Temperature-mediated diffusion of nanoparticles in semidilute polymer solutions.

The temperature is often a critical factor affecting the diffusion of nanoparticles in complex physiological media, but its specific effects are still to be fully understood. Here, we constructed a temperature-regulated model of semidilute polymer solution and experimentally investigated the temperature-mediated diffusion of nanoparticles using the particle tracking method. By examining the ensemble-averaged mean square displacements (MSDs), we found that the MSD grows gradually as the temperature increases while the transition time from sublinear to linear stage in MSD decreases. Meanwhile, the temperature-dependent measured diffusivity of the nanoparticles shows an exponential growth. We revealed that these temperature-mediated changes are determined by the composite effect of the macroscale property of polymer solution and the microscale dynamics of polymer chain as well as nanoparticles. Furthermore, the measured non-Gaussian displacement probability distributions were found to exhibit non-Gaussian fat tails, and the tailed distribution is enhanced as the temperature increases. The non-Gaussianity was calculated and found to vary in the same trend with the tailed distribution, suggesting the occurrence of hopping events. This temperature-mediated non-Gaussian feature validates the recent theory of thermally induced activated hopping. Our results highlight the temperature-mediated changes in diffusive transport of nanoparticles in polymer solutions and may provide the possible strategy to improve drug delivery in physiological media.

Weakly Supervised Building Semantic Segmentation Based on Spot-Seeds and Refinement Process.

Automatic building semantic segmentation is the most critical and relevant task in several geospatial applications. Methods based on convolutional neural networks (CNNs) are mainly used in current building segmentation. The requirement of huge pixel-level labels is a significant obstacle to achieve the semantic segmentation of building by CNNs. In this paper, we propose a novel weakly supervised framework for building segmentation, which generates high-quality pixel-level annotations and optimizes the segmentation network. A superpixel segmentation algorithm can predict a boundary map for training images. Then, Superpixels-CRF built on the superpixel regions is guided by spot seeds to propagate information from spot seeds to unlabeled regions, resulting in high-quality pixel-level annotations. Using these high-quality pixel-level annotations, we can train a more robust segmentation network and predict segmentation maps. To iteratively optimize the segmentation network, the predicted segmentation maps are refined, and the segmentation network are retrained. Comparative experiments demonstrate that the proposed segmentation framework achieves a marked improvement in the building's segmentation quality while reducing human labeling efforts.

An Efficient Supervised Deep Hashing Method for Image Retrieval.

In recent years, searching and retrieving relevant images from large databases has become an emerging challenge for the researcher. Hashing methods that mapped raw data into a short binary code have attracted increasing attention from the researcher. Most existing hashing approaches map samples to a binary vector via a single linear projection, which restricts the flexibility of those methods and leads to optimization problems. We introduce a CNN-based hashing method that uses multiple nonlinear projections to produce additional short-bit binary code to tackle this issue. Further, an end-to-end hashing system is accomplished using a convolutional neural network. Also, we design a loss function that aims to maintain the similarity between images and minimize the quantization error by providing a uniform distribution of the hash bits to illustrate the proposed technique's effectiveness and significance. Extensive experiments conducted on various datasets demonstrate the superiority of the proposed method in comparison with state-of-the-art deep hashing methods.

[Formulation optimization of emodin nanostructured lipid carriers by Box-Behnken response surface method and in vitro quality evaluation].

