RESUMEN
This paper explores the potential benefits of integrating a brain-computer interface (BCI) utilizing the visual-evoked potential paradigm (SSVEP) with a six-degrees-of-freedom (6-DOF) robotic arm to enhance rehabilitation tools. The SSVEP-BCI employs electroencephalography (EEG) as a method of measuring neural responses inside the occipital lobe in reaction to pre-established visual stimulus frequencies. The BCI offline and online studies yielded accuracy rates of 75% and 83%, respectively, indicating the efficacy of the system in accurately detecting and capturing user intent. The robotic arm achieves planar motion by utilizing a total of five control frequencies. The results of this experiment exhibited a high level of precision and consistency, as indicated by the recorded values of ±0.85 and ±1.49 cm for accuracy and repeatability, respectively. Moreover, during the performance tests conducted with the task of constructing a square within each plane, the system demonstrated accuracy of 79% and 83%. The use of SSVEP-BCI and a robotic arm together shows promise and sets a solid foundation for the development of assistive technologies that aim to improve the health of people with amyotrophic lateral sclerosis, spina bifida, and other related diseases.
Asunto(s)
Interfaces Cerebro-Computador , Procedimientos Quirúrgicos Robotizados , Dispositivos de Autoayuda , Humanos , Electroencefalografía/métodos , Potenciales Evocados Visuales , Estimulación LuminosaRESUMEN
Peripheral nerves have the capacity to conduct action potentials along great distances and quickly recover following damage which is mainly due to Schwann cells (SCs), the most abundant glial cells of the peripheral nervous system (PNS). SCs wrap around an axonal segment multiple times, forming a myelin sheath, allowing for a significant increase in action potential conduction by insulating the axons. Mature myelin consists of compact and non-compact (or cytoplasmic) myelin zones. Non-compact myelin is found in paranodal loops bordering the nodes of Ranvier, and in the inner and outermost cytoplasmic tongues and is the region in which Schmidt-Lanterman incisures (SLI; continuous spirals of overlapping cytoplasmic expansions within areas of compact myelin) are located. Using different technologies, it was shown that the layers of non-compact myelin could be connected to each other by gap junction channels (GJCs), formed by connexin 32 (Cx32), and their relative abundance allows for the transfer of ions and different small molecules. Likewise, Cx29 is expressed in the innermost layer of the myelin sheath. Here it does not form GJCs but colocalizes with Kv1, which implies that the SCs play an active role in the electrical condition in mammals. The critical role of GJCs in the functioning of myelinating SCs is evident in Charcot-Marie-Tooth disease (CMT), X-linked form 1 (CMTX1), which is caused by mutations in the gap junction protein beta 1 (GJB1) gene that codes for Cx32. Although the management of CMT symptoms is currently supportive, there is a recent method for targeted gene delivery to myelinating cells, which rescues the phenotype in KO-Cx32 mice, a model of CMTX1. In this mini-review article, we discuss the current knowledge on the role of Cxs in myelin-forming SCs and summarize recent discoveries that may become a real treatment possibility for patients with disorders such as CMT.
RESUMEN
The pathological hallmarks of Alzheimer's disease (AD) are amyloid-ß (Aß) plaques, neurofibrillary tangles, and glia activation. The pathology also includes vascular amyloidosis and cerebrovascular disease. Vascular compromise can result in hypoperfusion, local tissue hypoxia, and acidosis. Activated microglia and astrocytes can phagocytose Aß through membrane receptors that include scavenger receptors. Changes in glial cells induced by extracellular acidosis could play a role in the development of AD. Here, we assess whether extracellular acidosis changes glial cell properties relevant for Aß clearance capacity. Incubation of glial cells on acidified culture medium (pH 6.9 or 6.5) for 24-48âh resulted in decreased cell diameter, with thinner branches in astrocytes, slight reduction in cell body size in microglia, a transient decrease in astrocyte adhesion to substrates, and a persistent decrease in microglia adhesion compared with control media (pH 7.4). Astrocyte Aß phagocytosis decreased at pH 6.9 and 6.5, whereas microglia phagocytosis only transiently decreased in acidified media. Scavenger receptors class B member I (SR-BI) increased and scavenger receptors-macrophage receptors with collagenous structures (SR-MARCO) decreased in astrocytes cultured at pH 6.5. In contrast, in microglia exposed to pH 6.5, expression of SR-BI and SR-MARCO increased and fatty acid translocase (CD-36) decreased. In conclusion, the acidic environment changed the adhesiveness and morphology of both microglia and astrocytes, but only astrocytes showed a persistent decrease in Aß clearance activity. Expression of scavenger receptors was affected differentially in microglia and astrocytes by acidosis. These changes in scavenger receptor patterns can affect the activation of glia and their contribution to neurodegeneration.
