update bibliography and formating

_bibliography/papers.bib

@@ -9,6 +9,7 @@ @article{dzyubenko_role_2018
 	volume = {11},
 	issn = {1756-2864, 1756-2864},
 	url = {http://journals.sagepub.com/doi/10.1177/1756286418818092},
+	html = {http://journals.sagepub.com/doi/10.1177/1756286418818092},
 	doi = {10.1177/1756286418818092},
 	abstract = {Neuroinflammation is one of the key components contributing to the devastating outcome of ischemic stroke. Starting with stroke onset, inflammatory processes contribute both to cell damage and tissue remodeling. The early release of alarmins triggers the upregulation of multiple proinflammatory cytokines, resulting in the compromised integrity of the blood–brain barrier. From this moment on, the infiltration of peripheral immune cells, reactive gliosis and extracellular matrix (ECM) alterations become intricately intertwined and act as one unit during the tissue remodeling. While the mechanisms of leukocyte and glia activation are amply reviewed, the field of ECM modification remains as yet under explored. In this review, we focus on the interplay between neuroinflammatory cascades and ECM in the ischemic brain. By summarizing the currently available evidence obtained by in vitro research, animal experimentation and human studies, we aim to propose a new direction for the future investigation of stroke recovery.},
 	language = {en},
@@ -26,6 +27,7 @@ @misc{manrique-castano_dissecting_2023
 	title = {Dissecting glial scar formation by spatial point pattern and topological data analysis},
 	copyright = {© 2023, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution 4.0 International), CC BY 4.0, as described at http://creativecommons.org/licenses/by/4.0/},
 	url = {https://www.biorxiv.org/content/10.1101/2023.10.04.560910v1},
+	html = {https://www.biorxiv.org/content/10.1101/2023.10.04.560910v1},
 	doi = {10.1101/2023.10.04.560910},
 	abstract = {Glial scar formation represents a fundamental response to central nervous system (CNS) injury. It is mainly characterized by a well-defined spatial rearrangement of reactive astrocytes and microglia. The mechanisms underlying glial scar formation have been extensively studied, yet quantitative descriptors of the spatial arrangement of reactive glial cells remain limited. Here, we present a novel approach using point pattern analysis (PPA) and topological data analysis (TDA) to quantify spatial patterns of reactive glial cells after experimental ischemic stroke in mice. We provide open and reproducible tools using R and Julia to quantify spatial intensity, cell covariance and conditional distribution, cell-to-cell interactions, and short/long-scale arrangement, which collectively disentangle the arrangement patterns of the glial scar. This approach unravels a substantial divergence in the distribution of reactive astrocytes and microglia after injury that conventional analysis methods cannot fully characterize. PPA and TDA are valuable tools for studying the complex spatial arrangement of reactive glia and other nervous cells following CNS injuries and have potential applications for evaluating glial-targeted restorative therapies.},
 	language = {en},
@@ -66,6 +68,7 @@ @article{dzyubenko_tenascin-c_2022
 	volume = {110},
 	issn = {0945-053X},
 	url = {https://www.sciencedirect.com/science/article/pii/S0945053X22000555},
+	html = {https://www.sciencedirect.com/science/article/pii/S0945053X22000555},
 	doi = {10.1016/j.matbio.2022.04.003},
