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A bstract We provide mass/energy formulas for the extended thermodynamics, mixed thermodynamics, and holographic conformal field theory (CFT) thermodynamics for the charged and rotating Kerr-Newman Anti-de Sitter black holes. Then for the CFT thermal states dual to the black hole, we find the first-order phase transitions and criticality phenomena in the canonical ensemble with fixed angular momentum, volume, and central charge. We observe that the CFT states cannot be analogous to the Van der Waals fluids, despite the critical exponents falling into the universality class predicted by the mean field theory. Additionally, we examine the (de)confinement phase transitions within the grand canonical ensemble with fixed angular velocity, volume, and central charge of the CFT. Our findings suggest that the near zero temperature (de)confinement phase transitions can occur with the angular velocity of the CFT that solely depends on the CFT volume.

In view of a previous study of the intermediate principal stress effect at a limited σ2 range, a series of true triaxial tests, covering a full range of intermediate principal stresses that vary from the generalized triaxial compression stress state (σ2 = σ3) to the generalized triaxial tensile stress state (σ1 = σ2), was carried out on sandstone and granite samples. The experimental results revealed that the deformation, failure strength and failure mode have a significant dependence on the stress state. As an effect of the intermediate principal stress on crack evolution, the deformation difference known as stress-induced deformation anisotropy occurred and should be considered when developing the mechanical model. Moreover, a post-peak deformation with a step-shaped stress drop is observed and illustrates that there will be a multi-stage bearing capacity after the rock failure. The peak strength is non-symmetrical with the increasing σ2 and is closely related to the Lode angle. Based on the final fracture surface and SEM analysis under true triaxial compression, three failure modes and failure zones, including tension failure, shear failure and mixed failure, are delineated and discussed. Combining the failure mode and the strength under true triaxial compression, it is found that the strength variation exhibited a close relationship to the failure mechanism.

The purpose of this ISRM Suggested Method is to introduce a guideline on determining deformation and failure characteristics of rocks subjected to true triaxial compression on different stress path. The true triaxial testing apparatus was reviewed by means of the function and engineering application. Some key techniques, such as stress and strain measurements, and reduction of end effect between specimen and metal platens, preventing metal platens interference, were stated and suggested in detail. Methodology of specimen processing, specimen shape, and testing procedure are characterized. There is an explanation of the experimental data processing on stress–strain curves, strength, and fracture mode.

Ischemic stroke (IS) is a common neurological disorder associated with high disability rates and mortality rates. At present, recombinant tissue plasminogen activator (r-tPA) is the only US(FDA)-approved drug for IS. However, due to the narrow therapeutic window and risk of intracerebral hemorrhage, r-tPA is currently used in less than 5% of stroke patients. Natural compounds have been widely used in the treatment of IS in China and have a wide range of therapeutic effects on IS by regulating multiple targets and signaling pathways. The keywords “ischemia stroke, traditional Chinese Medicine, Chinese herbal medicine, natural compounds” were used to search the relevant literature in PubMed and other databases over the past five years. The results showed that JAK/STAT, NF-κB, MAPK, Notch, Nrf2, and PI3K/Akt are the key pathways, and SIRT1, MMP9, TLR4, HIF-α are the key targets for the natural compounds from traditional Chinese medicine in treating IS. This study aims to update and summarize the signaling pathways and targets of natural compounds in the treatment of IS, and provide a base of information for the future development of effective treatments for IS.

The observational association between gut microbiome and systemic lupus erythematosus (SLE) has been well documented. However, whether the association is causal remains unclear. The present study used publicly available genome-wide association study (GWAS) summary data to perform two-sample Mendelian randomization (MR), aiming to examine the causal links between gut microbiome and SLE. Two sets of MR analyses were conducted. A group of single nucleotide polymorphisms (SNPs) that less than the genome-wide statistical significance threshold (5 × 10 -8 ) served as instrumental variables. To obtain a comprehensive conclusion, the other group where SNPs were smaller than the locus-wide significance level (1 × 10 -5 ) were selected as instrumental variables. Based on the locus-wide significance level, the results indicated that there were causal effects of gut microbiome components on SLE risk. The inverse variance weighted (IVW) method suggested that Bacilli and Lactobacillales were positively correlated with the risk of SLE and Bacillales , Coprobacter and Lachnospira were negatively correlated with SLE risk. The results of weighted median method supported that Bacilli , Lactobacillales , and Eggerthella were risk factors for SLE and Bacillales and Coprobacter served as protective factors for SLE. The estimates of MR Egger suggested that genetically predicted Ruminiclostridium6 was negatively associated with SLE. Based on the genome-wide statistical significance threshold, the results showed that Actinobacteria might reduce the SLE risk. However, Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) detected significant horizontal pleiotropy between the instrumental variables of Ruminiclostridium6 and outcome. This study support that there are beneficial or detrimental causal effects of gut microbiome components on SLE risk.

