Body mass index, smoking behavior, and depression mediated the effects of schizophrenia on chronic obstructive pulmonary disease: trans-ethnic Mendelian-randomization analysis.

Background: Previous studies have highlighted the association between schizophrenia (SCZ) and chronic obstructive pulmonary disease (COPD), yet the causal relationship remains unestablished. Methods: Under the genome-wide significance threshold (P<5×10-8), data from individuals of European (EUR) and East Asian (EAS) ancestries with SCZ were selected for analysis. Univariable Mendelian randomization (MR) explored the causal relationship between SCZ and COPD. Linkage disequilibrium score (LDSC) regression was used to calculate genetic correlation, while multivariable and mediation MR further investigated the roles of six confounding factors and their mediating effects. The primary method utilized was inverse-variance weighted (IVW), complemented by a series of sensitivity analyses and false discovery rate (FDR) correction. Results: LDSC analysis revealed a significant genetic correlation between SCZ and COPD within EUR ancestry (rg = 0.141, P = 6.16×10-7), with no such correlation found in EAS ancestry. IVW indicated a significant causal relationship between SCZ and COPD in EUR ancestry (OR = 1.042, 95% CI 1.013-1.071, P = 0.003, PFDR = 0.015). Additionally, replication datasets provide evidence of consistent causal associations(P < 0.05 & PFDR < 0.05). Multivariable and mediation MR analyses identified body mass index (BMI)(Mediation effect: 50.57%, P = 0.02), age of smoking initiation (Mediation effect: 27.42%, P = 0.02), and major depressive disorder (MDD) (Mediation effect: 60.45%, P = 6.98×10-5) as partial mediators of this causal relationship. No causal associations were observed in EAS (OR = 0.971, 95% CI 0.875-1.073, P = 0.571, PFDR = 0.761) ancestry. No causal associations were found in the reverse analysis across the four ancestries (P > 0.05 & PFDR > 0.05). Conclusions: This study confirmed a causal relationship between SCZ and the risk of COPD in EUR ancestry, with BMI, smoking, and MDD serving as key mediators. Future research on a larger scale is necessary to validate the generalizability of these findings across other ancestries.

Exogenous hormone therapy and non-melanoma skin cancer (keratinocyte carcinoma) risk in women: a systematic review and meta-analysis.

Previous studies reported inconsistent results regarding the association between keratinocyte carcinoma (KC) and exogenous hormone therapy. This study aimed to investigate the association between the use of exogenous sex hormones and the risk of KC among women. The databases of PubMed, Ovid Medline, Cochrane, and Web of Science were searched until May 2023. A total of 5293 patients with KC and 106,424 controls were included for analysis. The meta-analysis indicated that oral contraceptives (OC) and hormonal replacement therapy (HRT) use were associated with an increased risk of squamous cell carcinoma (SCC) (OR/RR = 1.25, 95% CI 1.10 to 1.43, I2 = 41.6%, p = 0.080). Subgroup analysis showed that OC use increased the risk of SCC (OR/RR = 1.37, 95% CI 1.15 to 1.63), whereas no significant association was shown between HRT use and risk of SCC (OR/RR = 1.13, 95% CI 0.93 to 1.37). Additionally, OC and HRT use were linked to an increased risk of basal cell carcinoma (BCC) (OR/RR = 1.16, 95% CI 1.09 to 1.25, I2 = 30.1%, p = 0.188). Further subgroup analysis suggested both OC and HRT use were associated with an increased risk of BCC (OC: OR/RR = 1.13, 95% CI 1.01 to 1.25; HRT: OR/RR = 1.19, 95% CI 1.09 to 1.30). In conclusion, our findings support the hypothesis that the risk of KC among women may be affected by the use of exogenous hormones.

The diagnostic role and mechanistic functions of exosomal lncRNAs in prostate cancer.

