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An unprecedented method for the synthesis of biaryl aldehydes bearing both axial and central chirality is presented.

Chenlu Huang,1,* Weixia Li,2,* Chong Chen,2,* Wei Xu,1 Ling Fei,1 Shuai Tao,3 Qiankun Hu,1 Xudong Xie,1 Xiongyue Cao,1 Xiao-Yu Zhang,1,4 Liang Chen,1 Qiang Li,1 Yuxian Huang1 1Department of Liver Disease, Shanghai Public Health Clinical Center, Fudan University, Shanghai, People’s Republic of China; 2Department of Infectious Disease, Shanghai Public Health Clinical Center, Fudan University, Shanghai, People’s Republic of China; 3Research Unit, Shanghai Public Health Clinical Center, Fudan University, Shanghai, People’s Republic of China; 4Section of Education, Shanghai Public Health Clinical Center, Fudan University, Shanghai, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yuxian Huang; Qiang Li, Email yxhuang@fudan.edu.cn; liqiang66601@163.comAim: The early prognosis evaluation of acute-on-chronic liver failure (ACLF) is important to decrease its mortality. We aimed to develop a new score to accurately predict the outcome of patients with ACLF.Methods: A derivation set of 408 patients with hepatitis B virus-related ACLF (HBV-ACLF) based on the Asian Pacific Association for the Study of the Liver criteria is used to develop a prognostic score that was validated in 209 patients with HBV-ACLF and 195 patients with non-HBV-ACLF.Results: Seven factors were significantly related to the 28-day mortality and constituted a new score (CHINAT-CD4 = 0.320 × ln (creatinine) + 0.668 × hepatic encephalopathy score + 0.745 × ln (international normalized ratio) + 0.476 × ln (neutrophil) + 0.251 × ln (aspartate aminotransferase) + 0.411 × ln (total bilirubin) - 0.605 × ln (CD4+ T cells count)). The C-indices of the new score for the 28-/90-day mortality (0.810/0.806) outperformed those of the other seven scores (p≤ 0.05). The results were confirmed in a validation set (0.798/793 for HBV-ACLF; 0.790/0.788 for non-HBV-ACLF). The novel score based on CD4+ T cell count showed high predictive performance for the 28-/90-day mortality of ACLF.Conclusion: The novel score based on CD4+ T cell count can accurately predict the 28-/90-day mortality for patients with ACLF.Keywords: liver failure, chronic liver disease, prognostic score, risk stratification, inflammatory markers

Catalytic asymmetric 1,3-dipolar cycloaddition reactions of activated isocyanides with various 2π dipolarophiles have been intensively studied, affording a wide range of enantioenriched five-membered N-heterocycles. In sharp contrast, the catalytic enantioselective higher-order cycloaddition of activated isocyanides has not been achieved yet. We present here our recent work on the development of an unprecedented silver-catalyzed highly diastereo- and enantioselective [3+3] cycloaddition of activated isocyanides with azomethine imines. This method features high efficiency, good to excellent stereocontrol, wide substrate scope, as well as operational simplicity. It is also noteworthy that the same catalytic system was proved to be suitable for not only the late-stage functionalization of complex bioactive molecules but also the kinetic resolution of racemic azomethine imines.1 Introduction2 Results and Discussion3 Summary and Outlook

Bone metastasis is one of the main complications of lung cancer and most important factors that lead to poor life quality and low survival rate in lung cancer patients. However, the regulatory mechanisms underlying lung cancer bone metastasis are still poor understood. Here, we report that microRNA-182 (miR-182) plays a critical role in regulating osteoclastic metastasis of lung cancer cells. We found that miR-182 was significantly upregulated in both bone-metastatic human non–small cell lung cancer (NSCLC) cell line and tumor specimens. We further demonstrated that miR-182 markedly enhanced the ability of NSCLC cells for osteolytic bone metastasis in nude mice. Mechanistically, miR-182 promotes NSCLC cells to secrete Interleukin-8 (IL-8) and in turn facilitates osteoclastogenesis via activating STAT3 signaling in osteoclast progenitor cells. Importantly, systemically delivered IL-8 neutralizing antibody inhibits NSCLC bone metastasis in nude mice. Collectively, our findings identify the miR-182/IL-8/STAT3 axis as a key regulatory pathway in controlling lung cancer cell-induced osteolytic bone metastasis and suggest a promising therapeutic strategy that targets this regulatory axis to interrupt lung cancer bone metastasis.

