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Autism spectrum disorder (ASD) is defined by persistent deficits in social communication/interaction and stereotypic behaviors with many diagnosed persons experiencing a developmental regression at >1 year‑old. It was hypothesized that progressive childhood encephalopathy is an important etiological factor in ASD pathogenesis. This hypothesis‑testing study examined the relationship between diagnosed childhood encephalopathy and ASD. The Independent Healthcare Research Database is composed of de‑identified linked eligibility and claim healthcare records prospectively generated from the Florida Medicaid system. A cohort of 101,736 persons eligible for Florida Medicaid from 1990‑2009 and continuously eligible with ≥10 outpatient office visits during the 120 month period following birth were examined using SAS software. There were 1,397 persons (7,223 person‑years) in the ASD diagnosed cohort and 100,339 persons (980,786 person‑years) in the undiagnosed cohort. The incidence rate of encephalopathy was examined using Cox proportional hazards ratio models. In the ASD cohort relative to the undiagnosed cohort, a significantly increased incidence rate of diagnosed encephalopathy was observed in the unadjusted and adjusted models. The risk for an encephalopathy diagnosed at >1 year‑old was greater than for an encephalopathy diagnosed at 1 year‑old.The catecholamine norepinephrine (NE) links hindbrain metabolic‑sensory neurons with downstream gluco‑regulatory loci, including the ventromedial hypothalamic nucleus (VMN). Exogenous NE up‑regulates VMN expression of glutamate decarboxylase (GAD), biomarker for the gluco‑inhibitory transmitter γ‑aminobutryic acid (GABA). Brain glycogen phosphorylase (GP)‑muscle (GPmm) and ‑brain (GPbb) variants are stimulated in vitro by NE or energy deficiency, respectively. Current research investigated whether lactoprivic‑driven VMN NE signaling regulates GABA and if VMN GPmm and GPbb profiles react differently to that deficit cue. Male rats were pretreated by caudal fourth ventricle delivery of the selective catecholamine neurotoxin 6‑hydroxydopamine (6OHDA) ahead of the monocarboxylate transporter inhibitor alpha‑cyano‑4‑hydroxycinnamic acid (4CIN). Micropunch‑dissected VMN tissue was analyzed by Western blot and ELISA to assess NE‑dependent 4CIN regulation of GAD and GP variant protein expression and NE activity. 4CIN caused 6OHDA‑reversible augmentation of VMN NE content and plasma glucose and counter‑regulatory hormone levels. 6OHDA stimulated basal VMN GAD expression, but prevented 4CIN stimulation of this profile. Neurotoxin inhibited or increased baseline VMN GPmm and GPbb levels, respectively, in non‑4CIN‑injected rats. 6OHDA deterred 4CIN inhibition of GPmm, but did not prevent drug stimulation of GPbb. Results affirm hindbrain lactoprivic regulation of glucostasis. Hindbrain NE exerts opposite effects on VMN GABA transmission during hindbrain lactostasis vs. ‑privation. VMN norepinephrine‑ vs. energy‑sensitive GP variants are subject to dissimilar NE regulation during energy homeostasis, and respond differently to hindbrain lactoprivation.Adult‑onset hypothyroidism is associated with an increase in cell atrophy of the hippocampal pyramidal neurons. Physical exercise implies diverse actions on the neural tissue that promote neuron proliferation and survival. The beneficial effects of exercise seem to be inversely linked to its intensity, so that strenuous exercise has reduced protective effects. In this study we evaluated the capacity of a moderate forced‑exercise routine to counteract the neurodegenerative effects of a hypothyroid condition induced during adulthood. Simultaneously with a chronic anti‑thyroid chemical treatment, a group of rats was forced to walk in a motorized wheel for 30 min daily five times a week. In four weeks of treatment the rats developed a plain hypothyroid condition that in non‑exercised rats was accompanied by a marked increase in the number of atrophic cells in all CA regions of the hippocampus. The forced‑exercise treatment did not counter the development of hypothyroidism and its signs, but it did prevent almost completely the associated neuronal damage in all CA regions. The forced exercise also improved the cognitive function in a spatial‑learning test. These results indicate that moderate exercise has the potential to prevent the structural and functional deficits associated with a hypothyroid condition.Following nerve tissue damage, various events, such as inflammatory responses, microglial activation, endoplasmic reticulum stress, and apoptosis, can occur, which all lead to cell death, prevent axonal growth, and cause axonal circumvolution. So far, several researchers have tended to adopt strategies to reduce the harmful conditions associated with neurological disorders, and stem‑cell‑based therapy is one of those promising strategies. Epidermal neural crest stem cells (EPI‑NCSCs) are a type of stem cell that has widely been employed for the treatment of various neurological disorders. It has been suggested that these stem cells perform their supportive actions primarily through the release of different neurotrophic factors. Hence, in this study, the neuroprotective impacts of valproic acid (VPA) and crocin were evaluated on the mRNA expression levels of brain‑derived neurotrophic factor (BDNF) and glial‑cell‑derived neurotrophic factor (GDNF) in EPI‑NCSCs. In this research, we isolated EPI‑NCSCs from the us neurological disorders, such as spinal cord injury.The effect of C60 fullerene aqueous colloid solution (C60FAS) on the intensity of long‑lasting (persisting for one hour) rotational movements in non‑anesthetized rats was investigated. For this purpose, an experimental hemiparkinsonic animal model was used in the study. Rotational movements in hemiparkinsonic animals were initiated by the intraperitoneal administration of the dopamine