Exosomes are small membrane-enclosed vesicles that are released by most living cells and harbor a diverse array of proteins, nucleic acids, and lipid cargos. These exosomes offer valuable biomarkers that may offer insights regarding as a range of physiological and pathological processes, including immune responses, cancer development, pregnancy, and diseases of the central nervous system. With the development of high-throughput technologies, the vital functions of long non-coding RNAs (lncRNAs) have been gradually entered people's vision and become new research hotspots. Nowadays, lncRNAs can play important roles in cancer progression by combining with miRNAs, activating molecular targets and other ways, and are also related to the diagnosis, treatment and prognosis for cancer, such as prostate cancer. Current review focused on the summary of diagnostic roles and mechanistic functions about exosomal lncRNAs in prostate cancer.

Siglec10-An immunosuppressor and negative predictor of survival prognosis in gliomas.

Glioma is a type of tumor occurring in the central nervous system. In recent decades, specific gene mutations and molecular aberrations have been used to conduct the glioma classification and clinical decisions. Siglec10 is a member of the sialic acid-binding immunoglobulin superfamily. In this study, we investigated the expression and functions of siglec10 in gliomas. We analyzed the siglec10 expression in glioma patients with immunohistochemical (IHC) staining and evaluated the survival prognosis. The high siglec10 expression had a shorter survival prognosis than the low siglec10 expression in patients, especially in malignant gliomas. Bioinformatic datasets, including TCGA and CGGA, validated the IHC results and discovered the expression of siglec10 was higher in the malignant subtype than a benign subtype of gliomas. So, siglec10 is associated with the poor prognosis of gliomas. Furthermore, the related mechanisms of siglec10 in gliomas were investigated by functional enrichment analysis, including GSEA, GO, and KEGG analysis. Siglec10 was correlated with inflammatory mediators, inflammatory cells, and inflammatory pathways in gliomas. Siglec10 might take part in the immune response in the tumor microenvironment to induce glioma's progression and metastasis. This study showed siglec10 was a biomarker in glioma, and it might be the potential target of glioma immunotherapy in the future.

Functions and mechanisms of N6­methyladenosine in prostate cancer (Review).

Prostate cancer (PCa) has long been a major public health problem affecting men worldwide. Even with treatment, it can develop into castration­resistant PCa. With the continuous advancement in epigenetics, researchers have explored N6­methyladenosine (m6A) in search of a more effective and lasting treatment for PCa. m6A is widely distributed in mammalian cells and influences various aspects of mRNA metabolism. Recently, it has been associated with the development or suppression of various types of cancer, including PCa. This review summarizes the recent findings on m6A regulation and its functions and mechanisms in cells, focusing on the various functional proteins operating within m6A in PCa cells. Moreover, the potential clinical value of exploiting m6A modification as an early diagnostic marker in PCa diagnosis and therapeutics was discussed. m6A may also be used as an indicator to evaluate treatment outcome and prognosis.

N-glycosylation of GDF15 abolishes its inhibitory effect on EGFR in AR inhibitor-resistant prostate cancer cells.

Castration-resistance of prostate cancer is one of the most challenging clinical problems. In the present study, we have performed proteomics and glycomics using LNCaP model. Growth differentiation factor-15 (GDF15) level is increased in androgen receptor (AR) inhibitor-resistant cells and the inhibitory effect of GDF15 on epithelial growth factor receptor (EGFR) pathway is relieved by GDF15 N70 glycosylation. Interference of GDF15 (siRNA or N70Q dominant negative) or EGFR pathway (inhibitor or siRNA for EGFR, SRC or ERK) decreases the resistant-cell survival in culture and tumor growth in mice. Our study reveals a novel regulatory mechanism of prostate cancer AR inhibitor resistance, raises the possibility of AR/SRC dual-targeting of castration-resistance of prostate cancer, and lays foundation for the future development of selective inhibitors of GDF15 glycosylation.

High Expression Levels of SIGLEC9 Indicate Poor Outcomes of Glioma and Correlate With Immune Cell Infiltration.