Supplementary Figure S1. No significant difference in the serum levels of IL-4, IL-6, TNF-a and TGF-B between NSCLC patients and healthy controls. Supplementary Figure S2. Repression of mir-101 is involved in the tumorigenic activity of IL-1B in NSCLC cells. Supplementary Figure S3. IL-1B down-regulates mir-101 via the COX-2/HIF-1alpha pathway in NSCLC cells. Supplementary Figure S4. miR-101 up-regulates let-7 family miRNAs by targeting Lin28B in NSCLC cells. Supplementary Figure S5. Comparison of the expression of Lin28B and miR-101 in A549 and H1299 cells. Supplementary Figure S6. miR-101 plays a tumor suppressive role in NSCLC cells. Supplementary Figure S7. Repression of miR-101 is critical to IL-1B-mediated induction of Cox-2 and Lin28B in NSCLC cells. Supplementary Table S1 Sequences of chemically synthesized DNA and RNA oligonucleotides.

Current drugs do not provide an absolute cure or modify the course of asthma. Hyssopus cuspidatus Boriss extract (SXCF) has been used as Uyghur medicine for several years to treat bronchial asthma. However, very limited research has been conducted on the therapeutic mechanisms of SXCF. Disruptions in the metabolic network of lipid mediators (LMs) are closely linked to the development of asthma. Here, we explored the therapeutic mechanism of SXCF in asthma based on the metabolic network of LMs, aiming to contribute to the understanding of SXCF in asthma treatment at the molecular level. The UHPLC-MRM strategy was used for the quantitative detection of LMs in the lung tissue and in the peripheral circulatory system (serum). ELISA was used to detect IgE in serum and cytokines in BALF. The lung tissue sections were stained with H&E to observe the infiltration of inflammatory cells, and behavioural changes in mice were observed and recorded throughout the animal experiment. In contrast to the asthma group, the opposite result was observed in the SXCF groups, where the perturbed LMs metabolic network was partly restored in a dose-dependent manner with a significant elevation of anti-inflammatory metabolites, while pro-inflammatory lipids were decreased. As significant downregulation of IgE and pro-inflammatory cytokines was observed, IgE and cytokines analysis also supported the anti-inflammatory effects of SXCF. It was also noticed that SXCF treatment reduced the number of coughs and decreased the inflammatory cell infiltration around the bronchus in mice. These results suggested that SXCF has a significant ameliorative effect on ovalbumin (OVA)-induced asthma. The modulation of LMs is a possible underlying mechanism of the SXCF effects.

Pyroptosis refers to the programmed cell death. This study evaluated the mechanism of miR-126 in hypoxia-reoxygenation (HR)-induced cardiomyocyte pyroptosis.The HR rat cardiomyocyte models were established. The cell viability, cytotoxicity, and levels of miR-126, pro-caspase-1 (p45), activated caspase-1 (p20/p10), caspase-11, gasdermin D (GSDMD), and GSDMD-N were detected. The cells were transfected with miR-126 mimics to verify the effect on rat cardiomyocyte pyroptosis, and added with HMGB1 inhibitor (Glycyrrhizin) or NLRP3 inhibitor (S3680) to explore the regulatory mechanisms on rat cardiomyocyte pyroptosis. The binding relationship of miR-126 and HMGB1 was explored. The regulatory effect of miR-126 and HMGB1 on HR-stimulated cardiomyocytes was verified through co-transfection with miR-126 mimics and pcDNA3.1-HMGB1.HR treatment inhibited rat cardiomyocyte viability and increased cytotoxicity. After HR treatment, pro-caspase-1 (p45), activated caspase-1 (p20/p10), caspase-11, GSDMD, and GSDMD-N were elevated in rat cardiomyocytes, while miR-126 was evidently downregulated in rat cardiomyocytes. miR-126 overexpression, and inhibition of HMGB1 or NLRP3 partially reversed HR-induced rat cardiomyocyte cytotoxicity and pyroptosis. miR-126 targeted HMGB1 and HMGB1 overexpression partly reversed the inhibition of miR-126 overexpression on HR-induced cardiomyocyte pyroptosis.miR-126 inhibits HMGB1/NLRP3 activity and the caspase-1/11 activation and reduces the GSDMD-N cleaved from GSDMD, ultimately inhibiting HR-induced cardiomyocyte pyroptosis.

