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  1. Article ; Online: Optogenetic strategies for high-efficiency all-optical interrogation using blue-light-sensitive opsins.

    Forli, Angelo / Pisoni, Matteo / Printz, Yoav / Yizhar, Ofer / Fellin, Tommaso

    eLife

    2021  Volume 10

    Abstract: All-optical methods for imaging and manipulating brain networks with high spatial resolution are fundamental to study how neuronal ensembles drive behavior. Stimulation of neuronal ensembles using two-photon holographic techniques requires high- ... ...

    Abstract All-optical methods for imaging and manipulating brain networks with high spatial resolution are fundamental to study how neuronal ensembles drive behavior. Stimulation of neuronal ensembles using two-photon holographic techniques requires high-sensitivity actuators to avoid photodamage and heating. Moreover, two-photon-excitable opsins should be insensitive to light at wavelengths used for imaging. To achieve this goal, we developed a novel soma-targeted variant of the large-conductance blue-light-sensitive opsin CoChR (stCoChR). In the mouse cortex in vivo, we combined holographic two-photon stimulation of stCoChR with an amplified laser tuned at the opsin absorption peak and two-photon imaging of the red-shifted indicator jRCaMP1a. Compared to previously characterized blue-light-sensitive soma-targeted opsins in vivo, stCoChR allowed neuronal stimulation with more than 10-fold lower average power and no spectral crosstalk. The combination of stCoChR, tuned amplified laser stimulation, and red-shifted functional indicators promises to be a powerful tool for large-scale interrogation of neural networks in the intact brain.
    MeSH term(s) Animals ; Cerebral Cortex/cytology ; Cerebral Cortex/metabolism ; Cerebral Cortex/radiation effects ; Light ; Mice ; Neurons/radiation effects ; Opsins/metabolism ; Optogenetics ; Photons
    Chemical Substances Opsins
    Language English
    Publishing date 2021-05-25
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.63359
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Role of Female Sex Hormones in ADPKD Progression and a Personalized Approach to Contraception and Hormonal Therapy.

    Petrone, Micaela / Catania, Martina / De Rosa, Liliana Italia / Degliuomini, Rebecca S / Kola, Kristiana / Lupi, Chiara / Brambilla Pisoni, Matteo / Salvatore, Stefano / Candiani, Massimo / Vezzoli, Giuseppe / Sciarrone Alibrandi, Maria Teresa

    Journal of clinical medicine

    2024  Volume 13, Issue 5

    Abstract: This review navigates the intricate relationship between gender, hormonal influences, and the progression of autosomal dominant polycystic kidney disease (ADPKD), highlighting the limited literature on this crucial topic. The study explores the impact of ...

    Abstract This review navigates the intricate relationship between gender, hormonal influences, and the progression of autosomal dominant polycystic kidney disease (ADPKD), highlighting the limited literature on this crucial topic. The study explores the impact of female sex hormones on liver and renal manifestations, uncovering gender-specific differences in disease progression. Actually, hormonal therapy in women with ADPKD remains a challenging issue and is a source of concern regarding its potential impact on disease outcomes, particularly at the hepatic level. Notably, women with ADPKD exhibit a slower renal disease progression compared to men, attributed to hormonal dynamics. This review sheds light on the role of estrogen in regulating pathways of the renin-angiotensin-aldosterone system, revealing its complex interplay and implications for cardiovascular and renal health. Therapeutic considerations for fertile women with ADPKD, including contraception options, are discussed, emphasizing the necessity for personalized approaches. In the postmenopausal phase, the review evaluates the role of hormonal replacement therapy, considering its potential benefits and risks in the context of ADPKD. The review concludes by underscoring the imperative need for tailored treatment approaches for ADPKD patients, considering individual risks and benefits. The scarcity of literature underlines the call for further research to enhance our understanding of optimal hormonal therapies in the context of ADPKD, ultimately paving the way for innovative and personalized therapeutic interventions.
    Language English
    Publishing date 2024-02-22
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2662592-1
    ISSN 2077-0383
    ISSN 2077-0383
    DOI 10.3390/jcm13051257
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Early IGF-1 receptor inhibition in mice mimics preterm human brain disorders and reveals a therapeutic target.

