Study on the Infrared and Raman spectra of Ti3AlB2, Zr3AlB2, Hf3AlB2, and Ta3AlB2 by first-principles calculations.

In this paper, the crystal geometry, electronic structure, lattice vibration, Infrared and Raman spectra of ternary layered borides M3AlB2 (M = Ti, Zr, Hf, Ta) are studied by using first principles calculation method based on the density functional theory. The electronic structure of M3AlB2 indicates that they are all electrical conductors, and the d orbitals of Ti, Zr, Hf, and Ta occupy most of the bottom of the conduction band and most of the top of the valence band. Al and B have lower contributions near their Fermi level. The lightweight and stronger chemical bonds of atom B are important factors that correspond to higher levels of peak positions in the Infrared and Raman spectra. However, the vibration frequencies, phonon density of states, and peak positions of Infrared and Raman spectra are significantly lower because of heavier masses and weaker chemical bonds for M and Al atoms. And, there are 6 Infrared active modes A2u and E1u, and 7 Raman active modes, namely A1g, E2g, and E1g corresponding to different vibration frequencies in M3AlB2. Furthermore, the Infrared and Raman spectra of M3AlB2 were obtained respectively, which intuitively provided a reliable Infrared and Raman vibration position and intensity theoretical basis for the experimental study.

Structure, bonding and electronic characteristics of amorphous Se.

Ovonic threshold switching (OTS) selectors can effectively improve the storage density and suppress the leakage current of advanced phase-change memory devices. As a prototypical OTS material, amorphous GeSe is widely investigated. But the attention paid to amorphous Se (i.e., the functional constituent in amorphous GeSe) has been very limited up to now. Here we have explored the structure, bonding and electronic characteristics of amorphous Se using ab initio molecular dynamics simulations. The results reveal that the Se atoms in amorphous Se tend to form 2-coordinated configurations, and they connect with each other to form long chains. The fraction of the vibrational density of state located in the high frequency range is relatively large, and the formation energy of the Se-Se bond is as large as 4.44 eV, hinting that the Se-Se bonds in chains possess high stability. In addition, the mid-gap state related to the OTS behavior is also found in amorphous Se despite the small proportion. Our findings enrich the knowledge of amorphous Se, which aids the applications of Se-based OTS selectors.

The potential roles of stress-induced phosphoprotein 1 and connexin 43 in rats with reperfusion arrhythmia.

OBJECTIVE: Connexin 43 (Cx43) is a critical gene for maintaining myocardial homeostasis. Interestingly, Cx43 and stress-induced phosphoprotein 1 (STIP1) were recorded to be lowly expressed in ischemia/reperfusion (I/R). However, their impacts on reperfusion arrhythmia (RA) remain to be explored. Our study aimed to find out the related underlying mechanisms. METHODS: After the establishment of an isolated heart model through Langendorff perfusion, the heart rate, conduction activation time, conduction velocity, and conduction direction of the left ventricle were evaluated, along with the apoptotic rate detection in the collected myocardial tissues. After the construction of a hypoxia/reoxygenation (H/R)-induced cellular model, cell apoptosis, intercellular communication, cell viability, and the content of reactive oxygen species, superoxide dismutase, malondialdehyde, and lactic dehydrogenase were measured. The expression of Cx43 and STIP1 was determined in both rat heart and cell models. The bindings of STIP3 and Cx43 to  heat shock protein 90 (HSP90) and heat shock protein 70 (HSP70) were verified. RESULTS: Relative to the corresponding controls, Cx43 and STIP1 were decreased in myocardial tissues of RA rats and H/R-stimulated H9C2 cells, where Cx43-binding HSP70 and HSP90 were respectively increased and decreased, and ubiquitination level of Cx43 was enhanced. STIP1 overexpression promoted protein expression of Cx43, intercellular communication, and cell viability, and reduced cell apoptosis and oxidative stress in H/R-stimulated H9C2 cells. CONCLUSION: STIP1 promoted Cx43 expression to improve intercellular communication and reduce oxidative stress in H/R-stimulated H9C2 cells.

Sevoflurane exerts protection against myocardial ischemia-reperfusion injury and pyroptosis through the circular RNA PAN3/microRNA-29b-3p/stromal cell-derived factor 4 axis.

OBJECTIVE: Sevoflurane is suggested to exert protective functions against myocardial ischemia-reperfusion injury (MIRI). However, the particular mechanism remains elusive. Therefore, this research explored the mechanism of sevoflurane in MIRI-induced damage and pyroptosis. METHODS: Subsequent to gain-or loss-of-function assays or/and sevoflurane treatment, the MIRI model was developed in rats. Cardiac function and body and heart weight of rats were evaluated, followed by measurement of apoptosis and creatine kinase MB (CK-MB), lactate dehydrogenase (LDH), and pyroptosis-related protein levels. After loss-of-function assays or/and sevoflurane treatment in human cardiomyocytes (HCMs), the hypoxia/reoxygenation (H/R) model was constructed. In HCMs, cell viability, apoptosis, and pyroptosis-related proteins were detected. Circular RNA PAN3 (circPAN3), microRNA (miR)-29b-3p, and stromal cell-derived factor 4 (SDF4) expression was determined in rat myocardial tissues and HCMs. Mechanistically, interactions among circPAN3, miR-29b-3p, and SDF4 were analyzed. RESULTS: MIRI modeling increased miR-29b-3p expression and diminished circPAN3 and SDF4 expression in H/R-treated HCMs and MIRI rats, which was nullified by sevoflurane preconditioning. Mechanistically, circPAN3 negatively targeted miR-29b-3p to upregulate SDF4. Moreover, sevoflurane preconditioning reduced heart weight/body weight ratio, LDH, CK-MB, myocardial infarct size, left ventricular end-diastolic pressure, apoptosis, and pyroptosis, while elevating the increase and decrease of left ventricular pressure (±dp/dt max) and left ventricular systolic pressure in MIRI rats. In addition, sevoflurane preconditioning augmented viability while diminishing apoptosis and pyroptosis in H/R-treated HCMs. Moreover, circPAN3 silencing or miR-29b-3p overexpression abrogated alleviatory effects of sevoflurane on myocardial injury and pyroptosis in vitro. CONCLUSION: Sevoflurane treatment ameliorated myocardial injury and pyroptosis in MIRI via circPAN3/miR-29b-3p/SDF4 axis.