Objective: This study aimed to investigate the diagnostic value and underlying mechanisms of sialic acid-binding Ig-like lectin 9 (SIGLEC9) in gliomas. Patients and Methods: The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA) databases were used to analyze the association of SIGLEC9 expression levels with tumor stages and survival probability. Immunohistochemical staining of SIGLEC9 and survival analysis were performed in 177 glioma patients. Furthermore, related mechanisms were discovered about SIGLEC9 in glioma tumorigenesis, and we reveal how SIGLEC9 functions in macrophages through single-cell analysis. Results: TCGA and CGGA databases indicated that patients with high SIGLEC9 expression manifested a significantly shorter survival probability than those with low SIGLEC9 expression. SIGLEC9 was upregulated significantly in malignant pathological types, such as grade III, grade IV, mesenchymal subtype, and isocitrate dehydrogenase wild-type gliomas. The immunohistochemical staining of tissue sections from 177 glioma patients showed that high-SIGLEC9-expression patients manifested a significantly shorter survival probability than low-SIGLEC9-expression patients with age ≧60 years, grade IV, glioblastoma multiforme, alpha thalassemia/intellectual disability syndrome X-linked loss, and without radiotherapy or chemotherapy. Furthermore, the SIGLEC9 expression level was positively correlated with myeloid-derived suppressor cell infiltration and neutrophil activation. The SIGLEC9 expression was also positively correlated with major immune checkpoints, such as LAIR1, HAVCR2, CD86, and LGALS9. Through single-cell analysis, we found that the SIGLEC9 gene is related to the ability of macrophages to process antigens and the proliferation of macrophages. Conclusion: These findings suggested that SIGLEC9 is a diagnostic marker of poor outcomes in glioma and might serve as a potential immunotherapy target for glioma patients in the future.

Lysine demethylase 5A promotes prostate adenocarcinoma progression by suppressing microRNA-330-3p expression and activating the COPB2/PI3K/AKT axis in an ETS1-dependent manner.

Lysine demethylase 5A (KDM5A) is a histone demethylase frequently involved in cancer progression. This research aimed to explore the function of KDM5A in prostate adenocarcinoma (PRAD) and the molecular mechanism. KDM5A was highly expressed in collected PRAD tissues and acquired PRAD cells. High KDM5A expression was correlated with reduced survival and poor prognosis of patients with PRAD. Knockdown of KDM5A suppressed the proliferation, colony formation, migration, and invasiveness of PRAD cells and reduced angiogenesis ability of endothelial cells. Downstream molecules implicated in KDM5A mediation were predicted using integrated bioinformatic analyses. KDM5A enhanced ETS proto-oncogene 1 (ETS1) expression through demethylation of H3K4me2 at its promoter. ETS1 suppressed the transcription activity of miR-330-3p, and either further ETS1 overexpression or miR-330-3p inhibition blocked the functions of KDM5A knockdown in PRAD. miR-330-3p targeted coatomer protein complex subunit ß2 (COPB2) mRNA. Downregulation of miR-330-3p restored the expression of COPB2 and activated the PI3K/AKT pathway in PRAD. The results in vitro were reproduced in vivo where KDM5A downregulation suppressed the growth and metastasis of xenograft tumors in nude mice. In conclusion, this study demonstrated that KDM5A promoted PRAD by suppressing miR-330-3p and activating the COPB2/PI3K/AKT axis in an ETS1-dependent manner.

Upregulation of COPB2 Promotes Prostate Cancer Proliferation and Invasion Through the MAPK/TGF-ß Signaling Pathway.

