Benjaminkramer9890

Results of diffusion tensor tractography (DTT) for the ARAS showed decreased neural connectivity in the left lower dorsal ARAS, both lower ventral ARAS, and both upper ARAS. To the best of our knowledge, this is the first report of injury to the ARAS in bilateral pontine infarction diagnosed by DTT. We presume that our report would provide clinicians a better understanding of the mechanism of impaired consciousness in patients with pontine infarction.Peripheral nerve injury is a life-changing disability with significant socioeconomic consequences. In this rat model, we propose that partial enzyme digestion can facilitate the functional recovery of a crushed nerve. The sciatic nerves were harvested and in vitro cultured with the addition of Liberase to determine the appropriate enzyme amount in the hyaluronic acid (HA) membrane. Then, the sciatic nerve of adult male Sprague-Dawley rats was exposed, crushed, and then treated with partial enzyme digestion (either 0.001 or 0.002 unit/mm2 Liberase-HA membrane). The sciatic function index (SFI) for functional recovery of the sciatic nerve was evaluated. After 2 h of in vitro digestion, fascicles and axons were separated from each other, with the cells mobilized. Greater destruction of histology structures occurred in the high enzyme (Liberase-HA membrane at 0.002 unit/mm2) group at 24 h than in the low enzyme (0.001 unit/mm2) group at 48 h. In the SFI evaluation, the improvement in 0.001 unit/mm2 Liberase group was significantly better than control and 0.002 unit/mm2 Liberase group. Our study demonstrated that appropriate enzyme digestion had a significantly faster and earlier recovery.Transcription factor EB (TFEB)-based gene therapy is a promising therapeutic strategy in treating neurodegenerative diseases by promoting autophagy/lysosome-mediated degradation and clearance of misfolded proteins that contribute to the pathogenesis of these diseases. However, recent findings have shown that TFEB has proinflammatory properties, raising the safety concerns about its clinical application. To investigate whether TFEB induces significant inflammatory responses in the brain, male C57BL/6 mice were injected with phosphate-buffered saline (PBS), adeno-associated virus serotype 8 (AAV8) vectors overexpressing mouse TFEB (pAAV8-CMV-mTFEB), or AAV8 vectors expressing green fluorescent proteins (GFPs) in the barrel cortex. The brain tissue samples were collected at 2 months after injection. Western blotting and immunofluorescence staining showed that mTFEB protein levels were significantly increased in the brain tissue samples of mice injected with mTFEB-overexpressing vectors compared with those injected with PBS or GFP-overexpressing vectors. check details pAAV8-CMV-mTFEB injection resulted in significant elevations in the mRNA and protein levels of lysosomal biogenesis indicators in the brain tissue samples. No significant changes were observed in the expressions of GFAP, Iba1, and proinflammation mediators in the pAAV8-CMV-mTFEB-injected brain compared with those in the control groups. Collectively, our results suggest that AAV8 successfully mediates mTFEB overexpression in the mouse brain without inducing apparent local inflammation, supporting the safety of TFEB-based gene therapy in treating neurodegenerative diseases.

Inflammation is involved in cerebral ischemia/reperfusion (I/R)-induced neurological damage. Saikosaponin A (SSa), extracted from

, has been reported to exert anti-inflammatory effects. This article aimed to investigate whether SSa could ameliorate neuroinflammation mediated by ischemic stroke and the underlying mechanism.

Rat middle cerebral artery occlusion (MCAO) model was employed in this study, and the cognitive and motor functions were detected by behavioral tests. Inflammatory cytokines in the serum were detected by ELISA kits. The expression levels of Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), and high-mobility group box 1 (HMGB1) in the brain tissues were assayed with Western blot.

Our results showed that SSa pretreatment could significantly reduce brain damage, improve neurological function recovery, and decrease the water content of brain tissues when compared with the model group. SSa pretreatment significantly reduced the serum HMGB1 level and downregulated the contents of inflammatory cytokines including tumor necrosis factor-α, interleukin-1 beta, and interleukin-6. Furthermore, SSa pretreatment could attenuate the decreased TLR4 and nucleus NF-κB in the brain of MCAO rats. The protein level of HMGB1 in the nucleus was significantly upregulated in the SSa pretreatment group.

Our results suggested that the pretreatment with SSa provided significant protection against cerebral I/R injury in rats via its anti-inflammation property by inhibiting the nucleus HMGB1 release.

Our results suggested that the pretreatment with SSa provided significant protection against cerebral I/R injury in rats via its anti-inflammation property by inhibiting the nucleus HMGB1 release.

Sevoflurane, a volatile anesthetic, is known to induce widespread neuronal degeneration and apoptosis. Recently, the stress-inducible protein sestrin 2 and adenosine monophosphate-activated protein kinase (AMPK) have been found to regulate the levels of intracellular reactive oxygen species (ROS) and suppress oxidative stress. Notoginsenoside R1 (NGR1), a saponin isolated from

, has been shown to exert neuroprotective effects. The effects of NGR1 against neurotoxicity induced by sevoflurane were assessed.