Emodin nanostructured lipid carriers(ED-NLC) were prepared and their quality was evaluated in vitro. Based on the results of single-factor experiments, the ED-NLC formulation was optimized by Box-Behnken response surface method with the dosages of emodin, isopropyl myristate and poloxamer 188 as factors and the nanoparticle size, encapsulation efficiency and drug loading as evaluation indexes. Then the evaluation was performed on the morphology, size and in vitro release of the nanoparticles prepared by emulsification-ultrasonic dispersion method in line with the optimal formulation, i.e., 3.27 mg emodin, 148.68 mg isopropyl myristate and 173.48 mg poloxamer 188. Under a transmission electron microscope(TEM), ED-NLC were spherical and their particle size distribution was uniform. The particle size of ED-NLC was(97.02±1.55) nm, the polymer dispersion index 0.21±0.01, the zeta potential(-38.96±0.65) mV, the encapsulation efficiency 90.41%±0.56% and the drug loading 1.55%±0.01%. The results of differential scanning calorimeter(DSC) indicated that emodin may be encapsulated into the nanostructured lipid carriers in molecular or amorphous form. In vitro drug release had obvious characteristics of slow release, which accorded with the first-order drug release equation. The fitting model of Box-Behnken response surface methodology was proved accurate and reliable. The optimal formulation-based ED-NLC featured concentrated particle size distribution and high encapsulation efficiency, which laid a foundation for the follow-up study of ED-NLC in vivo.

MicroRNA-34a promotes MICB expression in hepatocytes.

MicroRNA-34a (miR-34a) behaves as a tumor suppressor by decreasing the expression of oncogenes involved in multiple carcinogenic pathways. Intravenous delivery of miR-34a mimics has been investigated in clinical trials as a potential treatment for advanced cancers; however, the effect of miR-34a on cancer immune surveillance is controversial. In the current study, we found that miR-34a plays a dual role in the regulation of major histocompatibility complex class I-related sequence B (MICB) protein, a ligand of the NKG2D receptor. MiR-34a could both induce and reduce MICB expression by upregulating ataxia telangiectasia and Rad3-related (ATR) protein kinase and downregulating the transcription factor E2F1, respectively. The net effect of miR-34a on MICB expression depended on endogenous E2F1 levels. Overexpression of miR-34a promoted MICB expression in hepatocytes and hepatocellular carcinoma (HCC) cells that have low E2F1 levels but not in HCC cells that have high E2F1 levels. In HCC patients, the expression of miR-34a and MICB showed positive correlation in paratumor liver tissues, which have low E2F1 levels, but not in HCC tissues, which have high E2F1 levels. We showed that miR-34a overexpression in non-transformed liver cells enhanced cytolysis and interferon-γ production by NK-92MI cells. Furthermore, higher miR-34a expression in tumor and paratumor tissues was associated with positive and negative outcomes, respectively, in HCC patients. Our findings suggest that miR-34a induces MICB expression in paratumor liver tissues, which may cause liver damage and serious cytokine release syndrome, thus disclosing potential side effects of systemic administration of miR-34a in anticancer therapy.

Acylated Aminooligosaccharides with Inhibitory Effects against α-Amylase from Streptomyces sp. HO1518.

Five new acylated aminooligosaccharides (1⁻5), together with one known related analogue (6), were isolated from Streptomyces sp. HO1518. Their structure was identified by extensive spectroscopic analysis, including 1D and 2D NMR data and high resolution electrospray ionization mass spectrometry (HRESIMS), and by comparison with those reported in the literature. All of the new compounds showed more promising porcine pancreatic α-amylase (PPA) inhibitory activities than the clinical drug acarbose, indicating them as potential pharmaceutical drug leads toward type II diabetes.

Dicer regulates non-homologous end joining and is associated with chemosensitivity in colon cancer patients.

DNA double-strand break (DSB) repair is an important mechanism underlying chemotherapy resistance in human cancers. Dicer participates in DSB repair by facilitating homologous recombination. However, whether Dicer is involved in non-homologous end joining (NHEJ) remains unknown. Here, we addressed whether Dicer regulates NHEJ and chemosensitivity in colon cancer cells. Using our recently developed NHEJ assay, we found that DSB introduction by I-SceI cleavage leads to Dicer upregulation. Dicer knockdown increased SIRT7 binding and decreased the level of H3K18Ac (acetylated lysine 18 of histone H3) at DSB sites, thereby repressing the recruitment of NHEJ factors to DSB sites and inhibiting NHEJ. Dicer overexpression reduced SIRT7 binding and increased the level of H3K18Ac at DSB sites, promoting the recruitment of NHEJ factors to DSBs and moderately enhancing NHEJ. Dicer knockdown and overexpression increased and decreased, respectively, the chemosensitivity of colon cancer cells. Dicer protein expression in colon cancer tissues of patients was directly correlated with chemoresistance. Our findings revealed a function of Dicer in NHEJ-mediated DSB repair and the association of Dicer expression with chemoresistance in colon cancer patients.