There is increasing evidence that coatomer protein complex subunit beta 2 (COPB2) plays an important role in various cancer types. This study explored the role and the downstream mediators of COPB2 in prostate cancer (PCa). The expression of COPB2 was determined by the Cancer Genome Atlas database and enzyme-linked immunosorbent assay. COPB2 expression was upregulated in PCa tissues and correlated with Gleason score, biochemical recurrence, and poor prognosis. The functional roles of COPB2 in PCa were verified through a series of experiments. Knocking down COPB2 expression inhibited the growth and clonogenesis of PCa cells, promoted cell apoptosis, and inhibited the ability of scratch repair, invasion of PCa cells, and tumor growth in Nude mice. To analyze downstream signaling pathways, ingenuity pathway analysis, GSEA, and whole-genome expression spectrum GeneChip analysis were used. Western blot revealed that COPB2 expression promoted the proliferation and invasion of PCa cells by regulating the MAPK/TGF-ß signaling pathway. The interacting protein (nuclear protein 1, NUPR1) was identified via Co-IP, real-time PCR, Western blot, and TCGA database in sampled tissues. The expressions of the interaction proteins NUPR1 and COPB2 were negatively regulated by each other. COPB2 could be a new biomarker for PCa diagnosis and monitoring and to provide a theoretical basis for identifying effective drug intervention targets through in-depth mechanistic studies.

Comprehensive Analysis of 29,464 Cancer Cases and 35,858 Controls to Investigate the Effect of the Cytotoxic T-Lymphocyte Antigen 4 Gene rs231775 A/G Polymorphism on Cancer Risk.

In our previous studies, we found that the rs231775 polymorphism of cytotoxic T-lymphocyte antigen 4 (CTLA-4) is associated with risks of different cancer types; however, the association remains controversial and ambiguous, so we conducted an in-depth meta-analysis to verify the association. A complete search of the PubMed, Google Scholar, Embase, Chinese databases, and Web of Science was conducted without regard to language limitations, covering all publications since November 20, 2021. The search criteria for cancer susceptibility associated with the polymorphism in the CTLA-4 gene rs231775 resulted in 87 case-control studies with 29,464 cases and 35,858 controls. The association strength was analyzed using odds ratios and 95% confidence intervals. Overall, we found that the CTLA-4 rs231775 polymorphism may reduce cancer risk. A stratified cancer type analysis showed that CTLA-4 rs231775 polymorphism was a risk factor for colorectal cancer and thyroid cancer; on the other hand, it was a protective factor for breast cancer, liver cancer, cervical cancer, bone cancer, head and neck, and pancreatic cancer. We also classified cancer into five systems and observed an increased association with digestive tract cancer, decreased associations with orthopedic tumors, tumors of the urinary system, and gynecological tumors. In the subgroup based on race, decreased relationships were observed in both Asians and Caucasians. The same decreased association was also shown in the analysis of the source of control analysis. Our present study indicates that the CTLA-4 rs231775 polymorphism contributes to cancer development and aggression.

Berberine-Based Heterogeneous Linear Supramolecules Neutralized the Acute Nephrotoxicity of Aristolochic Acid by the Self-Assembly Strategy.

Aristolochic acid (AA) has been reported to cause a series of health problems, including aristolochic acid nephropathy and liver cancer. However, AA-containing herbs are highly safe in combination with berberine (Ber)-containing herbs in traditional medicine, suggesting the possible neutralizing effect of Ber on the toxicity of AA. In the present study, in vivo systematic toxicological experiments performed in zebrafish and mice showed that the supramolecule self-assembly formed by Ber and AA significantly reduced the toxicity of AA and attenuated AA-induced acute kidney injury. Ber and AA can self-assemble into linear heterogenous supramolecules (A-B) via electrostatic attraction and π-π stacking, with the hydrophobic groups outside and the hydrophilic groups inside during the drug combination practice. This self-assembly strategy may block the toxic site of AA and hinder its metabolism. Meanwhile, A-B linear supramolecules did not disrupt the homeostasis of gut microflora as AA did. RNA-sequence analysis, immunostaining, and western blot of the mice kidney also showed that A-B supramolecules almost abolished the acute nephrotoxicity of AA in the activation of the immune system and tumorigenesis-related pathways.

The protective effect of L-glutamine against acute Cantharidin-induced Cardiotoxicity in the mice.

