Antti-Juhana Mäki

Dr. Antti-Juhana Mäki

Tampere University, Tampere, Pirkanmaa, Finland
orcid

Research Focus & Metrics

Academic Career Length

13Years (2014-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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29 September 2017 in Biomacromolecules
Verified
Journal Article
Closed access
ASAnne Skogberg
Anne Skogberg
AMAntti-Juhana Mäki
Antti-Juhana Mäki
MMMarja Mettänen
Marja Mettänen
PLPanu Lahtinen
Panu Lahtinen
Pasi KallioPasi Kallio
Pasi Kallio

1 December 2015 in Chemical Engineering Science
Verified
Journal Article
Closed access
AMAntti-Juhana Mäki
Antti-Juhana Mäki
MPM. Peltokangas
M. Peltokangas
JKJ. Kreutzer
J. Kreutzer
SAS. Auvinen
S. Auvinen
Pasi KallioPasi Kallio
Pasi Kallio

1 March 2017 in Journal of Neuroscience Methods
Verified
Journal Article
Closed access
JKJoose Kreutzer
Joose Kreutzer
LYLaura Ylä-Outinen
Laura Ylä-Outinen
AMAntti-Juhana Mäki
Antti-Juhana Mäki
MRMervi Ristola
Mervi Ristola
SNSusanna Narkilahti
Susanna Narkilahti
Pasi KallioPasi Kallio
Pasi Kallio

8 October 2014 in Journal of Fluids Engineering
Verified
Journal Article
Closed access
PDF file
AMAntti-Juhana Mäki
Antti-Juhana Mäki
SHSamu Hemmilä
Samu Hemmilä
JHJuha Hirvonen
Juha Hirvonen
NGNathaniel Narra Girish
Nathaniel Narra Girish
JKJoose Kreutzer
Joose Kreutzer
Pasi KallioPasi Kallio
Pasi Kallio
Passive pumping using gravity-driven flow is a fascinating approach for microfluidic systems. When designing a passive pumping system, generated flow rates should be known precisely. While reported models used to estimate the flow rates do not usually consider capillary forces, this paper shows that their exclusion is unrealistic in typical gravity-driven systems. Therefore, we propose a new analytical model to estimate the generated flow rates. An extensive set of measurements is used to verify that the proposed model provides a remarkably more precise approximation of the real flow rates compared to the previous models. It is suggested that the developed model should be used when designing a gravity-driven pumping system.

30 November 2021 in Nanoscale
Verified
Journal Article
Open access
PDF file
ASAnne Skogberg
Anne Skogberg
SSSanna Siljander
Sanna Siljander
AMAntti-Juhana Mäki
Antti-Juhana Mäki
MHMari Honkanen
Mari Honkanen
AEAlexander Efimov
Alexander Efimov
Pasi KallioPasi Kallio
Pasi Kallio
C-CNFs were used as an aid to disperse CNTs, and additional c-CNFs guided the self-assembly between nanocomponents resulting in a nanocomposite film with anisotropic properties.

19 March 2022 in Cells
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Journal Article
Open access
PDF file
MAHMOUD GABALLAMAHMOUD GABALLA
MAHMOUD GABALLA
KPKirsi Penttinen
Kirsi Penttinen
JKJoose Kreutzer
Joose Kreutzer
AMAntti-Juhana Mäki
Antti-Juhana Mäki
Pasi KallioPasi Kallio
Pasi Kallio
KAKatriina Aalto-Setala
Katriina Aalto-Setala
Ischemic heart disease (IHD) is one of the leading causes of mortality worldwide. Preserving functionality and preventing arrhythmias of the heart are key principles in the management of patients with IHD. Levosimendan, a unique calcium (Ca2+) enhancer with inotropic activity, has been introduced into clinical usage for heart failure treatment. Human-induced pluripotent cell-derived cardiomyocytes (hiPSC-CMs) offer an opportunity to better understand the pathophysiological mechanisms of the disease as well as to serve as a platform for drug screening. Here, we developed an in vitro IHD model using hiPSC-CMs in hypoxic conditions and defined the effects of the subsequent hypoxic stress on CMs functionality. Furthermore, the effect of levosimendan on hiPSC-CMs functionality was evaluated during and after hypoxic stress. The morphology, contractile, Ca2+-handling, and gene expression properties of hiPSC-CMs were investigated in response to hypoxia. Hypoxia resulted in significant cardiac arrhythmia and decreased Ca2+ transient amplitude. In addition, disorganization of sarcomere structure was observed after hypoxia induction. Interestingly, levosimendan presented significant antiarrhythmic properties, as the arrhythmia was abolished or markedly reduced with levosimendan treatment either during or after the hypoxic stress. Moreover, levosimendan presented significant protection from the sarcomere alterations induced by hypoxia. In conclusion, this chip model appears to be a suitable preclinical representation of IHD. With this hypoxia platform, detailed knowledge of the disease pathophysiology can be obtained. The antiarrhythmic effect of levosimendan was clearly observed, suggesting a possible new clinical use for the drug.