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Anxiety after surgery can be a major factor leading to postoperative cognitive dysfunction, particularly in elderly patients. The role of inhibitory neurons in the basolateral amygdala (BLA) in anxiety-like behaviors in aged mice following isoflurane anesthesia remains unclear. Therefore, the present study aimed to investigate the role of inhibitory neurons in isoflurane-treated mice. A total of 30 C57BL/6 mice (age, 13 months) were allocated into the control and isoflurane anesthesia groups (15 mice/group) and were then subjected to several neurological assessments. Behavioral testing using an elevated plus maze test showed that aged mice in the isoflurane anesthesia group displayed significant anxiety-like behavior, since they spent more time in the closed arm, exhibited more wall climbing behavior and covered more distance. In addition, whole-cell patch-clamp recording revealed that the excitability of the BLA excitatory neurons was notably increased following mice anesthesia with isoflurane, while that of inhibitory neurons was markedly reduced. Following mice treatment with diazepam, the excitability of the BLA inhibitory neurons was notably increased compared with that of the excitatory neurons, which was significantly attenuated. Overall, the results of the current study indicated that anxiety-like behavior could occur in aged mice after isoflurane anesthesia, which could be caused by a reduced excitability of the inhibitory neurons in the BLA area. This process could enhance excitatory neuronal activity in aged mice, thus ultimately promoting the onset of anxiety-like behaviors. [ABSTRACT FROM AUTHOR]

A new method to build a stochastic model of as-received coalbed gas content was proposed, and the workflow is explained in detail in this paper. First, dry-ash-free gas content model was obtained by combining the trend property and residual property to reflect the main control factor of depth and inherent heterogeneity of coal seams. Second, ash model was converted from logging density model with relative density as an intermediate variable for overcoming the shortage of core data. Third, moisture model was built. Finally, the model of as-received gas content was obtained by a simple arithmetic conversion. This method was applied in Harcourt coalbed gas field of Bowen Basin, Australia, with a satisfactory result. [ABSTRACT FROM AUTHOR]

Background and Purpose: The prevalence of elderly patients prompts anesthesiologists to determine the optimal dose of medication due to the altered pharmacokinetics and pharmacodynamics of this population. The present study aimed to determine the 95% effective dose (ED 95 ) of remimazolam tosylate in anesthesia induction to inhibit endotracheal intubation-related cardiovascular reaction in frail and non-frail senile patients. Methods: A prospective sequential allocation dose-finding study of remimazolam tosylate was conducted on 80 elderly patients who received general anesthesia between May and June 2022 at the First Affiliated Hospital of Nanchang University. The initial dose was 0.3 mg/kg. The blood pressure and heart rate fluctuations during intubation were either <20% (negative cardiovascular response) or ≥20% (positive cardiovascular response). If positive, the dose of the next patient was increased by 0.02 mg/kg, while if negative, it was reduced by 0.02 mg/kg according to the 95:5 biased coin design (BCD). The ED 95 and 95% confidence intervals (CIs) were determined using R-Foundation isotonic regression and bootstrapping methods. Results: The ED 95 of remimazolam tosylate to inhibit the response during tracheal intubation was 0.297 mg/kg (95% CI: 0.231-0.451 mg/kg) and 0.331 mg/kg (95% CI: 0.272-0.472 mg/kg) in frail and non-frail senile patients, respectively. Conculation and Implications: The CI of the two groups overlap, and no difference was detected in the ED 95 of remimazolam tosylate in inhibiting endotracheal intubation-related cardiovascular response in frail and non-frail senile patients. These results suggested that remimazolam tosylate is an optimal anesthesia inducer for all elderly patients. Clinical Trial Registration: https://www.chictr.org.cn, identifier ChiCTR2200055709., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Qu, Liu, Ouyang, Li, Long, Jiang, Wang and Cheng.)

Objective: To investigate the effects of stachydrine (STA) on apoptosis of Aβ 25-35 -induced PC12 cells mimicking Alzheimer's disease and explore the mechanisms., Methods: The differential genes of STA were analyzed based on GSE85871 data, and the target genes of STA were identified using STITCH database. PC12 cells were treated with Aβ 25-35 to establish a cell model of Alzheimer's disease, and the changes in cell viability and cell cycle in response to STA treatment were assessed using MTT assay and flow cytometry, respectively. RT-PCR and Western blotting were used to detect the relevant gene or protein expressions in the treated cells., Results: GSE85871 data showed 37 up-regulated genes and 48 down-regulated genes in cells following treatment with STA. Analysis of the data from the STITCH database indicated that RPS8 and EED were the target genes of STA. Treatment of PC12 cells with Aβ 25-35 significantly lowered the cell viability ( P &lt; 0.05) and the expressions of RPS8 and EED at both the mRNA and protein levels ( P &lt; 0.05), and obviously inhibited the expression of apoptosis-related proteins Bcl-2 and p53 ( P &lt; 0.05). STA treatment of the cells significantly reversed the effect of Aβ 25-35 and induced cell cycle arrest in G2/M phase, causing also significantly increases in the expression levels of RPS8, EED, Bcl-2 and p53 ( P &lt; 0.05)., Conclusions: STA plays an important role in inhibiting the apoptosis of PC12 cells induced by Aβ 25-35 possibly by regulating RPS8 and EED expression to promote the expressions of Bcl-2 and p53.

