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  1. Article ; Online: Unicompartmental knee arthroplasty vs. high tibial osteotomy for medial knee osteoarthritis (UNIKORN): a study protocol of a randomized controlled trial.

    Siren, Juuso / Rämö, Lasse / Rantasalo, Mikko / Komulainen, Olli / Skants, Noora / Reito, Aleksi / Kosola, Jussi / Lindahl, Jan

    Trials

    2023  Volume 24, Issue 1, Page(s) 256

    Abstract: Background: Medial knee osteoarthritis (OA) is a common health problem resulting in knee pain and limiting patients' physical activity. After failed conservative treatment, unicompartmental knee arthroplasty (UKA) and high tibial osteotomy (HTO) are ... ...

    Abstract Background: Medial knee osteoarthritis (OA) is a common health problem resulting in knee pain and limiting patients' physical activity. After failed conservative treatment, unicompartmental knee arthroplasty (UKA) and high tibial osteotomy (HTO) are possible surgical treatment options for this condition. There is a paucity of high-quality evidence in the literature comparing objective and subjective outcomes of these procedures. Also, there is no common agreement on whether these procedures provide comparable results in late-stage medial knee OA patients.
    Methods: We will perform a prospective randomized controlled trial comparing HTO and UKA in patients with late-stage medial knee OA. 100 patients with isolated medial knee OA (KL III-IV) are assigned to either UKA (n = 50) or HTO (n = 50) procedure in patients 45-65 years of age. Our primary outcome will be KOOS
    Ethics and dissemination: The institutional review board of the Helsinki and Uusimaa Hospital District has approved the protocol. We will disseminate the findings through peer-reviewed publications.
    Trial registration: ClinicalTrials.gov/TooloH NCT05442242. Registered on 7/1/2022.
    MeSH term(s) Humans ; Arthroplasty, Replacement, Knee/adverse effects ; Arthroplasty, Replacement, Knee/methods ; Osteoarthritis, Knee/diagnostic imaging ; Osteoarthritis, Knee/surgery ; Prospective Studies ; Treatment Outcome ; Knee Joint/diagnostic imaging ; Knee Joint/surgery ; Osteotomy/adverse effects ; Osteotomy/methods ; Pain/etiology ; Retrospective Studies ; Randomized Controlled Trials as Topic
    Language English
    Publishing date 2023-04-05
    Publishing country England
    Document type Clinical Trial Protocol ; Journal Article
    ZDB-ID 2040523-6
    ISSN 1745-6215 ; 1468-6694 ; 1745-6215
    ISSN (online) 1745-6215
    ISSN 1468-6694 ; 1745-6215
    DOI 10.1186/s13063-023-07263-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Deficiency of heme oxygenase 1a causes detrimental effects on cardiac function.

    Wang, Hong / Siren, Juuso / Perttunen, Sanni / Immonen, Katariina / Chen, Yu-Chia / Narumanchi, Suneeta / Kosonen, Riikka / Paavola, Jere / Laine, Mika / Tikkanen, Ilkka / Lakkisto, Päivi

    Journal of cellular and molecular medicine

    2024  Volume 28, Issue 7, Page(s) e18243

    Abstract: Humans lacking heme oxygenase 1 (HMOX1) display growth retardation, haemolytic anaemia, and vulnerability to stress; however, cardiac function remains unclear. We aimed to explore the cardiac function of zebrafish lacking hmox1a at baseline and in ... ...