receptor agonist apomorphine. It was shown that a preliminary injection of C60FAS (a substance with powerful antioxidant properties) in hemiparkinsonic rats induced distinct changes in animal motor behavior. It was revealed that fullerene‑pretreated animals, in comparison with non‑pretreated or vehicle‑pretreated rats, rotated for 1 h at an approximately identical speed until the end of the experiment, whereas the rotation speed of control rats gradually decreased to 20-30% of the initial value. One can assume that the observed changes in the movement dynamics of the hemiparkinsonic rats after C60FAS pretreatment presumably can be induced by the influence of C60FAS on the dopaminergic system, although the isolated potentiation of the action of apomorphine C60FAS cannot be excluded. Nevertheless, earlier data on the action of C60FAS on muscle dynamics has suggested that C60FAS can activate a protective action of the antioxidant system in response to long‑lasting muscular activity and that the antioxidant system in turn may directly decrease fatigue‑relate d changes during long‑lasting muscular activity.The efficacy of pseudoephedrine (PSE) as a nasal decongestant has been well‑demonstrated; however, PSE is strictly prescribed as a control substance due to its controversial psychostimulant effects. Although standard stimulatory drugs increase exploratory behavior and stimulate the dopamine system, the exact effects of PSE on locomotion and electrical activity in the striatum have not been determined. This study aimed to examine and compare the locomotor activities, local field potential (LFP) and sleep‑wake patterns produced by PSE and morphine, which is a standard drug used to promote psychomotor activity. Male Swiss albino mice were anesthetized and implanted with an intracranial electrode into the striatum. Animals were divided into four groups, which received either saline, PSE or morphine. Locomotor activity and LFP signals were continuously monitored following pseudoephedrine or morphine treatment. One‑way ANOVA revealed that locomotor count was significantly increased by morphine, but not PSE. CID44216842 solubility dmso Frequency analyses of LFP signals using fast Fourier transform also revealed significant increases in spectral powers of low‑ and high‑gamma waves following treatment with morphine, but not PSE. Sleep‑wake analysis also confirmed significant increases in waking and decreases in both non‑rapid eye movement and rapid eye movement sleep following morphine treatment. Sleep‑wakefulness did not appear to be disturbed by PSE treatment. These findings indicate that acute PSE administration, even at high doses, does not have psychostimulatory effects and may be relatively safe for the treatment of non‑chronic nasal congestion.Poly (lactide‑co‑glycolide) (PLGA) nanoparticles (NPs) are biodegradable carriers that participate in the transport of neuroprotective drugs across the blood brain barrier (BBB). Targeted brain‑derived neurotrophic factor (BDNF) delivery across the BBB could provide neuroprotection in brain injury. We tested the neuroprotective effect of PLGA nanoparticle‑bound BDNF in a permanent middle cerebral artery occlusion (pMCAO) model of ischemia in rats. Sprague‑Dawley rats were subjected to pMCAO. Four hours after pMCAO, two groups were intravenously treated with BDNF and NP‑BDNF, respectively. Functional outcome was assessed at 2 and 24 h after pMCAO, using the modified neurologic severity score (mNSS) and rotarod performance tests. Following functional assessments, rats were euthanized blood was taken to assess levels of the neurobiomarkers neuron‑specific enolase and S100 calcium‑binding protein β (S100β), and the brain was evaluated to measure the infarct volume. The NP‑BDNF‑treated group showed significant improvement in mNSS compared with pMCAO and BDNF‑treated groups and showed improved rotarod performance. The infarct volume in rats treated with NP‑BDNFs was also significantly smaller. These results were further corroborated by correlating differences in estimated NSE and S100β. NP‑BDNFs exhibit a significant neuroprotective effect in the pMCAO model of ischemia in rats.The broad applications of ultrawide-band signals and terahertz waves in quantum measurements1,2, imaging and sensing techniques3,4, advanced biological treatments5, and very-high-data-rate communications6 have drawn extensive attention to ultrafast electronics. In such applications, high-speed operation of electronic switches is challenging, especially when high-amplitude output signals are required7. For instance, although field-effect and bipolar junction devices have good controllability and robust performance, their relatively large output capacitance with respect to their ON-state current substantially limits their switching speed8. Here we demonstrate a novel on-chip, all-electronic device based on a nanoscale plasma (nanoplasma) that enables picosecond switching of electric signals with a wide range of power levels. The very high electric field in the small volume of the nanoplasma leads to ultrafast electron transfer, resulting in extremely short time responses. We achieved an ultrafast switching speed, higher than 10 volts per picosecond, which is about two orders of magnitude larger than that of field-effect transistors and more than ten times faster than that of conventional electronic switches. We measured extremely short rise times down to five picoseconds, which were limited by the employed measurement set-up. By integrating these devices with dipole antennas, high-power terahertz signals with a power-frequency trade-off of 600 milliwatts terahertz squared were emitted, much greater than that achieved by the state of the art in compact solid-state electronics. The ease of integration and the compactness of the nanoplasma switches could enable their implementation in several fields, such as imaging, sensing, communications and biomedical applications.