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A localized surface plasmon resonance (LSPR) sensor based on tapered optical fiber (TOF) using hollow gold nanoparticles (HAuNPs) for measuring the refractive index (RI) is presented. This optical fiber sensor is a good candidate for a label-free RI biosensor. In practical biosensors, bioreceptors are immobilized on nanoparticles (NPs) that only absorb specific biomolecules. The binding of these biomolecules to the receptors changes the local RI around the sensor and this change is detected by the transmittance spectrum of the fiber. Fast, accurate, easy and low-cost disease diagnosis are the advantages of optical fiber biosensors. In this paper, the structure theory is reviewed and the sensor is simulated by the finite difference time domain (FDTD) method and the finite element method (FEM) and the effect of the thickness and diameter of the HAuNPs and the waist diameter of the TOF is investigated. For the structure with HAuNPs thickness (2.5 nm), diameter (50 nm), and the fiber waist diameter of 10 μm, the wavelength sensitivity of 489.8 nm/RIU and full width at half maximum (FWHM) of 50 nm are obtained, which are better than those specifications in some other LSPR fiber sensors. In addition, the sensitivity of the sensor increases about 2–3 times compared to those of sensors with the same structure. Although there are many parameters in human blood that can change its RI, in practical work, the special bioreceptors on the sensor can deactivate other markers except the specific cancer markers, which changes the effective RI. Therefore, this optical fiber sensor is used for label-free detecting the RI of cancer cells and can be used as a biosensor for the detection of early stages of cancers in a non-invasive way, just using human blood samples. [ABSTRACT FROM AUTHOR]

Introduction: The developing and promising optogenetic stimulation method can aid functional recovery by carefully regulating neuronal activity in brain circuits damaged by a stroke lesion. This investigation assesses the potential pretreatment effects of optogenetic stimulation on an ischemic stroke animal model. Methods: Lentiviruses containing pLenti-CaMKIIa-hChR2 (H134R)-mCherry-WPRE were administered to adult male Wistar rats. It was injected into the right striatum for this purpose. Twenty-six days after the virus injection, the animals were exposed to blue laser light for six days in a row for 30 minutes at a time. Twenty-four hours after the final light stimulation, the transient middle cerebral artery occlusion (tMCAO) was done. One day after reperfusion, the neurological processes and the size of the brain infarcts in ischemic rats were evaluated. The transcript levels of microRNAs 21 and 124a--epigenetic indicators for neuroprotection and neurogenesis--were also assessed in the striatum and hippocampus. Results: Our findings suggested that pretreatment with glutamatergic striatum optogenetic stimulation could reduce neurological impairments in rats and boost neuronal survival in both striatum and hippocampal regions. Also, the expression of microRNA-21 (miR-21) in the striatum was significantly increased in rats that had been optogenetically stimulated. Additionally, miR-124a expression was elevated in both regions in rats given tMCAO, and pretreatment with optical stimulations may considerably lower its expression in the hippocampus. Conclusion: According to our findings, optogenetic stimulation pretreatment of the striatum positively affects stroke recovery. The effect is partially mediated by altering miRNAs involved in neurogenesis and subsequently activating its downstream signaling cascade. [ABSTRACT FROM AUTHOR]

Degenerative eye diseases cause partial or complete blindness due to photoreceptor degeneration. Optogenetic gene therapy is a revolutionary technique combining genetics and optical methods to control the function of neurons. Due to the inherent risk of photochemical damage, the light intensity necessary to activate Opto-mGluR6 surpasses the safe threshold for retinal illumination. Conversely, red-shifted lights pose a significantly lower risk of inducing such damage compared to blue lights. We designed red-shifted Opto-mGluR6 photopigments with a wide, red-shifted working spectrum compared to Opto-mGluR6 and examined their excitation capability in vitro. ROM19, ROM18 and ROM17, red-shifted variants of Opto-mGluR6, were designed by careful bioinformatics/computational studies. The predicted molecules with the best scores were selected, synthesised and cloned into the pAAV-CMV-IRES-EGFP vector. Expression of constructs was confirmed by functional assessment in engineered HEK-GIRK cells. Spectrophotometry and patch clamp experiments demonstrated that the candidate molecules were sensitive to the desired wavelengths of the light and directly coupled light stimuli to G-protein signalling. Herein, we introduce ROM17, ROM18 and ROM19 as newly generated, red-shifted variants with maximum excitation red-shifted of ~ 40nm, 70 nm and 126 nm compared to Opto-mGluR6. [ABSTRACT FROM AUTHOR]