The risk of early mortality of patients who start dialysis urgently is high; however, in patients with diabetes undergoing urgent-start peritoneal dialysis (USPD), the risk of, and risk factors for, early mortality are unknown.To identify risk factors for mortality during high-risk periods in patients with diabetes undergoing USPD.This retrospective cohort study enrolled 568 patients with diabetes, aged ≥ 18 years, who underwent USPD at one of five Chinese centers between 2013 and 2019. We divided the follow-up period into two survival phases: The first 6 mo of USPD therapy and the months thereafter. We compared demographic and baseline clinical data of living and deceased patients during each period. Kaplan-Meier survival curves were generated for all-cause mortality according to the New York Heart Association (NYHA) classification. A multivariate Cox proportional hazard regression model was used to identify risk factors for mortality within the first 6 mo and after 6 mo of USPD.Forty-one patients died within the first 6 mo, accounting for the highest proportion of mortalities (26.62%) during the entire follow-up period. Cardiovascular disease was the leading cause of mortality within 6 mo (26.83%) and after 6 mo (31.86%). The risk of mortality not only within the first 6 mo but also after the first 6 mo was higher for patients with obvious baseline heart failure symptoms than for those with mild or no heart failure symptoms. Independent risk factors for mortality within the first 6 mo were advanced age [hazard ratio (HR: 1.908; 95%CI: 1.400-2.600;To reduce the risk of mortality within the first 6 mo of USPD in patients with diabetes, controlling the serum phosphorus level and improving cardiac function are recommended.

Sirtuin 6 (SIRT6), a DNA repair-related gene, has undergone an extremely thorough study for its involvement in the development of many different cancers. The objective of our study was to explore the function and mechanism of SIRT6-induced regulation of prostate cancer (PCa). RT-PCR was performed to validate the levels of SIRT6 in PCa cell lines. Cell proliferation, migration, and invasion of cells with SIRT6 knockdown were assessed using CCK-8 assay, colony formation assay, wound-healing assay, and transwell assay. Western blot was applied to assess the related proteins. We found that SIRT6 expression was distinctly upregulated in PCa specimens and cells. Loss-of-functional assays revealed that SIRT6 silence suppressed the proliferation and metastasis of PCa cells. Mechanistic studies revealed that SIRT6 silence inhibited Wnt/β‐catenin signaling and EMT progress. Overall, the study confirmed the upregulation of SIRT6 in patients with PCa and its association with the progression. SIRT6 promoted PCa progression by regulating Wnt/β‐catenin signaling, providing a promising biomarker and treatment approach for preventing PCa.

Objective To investigate the predictive value of preoperative neutrophil to lymphocyte ratio (NLR) on acute kidney injury (AKI) after on-pump coronary artery bypass (ONCAB). Methods Patients who underwent elective ONCAB for coronary heart disease were included. NLR was calculated according to the results of preoperative routine blood test, patients were divided into non-AKI and AKI groups, and the differences in clinical baseline data between the two groups were compared. Results A total of 154 patients were included in this study, including 57 (37%) with postoperative AKI and 97 (63%) without AKI. Compared with the patients in non-AKI group, those in AKI group had higher NLR (2.63 (1.83, 3.505) vs. 2.06 (1.7, 2.56), p = 0.002), higher serum creatinine (78 (67, 98.5) vs. 70.9 ± 16.8 umol/L, p p for trend = 0.003). Patients in Tertile2 and Tertile3 had higher NLR compared to those in Tertile1 (p Conclusion Elevated preoperative NLR is associated with AKI after ONCAB, and had prognostic utility independent of other recognized risk factors.