Myeloid-specific disruption of recombination signal binding protein Jκ ameliorates hepatic fibrosis by attenuating inflammation through cylindromatosis in mice.

UNLABELLED: Macrophages play multidimensional roles in hepatic fibrosis, but their control has not been fully understood. The Notch pathway mediated by recombination signal binding protein Jκ (RBP-J), the transcription factor transactivated by signals from four mammalian Notch receptors, is implicated in macrophage activation and plasticity. In this study, by using mouse hepatic fibrosis models, we show that myeloid-specific disruption of RBP-J resulted in attenuated fibrosis. The activation of hepatic stellate cells and production of profibrotic factors including platelet-derived growth factor (PDGF)-B and transforming growth factor beta1 (TGF-ß1) reduced significantly in myeloid-specific RBP-J deficient mice. The infiltration of inflammatory cells and production of proinflammatory factors were reduced in liver of myeloid-specific RBP-J-deficient mice during fibrosis. In RBP-J-deficient macrophages, the nuclear factor kappa B (NF-κB) activation was remarkably attenuated as compared with the control. This could be attributed to the up-regulation of cylindromatosis (CYLD), a negative regulator of NF-κB, in Notch signal-compromised macrophages, because the knockdown of CYLD in RBP-J-deficient macrophages or overexpression of p65 in RBP-J knockdown cells both restored NF-κB activation and the production of proinflammatory and/or profibrotic factors by macrophages. In human hepatic fibrosis biopsies, stronger Notch activation is correlated with more severe fibrosis, which is accompanied by a lower level of CYLD but irrespective of etiological reasons. CONCLUSION: RBP-J-mediated Notch signaling is required for macrophages to promote hepatic fibrosis by up-regulation of NF-κB activation through CYLD.

FHL1C induces apoptosis in Notch1-dependent T-ALL cells through an interaction with RBP-J.

BACKGROUND: Aberrantly activated Notch signaling has been found in more than 50% of patients with T-cell acute lymphoblastic leukemia (T-ALL). Current strategies that employ γ-secretase inhibitors (GSIs) to target Notch activation have not been successful. Many limitations, such as non-Notch specificity, dose-limiting gastrointestinal toxicity and GSI resistance, have prompted an urgent need for more effective Notch signaling inhibitors for T-ALL treatment. Human four-and-a-half LIM domain protein 1C (FHL1C) (KyoT2 in mice) has been demonstrated to suppress Notch activation in vitro, suggesting that FHL1C may be new candidate target in T-ALL therapy. However, the role of FHL1C in T-ALL cells remained unclear. METHODS: Using RT-PCR, we amplified full-length human FHL1C, and constructed full-length and various truncated forms of FHL1C. Using cell transfection, flow cytometry, transmission electron microscope, real-time RT-PCR, and Western blotting, we found that overexpression of FHL1C induced apoptosis of Jurkat cells. By using a reporter assay and Annexin-V staining, the minimal functional sequence of FHL1C inhibiting RBP-J-mediated Notch transactivation and inducing cell apoptosis was identified. Using real-time PCR and Western blotting, we explored the possible molecular mechanism of FHL1C-induced apoptosis. All data were statistically analyzed with the SPSS version 12.0 software. RESULTS: In Jurkat cells derived from a Notch1-associated T-ALL cell line insensitive to GSI treatment, we observed that overexpression of FHL1C, which is down-regulated in T-ALL patients, strongly induced apoptosis. Furthermore, we verified that FHL1C-induced apoptosis depended on the RBP-J-binding motif at the C-terminus of FHL1C. Using various truncated forms of FHL1C, we found that the RBP-J-binding motif of FHL1C had almost the same effect as full-length FHL1C on the induction of apoptosis, suggesting that the minimal functional sequence in the RBP-J-binding motif of FHL1C might be a new drug candidate for T-ALL treatment. We also explored the molecular mechanism of FHL1C overexpression-induced apoptosis, which suppressed downstream target genes such as Hes1 and c-Myc and key signaling pathways such as PI3K/AKT and NF-κB of Notch signaling involved in T-ALL progression. CONCLUSIONS: Our study has revealed that FHL1C overexpression induces Jurkat cell apoptosis. This finding may provide new insights in designing new Notch inhibitors based on FHL1C to treat T-ALL.

