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1.
Int J Mol Sci ; 22(11)2021 May 26.
Artigo em Inglês | MEDLINE | ID: mdl-34073593

RESUMO

Ischemic stroke is a leading cause of mortality and chronic disability. Either recovery or progression towards irreversible failure of neurons and astrocytes occurs within minutes to days, depending on remaining perfusion levels. Initial damage arises from energy depletion resulting in a failure to maintain homeostasis and ion gradients between extra- and intracellular spaces. Astrocytes play a key role in these processes and are thus central players in the dynamics towards recovery or progression of stroke-induced brain damage. Here, we present a synopsis of the pivotal functions of astrocytes at the tripartite synapse, which form the basis of physiological brain functioning. We summarize the evidence of astrocytic failure and its consequences under ischemic conditions. Special emphasis is put on the homeostasis and stroke-induced dysregulation of the major monovalent ions, namely Na+, K+, H+, and Cl-, and their involvement in maintenance of cellular volume and generation of cerebral edema.


Assuntos
Astrócitos/metabolismo , Edema Encefálico/metabolismo , Lesões Encefálicas/metabolismo , Homeostase , Acidente Vascular Cerebral/metabolismo , Astrócitos/patologia , Edema Encefálico/patologia , Lesões Encefálicas/patologia , Humanos , Transporte de Íons , Acidente Vascular Cerebral/patologia
2.
NeuroRehabilitation ; 48(4): 513-522, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33967063

RESUMO

BACKGROUND: In hemiparetic patients, the skeletal muscle is mainly affected with a combination of abnormalities (denervation, remodeling, spasticity, and eventually muscular atrophy). OBJECTIVE: This study examined the role of eccentric exercise in strengthening muscles of the lower extremity and ultimately improving autonomy in patients with post-stroke hemiparesis during gait. METHODS: Thirty-seven patients hemiparetic adults were recruited, randomized into a control group (n = 19) and an intervention group receiving eccentric muscle strengthening (n = 18). The protocol consisted of three sets of five repetitions of eccentric contraction of the paretic limb after determining the maximum repetition (1 MRI). Evaluation of the 1RM, 10 meters and 6WMT was performed before and after the exercise for each group. Manova test was used to compare the differences between the control and intervention groups. RESULTS: The paretic limb showed significant increase in one-repetition maximum (1RM) between before and after rehabilitation (p≤0.00003). The two groups of Patients increased their walking speed (p≤0.0005), but we observed a significant difference between groups only for the 6MWT and not on the 10 meters Test. CONCLUSIONS: Eccentric training can be useful in strengthening the muscles of the lower limbs, and promoting gait performance. Eccentric training could complement other methods of managing patients with post-stroke hemiparesis.


Assuntos
Terapia por Exercício/métodos , Paresia/reabilitação , Reabilitação do Acidente Vascular Cerebral/métodos , Acidente Vascular Cerebral/complicações , Velocidade de Caminhada , Adulto , Idoso , Humanos , Masculino , Pessoa de Meia-Idade , Músculo Esquelético/fisiopatologia , Paresia/etiologia , Acidente Vascular Cerebral/patologia
3.
Food Chem ; 360: 130145, 2021 Oct 30.
Artigo em Inglês | MEDLINE | ID: mdl-34034049

RESUMO

Green leafy vegetables (GLVs) are a key element of healthy eating patterns and are an important source of lutein. To clarify the evidence for associations between GLVs and lutein intake and multiple health outcomes, we performed a review. A total of 24 meta-analyses with 29 health outcomes were identified by eligibility criteria. Dose-response analyses revealed that, per 100 g/d GLV intake was associated with a decreased risk (ca. 25%) of all-cause mortality, coronary heart disease and stroke. Beneficial effects of GLV intake were found for cardiovascular disease and bladder and oral cancer. Dietary lutein intake was inversely associated with age-related macular degeneration, age-related cataracts, coronary heart disease, stroke, oesophageal cancer, non-Hodgkin lymphoma, metabolic syndrome, and amyotrophic lateral sclerosis. Caution was warranted for contamination with potentially pathogenic organisms, specifically Escherichia coli. GLV consumption and lutein intake therein are generally safe and beneficial for multiple health outcomes in humans.