    Potenzieri, Alberto / Uccella, Sara / Preiti, Deborah / Pisoni, Matteo / Rosati, Silvia / Lavarello, Chiara / Bartolucci, Martina / Debellis, Doriana / Catalano, Federico / Petretto, Andrea / Nobili, Lino / Fellin, Tommaso / Tucci, Valter / Ramenghi, Luca A / Savardi, Annalisa / Cancedda, Laura

    Science advances

    2024  Volume 10, Issue 9, Page(s) eadk8123

    Abstract: Besides recent advances in neonatal care, preterm newborns still develop sex-biased behavioral alterations. Preterms fail to receive placental insulin-like growth factor-1 (IGF-1), a major fetal growth hormone in utero, and low IGF-1 serum levels ... ...

    Abstract Besides recent advances in neonatal care, preterm newborns still develop sex-biased behavioral alterations. Preterms fail to receive placental insulin-like growth factor-1 (IGF-1), a major fetal growth hormone in utero, and low IGF-1 serum levels correlate with preterm poor neurodevelopmental outcomes. Here, we mimicked IGF-1 deficiency of preterm newborns in mice by perinatal administration of an IGF-1 receptor antagonist. This resulted in sex-biased brain microstructural, functional, and behavioral alterations, resembling those of ex-preterm children, which we characterized performing parallel mouse/human behavioral tests. Pharmacological enhancement of GABAergic tonic inhibition by the U.S. Food and Drug Administration-approved drug ganaxolone rescued functional/behavioral alterations in mice. Establishing an unprecedented mouse model of prematurity, our work dissects the mechanisms at the core of abnormal behaviors and identifies a readily translatable therapeutic strategy for preterm brain disorders.
    MeSH term(s) United States ; Child ; Humans ; Infant, Newborn ; Pregnancy ; Female ; Animals ; Mice ; Insulin-Like Growth Factor I ; Receptor, IGF Type 1 ; Placenta ; Infant, Premature ; Brain Diseases/drug therapy
    Chemical Substances Insulin-Like Growth Factor I (67763-96-6) ; Receptor, IGF Type 1 (EC 2.7.10.1)
    Language English
    Publishing date 2024-03-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adk8123
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Rational design of a mutation to investigate the role of the brain protein TRIP8b in limiting the cAMP response of HCN channels in neurons.

    Porro, Alessandro / Binda, Anna / Pisoni, Matteo / Donadoni, Chiara / Rivolta, Ilaria / Saponaro, Andrea

    The Journal of general physiology

    2020  Volume 152, Issue 9

    Abstract: TRIP8b (tetratricopeptide repeat-containing Rab8b-interacting protein) is the neuronal regulatory subunit of HCN channels, a family of voltage-dependent cation channels also modulated by direct cAMP binding. TRIP8b interacts with the C-terminal region of ...

    Abstract TRIP8b (tetratricopeptide repeat-containing Rab8b-interacting protein) is the neuronal regulatory subunit of HCN channels, a family of voltage-dependent cation channels also modulated by direct cAMP binding. TRIP8b interacts with the C-terminal region of HCN channels and controls both channel trafficking and gating. The association of HCN channels with TRIP8b is required for the correct expression and subcellular targeting of the channel protein in vivo. TRIP8b controls HCN gating by interacting with the cyclic nucleotide-binding domain (CNBD) and competing for cAMP binding. Detailed structural knowledge of the complex between TRIP8b and CNBD was used as a starting point to engineer a mutant channel, whose gating is controlled by cAMP, but not by TRIP8b, while leaving TRIP8b-dependent regulation of channel trafficking unaltered. We found two-point mutations (N/A and C/D) in the loop connecting the CNBD to the C-linker (N-bundle loop) that, when combined, strongly reduce the binding of TRIP8b to CNBD, leaving cAMP affinity unaltered both in isolated CNBD and in the full-length protein. Proof-of-principle experiments performed in cultured cortical neurons confirm that the mutant channel provides a genetic tool for dissecting the two effects of TRIP8b (gating versus trafficking). This will allow the study of the functional role of the TRIP8b antagonism of cAMP binding, a thus far poorly investigated aspect of HCN physiology in neurons.
    MeSH term(s) Brain/metabolism ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels/metabolism ; Ion Channel Gating ; Mutation ; Neurons/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics
    Chemical Substances Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels ; Receptors, Cytoplasmic and Nuclear
    Language English
    Publishing date 2020-06-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3118-5
    ISSN 1540-7748 ; 0022-1295
    ISSN (online) 1540-7748
    ISSN 0022-1295
    DOI 10.1085/jgp.202012596
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.150: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: [The Management of Patients with Adult Autosomal Dominant Polycystic Kidney Disease (ADPKD) Requires a Multidisciplinary Approach].