    Abstract Humans lacking heme oxygenase 1 (HMOX1) display growth retardation, haemolytic anaemia, and vulnerability to stress; however, cardiac function remains unclear. We aimed to explore the cardiac function of zebrafish lacking hmox1a at baseline and in response to stress. We generated zebrafish hmox1a mutants using CRISPR/Cas9 genome editing technology. Deletion of hmox1a increases cardiac output and further induces hypertrophy in adults. Adults lacking hmox1a develop myocardial interstitial fibrosis, restrain cardiomyocyte proliferation and downregulate renal haemoglobin and cardiac antioxidative genes. Larvae lacking hmox1a fail to respond to hypoxia, whereas adults are insensitive to isoproterenol stimulation in the heart, suggesting that hmox1a is necessary for cardiac response to stress. Haplodeficiency of hmox1a stimulates non-mitochondrial respiration and cardiac cell proliferation, increases cardiac output in larvae in response to hypoxia, and deteriorates cardiac function and structure in adults upon isoproterenol treatment. Intriguingly, haplodeficiency of hmox1a upregulates cardiac hmox1a and hmox1b in response to isoproterenol. Collectively, deletion of hmox1a results in cardiac remodelling and abrogates cardiac response to hypoxia and isoproterenol. Haplodeficiency of hmox1a aggravates cardiac response to the stress, which could be associated with the upregulation of hmox1a and hmox1b. Our data suggests that HMOX1 homeostasis is essential for maintaining cardiac function and promoting cardioprotective effects.
    MeSH term(s) Animals ; Humans ; Heme Oxygenase (Decyclizing) ; Zebrafish/genetics ; Isoproterenol/pharmacology ; Heme Oxygenase-1/genetics ; Myocardium ; Cardiomyopathies ; Hypoxia ; Myocytes, Cardiac
    Chemical Substances Heme Oxygenase (Decyclizing) (EC 1.14.14.18) ; Isoproterenol (L628TT009W) ; Heme Oxygenase-1 (EC 1.14.14.18)
    Language English
    Publishing date 2024-03-20
    Publishing country England
    Document type Journal Article
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.18243
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5752: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  3. Article ; Online: Tankyrase Inhibition Attenuates Cardiac Dilatation and Dysfunction in Ischemic Heart Failure.

    Wang, Hong / Segersvärd, Heli / Siren, Juuso / Perttunen, Sanni / Immonen, Katariina / Kosonen, Riikka / Chen, Yu-Chia / Tolva, Johanna / Laivuori, Mirjami / Mäyränpää, Mikko I / Kovanen, Petri T / Sinisalo, Juha / Laine, Mika / Tikkanen, Ilkka / Lakkisto, Päivi

    International journal of molecular sciences

    2022  Volume 23, Issue 17

    Abstract: Hyperactive poly(ADP-ribose) polymerases (PARP) promote ischemic heart failure (IHF) after myocardial infarction (MI). However, the role of tankyrases (TNKSs), members of the PARP family, in pathogenesis of IHF remains unknown. We investigated the ... ...

    Abstract Hyperactive poly(ADP-ribose) polymerases (PARP) promote ischemic heart failure (IHF) after myocardial infarction (MI). However, the role of tankyrases (TNKSs), members of the PARP family, in pathogenesis of IHF remains unknown. We investigated the expression and activation of TNKSs in myocardium of IHF patients and MI rats. We explored the cardioprotective effect of TNKS inhibition in an isoproterenol-induced zebrafish HF model. In IHF patients, we observed elevated TNKS2 and DICER and concomitant upregulation of miR-34a-5p and miR-21-5p in non-infarcted myocardium. In a rat MI model, we found augmented TNKS2 and DICER in the border and infarct areas at the early stage of post-MI. We also observed consistently increased TNKS1 in the border and infarct areas and destabilized AXIN in the infarct area from 4 weeks onward, which in turn triggered Wnt/β-catenin signaling. In an isoproterenol-induced HF zebrafish model, inhibition of TNKS activity with XAV939, a TNKSs-specific inhibitor, protected against ventricular dilatation and cardiac dysfunction and abrogated overactivation of Wnt/β-catenin signaling and dysregulation of miR-34a-5p induced by isoproterenol. Our study unravels a potential role of TNKSs in the pathogenesis of IHF by regulating Wnt/β-catenin signaling and possibly modulating miRNAs and highlights the pharmacotherapeutic potential of TNKS inhibition for prevention of IHF.
    MeSH term(s) Animals ; Dilatation ; Heart Failure/drug therapy ; Isoproterenol/pharmacology ; MicroRNAs/genetics ; Rats ; Tankyrases/antagonists & inhibitors ; Tankyrases/metabolism ; Wnt Signaling Pathway ; Zebrafish/metabolism ; beta Catenin/metabolism
    Chemical Substances MIRN21 microRNA, zebrafish ; MicroRNAs ; beta Catenin ; mirn21 microRNA, rat ; Tankyrases (EC 2.4.2.30) ; Isoproterenol (L628TT009W)
    Language English
    Publishing date 2022-09-02
    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/ijms231710059
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  4. Article ; Online: PLASMA HEME OXYGENASE-1 IN PATIENTS RESUSCITATED FROM OUT-OF-HOSPITAL CARDIAC ARREST.

    Siren, Juuso / Vaahersalo, Jukka / Skrifvars, Markus / Pettilä, Ville / Tiainen, Marjaana / Tikkanen, Ilkka / Lakkisto, Päivi

    Shock (Augusta, Ga.)

