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These results suggest that RA-VII tightly stabilizes the GTP•eEF2 complex structure, which is able to bind to the ribosomal functional site, but seems to suppress normal turnover of eEF2 after translocation. The properties of RA-VII make it a novel ligand for probing the action of eEF2 in the process of translocation on the ribosome.Hepatocyte nuclear factor 4α (HNF4α) has essential roles in controlling the expression of a variety of genes involved in key metabolic pathways, including gluconeogenesis in the liver. The mechanistic and physiological significance of peroxisome proliferator-activated receptor gamma co-activator-1α (PGC-1α) for HNF4α-mediated transcriptional activation models for gluconeogenic genes is well characterized. However, the transcriptional repression of HNF4α for those genes remains to be examined. NGI1 In this study, we applied novel proteomic techniques to evaluate the interactions of HNF4α, including those with biochemically labile binding proteins. Based upon our experiments, we identified interferon regulatory factor 2 binding protein 2 (IRF2BP2) as a novel HNF4α co-repressor. This interaction could not be detected by conventional immunoprecipitation. IRF2BP2 repressed the transcriptional activity of HNF4α dependent on its E3 ubiquitin ligase activity. Deficiency of the IRF2BP2 gene in HepG2 cells induced gluconeogenic genes comparable to that of forskolin-treated wild-type HepG2 cells. Together, these results suggest that IRF2BP2 represents a novel class of nuclear receptor co-regulator.Nuclear receptor Pregnane X Receptor (PXR; NR1I2) has transcriptional regulation functions for energy homeostasis in the liver. Mouse PXR has a conserved phosphorylation motif at serine 347 (serine 350 in humans) within the ligand-binding domain. PXR phosphorylated at this motif is expressed in mouse livers in response to fasting. Mice with a PXR∗Ser347Ala knockin mutation (PXR KI) were generated to block phosphorylation, and utilized to investigate the role of Ser347 phosphorylation in vivo. PXR KI mice had decreased body weight at 8-weeks of age and had much greater weight loss after fasting compared with PXR WT mice. The cDNA microarray analysis of hepatic mRNAs showed that cell death or apoptotic signaling was induced in fasting PXR KI mice. Moreover, increasing hepatic lipids, triglycerides and the development of hypertriglyceridemia were observed in fasting PXR KI mice. These findings are indicative that blocking phosphorylation prevents mice from maintaining hepatic energy homeostasis. Thus, phosphorylated PXR may be an essential factor to prevent the liver from developing damage caused by fasting.Obesity is closely related to the occurrence of cardiovascular diseases, and an important reason for this is the induction of endothelial cell dysfunction. Mitochondria play an important role in maintaining the function of endothelial cells. In the present study, we examined the effects of the sodium-dependent glucose transporters 2 inhibitor dapagliflozin (DAPA) on the vascular endothelium in obese mice in vivo and on the structure and function of human umbilical vein endothelial cells (HUVECs) in vitro. The results revealed that DAPA rescued vascular endothelial damage in obese mice. Moreover, DAPA reversed the effects of palmitic acid (PA) on the reduction in angiogenesis and the increase in apoptosis in HUVECs. Furthermore, DAPA rescued the reduced mitochondrial membrane potential, mitochondrial viability, energy metabolism, mitochondrial biogenesis and the mitochondrial structural injury caused by PA. DAPA also activated the SIRT1/PGC-1α signaling pathway, while the SIRT1 inhibitor EX-527 abrogated the effects of DAPA on the mitochondria of HUVECs. In summary, our study suggests that DAPA improves endothelial cell mitochondrial function in obese mice by activating the SIRT1/PGC-1α pathway.MicroRNAs (miRNAs) play a crucial role in cancer progression due to their capability to modulate the expression of various target genes. However, given the heterogeneity of tumor cells, miRNAs have been confirmed to exert different regulatory effects. Here, bioinformatic analysis results indicated that expression of miR-330-5p is decreased in colorectal cancer (CRC) tissues and inversely correlated with SND1 expression. Notably, ectopic expression of miR-330-5p restrained tumor cell proliferation, migration, and enhance the sensitivity of CRC cells to 5-FU. Moreover, similar phenotypes were substantiated after inhibition of SND1 expression using RNA interference. Conversely, overexpression of SND1 facilitated the malignant phenotypes of CRC cells and restored miR-330-5p-mediated tumor-suppressive activities in CRC cells. Mechanistically, miR-330-5p directly binds to SND1-3'-untranslated region (3'-UTR), thus involving in inhibiting CRC cells proliferation and invasion and promoting apoptosis. Taken together, miR-330-5p may act as a tumor suppressor by targeting the expression of SND1, suggesting that the miR-330-5p/SND1 axis may be a meaningful regulator for CRC intervention.Endoplasmic reticulum stress (ER stress) plays a crucial role in the process of Alzheimer's disease (AD). Activating transcription factor 6 (ATF6) is a crucial sensor of ER stress. In AD patients, the homeostasis of the endogenous signal H2S produced by cystathionine γ-lyase (CTH) is in disbalance. However, the role of ATF6 and CTH in AD is rarely reported. Herein, we found that ATF6 and CTH were reduced in AD patients and APP/PS1 mice by immunohistochemistry and western blots. In LN229 and U87 MG cells, knockdown of ATF6 attenuated CTH expression, whereas overexpression of ATF6 resulted in upregulation of CTH. Brain-specific ATF6 knockout mice expressed significantly down-regulated CTH in the hippocampus and cortex compared to wild-type mice. Mechanistically, ATF6 and CTH increased H2S generation and autophagy-related proteins. Further we observed that CTH promoted the sulfhydration of αSNAP. This is probably to be the specific mechanism by which AFT6 promotes autophagy. Through in vivo studies, we found that αSNAP sulfhydration expression was significantly lower in ATF6 knockout mice than in wild-type mice. Decreased ATF6 impaired spatial memory retention, while addition of CTH rescued memory loss. Together, we demonstrate that ATF6 positively regulates the expression of CTH, which is closely related to the rescue of AD. Targeting the ATF6/CTH signal pathway may provide a new strategy for the treatment of AD.Electrophysiological and genetic studies reveal two major subclasses of layer 5 (L5) neocortical pyramidal neurons that differ in electrical parameters and afterhyperpolarization. KCa3.1 channels are identified as contributors to slow afterhyperpolarization (sAHP), and they are expressed by one subclass of L5 neurons. Yet, the impact of class-specific sAHP and KCa3.1 channels on coding abilities of the L5 neurons and dynamics of their action potentials (APs) remains poorly understood. Here, by comparing sAHP+ neurons to those with weak sAHP we investigate differences between the two groups in coding and AP features to address the question of whether those differences are due to contribution of KCa3.1 or other channels. Using patch clamp electrophysiology, channel blockers, and immunohistochemistry we demonstrate that Nav1.6 channels but not KCa3.1 channels affect the threshold of AP, its dynamics and coding abilities of the L5 cells. Immunohistochemical data show that KCa3.1+ and KCa3.1- neurons share the same pattern of Nav1.6 expression in the soma and axonal initial segment, thus they may differ in quantity of the channels expressed. Our study links the Nav1.6 function underlying regulation of voltage threshold to the abilities of L5 neurons to encode high frequencies.
Endoscopic port surgery is a promising alternative for the surgical treatment of intracerebral hypertensive basal ganglia hemorrhage (HBGH). The precise location of hematoma is a crucial step for surgery. The authors developed a simple, low-cost navigation method using an Android smartphone for the localization of HBGH.