Briarane diterpenes from the South China Sea gorgonian coral, Junceella gemmacea.

Four new briarane diterpenoids, junceellolides M-P (1-4), were isolated together with seven known analogs (5-11) from the South China Sea gorgonian, Junceella gemmacea. The structures of these compounds were elucidated by detailed spectroscopic analysis and comparison with the reported data. The absolute configuration of compounds 1-3 were determined based on an ECD experiment, while the absolute configuration of compound 4 was genetically determined. All the compounds were isolated for the first time from J. gemmacea. These compounds showed no growth inhibitory activity against A549, MG63 and SMMC-7721 cell lines in an in vitro bioassay.

Global Clue-Guided Cross-Memory Quaternion Transformer Network for Multisource Remote Sensing Data Classification.

Multisource remote sensing data classification is a challenging research topic, and how to address the inherent heterogeneity between multimodal data while exploring their complementarity is crucial. Existing deep learning models usually directly adopt feature-level fusion designs, most of which, however, fail to overcome the impact of heterogeneity, limiting their performance. As such, a multimodal joint classification framework, called global clue-guided cross-memory quaternion transformer network (GCCQTNet), is proposed for multisource data i.e., hyperspectral image (HSI) and synthetic aperture radar (SAR)/light detection and ranging (LiDAR) classification. First, a three-branch structure is built to extract the local and global features, where an independent squeeze-expansion-like fusion (ISEF) structure is designed to update the local and global representations by considering the global information as an agent, suppressing the negative impact of multimodal heterogeneity layer by layer. A cross-memory quaternion transformer (CMQT) structure is further constructed to model the complex inner relationships between the intramodality and intermodality features to capture more discriminative fusion features that fully characterize multimodal complementarity. Finally, a cross-modality comparative learning (CMCL) structure is developed to impose the consistency constraint on global information learning, which, in conjunction with a classification head, is used to guide the end-to-end training of GCCQTNet. Extensive experiments on three public multisource remote sensing datasets illustrate the superiority of our GCCQTNet with regards to other state-of-the-art methods.

Notch signal protects non-parenchymal cells from ischemia/reperfusion injury in vitro by repressing ROS.

BACKGROUND: We have previously reported that Notch signaling pathway protects hepatocytes from ischemia/ reperfusion (I/R) injury by repressing reactive oxygen species (ROS) production. However, apart from hepatocytes, non-parenchymal cells including vascular endothelia cells, Kupffer cells and hepatic stellate cells are also reported to be involved in hepatic I/R injury. AIM: To clarify the role of Notch signaling in non-parenchymal cells subjected to I/R injury. MATERIALS AND METHODS: Human Umbilical Vein Endothelial Cells (HUVECs), mouse macrophage line RAW264.7 and rat hepatic stellate cell line HSC-T6 were cultured and subjected to I/R injury, respectively. Activation of Notch signaling was assessed by NICD western blot. Then, pharmacological inhibitor (γ-secretase inhibitor GSI) was used to block Notch signaling of related cell lines in vitro. Intracellular ROS was detected and analyzed by FACS and apoptosis was examined by TUNEL staining and Annexin V staining. RESULTS: Notch signaling responded to I/R injury and I/R injury induced activation of Notch signaling in nonparenchymal cells. Notch signal deficiency led to overproduction of ROS and aggravated cell death of non-parenchymal cells subjected to I/R injury. CONCLUSION: Notch signal protects non-parenchymal cells from I/R injury by repressing ROS.

