DSP4 treatment also increased amyloid β (Aβ) deposition in the olfactory bulb of APP/PS1 mice, which correlated with olfactory memory, not with discrimination deficits... - Nitric oxide decreases the enzymatic activity of insulin degrading enzyme in APP/PS1 miceMarkus P Kummer
Clinical Neurosciences Unit, Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53105 Bonn, Germany
J Neuroimmune Pharmacol 7:165-72. 2012..These data suggest that NOS2 upregulation impairs amyloid β degradation through negative regulation of IDE activity and thus loss of NOS2 activity will positively influence amyloid β clearance... - Critical role of astroglial apolipoprotein E and liver X receptor-α expression for microglial Aβ phagocytosisDick Terwel
Department of Neurology, University of Bonn, 53127 Bonn, Germany
J Neurosci 31:7049-59. 2011..Together, these data suggest that astrocytic LXRα activation and subsequent release of ApoE by astrocytes is critical for the ability of microglia to remove fibrillar Aβ in response to treatment with TO901317... - Reduction of amyloid angiopathy and Abeta plaque burden after enriched housing in TgCRND8 mice: involvement of multiple pathwaysOliver Ambrée
University Hospital Munster, Institute of Neuropathology, Domagkstr 19, D 48149, Munster, Germany
Am J Pathol 169:544-52. 2006..In summary, this study demonstrates that the environment interacts with AD pathology at dif-ferent levels... - Neuroinflammatory and behavioural changes in the Atp7B mutant mouse model of Wilson's diseaseDick Terwel
Department of Neurology, Clinical Neurosciences, Bonn University, Bonn, Germany
J Neurochem 118:105-12. 2011..These mice can be used to evaluate therapeutic strategies to alleviate behavioural disturbances and cerebral pathology observed in WD... - NLRP3 is activated in Alzheimer's disease and contributes to pathology in APP/PS1 miceMichael T Heneka
Clinical Neuroscience Unit, Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
Nature 493:674-8. 2013..These results show an important role for the NLRP3/caspase-1 axis in the pathogenesis of Alzheimer's disease, and suggest that NLRP3 inflammasome inhibition represents a new therapeutic intervention for the disease... - Neuroinflammatory processes in Alzheimer's diseaseMichael T Heneka
Department of Neurology, Clinical Neurosciences, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
J Neural Transm 117:919-47. 2010.... - The oral antidiabetic pioglitazone protects from neurodegeneration and amyotrophic lateral sclerosis-like symptoms in superoxide dismutase-G93A transgenic miceBurkhard Schütz
Department of Psychiatry and Psychotherapy, University of Bonn, 53127 Bonn, Germany
J Neurosci 25:7805-12. 2005..Interestingly, mRNA levels of the suppressor of cytokine signaling 1 and 3 genes were increased by Pio, whereas both the mRNA and protein levels of endogenous mouse SOD1 and of transgenic human SOD1 remained unaffected... - Statins promote the degradation of extracellular amyloid {beta}-peptide by microglia via stimulation of exosome-associated insulin-degrading enzyme (IDE) secretionIrfan Y Tamboli
Departments of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
J Biol Chem 285:37405-14. 2010..These data demonstrate a novel pathway for the nonconventional secretion of IDE via exosomes. The modulation of this pathway could provide a new strategy to enhance the extracellular clearance of Aβ... - IFN-beta1a (Rebif) modifies the expression of microfilament-associated cell-cell contacts in C6 glioma cellsMichael Harzheim
Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, D 53105 Bonn, Germany
J Interferon Cytokine Res 23:83-9. 2003..This effect may also contribute to the therapeutic action of IFN-beta1a in MS... - Extracellular phosphorylation of the amyloid β-peptide promotes formation of toxic aggregates during the pathogenesis of Alzheimer's diseaseSathish Kumar
Department of Neurology, University of Bonn, Bonn, Germany