As a novel development concept and model, the cultural and creative industries have become an important sector of the global economy owing to their diverse development pathways. In particular, the animation industry surpasses traditional sectors in scale. This industry demonstrated unprecedented resilience during the COVID-19 pandemic, highlighting its critical significance in the global economy. In this study, the SWOT (strength, weakness, opportunity, and threat)-PEST (political, economic, social, and technological factor) analytical model was employed to systematically assess various properties of the animation industry in China. Through an in-depth analysis of both internal and external factors affecting the industry and in consideration of conditions in the post-pandemic era, industrial development strategies across macro, meso, and micro levels were proposed to improve the existing development system. It was found that policy guidance at the macro level, improving the industry chain, integrating technologies at the meso level, and expanding target markets and financial channels at the micro level are key strategies for the continued development of the industry. This study offers new insights and directions for the sustainable development of the animation industry in China.

Background The adaption of brain region is fundamental to the development and maintenance of nervous system disorders. The prelimbic cortex (PrL) participates in the affective components of the pain sensation. However, whether and how the adaptation of PrL contributes to the comorbidity of neuropathic pain and depression are unknown. Methods Using resting-state functional magnetic resonance imaging (rs-fMRI), genetic knockdown or overexpression, we systematically investigated the activity of PrL region in the pathogenesis of neuropathic pain/depression comorbid using the combined approaches of immunohistochemistry, electrophysiology, and behavior. Results The activity of PrL and the excitability of pyramidal neurons were decreased, and the osteoclastic tartrate-resistant acid phosphatase 5 (Acp5) expression in PrL neurons was upregulated following the acquisition of spared nerve injury (SNI)-induced comorbidity. Genetic knockdown of Acp5 in pyramidal neurons, but not parvalbumin (PV) neurons or somatostatin (SST) neurons, attenuated the decrease of spike number, depression-like behavior and mechanical allodynia in comorbidity rats. Overexpression of Acp5 in PrL pyramidal neurons decreased the spike number and induced the comorbid-like behavior in naïve rats. Moreover, the expression of interleukin-6 (IL-6), phosphorylated STAT3 (p-STAT3) and acetylated histone H3 (Ac-H3) were significantly increased following the acquisition of comorbidity in rats. Increased binding of STAT3 to the Acp5 gene promoter and the interaction between STAT3 and p300 enhanced acetylation of histone H3 and facilitated the transcription of Acp5 in PrL in the modeled rodents. Inhibition of IL-6/STAT3 pathway prevented the Acp5 upregulation and attenuated the comorbid-like behaviors in rats. Conclusions These data suggest that the adaptation of PrL mediated by IL-6/STAT3/Acp5 pathway contributed to the comorbidity of neuropathic pain/depression induced by SNI.

Skeletal muscle is an important motor organ with multinucleated myofibers as its smallest cellular units. Myofibers are formed after undergoing cell differentiation, cell–cell fusion, myonuclei migration, and myofibril crosslinking among other processes and undergo morphological and functional changes or lesions after being stimulated by internal or external factors. The above processes are collectively referred to as myogenesis. After myofibers mature, the function and behavior of skeletal muscle are closely related to the voluntary movement of the body. In this review, we systematically and comprehensively discuss the physiological and pathological processes associated with skeletal muscles from five perspectives: molecule basis, myogenesis, biological function, adaptive changes, and myopathy. In the molecular structure and myogenesis sections, we gave a brief overview, focusing on skeletal muscle‐specific fusogens and nuclei‐related behaviors including cell–cell fusion and myonuclei localization. Subsequently, we discussed the three biological functions of skeletal muscle (muscle contraction, thermogenesis, and myokines secretion) and its response to stimulation (atrophy, hypertrophy, and regeneration), and finally settled on myopathy. In general, the integration of these contents provides a holistic perspective, which helps to further elucidate the structure, characteristics, and functions of skeletal muscle. The article systematically and comprehensively reviews the physiological and pathological processes associated with skeletal muscles from five perspectives: molecule basis, myogenesis, biological function, poststimulation response, and myopathy. We primarily focus on nuclei‐related behaviors of skeletal muscle, cell–cell fusion, and nuclei migration in the first two sections and discuss the three biological functions of skeletal muscle (muscle contraction, thermogenesis, and myokines secretion) and its response to stimulation (atrophy, hypertrophy, and regeneration), and finally settle on myopathy.