BACKGROUND: Cantharidin (CTD) is a compound which have the potential to be exploited as an antitumor drug, and it has been demonstrated antitumor effects in a variety of cancers. However, the use is limited due to its severe toxicity. It has reported that it can induce fatal cardiac arrhythmias. Fortunately, we found that L-glutamine can alleviate cardiac toxicity caused by cantharidin in mice. METHODS: To investigate the protective effect of L-glutamine, we used a high dose of cantharidin in mice to create a model of cardiotoxicity. In the experimental mice, glutamine was given orally half an hour before they were administrated with cantharidin. The mice of control group were intraperitoneally injected with DMSO solution. The general state of all mice, cardiac mass index, electrocardiogram change and biological markers were determined. Hematoxylin-eosin staining (HE staining) of heart tissue was carried out in each group to reflect the protective effect of glutamine. To investigate the mechanisms underlying the injury and cardio-protection, multiple oxidative stress indexes were determined and succinate dehydrogenase activity was evaluated. RESULT: The results showed that L-glutamine (Gln) pretreatment reduced weight loss and mortality. It also decreased the biological markers (p < 0.05), improved electrocardiogram and histological changes that CTD induced cardiotoxicity in mice. Subsequently, the group pretreated with L-glutamine before CTD treatment increases in MDA but decreases in SOD and GSH, in comparison to the group treated with CTD alone. Besides, succinate dehydrogenase activity also was improved when L-glutamine was administrated before cantharidin compared to cantharidin. CONCLUSIONS: This study provided evidence that L-glutamine could protect cardiac cells against the acute cantharidin-induced cardiotoxicity and the protective mechanism of glutamine may be related to the myocardial cell membrane or the tricarboxylic acid cycle in the mitochondria.

Silencing miR-20a-5p inhibits axonal growth and neuronal branching and prevents epileptogenesis through RGMa-RhoA-mediated synaptic plasticity.

Epileptogenesis is a potential process. Mossy fibre sprouting (MFS) and synaptic plasticity promote epileptogenesis. Overexpression of repulsive guidance molecule a (RGMa) prevents epileptogenesis by inhibiting MFS. However, other aspects underlying the RGMa regulatory process of epileptogenesis have not been elucidated. We studied whether RGMa could be modulated by microRNAs and regulated RhoA in epileptogenesis. Using microRNA databases, we selected four miRNAs as potential candidates. We further experimentally confirmed miR-20a-5p as a RGMa upstream regulator. Then, in vitro, by manipulating miR-20a-5p and RGMa, we investigated the regulatory relationship between miR-20a-5p, RGMa and RhoA, and the effects of this pathway on neuronal morphology. Finally, in the epilepsy animal model, we determined whether the miR-20a-5p-RGMa-RhoA pathway influenced MFS and synaptic plasticity and then modified epileptogenesis. Our results showed that miR-20a-5p regulated RGMa and that RGMa regulated RhoA in vitro. Furthermore, in primary hippocampal neurons, the miR-20a-5p-RGMa-RhoA pathway regulated axonal growth and neuronal branching; in the PTZ-induced epilepsy model, silencing miR-20a-5p prevented epileptogenesis through RGMa-RhoA-mediated synaptic plasticity but did not change MFS. Overall, we concluded that silencing miR-20a-5p inhibits axonal growth and neuronal branching and prevents epileptogenesis through RGMa-RhoA-mediated synaptic plasticity in the PTZ-induced epilepsy model, thereby providing a possible strategy to prevent epileptogenesis.

Fibrinogen-Like Protein 2 (FGL2) is a Novel Biomarker for Clinical Prediction of Human Breast Cancer.