Background: Our previous study states that propofol suppresses proliferation and migration of papillary thyroid cancer (PTC) cells by downregulation of lncRNA ANRIL. This study intended to probe the downstream mechanism of ANRIL in PTC with potential microRNAs (miR) and genes., Methods: ANRIL expression was detected in normal thyroid epithelial cells (Nthy-ori 3-1) and PTC cells (TPC-1, FTC-133, K1 and BCPAP). ANRIL expression was inhibited in TPC-1 and BCPAP cells to explore the effects of si-ANRIL in PTC malignant behaviors. The gain-and loss-of functions of ANRIL/miR-320a were performed to measure their roles in PTC. Levels of ANRIL, miR-320a, HMGB1, apoptosis- and Wnt/β-catenin and NF-κB pathways-related proteins were measured. Dual-luciferase reporter gene assay and RNA pull-down assay were applied to verify ANRIL/miR-320a/HMGB1 relation. si-ANRIL was transplanted into xenograft tumors in nude mice., Results: ANRIL was upregulated in TPC-1 and BCPAP cells. miR-320a targeted HMGB1, and ANRIL bound to miR-320a. In TPC-1 and BCPAP cells, si-ANRIL prevented PTC cell malignant behaviors, and inactivated the Wnt/β-catenin and NF-κB pathways; while si-ANRIL + miR-320a inhibition showed opposite trends. Overexpressing miR-320a promoted malignant behaviors of TPC-1 cells. In 6 μg/mL propofol-treated TPC-1 cells, miR-320a inhibition weakened propofol's inhibitory effects on PTC cell growth. After ANRIL inhibition, the volume and weight of xenograft tumors were decreased., Conclusion: Propofol upregulated miR-320a and reduced HMGB1 by downregulating ANRIL and inactivating the Wnt/β-catenin and NF-κB pathways, thus preventing PTC cell malignant behaviors. This study may offer new insights in PTC prevention and treatment., Competing Interests: Declaration of Competing Interest All authors declare that there is no conflict of interests in this study., (Copyright © 2020 Elsevier GmbH. All rights reserved.)

Objective: To establish rat model of lung ischemia/reperfusion (IR) in vivo, and to explore the effects of acidification pretreatment for respiratory acidosis on the expression of matrix metalloproteinase-9 (MMP-9) and the possible mechanisms.
 Methods: A total of 36 male Sprague-Dawley rats were divided into a sham group (S group), a IR group, and an experiment group (RA group) (n=12 in each group). The rat left lung hilum in the S group was dissociated, followed by perfusion without ischemia. After the left lung hilum in the IR group was blocked for 45 min, the rats were followed by reperfusion for 180 min. After left lung hilum in the RA group was dissociated, the respiratory parameters were adjusted so that pressure of end tidal carbon dioxide (PETCO2) reached 56-65 mmHg (1 mmHg=0.133 kPa) for 5 min, then the rats was subjected to IR. Lung tissue wet/dry (W/D) and lung permeability index (LPI) were calculated, while the lung histopathology was observed and the MMP-9 protein expression were measured.
 Results: Compared with the control group, the W/D and LPI in the IR group and the RA group increased after reperfusion (both P<0.05), and the levels of W/D and LPI in the group RA were lower than that in the IR group (P<0.05). LPI and pathology scores were significantly lower in the RA group than those in the IR group (both P<0.01). After IR, the expression of MMP9 in the lung tissues in the IR group and the RA group increased significantly (both P<0.01). The expression of MMP-9 protein in the RA group was significantly lower than that in the IR group (P<0.01).
 Conclusion: After lung IR injury, the expression of MMP-9 protein, vascular permeability and inflammatory exudation is increased. The acidification pretreatment for respiratory acidosis can inhibit the expression of MMP-9 protein and reduce inflammatory exudation after lung IR, showing a protective effect on lung IR injury.

Objective: To observe the effects of low-intensity pulsed ultrasound (LIPUS) pretreatment on pulmonary expression of high mobility group box-1 (HMGB1) in a rat model of lung ischemia-reperfusion (IR)., Methods: Thirty-two male SpragueDawley rats weighing 250-300 g were randomly divided ( n =8) into sham-operated group, lung IR group, LIPUS pretreatment group and pretreatment with α7-nicotinic cholinergic receptor (α7nAChR) antagonist group. In the sham-operated group, the left pulmonary hilum was dissociated without occlusion; in the other 3 groups, the left pulmonary hilum was occluded for 45 min followed by reperfusion for 180 min; LIPUS pretreatment for 30 min and intraperitoneal injection of methyllycaconitine (2 mg/kg), an α7nAChR antagonist, were administered before the operation. The wet/dry weight ratio (W/D) and pulmonary permeability index (LPI) of the lung tissue were measured, and the lung histopathology was observed and scored. The contents of interleukin-1 (IL-1) and IL-6 in the lung tissues were measured using ELISA, and the pulmonary expression of HMGB1 protein was detected using immunofluorescence assay and Western blotting., Results: Compared with those in the sham-operated group, the W/D of the lung tissue, LPI, pathological scores, IL-1 and IL-6 contents in the lung tissue, and pulmonary HMGB1 expression all significantly increased in the other 3 groups ( P &lt; 0.05). LIPUS preconditioning significantly lowered the W/D values, LPI, pathological score, IL-1 and IL-6 contents and HMGB1 expression in the lung tissues following lung IR, and these effects were significantly inhibited by administration of methyllycaconitine., Conclusions: LIPUS preconditioning can reduce lung IR injury possibly by activating α7nAChR-dependent cholinergic anti-inflammatory pathway to reduce lung tissue HMGB1 expression.