 	abstract = {Cellular responses in glia play a key role in regulating brain remodeling post-stroke. However, excessive glial reactivity impedes post-ischemic neuroplasticity and hampers neurological recovery. While damage-associated molecular patterns and activated microglia were shown to induce astrogliosis, the molecules that restrain astrogliosis are largely unknown. We explored the role of tenascin-C (TnC), an extracellular matrix component involved in wound healing and remodeling of injured tissues, in mice exposed to ischemic stroke induced by transient intraluminal middle cerebral artery occlusion. In the healthy adult brain, TnC expression is restricted to neurogenic stem cell niches. We previously reported that TnC is upregulated in ischemic brain lesions. We herein show that the de novo expression of TnC post-stroke is closely associated with reactive astrocytes, and that astrocyte reactivity at 14 days post-ischemia is increased in TnC-deficient mice (TnC−/−). By analyzing the three-dimensional morphology of astrocytes in previously ischemic brain tissue, we revealed that TnC−/− reduces astrocytic territorial volume, branching point number, and branch length, which are presumably hallmarks of the homeostatic regulatory astrocyte state, in the post-acute stroke phase after 42 days. Interestingly, TnC−/− moderately increased aggrecan, a neuroplasticity-inhibiting proteoglycan, in the ischemic brain tissue at 42 days post-ischemia. In vitro in astrocyte-microglia cocultures, we showed that TnC−/− reduces the microglial migration speed on astrocytes and elevates intercellular adhesion molecule 1 (ICAM1) expression. Post-stroke, TnC−/− did not alter the ischemic lesion size or neurological recovery, however microglia-associated ICAM1 was upregulated in TnC−/− mice during the first week post stroke. Our data suggest that TnC plays a central role in restraining post-ischemic astrogliosis and regulating astrocyte-microglial interactions.},
 	urldate = {2024-03-01},
@@ -83,13 +86,14 @@ @article{daniel_manrique-castano_neurovascular_2021
 	title = {Neurovascular {Reactivity} in {Tissue} {Scarring} {Following} {Cerebral} {Ischemia}},
 	copyright = {Copyright (c) 2021 Daniel Manrique-Castano, PHD, Ayman ElAli, PHD},
 	url = {https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-neurovascular-reactivity},
+	html = {https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-neurovascular-reactivity},
 	doi = {10.36255/exonpublications.cerebralischemia.2021.neurovascularreactivity},
 	abstract = {ABSTRACT
 Tissue scarring upon cerebral ischemia entails a cascade of multifaceted cellular and molecular mechanisms that govern the remodeling of the neurovascular unit, which integrates neuronal, glial, and vascular functions.\  The process encompasses inflammation, glial reactivity, vascular reactivity, and neuronal remodeling. In this chapter we cover three major aspects involved in tissue scarring after cerebral ischemia. First, we outline the primary cellular mechanisms underlying glial scar formation, emphasizing on the interactions between astrocytes, microglia, and mural cells, including pericytes and fibroblasts at the injury core and perilesional areas. Next, we address the key routes of extracellular matrix deposition by reactive and fibrogenic cells, including proteoglycans, tenascins, fibronectin, and collagen. Finally, we discuss the promises and challenges of manipulating tissue scarring as a strategy to promote brain structural remodeling and neurological recovery.},
 	language = {en},
 	urldate = {2024-03-01},
 	journal = {Exon Publications},
-	author = {Daniel Manrique-Castano, P. H. D. and Ayman ElAli, P. H. D.},
+	author = {Daniel Manrique-Castano, and Ayman ElAli},
 	month = nov,
 	year = {2021},
 	keywords = {brain remodeling, cerebral ischemia, extracellular matrix, fibrotic scar, glial scar},
@@ -104,6 +108,7 @@ @article{lecordier_neurovascular_2021
 	issn = {1663-4365},
 	shorttitle = {Neurovascular {Alterations} in {Vascular} {Dementia}},
 	url = {https://www.frontiersin.org/articles/10.3389/fnagi.2021.727590},
+	html = {https://www.frontiersin.org/articles/10.3389/fnagi.2021.727590},