The risk factors for miscarriage of viable intrauterine pregnancies in patients with heterotopic pregnancy after surgical intervention.

To summarize the clinical characteristics and explore the risk factors for miscarriage of a viable intrauterine pregnancy following surgical intervention in patients with heterotopic pregnancy (HP). A total of 106 women diagnosed with HP that underwent surgical intervention in the Women's Hospital School of Medicine Zhejiang University between January 2014 and December 2021 were included in this retrospective study. They were divided into a miscarriage group (n = 13) and an ongoing pregnancy group (n = 93) according to the outcomes of the HP within 2 weeks after surgery. Data regarding clinical characteristics, surgical conditions, postoperative recovery, and complications were collected and compared between the groups. Logistic multivariate analysis was performed to explore the risk factors for miscarriage in patients with HP within 2 weeks of surgical intervention. Among the 106 women with HP, 80 had tubal HP, 8 had cornual HP, and 18 had interstitial HP. Eighty-seven (82.1%) patients developed clinical symptoms that manifested primarily as abnormal vaginal bleeding and/or abdominal pain, whereas 19 (17.9%) patients had no clinical symptoms. The mean gestational age on the day of surgery was 7.2 weeks (inter-quartile range, 6.4-8.3). The miscarriage rate within 2 weeks of surgical intervention was 12.3% in patients with HP. Compared to the ongoing pregnancy group, the miscarriage group had a higher body mass index, earlier gestational age at treatment, and higher volume of hemoperitoneum (P < .05 for all). Logistic multivariate analysis indicated that the women with a hemoperitoneum volume > 200 mL had significantly higher risk of miscarriage after adjusting covariates [OR (odds ratio) = 5.285, 95% CI (confidence interval) (1.152-24.238), P < .05]. Hemoperitoneum volume was independently associated with miscarriage of viable intrauterine pregnancies in patients with HP within 2 weeks of surgical intervention.

A Systematic Review and Meta-Analysis of Interventions to Promote Adjuvant Endocrine Therapy Adherence Among Breast Cancer Survivors.

PURPOSE: Adjuvant endocrine therapy (AET) adherence among breast cancer survivors is often suboptimal, leading to higher cancer recurrence and mortality. Intervention studies to promote AET adherence have burgeoned, more than doubling in number since this literature was last reviewed. The current aim is to provide an up-to-date systematic review and meta-analysis of interventions to enhance AET adherence and to identify strengths and limitations of existing interventions to inform future research and clinical care. METHODS: Systematic searches were conducted in three electronic databases. Studies were included in the systematic review if they examined an intervention for promoting AET adherence among breast cancer survivors. Studies were further included in the meta-analyses if they examined a measure of AET adherence (defined as compliance or persistence beyond initiation) and reported (or provided upon request) sufficient information to calculate an effect size. RESULTS: Of 5,045 unique records, 33 unique studies representing 375,951 women met inclusion criteria for the systematic review. Interventions that educated patients about how to manage side effects generally failed to improve AET adherence, whereas policy changes that lowered AET costs consistently improved adherence. Medication reminders, communication, and psychological/coping strategies showed varied efficacy. Of the 33 studies that met the inclusion criteria for the systematic review, 25 studies representing 367,873 women met inclusion criteria for the meta-analysis. The meta-analysis showed statistically significant effects of the adherence interventions overall relative to study-specified control conditions (number of studies [k] = 25; odds ratio, 1.412; 95% CI, 1.183 to 1.682; P = .0001). Subgroup analyses showed that there were no statistically significant differences in effect sizes by study design (randomized controlled trial v other), publication year, directionality of the intervention (unidirectional v bidirectional contact), or intervention type. CONCLUSION: To our knowledge, this is the first known meta-analysis to demonstrate a significant effect for interventions to promote AET adherence. The systematic review revealed that lowering medication costs and a subgroup of psychosocial and reminder interventions showed the most promise, informing future research, policy, and clinical directions.