EMBO J 30:2255-65. 2011..Phosphorylation of Aβ could represent an important molecular mechanism in the pathogenesis of the most common sporadic form of AD... - CNS-targeted production of IL-17A induces glial activation, microvascular pathology and enhances the neuroinflammatory response to systemic endotoxemiaJulian Zimmermann
Department of Neurology, Universitatsklinikum Bonn, Bonn, Germany
PLoS ONE 8:e57307. 2013..More likely IL-17A acts as a modulating factor in the network of induced cytokines. This novel mouse model will be a very useful tool to further characterize the role of IL-17A in neuroinflammatory disease models... - TLR2 is a primary receptor for Alzheimer's amyloid β peptide to trigger neuroinflammatory activationShirong Liu
Department of Neurology, University of the Saarland, 66421 Homburg Saar, Germany
J Immunol 188:1098-107. 2012..Our study demonstrated that TLR2 is a primary receptor for Aβ to trigger neuroinflammatory activation and suggested that inhibition of TLR2 in microglia could be beneficial in Alzheimer's disease pathogenesis... - Distinct modulation of microglial amyloid β phagocytosis and migration by neuropeptides (i)Sigal Fleisher-Berkovich
Division of Clinical Neurosciences, Dept of Neurology, University of Bonn Medical Center, Bonn, Germany
J Neuroinflammation 7:61. 2010..These results suggest that neuropeptides play an important role in chemotaxis and Aβ clearance and modulate the brain's response to neuroinflammatory processes... - Loss of gamma-secretase function impairs endocytosis of lipoprotein particles and membrane cholesterol homeostasisIrfan Y Tamboli
Department of Neurology, University of Bonn, 53127 Bonn, Germany
J Neurosci 28:12097-106. 2008..Thus, these data demonstrate a functional link between two major genetic factors that cause early-onset and late-onset Alzheimer's disease... - Neuroglia in neurodegenerationMichael T Heneka
Klinische Neurowissenschaften, Klinik und Poliklinik fur Neurologie, 53127 Bonn, Germany
Brain Res Rev 63:189-211. 2010..The complex of recently acquired knowledge allows us to regard the neurodegenerative diseases as primarily gliodegenerative processes, in which glial cells determine the progression and outcome of neuropathological process... - Selective loss of noradrenaline exacerbates early cognitive dysfunction and synaptic deficits in APP/PS1 miceThea Hammerschmidt
Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
Biol Psychiatry 73:454-63. 2013..Because the LC contains multiple neuromodulators known to affect amyloid β toxicity and cognitive function, the specific role of noradrenaline (NA) in AD is not well understood... - Mrp14 deficiency ameliorates amyloid β burden by increasing microglial phagocytosis and modulation of amyloid precursor protein processingMarkus P Kummer
Clinical Neurosciences Unit, Department of Neurology, University of Bonn, 53105 Bonn, Germany
J Neurosci 32:17824-9. 2012..We therefore conclude that Mrp14 promotes APP processing and Aβ accumulation under neuroinflammatory conditions... - Opposing roles for CXCR3 signaling in central nervous system versus ocular inflammation mediated by the astrocyte-targeted production of IL-12Marius Krauthausen
Department of Neurology, Universitatsklinikum Bonn, Bonn, Germany
Am J Pathol 179:2346-59. 2011..We conclude that the function of CXCR3 in cellular immune disease is driven by a common trigger and is controlled by tissue-specific factors... - Impact and Therapeutic Potential of PPARs in Alzheimer's DiseaseMichael T Heneka
University of Bonn, Department of Neurology, Clinical Neurosciences Unit, Bonn, Germany
Curr Neuropharmacol 9:643-50. 2011..Several clinical trials already revealed promising results using PPARγ agonists, therefore PPARγ represents an attractive therapeutic target for the treatment of AD... - Induction of apoptosis in human and rat glioma by agonists of the nuclear receptor PPARgammaThomas Zander
Department of Neurology, University Bonn, Germany