BACKGROUND Fibrinogen-like protein 2 (FGL2) is a member of the fibrinogen-like protein family and possesses important regulatory functions in both innate and adaptive immune responses. FGL2 is overexpressed in glioma, and its expression level is negatively associated with the prognosis of glioma patients. However, the diagnostic value of FGL2 is unknown in breast carcinoma. MATERIAL AND METHODS We comprehensively analyzed the expression pattern of FGL2 in breast cancer. Several online databases - TCGA, Oncomine, GEPIA, Kaplan-Meier plotter, and PrognoScan - were used in this study. RESULTS Based on the TCGA dataset and Oncomine database, we found that the expression level of FGL2 was remarkably lower in breast cancer compared with adjacent normal tissues. Clinical data showed that the expression level of FGL2 was significantly associated with radiation therapy, PR status, and tumor stage. Bioinformatics analysis of the GEPIA, Kaplan-Meier plotter, and PrognoScan databases showed that lower FGL2 expression levels were associated with a worse prognosis in breast cancer patients. Furthermore, the expression level of FGL2 was positively correlated with the immune cell infiltrations in breast cancer, especially those cells with high antitumor activities. GO, KEGG, and GSEA analyses also validated that FGL2 was closely related to genes involved in the immune response, signal transduction, and T cell receptor signaling pathway in breast cancer. CONCLUSIONS The results demonstrated that high expression of FGL2 is a useful marker for breast cancer treatment and appears to be correlated with enhanced antitumor activities in breast cancer patients.

FGL2 is positively correlated with enhanced antitumor responses mediated by T cells in lung adenocarcinoma.

Lung cancer is the most common malignant tumor, accounting for 25% of cancer-related deaths and 14% of new cancers worldwide. Lung adenocarcinoma is the most common type of pulmonary cancer. Although there have been some improvements in the traditional therapy of lung cancer, the outcome and prognosis of patients remain poor. Lung cancer is the leading cause of cancer-related deaths worldwide, with 1.8 million new cases being diagnosed each year. Precision medicine based on genetic alterations is considered a new strategy of lung cancer treatment that requires highly specific biomarkers for precision diagnosis and treatment. Fibrinogen-like protein 2 (FGL2) plays important roles in both innate and adaptive immunity. However, the diagnostic value of FGL2 in lung cancer is largely unknown. In this study, we systematically investigated the expression profile and potential functions of FGL2 in lung adenocarcinoma. We used the TCGA and Oncomine datasets to compare the FGL2 expression levels between lung adenocarcinoma and adjacent normal tissues. We utilized the GEPIA, PrognoScan and Kaplan-Meier plotter databases to analyze the relationship between FGL2 expression and the survival of lung adenocarcinoma patients. Then, we investigated the potential roles of FGL2 in lung adenocarcinoma with the TIMER database and functional enrichment analyses. We found that FGL2 expression was significantly lower in lung adenocarcinoma tissue compared with adjacent normal tissue. A high expression level of FGL2 was correlated with better prognostic outcomes of lung adenocarcinoma patients, including overall survival and progression-free survival. FGL2 was positively correlated with the infiltration of immune cells, including dendritic cells, CD8+ T cells, macrophages, B cells, and CD4+ T cells, in lung adenocarcinoma. Functional enrichment analyses also showed that a high expression level of FGL2 was positively correlated with enhanced T cell activities, especially CD8+ T cell activation. Thus, we propose that high FGL2 expression, which is positively associated with enhanced antitumor activities mediated by T cells, is a beneficial marker for lung adenocarcinoma treatment outcomes.

Effect of salvianolic acid A on the proliferation and apoptosis in esophageal cancer cells and the underlying mechanisms. / ä¸¹é šé ¸Aå¯¹é£Ÿç®¡ç™Œç»†èƒžå¢žæ®–ä¸Žå‡‹äº¡çš„å½±å“åŠå ¶æœºåˆ¶.