Asunto(s)
Acidosis/fisiopatología , Péptidos beta-Amiloides/metabolismo , Astrocitos/metabolismo , Regulación de la Expresión Génica/fisiología , Microglía/metabolismo , Fagocitosis/fisiología , Receptores Depuradores/genética , Animales , Animales Recién Nacidos , Astrocitos/efectos de los fármacos , Adhesión Celular/efectos de los fármacos , Células Cultivadas , Corteza Cerebral/citología , Medios de Cultivo Condicionados/farmacología , Medios de Cultivo Condicionados/toxicidad , Regulación de la Expresión Génica/efectos de los fármacos , Proteína Ácida Fibrilar de la Glía/metabolismo , Microglía/efectos de los fármacos , Óxido Nítrico Sintasa de Tipo II/metabolismo , Fagocitosis/efectos de los fármacos , Ratas , Receptores Depuradores/metabolismo , Factores de Tiempo , Proteínas de Transporte Vesicular/metabolismoRESUMEN
Impaired L-carnitine uptake correlates with higher blood pressure in adult men, and L-carnitine restores endothelial function in aortic rings from spontaneously hypertensive rat (SHR). Thus, endothelial dysfunction in hypertension could result from lower L-carnitine transport in this cell type. L-Carnitine transport is mainly mediated by novel organic cation transporters 1 (Octn1, Na(+)-independent) and 2 (Octn2, Na(+)-dependent); however, their kinetic properties and potential consequences in hypertension are unknown. We hypothesize that L-carnitine transport kinetic properties will be altered in aortic endothelium from spontaneously hypertensive rats (SHR). L-Carnitine transport was measured at different extracellular pH (pHo 5.5-8.5) in the absence or presence of sodium in rat aortic endothelial cells (RAECs) from non-hypertensive Wistar-Kyoto (WKY) rats and SHR. Octn1 and Octn2 mRNA relative expression was also determined. Dilation of endothelium-intact or denuded aortic rings in response to calcitonine gene related peptide (CGRP, 0.1-100 nmol/L) was measured (myography) in the absence or presence of L-carnitine. Total L-carnitine transport was lower in cells from SHR compared with WKY rats, an effect due to reduced Na(+)-dependent (Na(+) dep ) compared with Na(+)-independent (Na(+) indep ) transport components. Saturable L-carnitine transport kinetics show maximal velocity (V max), without changes in apparent K m for Na(+) indep transport in SHR compared with WKY rats. Total and Na(+) dep component of transport were increased, but Na(+) indep transport was reduced by extracellular alkalization in WKY rats. However, alkalization reduced total and Na(+) indep transport in cells from SHR. Octn2 mRNA was higher than Octn-1 mRNA expression in cells from both conditions. Dilation of artery rings in response to CGRP was reduced in vessels from SHR compared with WKY rats. CGRP effect was endothelium-dependent and restored by L-carnitine. All together these results suggest that reduced L-carnitine transport (likely via Na(+)-dependent Octn2) could limit this compound's potential beneficial effects in RAECs from SHR.