Assuntos
Dieta , Luteína/metabolismo , Verduras/metabolismo , Doenças Cardiovasculares/mortalidade , Doenças Cardiovasculares/patologia , Humanos , Luteína/química , Neoplasias/mortalidade , Neoplasias/patologia , Avaliação de Resultados em Cuidados de Saúde , Acidente Vascular Cerebral/mortalidade , Acidente Vascular Cerebral/patologia , Verduras/química
4.
BMC Neurol ; 21(1): 142, 2021 Mar 31.
Artigo em Inglês | MEDLINE | ID: mdl-33789591

RESUMO

BACKGROUND: Neuronal intranuclear inclusion disease (NIID) is a neurodegenerative disease, the clinical manifestations of which are complex and easily misdiagnosed. NIID clinical characteristics are varied, affecting the central and peripheral nervous systems and autonomic nerves. In this study, we present an NIID case with both stroke-like onset and encephalitic attacks, which is a rare case report. CASE PRESENTATION: A 68-year-old Chinese female presented with sudden aphasia and limb hemiplegia as the first symptoms, as well as fever, cognitive impairment and mental irritability from encephalitic attacks. During hospitalization, a brain magnetic resonance imaging (MRI) examination detected high signal intensity from diffusion-weighted imaging (DWI) of the bilateral frontal grey matter-white matter junction. Electrophysiological tests revealed the main site of injury was at the myelin sheath in the motor nerves. A skin biopsy revealed eosinophilic spherical inclusion bodies in the nuclei of small sweat gland cells, fibroblasts and fat cells, whilst immunohistochemistry revealed that p62 and ubiquitin antibodies were positive. From genetic analyses, the patient was not a carrier of the fragile X mental retardation 1 (FMR1) permutation, but repeated GGC sequences in the NOTCH2NLC gene confirmed an NIID diagnosis. Through antipsychotic and nutritional support therapy, the patient's symptoms were completely relieved within 3 weeks. CONCLUSIONS: This report of an NIID case with both stroke-like onset and encephalitic attacks provides new information for NIID diagnoses, and a comprehensive classification of clinical characteristics.


Assuntos
Encefalite/etiologia , Doenças Neurodegenerativas/complicações , Doenças Neurodegenerativas/diagnóstico , Acidente Vascular Cerebral/etiologia , Idoso , Encefalite/patologia , Feminino , Humanos , Corpos de Inclusão Intranuclear/genética , Mutação , Doenças Neurodegenerativas/genética , Receptor Notch2/genética , Acidente Vascular Cerebral/patologia
5.
Oxid Med Cell Longev ; 2021: 5545330, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33897941

RESUMO

Cerebral stroke is a serious worldwide health problem, as can be seen by the global epidemic of the disease. In this disorder, when the blood flow is compromised by ruptures or blocked arteries, sudden death of neurons is observed as a result of a lack of oxygen and nutrients. Numerous severe problems and frequent complications also exist in stroke patients; therefore, there is an urgent need to develop new therapeutic, diagnostic, and prognostic methods for the disease. At present, the diagnosis of stroke is based on a neurological examination, medical history, and neuroimaging, due to the fact that rapid and noninvasive diagnostic tests are unavailable. Nevertheless, oxidative stress and inflammation are considered key factors in stroke pathogenesis. Oxygen free radicals are responsible for oxidation of lipids, proteins, and DNA/RNA, which in turn contributes to oxidative damage of the brain. Toxic products of the oxidation reactions act cytostatically on the cell by damaging cell membranes and leading to neuronal death by apoptosis or necrosis. Thus, it seems that redox/inflammatory biomarkers might be used in the diagnosis of the disease. Nowadays, saliva is of increasing interest in clinical laboratory medicine. Redox biomarkers could be obtained easily, noninvasively, cheaply, and stress-free from saliva. This minireview is aimed at presenting the current knowledge concerning the use of salivary biomarkers of oxidative stress and inflammation in the diagnosis and prognosis of stroke.


Assuntos
Biomarcadores/metabolismo , Inflamação/imunologia , Estresse Oxidativo/imunologia , Saliva/metabolismo , Acidente Vascular Cerebral/diagnóstico , Humanos , Saliva/citologia , Acidente Vascular Cerebral/patologia
6.
Int J Mol Sci ; 22(6)2021 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-33804243

RESUMO

A growing body of preclinical evidence indicates that certain cannabinoids, including cannabidiol (CBD) and synthetic derivatives, may play a role in the myelinating processes and are promising small molecules to be developed as drug candidates for management of demyelinating diseases such as multiple sclerosis (MS), stroke and traumatic brain injury (TBI), which are three of the most prevalent demyelinating disorders. Thanks to the properties described for CBD and its interesting profile in humans, both the phytocannabinoid and derivatives could be considered as potential candidates for clinical use. In this review we will summarize current advances in the use of CBD and other cannabinoids as future potential treatments. While new research is accelerating the process for the generation of novel drug candidates and identification of druggable targets, the collaboration of key players such as basic researchers, clinicians and pharmaceutical companies is required to bring novel therapies to the patients.