J Neurochem 81:1052-60. 2002..Taken together, treatment of glioma cells with PPARgamma agonists may hold therapeutic potential for the treatment of gliomas... - Restraint stress increases neuroinflammation independently of amyloid β levels in amyloid precursor protein/PS1 transgenic miceBeatriz G Perez Nievas
Department of Neurology, Clinical Neuroscience Unit, University of Bonn Medical Center, Bonn, Germany
J Neurochem 116:43-52. 2011..Since inflammation may act as a factor that contributes disease progression, the stress-inflammation relation described here may be relevant to understand the initial mechanisms in underlying the risk enhancing action of stress on AD... - Clinical symptoms and risk factors in cerebral microangiopathy patientsSandra Okroglic
Department of Neurology, Clinical Neuroscience Unit, University of Bonn, Bonn, Germany
PLoS ONE 8:e53455. 2013..Hence, patterns of association among lesion topography and severity, clinical symptoms and demographic and disease risk factors were investigated retrospectively in a cohort of CM patients... - Glucose metabolism, gray matter structure, and memory decline in subjective memory impairmentLukas Scheef
Department of Radiology, University of Bonn, Bonn, Germany
Neurology 79:1332-9. 2012..To identify biological evidence for Alzheimer disease (AD) in individuals with subjective memory impairment (SMI) and unimpaired cognitive performance and to investigate the longitudinal cognitive course in these subjects... - Imaging microglial activation and glucose consumption in a mouse model of Alzheimer's diseaseSara Rapic
European Institute for Molecular Imaging, Westfalian Wilhelms University Munster, Munster, Germany
Neurobiol Aging 34:351-4. 2013.... - Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndromeChristof Thees
Department of Anaesthesiology and Intensive Care Medicine, University of Bonn, 53105 Bonn, Germany
Crit Care 11:R123. 2007..We hypothesized that cerebral haemodynamics and carbon dioxide reactivity would be impaired in patients with sepsis syndrome and pathological electroencephalogram patterns... - PPARs in Alzheimer's DiseaseMarkus P Kummer
Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
PPAR Res 2008:403896. 2008..Several clinical trials already revealed promising results using PPAR agonists, therefore PPARs represent an attractive therapeutic target for the treatment of AD... - Protection by pioglitazone in the MPTP model of Parkinson's disease correlates with I kappa B alpha induction and block of NF kappa B and iNOS activationThomas Dehmer
Neurodegeneration Laboratory, Center of Neurology and Hertie Institute for Clinical Brain Research, , , Germany
J Neurochem 88:494-501. 2004..In conclusion, treatment with pioglitazone may offer a treatment opportunity in PD to slow the progression of disease that is mediated by inflammation... - Noradrenaline deficiency in brain increases beta-amyloid plaque burden in an animal model of Alzheimer's diseaseSergey Kalinin
Department of Anesthesiology, University of Illinois, and Jesse Brown Veteran s Affairs Research Division, Chicago, IL 60612, United States
Neurobiol Aging 28:1206-14. 2007..These findings suggest that noradrenergic innervation from LC are needed to maintain adequate Abeta clearance, and therefore that LC degeneration could contribute to AD pathogenesis... - Peroxisome proliferator-activated receptor-gamma agonists prevent experimental autoimmune encephalomyelitisDouglas L Feinstein
Department of Anesthesiology, University of Illinois, 11819 West Polk Street, MC519, Chicago, IL 60612, USA
Ann Neurol 51:694-702. 2002..Pioglitazone also reduced the antigen-dependent interferon-gamma production from EAE-derived T cells. These results suggest that orally administered PPARgamma agonists could provide therapeutic benefit in demyelinating disease... - Inhibition of in vivo glioma growth and invasion by peroxisome proliferator-activated receptor gamma agonist treatmentChristian Grommes
Department of Neurosciences, Alzheimer Research Laboratory, Case Western Reserve University, Cleveland, Ohio, USA