 	abstract = {Vascular dementia (VaD) constitutes the second most prevalent cause of dementia in the world after Alzheimer’s disease (AD). VaD regroups heterogeneous neurological conditions in which the decline of cognitive functions, including executive functions, is associated with structural and functional alterations in the cerebral vasculature. Among these cerebrovascular disorders, major stroke, and cerebral small vessel disease (cSVD) constitute the major risk factors for VaD. These conditions alter neurovascular functions leading to blood-brain barrier (BBB) deregulation, neurovascular coupling dysfunction, and inflammation. Accumulation of neurovascular impairments over time underlies the cognitive function decline associated with VaD. Furthermore, several vascular risk factors, such as hypertension, obesity, and diabetes have been shown to exacerbate neurovascular impairments and thus increase VaD prevalence. Importantly, air pollution constitutes an underestimated risk factor that triggers vascular dysfunction via inflammation and oxidative stress. The review summarizes the current knowledge related to the pathological mechanisms linking neurovascular impairments associated with stroke, cSVD, and vascular risk factors with a particular emphasis on air pollution, to VaD etiology and progression. Furthermore, the review discusses the major challenges to fully elucidate the pathobiology of VaD, as well as research directions to outline new therapeutic interventions.},
 	urldate = {2024-03-01},
 	journal = {Frontiers in Aging Neuroscience},
@@ -118,6 +123,7 @@ @article{dzyubenko_inhibitory_2021
 	volume = {78},
 	issn = {1420-9071},
 	url = {https://doi.org/10.1007/s00018-021-03861-3},
+	html = {https://doi.org/10.1007/s00018-021-03861-3},
 	doi = {10.1007/s00018-021-03861-3},
 	abstract = {Inhibitory control is essential for the regulation of neuronal network activity, where excitatory and inhibitory synapses can act synergistically, reciprocally, and antagonistically. Sustained excitation-inhibition (E-I) balance, therefore, relies on the orchestrated adjustment of excitatory and inhibitory synaptic strength. While growing evidence indicates that the brain’s extracellular matrix (ECM) is a crucial regulator of excitatory synapse plasticity, it remains unclear whether and how the ECM contributes to inhibitory control in neuronal networks. Here we studied the simultaneous changes in excitatory and inhibitory connectivity after ECM depletion. We demonstrate that the ECM supports the maintenance of E-I balance by retaining inhibitory connectivity. Quantification of synapses and super-resolution microscopy showed that depletion of the ECM in mature neuronal networks preferentially decreases the density of inhibitory synapses and the size of individual inhibitory postsynaptic scaffolds. The reduction of inhibitory synapse density is partially compensated by the homeostatically increasing synaptic strength via the reduction of presynaptic GABAB receptors, as indicated by patch-clamp measurements and GABAB receptor expression quantifications. However, both spiking and bursting activity in neuronal networks is increased after ECM depletion, as indicated by multi-electrode recordings. With computational modelling, we determined that ECM depletion reduces the inhibitory connectivity to an extent that the inhibitory synapse scaling does not fully compensate for the reduced inhibitory synapse density. Our results indicate that the brain’s ECM preserves the balanced state of neuronal networks by supporting inhibitory control via inhibitory synapse stabilization, which expands the current understanding of brain activity regulation.},
 	language = {en},
@@ -138,6 +144,7 @@ @article{manrique-castano_tenascin-c_2021
 	volume = {91},
 	issn = {0889-1591},
 	url = {https://www.sciencedirect.com/science/article/pii/S0889159120323667},
+	html = {https://www.sciencedirect.com/science/article/pii/S0889159120323667},
 	doi = {10.1016/j.bbi.2020.10.016},