Assuntos
Canabidiol/uso terapêutico , Canabinoides/uso terapêutico , Cannabis/química , Doenças Desmielinizantes/tratamento farmacológico , Lesões Encefálicas Traumáticas/tratamento farmacológico , Lesões Encefálicas Traumáticas/patologia , Doenças Desmielinizantes/patologia , Humanos , Esclerose Múltipla/tratamento farmacológico , Esclerose Múltipla/patologia , Acidente Vascular Cerebral/tratamento farmacológico , Acidente Vascular Cerebral/patologia
7.
Int J Mol Sci ; 22(6)2021 Mar 13.
Artigo em Inglês | MEDLINE | ID: mdl-33805800

RESUMO

Cyclin-dependent kinases (CDKs) are involved in many crucial processes, such as cell cycle and transcription, as well as communication, metabolism, and apoptosis. The kinases are organized in a pathway to ensure that, during cell division, each cell accurately replicates its DNA, and ensure its segregation equally between the two daughter cells. Deregulation of any of the stages of the cell cycle or transcription leads to apoptosis but, if uncorrected, can result in a series of diseases, such as cancer, neurodegenerative diseases (Alzheimer's or Parkinson's disease), and stroke. This review presents the current state of knowledge about the characteristics of cyclin-dependent kinases as potential pharmacological targets.


Assuntos
Doença de Alzheimer/tratamento farmacológico , Ciclo Celular/genética , Quinases Ciclina-Dependentes/genética , Neoplasias/tratamento farmacológico , Doença de Parkinson/tratamento farmacológico , Inibidores de Proteínas Quinases/uso terapêutico , Doença de Alzheimer/enzimologia , Doença de Alzheimer/genética , Doença de Alzheimer/patologia , Animais , Antineoplásicos/uso terapêutico , Apoptose/efeitos dos fármacos , Apoptose/genética , Cardiomegalia/tratamento farmacológico , Cardiomegalia/enzimologia , Cardiomegalia/genética , Cardiomegalia/patologia , Fármacos Cardiovasculares/uso terapêutico , Ciclo Celular/efeitos dos fármacos , Quinases Ciclina-Dependentes/antagonistas & inibidores , Quinases Ciclina-Dependentes/metabolismo , Ciclinas/genética , Ciclinas/metabolismo , Regulação da Expressão Gênica , Humanos , Neoplasias/enzimologia , Neoplasias/genética , Neoplasias/patologia , Fármacos Neuroprotetores/uso terapêutico , Doença de Parkinson/enzimologia , Doença de Parkinson/genética , Doença de Parkinson/patologia , Saccharomyces cerevisiae/genética , Saccharomyces cerevisiae/metabolismo , Acidente Vascular Cerebral/tratamento farmacológico , Acidente Vascular Cerebral/enzimologia , Acidente Vascular Cerebral/genética , Acidente Vascular Cerebral/patologia
8.
Stem Cells ; 39(7): 904-912, 2021 07.
Artigo em Inglês | MEDLINE | ID: mdl-33704866

RESUMO

We have shown previously that transplanted bone marrow mononuclear cells (BM-MNC), which are a cell fraction rich in hematopoietic stem cells, can activate cerebral endothelial cells via gap junction-mediated cell-cell interaction. In the present study, we investigated such cell-cell interaction between mesenchymal stem cells (MSC) and cerebral endothelial cells. In contrast to BM-MNC, for MSC we observed suppression of vascular endothelial growth factor uptake into endothelial cells and transfer of glucose from endothelial cells to MSC in vitro. The transfer of such a small molecule from MSC to vascular endothelium was subsequently confirmed in vivo and was followed by suppressed activation of macrophage/microglia in stroke mice. The suppressive effect was absent by blockade of gap junction at MSC. Furthermore, gap junction-mediated cell-cell interaction was observed between circulating white blood cells and MSC. Our findings indicate that gap junction-mediated cell-cell interaction is one of the major pathways for MSC-mediated suppression of inflammation in the brain following stroke and provides a novel strategy to maintain the blood-brain barrier in injured brain. Furthermore, our current results have the potential to provide a novel insight for other ongoing clinical trials that make use of MSC transplantation aiming to suppress excess inflammation, as well as other diseases such as COVID-19 (coronavirus disease 2019).