Canonical notch pathway protects hepatocytes from ischemia/reperfusion injury in mice by repressing reactive oxygen species production through JAK2/STAT3 signaling.

UNLABELLED: Hepatic ischemia/reperfusion (I/R) injury is initiated by reactive oxygen species (ROS) accumulated during the early reperfusion phase after ischemia, but cellular mechanisms controlling ROS production and scavenging have not been fully understood. In this study, we show that blocking Notch signal by knockout of the transcription factor RBP-J or a pharmacological inhibitor led to aggravated hepatic I/R injury, as manifested by deteriorated liver function and increased apoptosis, necrosis, and inflammation, both in vitro and in vivo. Interruption of Notch signaling resulted in increased intracellular ROS in hepatocytes, and a ROS scavenger cured exacerbated hepatic I/R injury after Notch signaling blockade, suggesting that Notch signal deficiency aggravated I/R injury through increased ROS levels. Notch signal blockade resulted in down-regulation of Hes5, leading to reduced formation of the Hes5-STAT3 complex and hypophosphorylation of STAT3, which further attenuated manganese superoxide dismutase (MnSOD) expression and increased ROS and apoptosis. Indeed, overexpression of a constitutively active STAT3 rescued MnSOD expression and I/R injury-induced apoptosis in the absence of Notch signaling. Finally, forced Notch activation by ligand stimulation or Hes5 overexpression reduced intracellular ROS and protected hepatocytes from apoptosis after I/R injury through the activation of STAT3 and MnSOD expression. CONCLUSION: Notch signal protects hepatocytes from I/R injury by Hes5-dependent activation of STAT3, which activates the expression of MnSOD, leading to the scavenging of ROS.

A3 CLNN: Spatial, Spectral and Multiscale Attention ConvLSTM Neural Network for Multisource Remote Sensing Data Classification.

The problem of effectively exploiting the information multiple data sources has become a relevant but challenging research topic in remote sensing. In this article, we propose a new approach to exploit the complementarity of two data sources: hyperspectral images (HSIs) and light detection and ranging (LiDAR) data. Specifically, we develop a new dual-channel spatial, spectral and multiscale attention convolutional long short-term memory neural network (called dual-channel A3 CLNN) for feature extraction and classification of multisource remote sensing data. Spatial, spectral, and multiscale attention mechanisms are first designed for HSI and LiDAR data in order to learn spectral- and spatial-enhanced feature representations and to represent multiscale information for different classes. In the designed fusion network, a novel composite attention learning mechanism (combined with a three-level fusion strategy) is used to fully integrate the features in these two data sources. Finally, inspired by the idea of transfer learning, a novel stepwise training strategy is designed to yield a final classification result. Our experimental results, conducted on several multisource remote sensing data sets, demonstrate that the newly proposed dual-channel A 3 CLNN exhibits better feature representation ability (leading to more competitive classification performance) than other state-of-the-art methods.

Prognostic Significance of CCDC137 Expression and Its Association with Immune Infiltration in Hepatocellular Carcinoma.