ObjectivesPreoperative prediction of microvascular invasion (MVI) in patients with hepatocellular cancer (HCC) is important for surgery strategy making. We aimed to develop and validate a combined intratumoural and peritumoural radiomics model based on gadolinium-ethoxybenzyl-diethylenetriamine (Gd-EOB-DTPA)-enhanced magnetic resonance imaging (MRI) for preoperative prediction of MVI in primary HCC patients.MethodsThis study included a training cohort of 110 HCC patients and a validating cohort of 50 HCC patients. All the patients underwent preoperative Gd-EOB-DTPA-enhanced MRI examination and curative hepatectomy. The volumes of interest (VOIs) around the hepatic lesions including intratumoural and peritumoural regions were manually delineated in the hepatobiliary phase of MRI images, from which quantitative features were extracted and analysed. In the training cohort, machine-learning method was applied for dimensionality reduction and selection of the extracted features.ResultsThe proportion of MVI-positive patients was 38.2% and 40.0% in the training and validation cohort, respectively. Supervised machine learning selected ten features to establish a predictive model for MVI. The area under the receiver operating characteristic curve (AUC), sensitivity, specificity of the combined intratumoural and peritumoural radiomics model in the training and validation cohort were 0.85 (95% confidence interval (CI), 0.77–0.93), 88.2%, 76.2%, and 0.83 (95% CI, 0.71–0.95), 90.0%, 75.0%, respectively.ConclusionsWe evaluate quantitative Gd-EOB-DTPA-enhanced MRI image features of both intratumoural and peritumoural regions and provide an effective radiomics-based model for the prediction of MVI in HCC patients, and may therefore help clinicians make precise decisions regarding treatment before the surgery.Key Points• An effective radiomics model for prediction of microvascular invasion in HCC patients is established.• The radiomics model is superior to the radiologist in prediction of MVI.• The radiomics model can help clinicians in pretreatment decision making.

The biological functions of short open reading frame (sORF)‐encoded micropeptides remain largely unknown. Here, we report that LINC00998, a previously annotated lncRNA, was upregulated in multiple cancer types and the sORF on LINC00998 encoded a micropeptide named SMIM30. SMIM30 was localized in the membranes of the endoplasmic reticulum (ER) and mitochondria. Silencing SMIM30 inhibited the proliferation of hepatoma cells in vitro and suppressed the growth of tumor xenografts and N‐nitrosodiethylamine‐induced hepatoma. Overexpression of the 5′UTR‐sORF sequence of LINC00998, encoding wild‐type SMIM30, enhanced tumor cell growth, but this was abolished when a premature stop codon was introduced into the sORF via single‐base deletion. Gain‐ and loss‐of‐function studies revealed that SMIM30 peptide but not LINC00998 reduced cytosolic calcium level, increased CDK4, cyclin E2, phosphorylated‐Rb and E2F1, and promoted the G1/S phase transition and cell proliferation. The effect of SMIM30 silencing was attenuated by a calcium chelator or the agonist of sarco/endoplasmic reticulum calcium ATPase (SERCA) pump. These findings suggest a novel function of micropeptide SMIM30 in promoting G1/S transition and cell proliferation by enhancing SERCA activity and reducing cytosolic calcium level. LINC00998, a previously annotated lncRNA, encodes an ER‐localized micropeptide named SMIM30. The authors found that the peptide, but not the lncRNA, reduced cytosolic calcium level by enhancing SERCA activity, then increased CDK4, cyclin E2 and E2F1 levels, and consequently promoted the G1/S phase transition and cell proliferation. These data unravel a new function of SMIM30 in regulating cytosolic calcium and G1/S transition.