    2016  Volume 45, Issue 3, Page(s) 320–325

    Abstract: Heme oxygenase-1 (HO-1) is an enzyme induced by hypoxia and reperfusion injury, and is associated with organ dysfunction in critically ill patients. Patients resuscitated from out-of-hospital cardiac arrest (OHCA) are subjected to hypoxemia, brain injury, ...

    Abstract Heme oxygenase-1 (HO-1) is an enzyme induced by hypoxia and reperfusion injury, and is associated with organ dysfunction in critically ill patients. Patients resuscitated from out-of-hospital cardiac arrest (OHCA) are subjected to hypoxemia, brain injury, and organ dysfunction. Accordingly, we studied HO-1 among these patients. A total of 143 OHCA patients resuscitated from a shockable initial rhythm and admitted to an ICU were included, with plasma HO-1 measured at ICU admission and at 24 h. We analyzed the associations between plasma HO-1 and time to return of spontaneous circulation (ROSC), 90-day mortality, and 12-month Cerebral Performance Category (CPC). HO-1 plasma concentrations were higher after OHCA compared with controls. HO-1 concentrations at admission and on day 1 associated with ROSC (P = 0.002 to P = 0.003). Admission and day 1 HO-1 plasma concentrations were higher in 90-day non-survivors than in survivors (P = 0.017, 0.026). In addition, poor neurological outcome (CPC 3-5) was associated with higher HO-1 plasma levels at admission (P = 0.024). Admission plasma HO-1 levels had an AUC of 0.623 to predict 90-day mortality and an AUC of 0.611 to predict CPC 3 to 5. In conclusion, we found that higher HO-1 plasma levels are associated with longer ROSC and poor long-term outcome.
    MeSH term(s) Brain Injuries/blood ; Brain Injuries/etiology ; Brain Injuries/mortality ; Disease-Free Survival ; Heme Oxygenase-1/blood ; Hypoxia/blood ; Hypoxia/etiology ; Hypoxia/mortality ; Hypoxia/therapy ; Multiple Organ Failure/blood ; Multiple Organ Failure/etiology ; Multiple Organ Failure/mortality ; Out-of-Hospital Cardiac Arrest/blood ; Out-of-Hospital Cardiac Arrest/complications ; Out-of-Hospital Cardiac Arrest/mortality ; Out-of-Hospital Cardiac Arrest/therapy ; Resuscitation ; Survival Rate ; Time Factors
    Chemical Substances HMOX1 protein, human (EC 1.14.14.18) ; Heme Oxygenase-1 (EC 1.14.14.18)
    Language English
    Publishing date 2016-03
    Publishing country United States
    Document type Clinical Trial ; Journal Article ; Multicenter Study ; Observational Study
    ZDB-ID 1185432-7
    ISSN 1540-0514 ; 1073-2322
    ISSN (online) 1540-0514
    ISSN 1073-2322
    DOI 10.1097/SHK.0000000000000521
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3985: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  5. Article ; Online: Carbon monoxide releasing molecule improves structural and functional cardiac recovery after myocardial injury.

    Segersvärd, Heli / Lakkisto, Päivi / Hänninen, Mikko / Forsten, Hanna / Siren, Juuso / Immonen, Katariina / Kosonen, Riikka / Sarparanta, Mirkka / Laine, Mika / Tikkanen, Ilkka

    European journal of pharmacology

    2018  Volume 818, Page(s) 57–66

    Abstract: Carbon monoxide (CO), produced by heme oxygenase-1 (HO-1), is an endogenous paracrine factor involved in the regulation of cardiovascular structure and function. We studied the effects of a synthetic CO releasing molecule (CORM-3) on cardiac recovery and ...