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Aorta/metabolismo , Carnitina/metabolismo , Células Endoteliales/metabolismo , Endotelio Vascular/metabolismo , Hipertensión/metabolismo , Animales , Aorta/efectos de los fármacos , Aorta/patología , Transporte Biológico , Presión Sanguínea , Péptido Relacionado con Gen de Calcitonina/farmacología , Proteínas Portadoras/genética , Proteínas Portadoras/metabolismo , Células Cultivadas , Células Endoteliales/efectos de los fármacos , Células Endoteliales/patología , Endotelio Vascular/efectos de los fármacos , Endotelio Vascular/patología , Expresión Génica , Humanos , Concentración de Iones de Hidrógeno , Hipertensión/patología , Hipertensión/fisiopatología , Cinética , Masculino , Proteínas de la Membrana/genética , Proteínas de la Membrana/metabolismo , Proteínas de Transporte de Catión Orgánico/genética , Proteínas de Transporte de Catión Orgánico/metabolismo , Ratas , Ratas Endogámicas SHR , Ratas Endogámicas WKY , Sodio/metabolismo , Miembro 5 de la Familia 22 de Transportadores de Solutos , Proteínas Transportadoras de Solutos , Simportadores , Técnicas de Cultivo de Tejidos , Vasodilatación/efectos de los fármacosRESUMEN
Microvascular and macrovascular endothelial function maintains vascular reactivity. Several diseases alter endothelial function, including hypertension, obesity, and diabetes mellitus. In addition, micro- and macrovascular endothelial dysfunction is documented in GDM with serious consequences for the growing fetus. Increased l-arginine uptake via hCAT-1 and NO synthesis by eNOS is associated with GDM. These alterations are paralleled by activation of purinergic receptors and increased umbilical vein, but not arteries blood adenosine accumulation. GDM associates with NO-reduced adenosine uptake in placental endothelium, suggested to maintain and/or facilitate insulin vasodilation likely increasing hCAT-1 and eNOS expression and activity. It is proposed that increased umbilical vein blood adenosine concentration in GDM reflects a defective metabolic state of human placenta. In addition, insulin recovers GDM-alterations in hCAT-1 and eNOS in human micro- and macrovascular endothelium, and its biological actions depend on preferential activation of insulin receptors A and B restoring a normal-like from a GDM-like phenotype. We summarized existing evidence for a potential role of insulin/adenosine/micro- and macrovascular endothelial dysfunction in GDM. These mechanisms could be crucial for a better management of the mother, fetus and newborn in GDM pregnancies.
Asunto(s)
Adenosina/metabolismo , Diabetes Gestacional , Células Endoteliales , Insulina/metabolismo , Placenta , Arginina/metabolismo , Diabetes Gestacional/metabolismo , Diabetes Gestacional/patología , Diabetes Gestacional/fisiopatología , Células Endoteliales/metabolismo , Células Endoteliales/patología , Femenino , Humanos , Óxido Nítrico/biosíntesis , Óxido Nítrico Sintasa de Tipo III/biosíntesis , Placenta/irrigación sanguínea , Placenta/metabolismo , Placenta/patología , Placenta/fisiopatología , EmbarazoRESUMEN
Gestational diabetes mellitus (GDM) courses with increased fetal plasma adenosine concentration and reduced adenosine transport in placental macrovascular endothelium. Since insulin modulates human equilibrative nucleoside transporters (hENTs) expression/activity, we hypothesize that GDM will alter hENT2-mediated transport in human placental microvascular endothelium (hPMEC), and that insulin will restore GDM to a normal phenotype involving insulin receptors A (IR-A) and B (IR-B). GDM effect on hENTs expression and transport activity, and IR-A/IR-B expression and associated cell signalling cascades (p42/44 mitogen-activated protein kinases (p42/44(mapk)) and Akt) role in hPMEC primary cultures was assayed. GDM associates with elevated umbilical whole and vein, but not arteries blood adenosine, and reduced hENTs adenosine transport and expression. IR-A/IR-B mRNA expression and p42/44(mapk)/Akt ratios ('metabolic phenotype') were lower in GDM. Insulin reversed GDM-reduced hENT2 expression/activity, IR-A/IR-B mRNA expression and p42/44(mapk)/Akt ratios to normal pregnancies ('mitogenic phenotype'). It is suggested that insulin effects required IR-A and IR-B expression leading to differential modulation of signalling pathways restoring GDM-metabolic to a normal-mitogenic like phenotype. Insulin could be acting as protecting factor for placental microvascular endothelial dysfunction in GDM.