 	abstract = {As an endogenous activator of toll-like receptor-4 (Tlr4), the extracellular matrix glycoprotein tenascin-C (TnC) regulates chemotaxis, phagocytosis and proinflammatory cytokine production in microglia. The role of TnC for ischemic brain injury, post-ischemic immune responses and stroke recovery has still not been evaluated. By comparing wild type and TnC−/− mice exposed to transient intraluminal middle cerebral artery occlusion (MCAO), we examined the effects of TnC deficiency for ischemic injury, neurological deficits, microglia/macrophage activation and brain leukocyte infiltration using behavioural tests, histochemical studies, Western blot, polymerase chain reaction and flow cytometry. Histochemical studies revealed that TnC was de novo expressed in the ischemic striatum, which contained the infarct core, and overlapped with the area of strongest accumulation of Iba1 + microglia/macrophages. TnC deficiency increased overall Iba1 immunoreactivity in the perilesional cortex, suggesting that TnC might restrict the distribution of microglial cells to the infarct core. By analysing microglial morphology in 3D we found that the post-ischemic loss of microglial cell territory, branching and volume at 3 and 7 days post-ischemia was amplified in the brains of TnC deficient compared with wild type mice. Microglial cell number was not different between genotypes. Hence, TnC deficiency reduced tissue surveillance by microglial cells. Concomitantly, the number of infiltrating leukocytes and, more specifically, T cells was increased in the ischemic brain parenchyma of TnC deficient compared with wild type mice. Ischemic injury and neurological deficits were not affected by TnC deficiency. We propose that the reduced microglia surveillance in TnC deficient mice might favour leukocyte accumulation in the ischemic brain.},
 	urldate = {2024-03-01},
@@ -149,3 +156,61 @@ @article{manrique-castano_tenascin-c_2021
 	pages = {639--648},
 	pdf = {Tenascin-C preserves microglia surveillance and restricts leukocyte.pdf}
 }
+
+@article{manrique-castano_deactivation_2019,
+  abbr={Front. cell. neurosci},
+	title = {Deactivation of {ATP}-{Binding} {Cassette} {Transporters} {ABCB1} and {ABCC1} {Does} {Not} {Influence} {Post}-ischemic {Neurological} {Deficits}, {Secondary} {Neurodegeneration} and {Neurogenesis}, but {Induces} {Subtle} {Microglial} {Morphological} {Changes}},
+	volume = {13},
+	issn = {1662-5102},
+	url = {https://www.frontiersin.org/articles/10.3389/fncel.2019.00412},
+	html = {https://www.frontiersin.org/articles/10.3389/fncel.2019.00412},
+	abstract = {ATP-binding cassette (ABC) transporters prevent the access of pharmacological compounds to the ischemic brain, thereby impeding the efficacy of stroke therapies. ABC transporters can be deactivated by selective inhibitors, which potently increase the brain accumulation of drugs. Concerns have been raised that long-term ABC transporter deactivation may promote neuronal degeneration and, under conditions of ischemic stroke, compromise neurological recovery. To elucidate this issue, we exposed male C57BL/6 mice to transient intraluminal middle cerebral artery occlusion (MCAO) and examined the effects of the selective ABCB1 inhibitor tariquidar (8 mg/kg/day) or ABCC1 inhibitor MK-571 (10 mg/kg/day), which were administered alone or in combination with each other over up to 28 days, on neurological recovery and brain injury. Mice were sacrificed after 14, 28, or 56 days. The Clark score, RotaRod, tight rope, and open field tests revealed reproducible motor-coordination deficits in mice exposed to intraluminal MCAO, which were not influenced by ABCB1, ABCC1, or combined ABCB1 and ABCC1 deactivation. Brain volume, striatum volume, and corpus callosum thickness were not altered by ABCB1, ABCC1 or ABCB1, and ABCC1 inhibitors. Similarly, neuronal survival and reactive astrogliosis, evaluated by NeuN and GFAP immunohistochemistry in the ischemic striatum, were unchanged. Iba1 immunohistochemistry revealed no changes of the overall density of activated microglia in the ischemic striatum of ABC transporter inhibitor treated mice, but subtle changes of microglial morphology, that is, reduced microglial cell volume by ABCB1 deactivation after 14 and 28 days and reduced microglial ramification by ABCB1, ABCC1 and combined ABCB1 and ABCC1 deactivation after 56 days. Endogenous neurogenesis, assessed by BrdU incorporation analysis, was not influenced by ABCB1, ABCC1 or combined ABCB1 and ABCC1 deactivation. Taken together, this study could not detect any exacerbation of neurological deficits or brain injury after long-term ABC transporter deactivation in this preclinical stroke model.},