Assuntos
Comunicação Celular , Junções Comunicantes , Células Endoteliais da Veia Umbilical Humana/metabolismo , Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais , Acidente Vascular Cerebral , Aloenxertos , Animais , COVID-19/metabolismo , COVID-19/patologia , Junções Comunicantes/metabolismo , Junções Comunicantes/patologia , Células Endoteliais da Veia Umbilical Humana/patologia , Humanos , Células-Tronco Mesenquimais/metabolismo , Células-Tronco Mesenquimais/patologia , Camundongos , SARS-CoV-2/metabolismo , Acidente Vascular Cerebral/metabolismo , Acidente Vascular Cerebral/patologia , Acidente Vascular Cerebral/terapia
9.
Stem Cells ; 39(7): 904-912, 2021 07.
Artigo em Inglês | MEDLINE | ID: covidwho-1126519

RESUMO

We have shown previously that transplanted bone marrow mononuclear cells (BM-MNC), which are a cell fraction rich in hematopoietic stem cells, can activate cerebral endothelial cells via gap junction-mediated cell-cell interaction. In the present study, we investigated such cell-cell interaction between mesenchymal stem cells (MSC) and cerebral endothelial cells. In contrast to BM-MNC, for MSC we observed suppression of vascular endothelial growth factor uptake into endothelial cells and transfer of glucose from endothelial cells to MSC in vitro. The transfer of such a small molecule from MSC to vascular endothelium was subsequently confirmed in vivo and was followed by suppressed activation of macrophage/microglia in stroke mice. The suppressive effect was absent by blockade of gap junction at MSC. Furthermore, gap junction-mediated cell-cell interaction was observed between circulating white blood cells and MSC. Our findings indicate that gap junction-mediated cell-cell interaction is one of the major pathways for MSC-mediated suppression of inflammation in the brain following stroke and provides a novel strategy to maintain the blood-brain barrier in injured brain. Furthermore, our current results have the potential to provide a novel insight for other ongoing clinical trials that make use of MSC transplantation aiming to suppress excess inflammation, as well as other diseases such as COVID-19 (coronavirus disease 2019).


Assuntos
Comunicação Celular , Junções Comunicantes , Células Endoteliais da Veia Umbilical Humana/metabolismo , Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais , Acidente Vascular Cerebral , Aloenxertos , Animais , COVID-19/metabolismo , COVID-19/patologia , Junções Comunicantes/metabolismo , Junções Comunicantes/patologia , Células Endoteliais da Veia Umbilical Humana/patologia , Humanos , Células-Tronco Mesenquimais/metabolismo , Células-Tronco Mesenquimais/patologia , Camundongos , SARS-CoV-2/metabolismo , Acidente Vascular Cerebral/metabolismo , Acidente Vascular Cerebral/patologia , Acidente Vascular Cerebral/terapia
10.
Mayo Clin Proc ; 96(6): 1609-1621, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-33775421

RESUMO

Atrial fibrillation (AF) is the most common cardiac arrhythmia, and coronary atherosclerosis is the leading cause of death in the United States and worldwide. Endothelial dysfunction is the earliest clinically detectable form of atherosclerosis. Control of shared AF and coronary atherosclerosis risk factors improves both AF-free survival and vascular endothelial function. Decades of AF research have yielded fundamental insight into AF pathophysiology, but current pharmacological and catheter-based invasive AF therapies have limited long-term efficacy and substantial side effects, possibly because of incomplete understanding of underlying complex AF pathophysiology. We hereby discuss potential mechanistic links between endothelial dysfunction and AF (risk-factor-associated systemic inflammation and oxidative stress, myocardial ischemia, common gene variants, vascular shear stress, and fibroblast growth factor-23), explore a potential new vascular dimension to AF pathophysiology, highlight a growing body of evidence supporting an association between systemic vascular endothelial dysfunction, AF, and stroke, and discuss potential common effective therapies.


Assuntos
Fibrilação Atrial/etiologia , Endotélio Vascular/fisiopatologia , Fibrilação Atrial/patologia , Fibrilação Atrial/fisiopatologia , Doença da Artéria Coronariana/complicações , Doença da Artéria Coronariana/patologia , Doença da Artéria Coronariana/fisiopatologia , Endotélio Vascular/patologia , Humanos , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/patologia , Acidente Vascular Cerebral/fisiopatologia
11.
Medicine (Baltimore) ; 100(11): e25150, 2021 Mar 19.
Artigo em Inglês | MEDLINE | ID: mdl-33725999

RESUMO

BACKGROUND: The association between cytochrome P450 2C19 (CYP2C19) polymorphisms and neurological deterioration in stroke or transient ischemic attack (TIA) patients is not completely understood. Hence, we performed a systematic review and meta-analysis of prospective cohort studies to quantify this association. METHODS: PubMed, Cochrane Library, Excerpta Medica Database, China National Knowledge Infrastructure and WanFang databases were searched for studies published up to April 2019. Prospective cohort studies that reported an association between CYP2C19 polymorphisms and neurological deterioration in stroke/TIA patients were included. Data on risk ratio (RR) and 95% confidence intervals (CI) were extracted and pooled by the authors. Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines were followed. RESULTS: Twelve eligible studies were included. Twelve studies reported CYP2C19∗2, ∗3 loss-of-function alleles and 5 studies reported CYP2C19∗17 gain-of-function allele. Compared to non-carriers, carriers of CYP2C19∗2, ∗3 loss-of-function alleles had a significantly higher risk of neurological deterioration (RR, 1.63; 95%CI, 1.32-2.02). Conversely, carriers of CYP2C19∗17 gain-of-function allele had a significantly lower risk of neurological deterioration (RR, 0.520; 95%CI, 0.393-0.689) compared to non-carriers. CONCLUSIONS: This meta-analysis demonstrated that the carriers of CYP2C19∗2, ∗3 loss-of-function alleles have an increased risk of neurological deterioration compared to non-carriers in stroke or TIA patients. Additionally, CYP2C19∗17 gain-of-function allele can reduce the risk of neurological deterioration.