Introduction: Radiofrequency electromagnetic radiation (RFEMR) and extremely low-frequency electromagnetic fields (ELF-EMF) have emerged as noteworthy sources of environmental pollution in the contemporary era. The potential biological impacts of RF-EMR and ELF-EMF exposure on human organs, particularly the central nervous system (CNS), have garnered considerable attention in numerous research studies. Methods: This article presents a comprehensive yet summarized review of the research on the explicit/implicit effects of RF-EMR and ELF-EMF exposure on CNS performance. Results: Exposure to RF-EMR can potentially exert adverse effects on the performance of CNS by inducing changes in the permeability of the blood-brain barrier (BBB), neurotransmitter levels, calcium channel regulation, myelin protein structure, the antioxidant defense system, and metabolic processes. However, it is noteworthy that certain reports have suggested that RF-EMR exposure may confer cognitive benefits for various conditions and disorders. ELF-EMF exposure has been associated with the enhancement of CNS performance, marked by improved memory retention, enhanced learning ability, and potential mitigation of neurodegenerative diseases. Nevertheless, it is essential to acknowledge that ELF-EMF exposure has also been linked to the induction of anxiety states, oxidative stress, and alterations in hormonal regulation. Moreover, ELF-EMR exposure alters hippocampal function, notch signaling pathways, the antioxidant defense system, and synaptic activities. Conclusion: The RF-EMR and ELF-EMF exposures exhibit both beneficial and adverse effects. Nevertheless, the precise conditions and circumstances under which detrimental or beneficial effects manifest (either individually or simultaneously) remain uncertain. [ABSTRACT FROM AUTHOR]

Introduction: Introduction: Several studies have demonstrated that orexins may regulate different forms of affective and cognitive processes during wakefulness. The Orbitofrontal Cortex (OFC) and Anterior Cingulate Cortex (ACC), as an essential part of the Prefrontal Cortex (PFC), have a crucial role in cognitive processes such as reward and decision-making. They also have a high amount of orexin receptor type 1 (OX1Rs). Methods: In the present study, we inhibited OX1Rs in this area after a 10-min baseline recording to find out the role of OX1Rs in the OFC neuron’s firing rate. Next, we inhibited the lateral hypothalamus (LH) as the primary source of orexinergic neurons. Afterward, using a single-unit recording technique in rats, we detected the effects of the lateral hypothalamus on the firing rate and activity pattern of the ACC or OFC neurons. Results: Data showed that the blockade of OX1Rs in the OFC could excite 8 and inhibit 1 neuron(s) out of 11. In addition, the blockade of OX1Rs in the ACC could excite 6 and inhibit 3 neurons out of 10. LH inactivation excited 5 out of 12 neurons and inhibited 6 in the ACC. It also excited 8 and inhibited 6 neurons out of 14 in the OFC. These data suggest that the blockade of OX1Rs excites 72% of the neurons, but LH inactivation had a stimulating effect on only 50% of neurons in two main subregions of the PFC. Conclusion: Accordingly, PFC neurons may receive the orexinergic inputs from the LH and indirectly from other sources. [ABSTRACT FROM AUTHOR]

The use of electromagnetic fields (EMFs) is essential in daily life. Since 1970, concerns have grown about potential health hazards from EMF. Exposure to EMF can stimulate nerves and affect the central nervous system, leading to neurological and cognitive changes. However, current research results are often vague and contradictory. These effects include changes in memory and learning through changes in neuronal plasticity in the hippocampus, synapses and hippocampal neuritis, and changes in metabolism and neurotransmitter levels. Prenatal exposure to EMFs has negative effects on memory and learning, as well as changes in hippocampal neuron density and histomorphology of hippocampus. EMF exposure also affects the structure and function of glial cells, affecting gate dynamics, ion conduction, membrane concentration, and protein expression. EMF exposure affects gene expression and may change epigenetic regulation through effects on DNA methylation, histone modification, and microRNA biogenesis, and potentially leading to biological changes. Therefore, exposure to EMFs possibly leads to changes in cellular and molecular mechanisms in central nervous system and alter cognitive function. • Electromagnetic field (EMF) exposure alters neurogenesis and apoptosis. • EMF exposure affects epigenetic and non-epigenetic regulation of gene expression. • Exposure to EMF modifies the expression, function, and structure of ion channels. • EMF exposure changes synaptic transmission and glial function. • EMF exposure causes the neuronal network remodeling and behavioral consequences. [ABSTRACT FROM AUTHOR]