Mol Pharmacol 70:1524-33. 2006..Together, these data indicate that pioglitazone may be of potential use in treatment of malignant gliomas... - Beta-amyloid peptides decrease soluble guanylyl cyclase expression in astroglial cellsMaria Antonia Baltrons
Instituto de Biotecnología y Biomedicina V Villar Palasi, Departamento de Bioquímica Biologia Molecular, Universidad Autonoma de Barcelona, 08193, Bellaterra, Spain
Neurobiol Dis 10:139-49. 2002..A loss of sGC in reactive astrocytes surrounding beta-amyloid plaques could be a mechanism to prevent excess signalling via cGMP at sites of high NO production... - Noradrenergic regulation of inflammatory gene expression in brainDouglas L Feinstein
Department of Anesthesiology, University of Illinois, Chicago, IL, USA
Neurochem Int 41:357-65. 2002.... - Intrinsic regulation of brain inflammatory responsesElena Galea
Department of Anesthesiology, University of Illinois, Chicago, Illinois, USA
Cell Mol Neurobiol 23:625-35. 2003.... - Multitracer positron emission tomographic imaging of exogenous gene expression mediated by a universal herpes simplex virus 1 amplicon vectorChristiane Kummer
Laboratory for Gene Therapy and Molecualr Imaging, Max Planck Institute for Neurological Research, Center for Molecualr Medicine, and Department of Neurology, University of Cologne, Cologne, Germany
Mol Imaging 6:181-92. 2007..The d2r80A in combination with a specific binding compound passing the intact blood-brain barrier might be an alternative marker gene for the noninvasive assessment of vector-mediated gene expression in the brain using PET... - Interleukin-1 beta and lipopolysaccharide decrease soluble guanylyl cyclase in brain cells: NO-independent destabilization of protein and NO-dependent decrease of mRNACarlos E Pedraza
Institute of Biotechnology and Biomedicine V Villar Palasi, and Department of Biochemistry and Molecular Biology, Autonomous University of Barcelona, 08193 Bellaterra, Spain
J Neuroimmunol 144:80-90. 2003..Additionally, both agents induce a NO-dependent decrease of sGC subunit mRNA. Decreased sGC subunit protein and mRNA levels are also observed in adult rat brain after focal injection of IL-1beta or LPS... - Suppressive effects of ansamycins on inducible nitric oxide synthase expression and the development of experimental autoimmune encephalomyelitisPatricia Murphy
Department of Anesthesiology, University of Illinois, 1819 West Polk Street, Chicago, IL 60612, USA
J Neurosci Res 67:461-70. 2002..These results indicate that ansamycins can exert potent anti-inflammatory effects on brain glial cells which may provide therapeutic benefit in neuroinflammatory diseases... - The nonthiazolidinedione tyrosine-based peroxisome proliferator-activated receptor gamma ligand GW7845 induces apoptosis and limits migration and invasion of rat and human glioma cellsChristian Grommes
Department of Neurosciences, Alzheimer Research Laboratory, Case Western Reserve University, Cleveland, Ohio, USA
J Pharmacol Exp Ther 313:806-13. 2005..There was also a reduction of migration and invasion, assessed by Boyden chamber and spheroid experiments. Together, these data indicate that the PPARgamma agonist GW7845 may be of potential use in treatment of malignant gliomas... - Imaging-guided gene therapy of experimental gliomasAndreas H Jacobs
Laboratory for Gene Therapy and Molecular Imaging at the Max Planck Institute for Neurological Research, University of Cologne, Gleuelerstrasse 50, 50931 Cologne, Germany
Cancer Res 67:1706-15. 2007..This strategy will help in the development of safe and efficient gene therapy protocols for clinical application... - Norepinephrine increases I kappa B alpha expression in astrocytesVitaliy Gavrilyuk
Department of Anesthesiology, University of Illinois at Chicago, Chicago, Illinois 60612, USA
J Biol Chem 277:29662-8. 2002..These results demonstrate that I kappa B alpha expression is regulated by NE at both transcriptional and post-transcriptional levels, which could contribute to the observed anti-inflammatory properties of NE in vitro and in vivo...