Assuntos
Citocromo P-450 CYP2C19/genética , Ataque Isquêmico Transitório/patologia , Degeneração Neural/genética , Polimorfismo Genético/genética , Acidente Vascular Cerebral/patologia , Idoso , Feminino , Humanos , Ataque Isquêmico Transitório/genética , Mutação com Perda de Função/genética , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Acidente Vascular Cerebral/genética
12.
Life Sci ; 274: 119343, 2021 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-33716063

RESUMO

Aging is a risk factor for major central nervous system (CNS) disorders. More specifically, aging can be inked to neurodegenerative diseases (NDs) because of its deteriorating impact on neurovascular unit (NVU). Metformin, a first line FDA-approved anti-diabetic drug, has gained increasing interest among researchers for its role in improving aging-related neurodegenerative disorders. Additionally, numerous studies have illustrated metformin's role in ischemic stroke, a cerebrovascular disorder in which the NVU becomes dysfunctional which can lead to permanent life-threatening disabilities. Considering metformin's beneficial preclinical actions on various disorders, and the drug's role in alleviating severity of these conditions through involvement in commonly characterized cellular pathways, we discuss the potential of metformin as a suitable drug candidate for repurposing in CNS disorders.


Assuntos
Envelhecimento/efeitos dos fármacos , Isquemia Encefálica/tratamento farmacológico , Reposicionamento de Medicamentos/métodos , Hipoglicemiantes/uso terapêutico , Metformina/uso terapêutico , Doenças Neurodegenerativas/tratamento farmacológico , Acidente Vascular Cerebral/tratamento farmacológico , Envelhecimento/patologia , Animais , Isquemia Encefálica/patologia , Humanos , Doenças Neurodegenerativas/patologia , Acidente Vascular Cerebral/patologia
13.
Mol Med Rep ; 23(4)2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33604682

RESUMO

The inflammatory response and apoptosis are key factors in cerebral ischemia­reperfusion injury. The severity of the inflammatory reaction and apoptosis has an important impact on the prognosis of stroke. The ultrasmall superparamagnetic iron oxide particle has provided an effective magnetic resonance molecular imaging method for dynamic observation of the cell infiltration process in vivo. The aims of the present study were to investigate the inflammatory response of cerebral ischemia­reperfusion injury in mice using ferumoxytol­enhanced magnetic resonance imaging, and to observe the dynamic changes of inflammatory response and apoptosis. In the present study a C57BL/6n mouse cerebral ischemia­reperfusion model was established by blocking the right middle cerebral artery with an occluding suture. Subsequently, the mice were injected with ferumoxytol via the tail vein, and magnetic resonance scanning was performed at corresponding time points to observe the signal changes. Furthermore, blood samples were used to measure the level of serum inflammatory factors, and histological staining was performed to assess the number of iron­swallowing microglial cells and apoptotic cells. The present results suggested that there was no significant difference in the serum inflammatory factors tumor necrosis factor­α and interleukin 1ß between the middle cerebral artery occlusion (MCAO) and MCAO + ferumoxytol groups injected with ferumoxytol and physiological saline. The lowest signal ratio in the negative enhancement region was decreased 24 h after reperfusion in mice injected with ferumoxytol. The proportion of iron­swallowing microglial cells and TUNEL­positive cells were the highest at 24 h after reperfusion, and decreased gradually at 48 and 72 h after reperfusion. Therefore, the present results indicated that ferumoxytol injection of 18 mg Fe/kg does not affect the inflammatory response in the acute phase of cerebral ischemia and reperfusion. Ferumoxytol­enhanced magnetic resonance imaging can be used as an effective means to monitor the inflammatory response in the acute phase of cerebral ischemia­reperfusion injury. Furthermore, it was found that activation of the inflammatory response and apoptosis in the acute stage of cerebral ischemia­reperfusion injury is consistent.