BACKGROUND Liver cancer is one of the most highly malignant cancers, characterized by easy metastasis and chemoradiotherapy resistance. Emerging evidence indicates that long noncoding RNAs (LncRNAs), including Lnc524369, are highly involved in the initiation, progression, radioresistance, and chemoresistance of hepatocellular carcinoma (HCC). However, the function of Lnc524369 remains unclear. AIM To explore the function of Lnc524369 in HCC. METHODS To investigate the effect of Lnc524369, tissue from 41 HCC patients were analyzed using CCK8, migration, and invasion assays. Lnc524369 and YWHAZ (also named 14-3-3ζ) mRNA were detected by qPCR, and YWHAZ and RAF1 proteins were detected by western blot in liver cancer cell lines and human HCC tissues. The Cancer Cell Line Encyclopedia (CCLE) databases, STRING database, Human Protein Atlas database, and the TCGA database were used for bioinformatic analysis. RESULTS Lnc524369 was significantly upregulated in the nucleus of liver cancer cells and human HCC tissues. Overexpression of Lnc524369 was associated with the proliferation, migration, and invasion of liver cancer cells. YWHAZ and RAF1 proteins and YWHAZ mRNA were overexpressed in liver cancer, which could be attenuated by overexpression of Lnc524369. Lnc524369 and its downstream target YWHAZ and RAF1 proteins were negatively associated with overall survival time. CONCLUSION Lnc524369 might be a promising target of HCC as it can enhance liver cancer progression and decrease the overall survival time of HCC by activating the YWHAZ/RAF1 pathway.

Fusion transcripts are thought to be somatic and associated with cancer. However, they have been observed in healthy tissues at high recurrent frequencies. We have used SCIF (SplicingCodesIdentifyFusion Transcripts) to analyze RNA-Seq data from 727 multiple myeloma (MM) patients of the MMRF CoMMpass Study.MTG1-SCART1, SCART1-CYP2E1, andTPM4-KLF2have been detected in 96.1%, 95.7%, and 92.2% of 727 MM patients and formed fusion gene signatures.MTG1-SCART1andSCART1-CYP2E1are read-through from the same locus and the two most recurrent epigenetic fusion genes (EFGs) out of 187 EFGs detected in ≥10% of 727 MM patients.TPM4-KLF2fusion gene, which was initially thought to be somatic, has been shown by a monozygotic twin genetic model to be a hereditary fusion gene (HFG) and the dominant genetic factor associated with MM. This work provides the first line of evidence that HFGs are the genetic factors and EFGs reflect the consequences between genetics and environments during development.

OBJECTIVE This study aimed to investigate the clinical features and potential pathogenesis of a rare nonhereditary polyposis syndrome, Cronkhite-Canada syndrome (CCS). METHODS Medical records of eight patients with CCS who were admitted to our hospital from January 2005 to November 2019 were reviewed. Transcriptome profiling was performed in one patient to investigate its difference between gastric polyp tissue and normal mucosa. Differentially expressed genes (DEGs) were determined for functional analysis. The expression of inhibin beta A (INHBA) was further assessed by using immunohistochemistry. RESULTS All patients presented with gastrointestinal polyposis, accompanied by diarrhea, skin hyperpigmentation, hair loss and nail dystrophy. Hyperplastic polyps were observed in seven patients, tubular adenoma in two, inflammatory polyps in one and hamartomatous polyps in one, respectively. All patients underwent comprehensive treatment and five achieved clinical remission. A total of 2107 DEGs, including 1265 upregulated and 842 downregulated, were found in the gastric polyp. Gene ontology analysis showed that upregulated genes were significantly enriched in the positive regulation of cell proliferation, epithelium development and angiogenesis. A protein-protein interaction analysis suggested that INHBA was at the center of the interaction network and might play an important role in CCS. Immunohistochemistry confirmed that INHBA expression was upregulated in CCS gastric polyps. CONCLUSIONS CCS is a rare disease and its diagnosis mainly depends on typical clinical manifestations, endoscopic findings and histological features. INHBA upregulation may contribute to its pathogenesis.

In recent years, long noncoding RNAs (lncRNAs) have been demonstrated to be important tumor-associated regulatory factors. LncRNA growth arrest-specific transcript 5 (Gas5) acts as an anti-oncogene in most cancers. Whether Gas5 acts as an oncogene or anti-oncogene in hepatocellular carcinoma (HCC) remains unclear. In the present study, the expression and role of Gas5 in HCC were investigated in vitro and in vivo. Lower expression levels of Gas5 were determined in HCC tissues and cells by quantitative reverse transcription-polymerase chain reaction. Overexpressed Gas 5 lentiviral vectors were constructed to analyze their influence on cell viability, migration, invasion, and apoptosis. Fluorescence in situ hybridization was used to identify the subcellular localization of Gas5. Protein complexes that bound to Gas5 were isolated from HepG2 cells through pull-down experiments and analyzed by mass spectrometry. A series of novel Gas5-interacting proteins were identified and bioinformatics analysis was carried out. These included ribosomal proteins, proteins involved in protein folding, sorting, and transportation in the ER, some nucleases and protein enzymes involved in gene transcription, translation, and other proteins with various functions.78 kDa glucose-regulated protein (GRP78) was identified as a direct target of Gas5 by Rip-qPCR and Western blot analysis assay. Gas5 inhibited HepG2 cell growth and induced cell apoptosis via upregulating CHOP to activate the ER stress signaling pathway. Further studies indicated that the knockdown of CHOP by shRNA partially reversed Gas5-mediated apoptosis in HepG2 cells. Magnetic resonance imaging showed that the ectopic expression of Gas5 inhibited the growth of HCC in nude mice. These findings suggest that Gas5 functions as a tumor suppressor and induces apoptosis through activation of ER stress by targeting the CHOP signal pathway in HCC.