All patients' CT DICOM data were processed with an open-source software (3D Slicer). The volume of hematoma, angle, and length of trajectory were calculated automatically. A smartphone running the Android system and the Compass APP was used to help insert the inner introducer. An endoscopic port system was applied to create a working channel for neuro-endoscopic hematoma evacuation.

There were 27 patients enrolled in this study (mean age 56). All patients underwent successful surgical evacuation of HBGH with neuroendoscopic evacuation. The mean time taken for the surgical plan was 4min. The total operation time from skin incision to final suture was 82.6min. Compared with standard neuronavigation, mean error of trajectory was 5.1mm. The mean preoperative hematoma volume was 44.8ml. The optimal trajectory angle averaged 39.5°and the length was 71mm. Intraoperative blood loss was about 45ml. Post-operative hematoma volume was 2.9ml, and the average evacuation rate was 93.6%. One week after surgery, the mean GCS score was improved from 8.2 to 13.8 (p<0.01).

This simple, low-cost navigation method using 3D Slicer, an Android smartphone with the Compass APP, helps precisely insert the endoscopic working channel to the desired point, which is crucial for satisfactory evacuation of HBGH.
This simple, low-cost navigation method using 3D Slicer, an Android smartphone with the Compass APP, helps precisely insert the endoscopic working channel to the desired point, which is crucial for satisfactory evacuation of HBGH.The Hybrid Assistive Limb (HAL) is used in training to improve walking ability for stroke patients; however, the quality of the evidence for its effects has not been fully critiqued to date. This study conducted a systematic review of randomized controlled trials to investigate the effectiveness of post-stroke gait training with the HAL. PubMed, the Cochrane Library, the Physiotherapy Evidence Database (PEDro), and the Cumulative Index to Nursing and Allied Health Literature (CINAHL) were searched for randomized controlled clinical trials evaluating the effect of HAL on gait training in stroke patients, published from the inception of each database until March 2021. Two authors screened the titles and abstracts of articles returned in the initial search and reviewed the full text of articles that met the selection criteria. The risk of bias was assessed using the PEDro scale. Of 273 articles retrieved from the databases, three met all inclusion criteria. One study showed that gait training using HAL improves independence in walking; however, the quality of this study was rated as 4 (medium quality). Other studies did not show improvement with HAL in walking independence. This review did not provide strong evidence to support the effectiveness of HAL in improving walking ability.
Models of anxiety disorders and the rationale of exposure therapy (ET) are grounded on classical fear conditioning. Yet, it is unclear whether lower fear ratings of conditioned safety versus threat cues and corresponding neural markers of safety-learning and/or fear inhibition assessed before treatment would predict better outcomes of behavioral exposure.

Sixty-six patients with spider phobia completed pre-treatment clinical and experimental fear conditioning assessments, one session of virtual reality ET, a post-treatment clinical assessment, and a 6-month follow-up assessment. Tilted Gabor gratings served as conditioned stimuli (CS) that were either paired (CS+) or remained unpaired (CS-) with an aversive phobia-related and phobia-unrelated unconditioned stimulus (UCS). CS+/CS- differences in fear ratings and magnetoencephalographic event-related fields (ERFs) were related to percentual symptom reductions from pre- to post-treatment, as assessed via spider phobia questionnaire (SPQ), behavioral avoidance test (BAT), and remission status at 6-month follow-up.
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