Assuntos
Isquemia Encefálica/diagnóstico por imagem , Infarto da Artéria Cerebral Média/diagnóstico por imagem , Inflamação/diagnóstico por imagem , Traumatismo por Reperfusão/diagnóstico por imagem , Animais , Apoptose/efeitos dos fármacos , Encéfalo/diagnóstico por imagem , Encéfalo/efeitos dos fármacos , Isquemia Encefálica/sangue , Isquemia Encefálica/complicações , Isquemia Encefálica/patologia , Meios de Contraste/farmacologia , Modelos Animais de Doenças , Óxido Ferroso-Férrico/farmacologia , Infarto da Artéria Cerebral Média/complicações , Infarto da Artéria Cerebral Média/patologia , Inflamação/sangue , Inflamação/complicações , Inflamação/patologia , Interleucina-1beta/sangue , Imageamento por Ressonância Magnética , Masculino , Camundongos , Microglia/efeitos dos fármacos , Traumatismo por Reperfusão/complicações , Traumatismo por Reperfusão/patologia , Acidente Vascular Cerebral/sangue , Acidente Vascular Cerebral/complicações , Acidente Vascular Cerebral/diagnóstico por imagem , Acidente Vascular Cerebral/patologia , Fator de Necrose Tumoral alfa/sangue
14.
Nutr Metab Cardiovasc Dis ; 31(4): 1113-1120, 2021 04 09.
Artigo em Inglês | MEDLINE | ID: mdl-33549459

RESUMO

BACKGROUND AND AIMS: Most studies assess the relationship between alcohol and stroke at some point. Little is known about the effect on stroke of drinking status changes over time. This study aimed to examine the association of median 2.4-year drinking status changes with risk of stroke. METHODS AND RESULTS: We examined 22,691 adults from rural China. Drinking status was assessed at 2004-2006 and in 2008. Participants were divided into four change patterns: consistent non-drinkers, abstainers, starters, and consistent drinkers. A Cox proportional hazards model were performed. We observed 1215 cases of stroke during a median follow-up period of 11.8 years. A faint J-shaped association between alcohol consumption and risk of stroke was found in this population. Based on the amount of alcohol consumption, only current drinkers with ≥721 g/week at baseline in both males and females had a higher risk of stroke [hazard ratio (HR): 1.342; 95% confidence interval (CI): 1.070-1.683 and HR: 2.130; CI: 1.041-4.357, respectively]. Based on change patterns, Compared with consistent non-drinkers, the HR (95% CI) for consistent drinkers, abstainers and starters was 1.298 (1.070-1.576), 1.093 (0.877-1.362) and 1.263 (1.034-1.543), respectively. The same trend was observed in male. The HR (95% CI) for consistent drinkers, abstainers and starters was 1.360 (1.098-1.685), 1.139 (0.883-1.470) and 1.364 (1.092-1.703), respectively. No difference was observed in females. CONCLUSION: High alcohol consumption was associated with increased risk of stroke in both males and females. However, based on change patterns, consistent drinkers and starters were at higher risk of stroke only in males.


Assuntos
Abstinência de Álcool , Consumo de Bebidas Alcoólicas/efeitos adversos , Saúde da População Rural , Acidente Vascular Cerebral/patologia , Adulto , Consumo de Bebidas Alcoólicas/epidemiologia , China/epidemiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Fatores de Proteção , Medição de Risco , Fatores de Risco , Acidente Vascular Cerebral/diagnóstico , Acidente Vascular Cerebral/epidemiologia , Fatores de Tempo
15.
Am J Forensic Med Pathol ; 42(2): 160-163, 2021 Jun 01.
Artigo em Inglês | MEDLINE | ID: covidwho-1045797

RESUMO

ABSTRACT: The SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) pandemic has revealed diverse neurological manifestations of coronavirus disease 2019 (COVID-19). This case report begins with a background review of the neurological effects of COVID-19, focusing on stroke, neuroinflammation, and coagulopathy. It then describes the clinical course and autopsy findings of a young patient presenting with COVID-19-associated stroke. The formal neuropathological examination is presented, along with the systemic and brain histological features. Interesting aspects include multiterritory hemorrhagic infarctions, microinfarcts throughout the cortex and white matter, and prominent mixed inflammatory cell cuffing of intracerebral blood vessels distant from the infarcts.


Assuntos
COVID-19/complicações , Infarto da Artéria Cerebral Média/patologia , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/patologia , Adulto , Encéfalo/patologia , Morte Encefálica , Feminino , Humanos , Infarto da Artéria Cerebral Média/diagnóstico por imagem , Pulmão/patologia , Linfócitos/patologia , Macrófagos/patologia , Monócitos/patologia , Edema Pulmonar/patologia , Tomografia Computadorizada por Raios X
16.
Neurology ; 96(9): e1290-e1300, 2021 03 02.
Artigo em Inglês | MEDLINE | ID: mdl-33431517