BACKGROUND: Glioblastoma is the most common and most aggressive type of primary brain tumor. OBJECTIVE: The aim of this study was to investigate the efficacy and safety of intranasal granulocyte-macrophage colony stimulating factor (GM-CSF) administration combined with chemoradiotherapy in patients with glioblastoma who underwent surgery. METHODS: Ninety-two patients were randomly divided into two groups: a control group (n= 46), who received radiotherapy with adjuvant local delivery of nimustine hydrochloride (ACNU) and systemic administration of temozolomide, and an intervention group (n= 46), who received intranasal GM-CSF prior to each cycle of adjuvant chemotherapy in addition to the treatment of the control group. Karnofsky performance status (KPS) scores, progression-free survival (PFS), overall survival (OS), and adverse effects were calculated and compared between the two groups. RESULTS: Compared with the control group, the intervention group had longer PFS (7.8 vs. 6.9 months, P= 0.016) and OS (19.2 vs. 17.1 months, P= 0.045, without adjustment for interim analyses). The KPS scores were also higher in the intervention group than in the control group after 6 months (84.35 ± 8.86 vs. 80.65 ± 7.72; t= 4.552, P= 0.036). Furthermore, the patients in the intervention group had lower incidence of neutropenia and thrombocytopenia (8.7% vs. 29.5%, P= 0.012; 8.7% vs. 18.2%, P= 0.186). Other adverse events were similar in both groups, and most adverse events were grade I/II and resolved spontaneously. CONCLUSION: Intranasal GM-CSF enhances the efficacy of the local ACNU administration combined with oral temozolomide chemotherapy. The survival and performance status were significantly improved in patients with glioblastoma after surgery. Additionally, the GM-CSF therapy was able to reduce the occurrence of chemotherapy-related neutropenia and thrombocytopenia.

Catalytic asymmetric dynamic kinetic resolution of configurationally labile bridged biaryls is emerging as a powerful strategy for atropisomer synthesis. However, the reported examples suffer from an inherent challenge as the reactivity is highly dependent on the torsional strain of the biaryl substrates, which significantly narrows down the scope and hampers the application. Herein, we report our discovery and development of a torsional strain-independent reaction between biaryl thionolactones and activated isocyanides. By employing auto-tandem silver catalysis, a universal synthesis of both tri- and tetra-ortho-substituted thiazole-containing biaryls was realized in high yields with high enantioselectivities. In addition, these products could be facilely converted to a novel type of bridged biaryls bearing an eight-membered lactone. Mechanistic studies were carried out to elucidate the cause of this unusual torsional strain-independent reactivity.

Two new alkaloids, leptocarpinine B (1) and corydamine acid (2), with thirteen known alkaloid compounds (3–15), were isolated from Hypecoum leptocarpum. The structures of the isolated compounds were determined based on spectroscopic data analyses, including IR, ESI-MS, 1 D, and 2 D NMR. In addition, all the isolates were evaluated for cytotoxic activities. Compound 6 showed moderate cytotoxicity against human ovarian cancer cell lines (A2780), human cervical cancer cell lines (HeLa), and human hepatocellular carcinomas cell lines (HepG2).