Dexmedetomidine suppresses hippocampal astrocyte pyroptosis in cerebral hypoxic-ischemic neonatal rats by upregulating microRNA-148a-3p to inactivate the STAT/JMJD3 axis.

OBJECTIVE: Dexmedetomidine (DEX), a selective α2-adrenoceptor agonist, is an anesthetic and sedative agent and has been reported to confer neuroprotective effects after cerebral hypoxic ischemia (CHI). This study was undertaken to elucidate the mechanisms by which microRNA (miR)-148a-3p is involved in the neuroprotective effect of DEX on hypoxic-ischemic brain damage in neonatal rats. METHODS: Neonatal rats were exposed to CHI conditions, a miR-148a-3p inhibitor, and DEX. Hippocampal astrocytes were isolated to construct an oxygen-glucose deprivation (OGD) model. qRT-PCR and western blot were utilized to inspect miR-148a-3p, STAT1, STAT3, JMJD3, cleaved-Caspase-1, ASC, NLRP3, GSDMD, and GSDMD-N expression in rats and astrocytes. TUNEL staining was employed to measure astrocyte apoptosis rate, immunofluorescence to inspect cleaved-Caspase-1 and ASC levels, and ELISA to determine IL-1ß and IL-18 expression. The target genes of miR-148a-3p were predicted using online software and verified by a dual-luciferase reporter gene assay. RESULTS: A prominent increase in astrocyte apoptosis rate and the expression of pyroptosis- and inflammation-related factors were found in rats with CHI and OGD-treated astrocytes. DEX suppressed astrocyte apoptosis rate and decreased expression of pyroptosis- and inflammation-related factors. Knockdown of miR-148a-3p facilitated astrocyte pyroptosis, indicating that DEX exerted its protective effect by upregulating miR-148a-3p. miR-148a-3p negatively mediated STAT to inactivate JMJD3. Overexpression of STAT1 and STAT3 facilitated pyroptosis in astrocytes, which was negated by the overexpression of miR-148a-3p. CONCLUSION: DEX inhibited hippocampal astrocyte pyroptosis by upregulating miR-148a-3p to inactivate the STAT/JMJD3 axis, thereby alleviating cerebral damage in neonatal rats with CHI.

Molecular chaperones HSP40, HSP70, STIP1, and HSP90 are involved in stabilization of Cx43.

To investigate the involvement of stress induced phosphoprotein 1 (STIP1), heat shock protein (HSP) 70, and HSP90 in ubiquitination of connexin 43 (Cx43) in rat H9c2 cardiomyocytes. Co-immunoprecipitation was used to detect protein-protein interactions and Cx43 ubiquitination. Immunofluorescence was used for protein co-localization. The protein binding, Cx43 protein expression, and Cx43 ubiquitination were reanalyzed in H9c2 cells with modified STIP1 and/or HSP90 expression. STIP1 bound to HSP70 and HSP90, and Cx43 bound to HSP40, HSP70, and HSP90 in normal H9c2 cardiomyocytes. Overexpression of STIP1 promoted the transition of Cx43-HSP70 to Cx43-HSP90 and inhibited Cx43 ubiquitination; knockdown of STIP1 resulted in the opposite effects. Inhibition of HSP90 counteracted the inhibitory effect of STIP1 overexpression on Cx43 ubiquitination. STIP1 suppresses Cx43 ubiquitination in H9c2 cardiomyocytes by promoting the transition of Cx43-HSP70 to Cx43-HSP90.

Association between ABO blood groups and postoperative pain in children after adenotonsillectomy: a prospective cohort study.

BACKGROUND: It has been known that ABO blood groups are linked to the phenotypes of certain diseases; however, and the relationship between ABO blood groups and postoperative pain have not been extensively studied, especially in children. This study was to investigate whether there would be an association between the four major ABO blood groups and postoperative pain, as indicated by the differences in pain scores and rescue fentanyl requirements among blood groups in children after adenotonsillectomy. METHODS: A total of 124 children, aged 3-7 years, ASA I or II, and undergoing elective adenotonsillectomy were enrolled in the study. Postoperative pain was evaluated using the Children's Hospital of Eastern Ontario Pain Scale (CHEOPS) and the rescue fentanyl requirement in post anesthesia care unit (PACU) was analyzed. Pediatric Anesthesia Emergence Delirium (PAED) score and the duration of PACU were recorded. The postoperative nausea and vomiting (PONV) within 24 h were documented. RESULTS: Among four blood type groups, no significant differences were observed regarding surgery time, and the gaps of fentanyl given at the anesthesia induction and the first rescue fentanyl injection in PACU. However, patients from AB and B blood groups had significantly higher pain score at initial CHEOPS assessment and consequently, higher consumption of rescue fentanyl during PACU stay. A significantly higher percentage of patients had received > 1 µg/kg rescue fentanyl. Higher PAED scores were also observed in AB and B blood groups. CONCLUSION: Paediatric patients with AB and B blood type had higher postoperative CHEOPS pain score and required significantly more fentanyl for pain control than those with A and O blood type after T&A. The initial scores of PAED in patients with AB and B blood type were also higher than that in patients with A and O blood type.