RESUMO

OBJECTIVE: To test the hypothesis that bone mineral loss is mechanistically related to cerebral small vessel disease (SVD), we investigated the relationship between bone mineral density and the prevalence and intensity of SVD among patients with stroke. METHODS: We analyzed data of 1,190 consecutive patients with stroke who were >50 years of age and underwent both brain MRI and dual-energy x-ray absorptiometry from the stroke registry of Chung-Ang University Hospital in Seoul, Korea. The patients were categorized into 3 groups according to their bone mineral density (normal, osteopenia, and osteoporosis). White matter hyperintensities, silent lacunes, cerebral microbleeds, and extensive perivascular space were assessed from brain MRI. Multinomial logistic regression model was used to examine the association between osteoporosis and total SVD score. We also recruited 70 patients with stroke to study serum bone turnover markers and microRNAs related to both cerebral atherosclerosis and bone metabolism to understand bone and brain interaction. RESULTS: Osteoporosis was determined among 284 patients (23.9%), and 450 patients (37.8%) had osteopenia. As bone mineral density decreased, total SVD score and the incidence of every SVD phenotype increased except strictly lobar cerebral microbleeds. Multinomial logistic regression analysis showed that osteoporosis was independently associated with severe SVD burden. The levels of microRNA-378f were significantly increased among the patients with osteoporosis and maximal total SVD score and positively correlated with parathyroid hormone and osteocalcin. CONCLUSIONS: These findings suggest a pathophysiologic link between bone mineral loss and hypertensive cerebral arteriolar degeneration, possibly mediated by circulating microRNA.


Assuntos
Densidade Óssea , Doenças de Pequenos Vasos Cerebrais/patologia , Absorciometria de Fóton , Idoso , Idoso de 80 Anos ou mais , Doenças Ósseas Metabólicas/complicações , Encéfalo/diagnóstico por imagem , Doenças de Pequenos Vasos Cerebrais/complicações , Doenças de Pequenos Vasos Cerebrais/diagnóstico por imagem , Feminino , Humanos , Arteriosclerose Intracraniana/complicações , Arteriosclerose Intracraniana/diagnóstico por imagem , Hemorragias Intracranianas/diagnóstico por imagem , Imageamento por Ressonância Magnética , Masculino , MicroRNAs/genética , Pessoa de Meia-Idade , Osteocalcina/sangue , Osteoporose/complicações , Hormônio Paratireóideo/sangue , Acidente Vascular Cerebral/diagnóstico por imagem , Acidente Vascular Cerebral/patologia , Substância Branca/diagnóstico por imagem
17.
Neurosci Lett ; 747: 135662, 2021 03 16.
Artigo em Inglês | MEDLINE | ID: mdl-33484738

RESUMO

Stroke is one of the leading causes of death in adults worldwide. However, the mechanism causing neuronal death remains poorly understood. Our previous report showed that enolase1 (ENO1), a key glycolytic enzyme, alleviates cerebral ischemia-induced neuronal injury. It remained unclear whether enolase2 (ENO2) affects neuronal injury in stroke models. Here, we examined the effects of ENO2 in several stroke models. The results showed that the expression level of ENO2 was downregulated after 3 h of cerebral ischemia by middle cerebral artery occlusion (MCAO) in the mouse model. ENO2 was expressed in mouse brain and cultured hippocampus neurons. Overexpression of ENO2 in cultured hippocampus neurons did not affect neuronal injury in our oxygen-glucose deprivation (OGD) model. Interestingly, double knock-down (KD) of ENO1 and ENO2 increased neuronal injury while either KD of ENO1 or ENO2 failed to increase neuronal injury in OGD. Deletion of ENO1 did not affect anoxia-starvation (AS)-induced worm death in C. elegans. These findings demonstrated that ENO2 and ENO1 work together against neuronal injury in these stroke models.


Assuntos
Lesões Encefálicas/metabolismo , Isquemia Encefálica/metabolismo , Neurônios/metabolismo , Fosfopiruvato Hidratase/metabolismo , Acidente Vascular Cerebral/metabolismo , Animais , Apoptose/efeitos dos fármacos , Lesões Encefálicas/patologia , Isquemia Encefálica/patologia , Modelos Animais de Doenças , Infarto da Artéria Cerebral Média/metabolismo , Camundongos Endogâmicos C57BL , Acidente Vascular Cerebral/patologia
18.
Int Immunopharmacol ; 92: 107339, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33516048