The potential application of an experimentally synthesized superatom Ti@Si

With the development of economy and improvement of people's living standards, the incidence of obesity and type 2 diabetes mellitus (T2DM) has increased significantly and obesity has also become one of the most important risk factors of T2DM. In light of these trends, there have been many ways to take effect in losing weight. However, they also have corresponding deficiencies including inapparent curative effect, complex and incomplete reversible procedures and severe complications. Duodenal-Jejunal Bypass Liner (DJBL), which mimics Roux-en-Y gastric bypass (RYGB), is proved to play a key role in weight loss and control of T2DM. DJBL is reversible, less invasive and is more suitable for the treatment of obesity and T2DM, which is associated with multiple mechanisms, including incretin effect, gastric emptying mechanism, bile acid regulation, intestinal microbiota, inflammatory reaction mechanism and neural mechanism. In our review, we aimed to elaborate DJBL's clinical efficacy, safety and mechanisms in detail.

The study explored the differences in nightmare, insomnia, depression, anxiety, and cognitive deficits among adolescents and the chain mediating effects of insomnia, depression, and anxiety on the relationship between nightmares and cognitive deficits in adolescents.An online survey was used to collect demographic data of 6014 adolescents and assess nightmare, insomnia, depression, anxiety, and cognitive deficits using the Chinese Version of Nightmare Distress Questionnaire, Insomnia Severity Index, Patient Health Questionnaire 9, Generalized Anxiety Disorder 7, and Perceived Deficits Questionnaire-Depression. Spearman correlation analysis and the SPSS function "PROCESS macro" were used for correlation and mediation analyses, respectively.Female adolescents, senior high school, and poor academic performance had higher nightmare, insomnia, and cognitive deficit scores; those living in the city had higher depression and anxiety scores. Cognitive deficits were positively correlated with nightmares, insomnia, depression, and anxiety. Further, insomnia, depression, and anxiety had a chain mediating effect between nightmares and cognitive deficits in adolescents. Nightmares indirectly affect cognition deficits by affecting insomnia and then depression and anxiety symptoms.As this was a cross-sectional study, the causal relationship between the variables could not be determined. Moreover, reporting bias and volunteer bias might be present.These findings suggest that clinicians should identify adolescents with frequent nightmares early and provide timely treatment to minimize negative outcomes and possibly limit the chronicity of nightmare disorder. It is significant to maintain the physical and mental health development of adolescents to reduce the risk of insomnia, depression, anxiety, and cognitive deficits.

Biotreatment of acidic rare earth mining wastewater via acidophilic living organisms is a promising approach owing to their high tolerance to high concentrations of rare earth elements (REEs); however, simultaneous removal of both REEs and ammonium is generally hindered since most acidophilic organisms are positively charged. Accordingly, immobilization of acidophilic

Renal cell carcinoma (RCC) has the highest mortality rate among urological cancers and tumor angiogenesis that plays a critical role in RCC progress. Epidermal growth factor-like domain multiple 7 (EGFL7) has been recently identified as a regulator in RCC tumor angiogenesis and progression. Long noncoding RNA (LncRNA) HOTAIR has been considered as a pro-oncogene in multiple cancers, but its precise mechanism of tumor angiogenesis has rarely been reported. MicroRNA-126 (miR-126) functions as a tumor suppressor in RCC. However, the underlying tumor angiogenesis mechanism of HOTAIR/miR-126 axis in RCC has not been studied. The proliferation, migration, angiogenesis, and expression of EGFL7 and related proteins in extracellular signal-regulated kinase (ERK)/activators of transcription 3 (STAT3) signal pathway were determined to examine the effect and mechanism of HOTAIR and miR-126 on RCC progress. The regulatory relationship of HOTAIR and miR-126, as well as miR-126 and EGFL7 were tested using dual-luciferase reporter assay. Aenograft RCC mice model was used to examine the effect of HOTAIR on RCC tumor growth and metastasis in vivo. HOTAIR knockdown and miR-126 overexpression suppressed the proliferation, migration, and angiogenesis of RCC cells. HOTAIR regulated EGFL7 expression by competitively binding to miR-126. Knockdown of HOTAIR significantly suppressed the RCC tumor progression and lung metastasis in vivo. These findings suggest that lncRNA HOTAIR regulate RCC angiogenesis through miR-126/EGFL7 axis and provide a new perspective on the molecular pathways of angiogenesis in RCC development, which might be potential therapeutic targets for RCC treatment.

High oxygen content of microalgae-derived bio-oil limits their direct use in modern motors. In this study, instead of noble metal-catalyzed two-step hydrodeoxygenation, MgAl layered double hydroxid...