Asunto(s)
Adenosina/metabolismo , Diabetes Gestacional/metabolismo , Endotelio Vascular/metabolismo , Insulina/farmacología , Microvasos/metabolismo , Placenta/irrigación sanguínea , Adenosina/sangre , Adulto , Transporte Biológico/efectos de los fármacos , Endotelio Vascular/efectos de los fármacos , Tranportador Equilibrativo 1 de Nucleósido/metabolismo , Transportador Equilibrativo 2 de Nucleósido/genética , Transportador Equilibrativo 2 de Nucleósido/metabolismo , Femenino , Sangre Fetal/metabolismo , Regulación de la Expresión Génica/efectos de los fármacos , Humanos , Recién Nacido , Cinética , Microvasos/efectos de los fármacos , Modelos Biológicos , Embarazo , Regiones Promotoras Genéticas/genética , Isoformas de Proteínas/genética , Isoformas de Proteínas/metabolismo , Receptor de Insulina/genética , Receptor de Insulina/metabolismoRESUMEN
Gestational diabetes mellitus (GDM) is a syndrome compromising the health of the mother and the fetus. Endothelial damage and reduced metabolism of the vasodilator adenosine occur and fetal hyperinsulinemia associated with deficient insulin response and a metabolic rather than mitogenic phenotype is characteristic of this pathology. These phenomena lead to endothelial dysfunction of the fetoplacental unit. Major databases were searched for the relevant literature in the field. Special attention was placed on publications related with diabetes and hormone/metabolic disorders. We aimed to summarize the information regarding insulin sensitivity changes in GDM and the role of adenosine in this phenomenon. Evidence supporting the possibility that fetal endothelial dysfunction involves a functional link between adenosine and insulin signaling in the fetal endothelium from GDM pregnancies is summarized. Since insulin acts via membrane receptors type A (preferentially associated with mitogenic responses) or type B (preferentially associated with metabolic responses), a differential activation of these receptors in this syndrome is proposed.
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Adenosina/metabolismo , Diabetes Gestacional/fisiopatología , Insulina/metabolismo , Animales , Endotelio Vascular/patología , Femenino , Enfermedades Fetales/etiología , Humanos , Hiperinsulinismo/etiología , Circulación Placentaria , Embarazo , Receptor de Insulina/metabolismoRESUMEN
La hiperplasia angiolinfoide con eosinofilia es una rara enfermedad vascular, inflamatoria, benigna y de etiología desconocida que se caracterizapor una proliferación vascular formada por células endoteliales epitelioides grandes y un infiltrado inflamatorio de linfocitos, histiocitos yeosinófilos. Clínicamente se presenta como pápulas o nódulos subcutáneos, únicos o múltiples, de color rojo-marrón a violáceos que se localizan, en la mayoría de casos, en cabeza y cuello; algunas veces está asociada a prurito y dolor. Ocurre frecuentemente en mujeres entre la tercera y cuarta década de la vida. Existen múltiples modalidades de tratamiento pero es frecuente la recurrencia. Se presenta el caso de un paciente varón de 49 años de edad, con una lesión en placa indurada a nivel de antebrazo, pruriginosa y con diagnóstico de hiperplasia angiolinfoide con eosinofilia según histopatología. El interés del caso radica en la localización infrecuente de la lesión.
Angiolymphoid hyperplasia with eosinophilia is a rare benign inflammatory, vascular disease of unknown etiology, characterized by vascular proliferation composed of large epithelioid endothelial cells and an inflammatory infiltrate of lymphocytes, histiocytes and eosinophils. Clinically, it manifests as papules or subcutaneous nodules, single or multiple, red-brown to violet, which are located in most cases in the head and neck, sometimes associated with itching and pain. This patology occurs frequently in women between the third and fourth decade of life. There are multiple treatment modalities, but recurrence is common. We describe the case of a male patient aged 49 with a itching hardened plate injury at the forearm, with the disnosis of angiolymphoid hyperplasia with eosinophilia by histopathology. The interest of the case lies in the unusual location of the lesion.
Asunto(s)
Humanos , Masculino , Persona de Mediana Edad , Eosinofilia , Eosinófilos , Hiperplasia Angiolinfoide con EosinofiliaRESUMEN
Los siringomas son tumoraciones anexiales benignas bastante frecuentes en la población femenina de edad media, siendo la localización habitual la periorbitaria. Siringomas de localización vulvar han sido descritos cada vez más frecuentemente en la literatura, pero aún son considerados una patología inusual. Reportamos el caso de una mujer de 41 años que presentó múltiples siringomas vulvares, habiendo sido tratada por mucho tiempo sin éxito por prurito vulvar.