RESUMO

BACKGROUND: Inflammation and oxidative stress is closely associated with the development of ischemic brain stroke. Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1), a novel identified long non-coding RNA (lncRNA), has been suggested to play an important role in the development of many types of human cancers. However, the functional involvement of OIP5-AS1 in ischemic stroke is still unknown. METHODS: Quantitative real-time polymerase chain reaction and /or western blot were conducted to determine the expression profiles of OIP5-AS1, C1q/TNF-related protein 3 (CTRP3) and miR-186-5p in the serum of stroke patients, as well as in the ischemic penumbra of rats with middle cerebral artery occlusion/reperfusion (MCAO/R) injury and microglial cells treated with oxygen glucose deprivation/re-oxygenation (OGD/R). Upon selective regulation of OIP5-AS1 and miR-186-5p, the inflammation and oxidative stress responses in microglia/macrophage as well as neurologic functions in MCAO/R rats were detected. Furthermore, the interactions between OIP5-AS1 and miR-186-5p, miR-186-5p and CTRP3 were investigated by RNA immunoprecipitation (RIP) assay, luciferase report assay and bioinformation anaylsis. RESULTS: We observed markedly increased infarct volume, neuronal apoptosis, inflammation and oxidative stress responses in the infarcted lesions of MCAO/R rats, in line with down-regulated levels of OIP5-AS1 and CTRP3 while up-regulated miR-186-5p. Functional studies demonstrated that up-regulation of OIP5-AS1 attenuated infarct volume, neuronal apoptosis, microglia/macrophage inflammation and oxidative stress responses induced by MCAO/R or OGD/R. In terms of mechanism, we revealed that OIP5-AS1-miR-186-5p-CTRP3 axis played a vital role in modulating microglia/macrophage activation and neuronal apoptosis. CONCLUSION: Up-regulating lncRNA OIP5-AS1 protects neuron injury against MCAO/R induced inflammation and oxidative stress in microglia/macrophage through activating CTRP3 via sponging miR-186-5p.


Assuntos
Hipóxia-Isquemia Encefálica/complicações , Inflamação/prevenção & controle , MicroRNAs/genética , Neurônios/metabolismo , Estresse Oxidativo , RNA Longo não Codificante/genética , Fatores de Necrose Tumoral/metabolismo , Animais , Células Cultivadas , Modelos Animais de Doenças , Regulação Neoplásica da Expressão Gênica , Humanos , Inflamação/etiologia , Inflamação/metabolismo , Inflamação/patologia , Macrófagos/metabolismo , Macrófagos/patologia , Camundongos , Microglia/metabolismo , Microglia/patologia , Neurônios/patologia , Ratos , Transdução de Sinais , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/metabolismo , Acidente Vascular Cerebral/patologia , Acidente Vascular Cerebral/prevenção & controle
19.
Clin Nucl Med ; 46(3): e171-e172, 2021 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-33443953

RESUMO

ABSTRACT: A 50-year-old man with angioimmunoblastic T-cell lymphoma in complete response to treatment presented new hypermetabolic brain lesions on 18F-FDG PET/CT suggestive of malignancy. These findings were correlated by MRI that showed cortical-subcortical peripheral lesions typical of acute ischemic infarction. A restaging 18F-FDG PET/CT showed that hypermetabolic lesions were replaced by ametabolic areas, supporting chronic infarction. Early ischemia presents transitory FDG increase. Brain lymphomas are highly FDG avid and difficult to differentiate from acute cerebral infarction. In view of the discordance of abnormal areas of intracranial uptake on PET FDG, MRI confirmation is required to avoid misinterpretation.


Assuntos
Fluordesoxiglucose F18 , Transtornos Linfoproliferativos/complicações , Imageamento por Ressonância Magnética , Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada , Acidente Vascular Cerebral/complicações , Acidente Vascular Cerebral/diagnóstico por imagem , Diagnóstico Diferencial , Progressão da Doença , Humanos , Masculino , Pessoa de Meia-Idade , Acidente Vascular Cerebral/patologia
20.
Am J Forensic Med Pathol ; 42(2): 160-163, 2021 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-33491953

RESUMO

ABSTRACT: The SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) pandemic has revealed diverse neurological manifestations of coronavirus disease 2019 (COVID-19). This case report begins with a background review of the neurological effects of COVID-19, focusing on stroke, neuroinflammation, and coagulopathy. It then describes the clinical course and autopsy findings of a young patient presenting with COVID-19-associated stroke. The formal neuropathological examination is presented, along with the systemic and brain histological features. Interesting aspects include multiterritory hemorrhagic infarctions, microinfarcts throughout the cortex and white matter, and prominent mixed inflammatory cell cuffing of intracerebral blood vessels distant from the infarcts.


Assuntos
COVID-19/complicações , Infarto da Artéria Cerebral Média/patologia , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/patologia , Adulto , Encéfalo/patologia , Morte Encefálica , Feminino , Humanos , Infarto da Artéria Cerebral Média/diagnóstico por imagem , Pulmão/patologia , Linfócitos/patologia , Macrófagos/patologia , Monócitos/patologia , Edema Pulmonar/patologia , Tomografia Computadorizada por Raios X
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