Globally, hepatocellular carcinoma (HCC) is one of the most common causes of cancer-associated mortalities. The clinical outcome of HCC patients remains poor due to distant metastasis and recurrence. In recent years, growing evidences have confirmed that the coiled-coil domain-containing (CCDC) family proteins are involved in the progression of several diseases. However, the expression and clinical significance of the coiled-coil domain-containing 137 (CCDC137) in hepatocellular carcinoma (HCC) have not been investigated. Level 3 mRNA expression profiles and clinicopathological data were obtained in TCGA-LIHC. Differentially expressed genes (DEGs) were screened between 371 HCC and 50 nontumor specimens. The prognostic value of CCDC137 was analyzed in HCC patients. The correlations between CCDC137 and cancer immune infiltrates were investigated. In this study, a total of 2897 DEGs were obtained: 2451 genes were significantly upregulated and 446 genes were significantly downregulated. KEGG assays revealed that these DEGs were involved in tumor progression. Among 2897 DEGs, we found that CCDC137 expression was distinctly increased in HCC specimens compared with nontumor specimens. A high level of CCDC137 expression was related to an advanced tumor stage and grade. Moreover, patients with higher levels of CCDC137 expression had a shorter overall survival and disease-free survival than patients with lower CCDC137 levels. CCDC137 expression was positively correlated with infiltrating levels of several immune cells, such as CD8 T cells and Th2 cells. Finally, in vitro experiments confirmed that CCDC137 expression was highly expressed in HCC cells, and its knockdown suppressed the proliferation of HCC cells. Taken together, our findings revealed that CCDC137 might be used as a biomarker for immune infiltration and poor prognosis in HCC, which offered fresh insight on potential therapies for HCC.

Overexpression of SLC25A51 promotes hepatocellular carcinoma progression by driving aerobic glycolysis through activation of SIRT5.

Solute carrier family 25 member 20 (SLC25A51) is a newly identified mammalian mitochondrial NAD+ transporter. However, the clinicopathological and biological significance of SLC25A51 in human cancers, including hepatocellular carcinoma (HCC), remains unclear. The aim of this study was to define the role of SLC25A51 in HCC progression. Here we demonstrate that SLC25A51 is significantly overexpressed in human HCC specimens and cell lines, caused by, at least in partial, the decrease of miR-212-3p. SLC25A51 overexpression is positively correlated with the clinicopathological characteristics of vascular invasion and tumor diameter, as well as poor survival in patients with HCC. Knockdown of SLC25A51 attenuated, while overexpression of SLC25A51 enhanced the growth and metastasis of HCC cells both in vitro and in vivo. Mechanistically, glucose metabolism reprogramming from oxidative phosphorylation to glycolysis by activation of mitochondrial sirtuin 5 (SIRT5) was found to contribute to the promotion of growth and metastasis by SLC25A51 in HCC cells. Together, these findings reveal important roles of SLC25A51 in HCC tumorigenesis and suggest SLC25A51 as a promising prognostic marker and therapeutic target for treating HCC.

Transcervical Exploration via the Posterolateral Approach to Extract a Fishbone Embedded in the Paraglottic Space.

Ingested foreign bodies occasionally migrate to the paraglottic space. The external transcervical approach is almost always required to extract completely embedded foreign bodies. We report a case of an ingested fishbone embedded in the paraglottic space, which was successfully removed through transcervical exploration of the paraglottic space via the posterolateral approach. The posterolateral approach is safe and effective for the removal of foreign bodies completely embedded in the paraglottic space.

Sesquiterpene Lactams and Lactones With Antioxidant Potentials From Atractylodes macrocephala Discovered by Molecular Networking Strategy.

Atractylodes macrocephala rhizome (called Bái-zhú in China) has a long history as a functional food and herbal medicine in East Asia, especially China. Sesquiterpenoids are one of the main active compounds of Atractylodes macrocephala rhizome. This study aimed to explore the unknown sesquiterpenoids of A. macrocephala rhizome using a molecular networking strategy. Two new nitrogen-containing sesquiterpenoids, atractylenolactam A (1) and atractylenolactam B (2), and 2 new sesquiterpene lactones, 8-methoxy-atractylenolide V (6) and 15-acetoxyl atractylenolide III (7), along with 12 known analogs (3-5 and 8-16) were discovered and isolated. All the structures were assigned based on detailed spectroscopic analyses. The absolute configurations of 1, 2, 6, and 7 were established by time-dependent density functional theory ECD (TDDFT-ECD) calculations. All these compounds had different degrees of concentration-dependent activating effects on nuclear-factor-E2-related factor-2 (Nrf2).