OBJECTIVES: To explore the effect of salvianolic acid A (SalA) on the proliferation and apoptosis in esophageal cancer cell line KYSE-150 and the possible mechanisms. METHODS: The esophageal cancer cells were randomly divided into 4 groups: a control group, a 10 µmol/L SalA group, a 25 µmol/L SalA group, and a 50 µmol/L SalA group. Cell counting kit-8 (CCK-8) was used to detect the cell proliferation activity. Flow cytometry was used to detect cell cycle distribution and cell apoptosis rate. Western blotting was used to detect the protein expression of cell proliferation maker Ki-67, cyclin D1, cyclin-dependent kinase 4 (CDK4), CDK6, B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X (Bax), cleaved-caspase-9, cleaved-caspase-3, phosphatidylinositol 3-kinase (PI3K), phosphorylated protein kinase B (p-Akt) and mechanistic target of rapamycin (mTOR). RESULTS: Compared with the control group, the cell proliferation activity was significantly reduced (P<0.01); the cells in the G1 phase were significantly increased, and the S phase cells were significantly reduced (both P<0.01); the cell apoptosis rate was significantly increased (P<0.01) in the SalA groups at different concentration; the expression levels of Ki-67, cyclin D1, CDK4, CDK6, Bcl-2, PI3K, p-Akt and mTOR were decreased significantly, but the expression levels of p21, Bax, cl-caspase-9 and cl-caspase-3 were increased significantly in the SalA groups at different concentration (all P<0.01). CONCLUSIONS: SalA can inhibit the proliferation and induce G1 phase arrest and apoptosis in the esophageal cancer cell line KYSE-150, which may be related to the activation of PI3K/Akt/mTOR signal pathway.

Secondary Metabolites from Deep-Sea Derived Microorganisms.

Microorganisms obtained from the deep sea are a rich source of marine natural products with distinctive chemical structures and bioactivities. In this review, we will provide a retrospective of outstanding research within the scope of deep-sea (≥1000 m) microbial natural products, which has produced up to 442 compounds by the end of 2017. Approximetely, 60% of these structures have demonstrated various biological activities with more than 30% showing cytotoxic function. In this review, we particularly summarize those successful research on secondary metabolites produced by deep-sea derived microorganisms with inclusion of structural characteristics, biological activities, together with biogenetic origins and taxonomic features of the source microorganisms, from which, we expect to provide more comprehensive understanding of small molecules obtained from deep-sea environment and benefit the ongoing scholarly endeavors in the search for novel pharmaceutical agents from the deep-sea derived microorganisms.

Facile Synthesis of Nickel Cobalt Layered Double Hydroxide Nanosheets Intercalated with Sulfate Anion for High-Performance Supercapacitor.

Nickel-cobalt layered double hydroxide nanosheets intercalated with sulfate anion were fabricated via a facile hydrothermal method and investigated as high-performance electrode materials for supercapacitors. The morphology and electrochemical properties of the obtained samples could be controlled by changing molar ratios of the Ni and Co precursors. NiCo-LDHs with Ni/Co molar ratio of 0.35:0.65 exhibited high specific capacitance of 1551.1 F/g at the current density of 1 A/g and good cycling stability of 84.0% retention after 1000 charge/discharge cycles. On this basic, aqueous asymmetric supercapacitor (AAS) was successfully constructed by using the Ni0.35Co0.65-LDHs as the positive electrode and the activated carbon as the negative electrode. The as-built AAS was able to work in a working voltage window of 0~1.4 V and exhibited outstanding electrochemical performance. The Ni0.35Co0.65-LDHs//KOH activated cotton-derived carbon (ACDC) AAS showed the highest specific capacitance of 157.5 F/g, the satisfactory capacitance retention of 78.62% after 5000 cycles, the maximum energy density of 42.88 Wh/kg, and preferable combination of energy density of 30.63 Wh/kg with power density of 4.9 kW/kg at a current density of 7 A/g.

Anthraquinone Derivatives from a Marine-Derived Fungus Sporendonema casei HDN16-802.

Five new anthraquinone derivatives, auxarthrols D-H (1-5), along with two known analogues (6-7), were obtained from the culture of the marine-derived fungus Sporendonema casei. Their structures, including absolute configurations, were established on the basis of NMR, HRESIMS, and circular dichroism (CD) spectroscopic techniques. Among them, compound 4 represents the second isolated anthraquinone derivative with a chlorine atom, which, with compound 6, are the first reported anthraquinone derivatives with anticoagulant activity. Compounds 1 and 3 showed cytotoxic activities with IC50 values from 4.5 µM to 22.9 µM, while compounds 1, 3-4, and 6-7 showed promising antibacterial activities with MIC values from 12.5 µM to 200 µM. In addition, compound 7 was discovered to display potential antitubercular activity for the first time.