    Abstract Carbon monoxide (CO), produced by heme oxygenase-1 (HO-1), is an endogenous paracrine factor involved in the regulation of cardiovascular structure and function. We studied the effects of a synthetic CO releasing molecule (CORM-3) on cardiac recovery and myocardial microRNA expression after myocardial infarction (MI). Male Wistar rats with MI (n = 75) or sham-operated controls (n = 75) were treated from day 4 to day 14 after MI either with synthetic CORM-3 or with inactive iCORM and killed 2, 4 or 8 weeks post-MI. Infarct size, vascular and capillary densities, the amount of cardiomyocytes in the infarct area, and cardiomyocyte proliferation and apoptosis were determined. PCR was used for microRNA and mRNA quantification, western blotting to evaluate protein expression and echocardiography to assess cardiac structure and function. CORM-3 treatment increased vascular density (P< 0.05 vs. iCORM) and the proportion of cardiomyocytes (P< 0.05 vs. iCORM) in the infarct area. Ejection fraction improved (P< 0.05) and left ventricular volumes decreased (P< 0.05) in CORM-3 treated MI groups compared to iCORM treatment. CORM-3 treatment decreased the amount of proliferating Ki67 positive cardiomyocytes in the infarct/border area at week 2 after MI compared to iCORM treatment, whereas the amount of apoptotic cardiomyocytes did not differ between CORM-3 and iCORM groups. Compared to iCORM treatment, CORM-3 decreased expression on miR-206 in the remote area at week 2 after MI. The CO releasing molecule CORM-3 improved structural and functional cardiac recovery after MI. Modulation of HO-1-CO axis may prove novel drug targets to facilitate cardiac recovery after myocardial injury.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Body Weight/drug effects ; Capillaries/drug effects ; Capillaries/metabolism ; Cell Proliferation/drug effects ; Fibrosis ; Heart/drug effects ; Heart/physiopathology ; Heart Injuries/metabolism ; Heart Injuries/pathology ; Heart Injuries/physiopathology ; Male ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/pathology ; Organ Size/drug effects ; Organometallic Compounds/pharmacology ; Rats ; Rats, Wistar ; Recovery of Function/drug effects
    Chemical Substances Organometallic Compounds ; tricarbonylchloro(glycinato)ruthenium(II)
    Language English
    Publishing date 2018-01-05
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 80121-5
    ISSN 1879-0712 ; 0014-2999
    ISSN (online) 1879-0712
    ISSN 0014-2999
    DOI 10.1016/j.ejphar.2017.10.031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 522: Show issues Location:
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  6. Article ; Online: Vezf1 regulates cardiac structure and contractile function.

    Paavola, Jere / Alakoski, Tarja / Ulvila, Johanna / Kilpiö, Teemu / Sirén, Juuso / Perttunen, Sanni / Narumanchi, Suneeta / Wang, Hong / Lin, Ruizhu / Porvari, Katja / Junttila, Juhani / Huikuri, Heikki / Immonen, Katariina / Lakkisto, Päivi / Magga, Johanna / Tikkanen, Ilkka / Kerkelä, Risto

    EBioMedicine

    2020  Volume 51, Page(s) 102608

    Abstract: Background: Vascular endothelial zinc finger 1 (Vezf1) is a transcription factor previously shown to regulate vasculogenesis and angiogenesis. We aimed to investigate the role of Vezf1 in the postnatal heart.: Methods: The role of Vezf1 in regulating ...

    Abstract Background: Vascular endothelial zinc finger 1 (Vezf1) is a transcription factor previously shown to regulate vasculogenesis and angiogenesis. We aimed to investigate the role of Vezf1 in the postnatal heart.
    Methods: The role of Vezf1 in regulating cardiac growth and contractile function was studied in zebrafish and in primary cardiomyocytes.
    Findings: We find that expression of Vezf1 is decreased in diseased human myocardium and mouse hearts. Our experimental data shows that knockdown of zebrafish Vezf1 reduces cardiac growth and results in impaired ventricular contractile response to β-adrenergic stimuli. However, Vezf1 knockdown is not associated with dysregulation of cardiomyocyte Ca
    Interpretation: We demonstrate a role for Vezf1 in regulation of compensatory cardiac growth and cardiomyocyte contractile function, which may be relevant in human cardiac disease.
    MeSH term(s) Adrenergic Agents/pharmacology ; Animals ; Binding Sites ; Cardiomyopathies/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation/drug effects ; Genes, Reporter ; Humans ; Luciferases/metabolism ; Mice, Inbred C57BL ; Myocardial Contraction ; Myocardium/metabolism ; Myocardium/pathology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Myosin Heavy Chains/genetics ; Myosin Heavy Chains/metabolism ; Neovascularization, Physiologic/drug effects ; Promoter Regions, Genetic/genetics ; Protein Binding/drug effects ; Rats, Sprague-Dawley ; Transcription Factors/metabolism ; Zebrafish ; Zebrafish Proteins/metabolism
    Chemical Substances Adrenergic Agents ; DNA-Binding Proteins ; Transcription Factors ; VEZF1 protein, human ; Vezf1 protein, mouse ; Zebrafish Proteins ; vezf1b protein, zebrafish ; Luciferases (EC 1.13.12.-) ; Myosin Heavy Chains (EC 3.6.4.1)
    Language English
    Publishing date 2020-01-03
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2019.102608
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    Zs.A 7090: Show issues Location:
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