    Bucci, Romina / De Rosa, Liliana Italia / Brambilla Pisoni, Matteo / Farinone, Sara / Vespa, Marta / Joli, Giancarlo / Catania, Martina / Kola, Kristiana / Tunesi, Francesca / Brioni, Elena / Carrera, Paola / Mancassola, Giulia / Citterio, Lorena / Manunta, Paolo / Vezzoli, Giuseppe / Sciarrone Alibrandi, Maria Teresa

    Giornale italiano di nefrologia : organo ufficiale della Societa italiana di nefrologia

    2023  Volume 40, Issue 6

    Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic kidney disease. Its main feature is the progressive enlargement of both kidneys with progressive loss of kidney function. ADPKD is the fourth leading cause of terminal renal ... ...

    Abstract Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic kidney disease. Its main feature is the progressive enlargement of both kidneys with progressive loss of kidney function. ADPKD is the fourth leading cause of terminal renal failure in the world. Even today there are still uncertainties and poor information. Patients too often have a renunciatory and passive attitude toward the disease. However, there are currently no internationally accepted clinical practice guidelines, and there are significant regional variations in approaches to the diagnosis, clinical evaluation, prevention, and treatment of ADPKD. Therefore, we believe it is important to point out the conduct of our specialist outpatient clinic for ADPKD, which from the beginning has developed a multidisciplinary approach (nephrologists, geneticists, psychologists, radiologists, nutritionists) to face the disease at 360° and therefore not only from a purely nephrological point of view. Such a strategy not only enables patients to receive a timely and accurate diagnosis of the disease, but also ensures that they will receive a thorough and focused follow-up over time, that can prevent or at least slow down the disease in its evolution providing patients with a serene awareness of their condition as much as possible.
    MeSH term(s) Adult ; Humans ; Polycystic Kidney, Autosomal Dominant/complications ; Polycystic Kidney, Autosomal Dominant/therapy ; Kidney ; Kidney Failure, Chronic/etiology
    Language Italian
    Publishing date 2023-12-22
    Publishing country Italy
    Document type English Abstract ; Journal Article
    ZDB-ID 1237110-5
    ISSN 1724-5990 ; 0393-5590
    ISSN (online) 1724-5990
    ISSN 0393-5590
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4313: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: The HCN domain couples voltage gating and cAMP response in hyperpolarization-activated cyclic nucleotide-gated channels.

    Porro, Alessandro / Saponaro, Andrea / Gasparri, Federica / Bauer, Daniel / Gross, Christine / Pisoni, Matteo / Abbandonato, Gerardo / Hamacher, Kay / Santoro, Bina / Thiel, Gerhard / Moroni, Anna

    eLife

    2019  Volume 8

    Abstract: Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels control spontaneous electrical activity in heart and brain. Binding of cAMP to the cyclic nucleotide-binding domain (CNBD) facilitates channel opening by relieving a tonic inhibition ... ...

    Abstract Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels control spontaneous electrical activity in heart and brain. Binding of cAMP to the cyclic nucleotide-binding domain (CNBD) facilitates channel opening by relieving a tonic inhibition exerted by the CNBD. Despite high resolution structures of the HCN1 channel in the cAMP bound and unbound states, the structural mechanism coupling ligand binding to channel gating is unknown. Here we show that the recently identified helical HCN-domain (HCND) mechanically couples the CNBD and channel voltage sensing domain (VSD), possibly acting as a sliding crank that converts the planar rotational movement of the CNBD into a rotational upward displacement of the VSD. This mode of operation and its impact on channel gating are confirmed by computational and experimental data showing that disruption of critical contacts between the three domains affects cAMP- and voltage-dependent gating in three HCN isoforms.
    MeSH term(s) Binding Sites ; Cyclic AMP/chemistry ; Cyclic AMP/metabolism ; Electrophysiology ; HEK293 Cells/physiology ; Humans ; Hydrophobic and Hydrophilic Interactions ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels/chemistry ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels/genetics ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels/metabolism ; Ion Channel Gating ; Kinetics ; Molecular Dynamics Simulation ; Protein Conformation ; Protein Domains ; Protein Isoforms ; Thermodynamics
    Chemical Substances Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels ; Protein Isoforms ; Cyclic AMP (E0399OZS9N)
    Language English
    Publishing date 2019-11-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.49672
    Database MEDical Literature Analysis and Retrieval System OnLINE

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