Sprague-Dawley rat pups on postnatal day 7 (PD7) were exposed to sevoflurane (3%) anesthesia for 6 h. NGR1 at doses of 12.5, 25, or 50 mg/kg body weight was orally administered to pups from PD2 to PD7.

Pretreatment with NGR1 attenuated sevoflurane-induced generation of ROS and reduced apoptotic cell counts. Western blotting revealed decreased cleaved caspase 3 and Bad and Bax pro-apoptotic protein expression. NGR1 substantially upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) expression along with increased heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase-1 levels, suggesting Nrf2 signaling activation. Enhanced sestrin-2 and phosphorylated AMPK expression were noticed following NGR1 pretreatment.

This study revealed the neuroprotective effects of NGR1 through effective suppression of apoptosis and ROS via regulation of apoptotic proteins and activation of Nrf2/HO-1 and sestrin 2/AMPK signaling cascades.

This study revealed the neuroprotective effects of NGR1 through effective suppression of apoptosis and ROS via regulation of apoptotic proteins and activation of Nrf2/HO-1 and sestrin 2/AMPK signaling cascades.Reversible splenial lesion syndrome (RESLES) is a single-stage non-specific syndrome with unclear pathogenesis. There has been no report on answer delay in patients with RESLES. We report a female patient who was admitted to our department for mixed aphasia accompanied by cognitive impairment. During the rapid improvement of aphasia, there was a clear phase of language output response delay accompanied by resolution of imaging lesions. We analyzed the course and the examination results of the patient and speculated the cause and pathogenesis. RESLES-relevant knowledge was systematically reviewed, which will help doctors in the classification of cerebral function and the diagnosis of RESLES. The specific language and cognitive impairment may be associated with the damage of contact fibers in the bilateral primary and secondary sensory and motor cortices.Most research has mainly focused on the decline of the subjective experience in Alzheimer's disease (AD). However, few attempts have been made to evaluate whether subjective experience may be maintained in AD. In this narrative review, we attempt to provide a positive view, according to which patients with AD can enjoy, to some extent, subjective experience during memory retrieval. Memory and expression difficulties (e.g., aphasia) limit the ability of patients with AD to describe their memories, resulting in a little specificity of reported memories. However, according to the "authentic subjective experience" view, we propose in this study that the ability to mentally relive these memories could be preserved in the patients. By proposing the authentic subjective experience view, we attempt to provide an alternative view to the general consideration that the patients suffer a diminished subjective experience. This view can contribute to a larger clinical framework that gives a positive meaning to the subjective experience of patients with AD. Furthermore, several clinical and empirical implications can be drawn from the authentic subjective experience view, including the possibility to evaluate behavioral correlates of the subjective experience in AD.The purpose of this study was to quantify head motion between isometric erector spinae (ES) contraction strategies, paradigms, and intensities in the development of a neuroimaging protocol for the study of neural activity associated with trunk motor control in individuals with low back pain. Ten healthy participants completed two contraction strategies; (1) a supine upper spine (US) press and (2) a supine lower extremity (LE) press. Each contraction strategy was performed at electromyographic (EMG) contraction intensities of 30, 40, 50, and 60% of an individually determined maximum voluntary contraction (MVC) (±10% range for each respective intensity) with real-time, EMG biofeedback. A cyclic contraction paradigm was performed at 30% of MVC with US and LE contraction strategies. Inertial measurement units (IMUs) quantified head motion to determine the viability of each paradigm for neuroimaging. US vs LE hold contractions induced no differences in head motion. Hold contractions elicited significantly less head motion relative to cyclic contractions. Contraction intensity increased head motion in a linear fashion with 30% MVC having the least head motion and 60% the highest. The LE hold contraction strategy, below 50% MVC, was found to be the most viable trunk motor control neuroimaging paradigm.[This corrects the article on p. 4 in vol. 11, PMID 32104589.].The present study was performed to evaluate the effects of ormosanine against spinal cord injury (SCI) in rats and to examine the possible molecular mechanism of action. SCI was induced using an impactor device, and rats were treated with ormosanine 10, 50 or 100 mg/kg, p.o., for 10 days after induction of SCI. The effect of ormosanine on SCI was determined by estimating neurological functions and cytokines and parameters of oxidative stress level were estimated in SCI rats. Quantitative reverse transcription polymerase chain reaction, Western blotting analysis and histopathological study were performed on spinal tissue of SCI rats. The data suggested that treatment with ormosanine reversed the alterations of neurological function in SCI rats. Moreover, the levels of cytokines, oxidative stress and reactive oxygen species production were reduced in the ormosanine treatment group compared to the SCI group. The levels of calpain and neuronal nitric oxide synthase activity were significantly reduced in the spinal tissue of the ormosanine treatment group compared to the SCI group.