+	urldate = {2024-03-01},
+	journal = {Frontiers in Cellular Neuroscience},
+	author = {Manrique-Castano, Daniel and Sardari, Maryam and Silva de Carvalho, Tayana and Doeppner, Thorsten R. and Popa-Wagner, Aurel and Kleinschnitz, Christoph and Chan, Andrew and Hermann, Dirk M.},
+	year = {2019},
+	pdf = {Manrique-Castano et al. - 2019 - Deactivation of ATP-Binding Cassette Transporters .pdf},
+}
+
+@article{manrique-castano_encods_2019,
+	title = {{ENCODS}: {A} novel initiative to inspire young neuroscientists},
+	volume = {49},
+	copyright = {© 2019 Federation of European Neuroscience Societies and John Wiley \& Sons Ltd},
+	issn = {1460-9568},
+	shorttitle = {{ENCODS}},
+	url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.14428},
+	html = {https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.14428},
+	doi = {10.1111/ejn.14428},
+	language = {en},
+	number = {9},
+	urldate = {2024-03-01},
+	journal = {European Journal of Neuroscience},
+	author = {Manrique-Castano, Daniel and van Casteren, Adriana and Bouazza-Arostegui, Boris and MacDonald, Donald Iain and Pfeiffer, Paul},
+	year = {2019},
+	note = {\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1111/ejn.14428},
+	keywords = {ENCODS, neuroscience conference, scientific training, unconference},
+	pages = {1077--1083},
+	pdf = {Manrique-Castano et al. - 2019 - ENCODS A novel initiative to inspire young neuros.pdf},
+}
+
+@article{arango-davila_evaluacion_2016,
+	title = {Evaluación de la diásquisis transcallosa en un modelo murino de isquemia cerebral focal},
+	volume = {47},
+	copyright = {Copyright (c) 2016 Universidad del Valle},
+	issn = {1657-9534},
+	url = {https://colombiamedica.univalle.edu.co/index.php/comedica/article/view/2146},
+	html = {https://colombiamedica.univalle.edu.co/index.php/comedica/article/view/2146},
+	doi = {10.25100/cm.v47i2.2146},
+	abstract = {Objetivo:Evaluar los cambios exofocales transcallosos después de lesión isquémica focal en ratas, mediante marcación inmunohistoquímica con el anticuerpo monoclonal anti-NeuN (Mouse Anti-Neuronal Nuclei).Métodos:Se intervinieron 28 ratas machos Wistar adultas. Mediante el modelo experimental de isquemia cerebral focal del territorio de la arteria cerebral media por filamento intraluminal, se les ocasionó una lesión focal en el hemisferio derecho. Posteriormente se evaluó el hemisferio contralateral, marcando la población neuronal con el anticuerpo monoclonal anti-NeuN. Se definieron cinco grupos de evaluación: uno de control, 24 horas, 96 horas, 10 días y 20 días. Se evaluaron los cambios neuronales exofocales después de la lesión con base en la observación de los cambios en la inmunoreactividad de las neuronas al NeuN.Resultados:Se redujo la inmunoreactividad en la corteza contralateral a la lesión. Este fenómeno fue más notable en las capas supragranulares después de 24 horas post isquemia. Después de 96 horas hubo una disminución generalizada de la inmmunoreactivity en las capas supra e infragranulares. A los 10 y 20 días, el tejido recobró alguna inmunoreactividad NeuN, estos cambios se dieron en la capa VI.Conclusiones:Los cambios inmunorreactivos a NeuN apoyan el proceso de diasquisis interhemisférica. Los cambios en la inmunorreactividad podrían indicar estrés metabólico secundario a la interrupción en la conectividad con el sitio de la lesión.},
+	language = {es},
+	number = {2},
+	urldate = {2024-03-01},
+	journal = {Colombia Medica},
+	author = {Arango-Dávila, Cesar Augusto and Munoz, Beatriz E. and Castaño, Daniel Manrique and Potes, Laura and Umbarila, John},
+	month = jun,
+	year = {2016},
+	note = {Number: 2},
+	keywords = {apoptosis, Brain Injury, Brain Ischemia, Immunohistochemistry, Physiological stress},
+	pages = {87--93},
+	pdf = {Arango-Dávila et al. - 2016 - Evaluación de la diásquisis transcallosa en un mod.pdf},
+}