Cancer-Associated Fibroblast-Secreted Exosomes Promote Gastric Cancer Cell Migration and Invasion via the IL-32/ESR1 Axis.

Exosomes secreted by cancer-associated fibroblasts (CAFs) play a critical part in cancer progression. This study aimed to explore the effects of CAF-exosomes on gastric cancer (GC) cell metastasis. AGS and HGC-27 cells were treated with exosomes and cell viability, migration, and invasion were evaluated using Cell-Counting Kit-8 and Transwell assays. Exosome-regulated mRNAs were explored using quantitative real-time PCR. The relationship between interleukin (IL)32 and estrogen receptor 1 (ESR1) was evaluated using co-immunoprecipitation and dual-luciferase reporter assays. The results of this study show that CAF-derived exosomes promote GC cell viability, migration, and invasion. Exosome treatment increased the levels of IL32, which interacted with ESR1 and negatively regulated ESR1 levels. Rescue experiments were conducted to demonstrate that CAF-exosomes promoted biological behaviors of GC cells by upregulating IL32 and downregulating ESR1 expression. In conclusion, CAF-derived exosomes promote GC cell viability, migration, and invasion by elevating the IL32/ESR1 axis, suggesting a novel strategy for metastatic GC treatment.

Complexation of uranyl with benzoic acid in aqueous solution at variable temperatures: potentiometry, spectrophotometry and DFT calculations.

Investigation of the fundamental coordination chemistry between U(VI) and simple organic ligands is important to understand the chemical behavior of U(VI) in the natural environment and separation processes. In this work, the complexation of U(VI) with a common carboxylic acid, benzoic acid, has been systematically investigated through potentiometry, spectrometry and DFT calculations. Three successive complexes (UO2L+, UO2L2 and UO2L3-, L = benzoate ion) between U(VI) and benzoic acid are successfully identified in aqueous solution and their corresponding thermodynamic parameters (stability constant, enthalpy and entropy) are determined. Notably, this is the first time that the previously missing 1 : 2 and 1 : 3 (U to L) complexes in aqueous solution and their complexation thermodynamics have been reported, which would aid in more accurate prediction of the chemical behavior of U(VI) in the presence of benzoic acid. Moreover, the structures of the complexes are elucidated using DFT calculations, which show that benzoic acid coordinates to U(VI) in a bidentate form in all the complexes.

Esculetin Alleviates Inflammation, Oxidative Stress and Apoptosis in Intestinal Ischemia/Reperfusion Injury via Targeting SIRT3/AMPK/mTOR Signaling and Regulating Autophagy.

Aim: Intestinal ischemia/reperfusion (I/R) injury is a challenging pathological phenomenon accountable for significant mortality in clinical scenarios. Substantial evidence has supported the protective role of esculetin in myocardial I/R injury. This study is designed to reveal the specific impacts of esculetin on intestinal I/R injury and disclose the underlying mechanism. Methods: First, intestinal I/R injury model and intestinal epithelial cell line hypoxia/reoxygenation (H/R) model were established. Pathologic damages to intestinal tissues were observed through H&E staining. Serum diamine oxidase (DAO) levels were examined. RT-qPCR and Western blot examined the expression of inflammatory mediators. Commercial kits were used for detecting the levels of oxidative stress markers. TUNEL assay and caspase 3 activity assay measured cell apoptosis. Immunofluorescence (IF) staining measured autophagy levels. Western blot analyzed the expression of apoptosis-, Sirtuin 3 (SIRT3)/AMP activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling- and autophagy-related proteins. Molecular docking verified the interaction of esculetin with SIRT3. Cell viability was explored via CCK-8 assay. Results: The experimental results revealed that esculetin treatment mitigated pathological damage of intestinal tissues, reduced serum DAO level, ameliorated inflammation, oxidative stress and apoptosis and promoted autophagy in intestinal I/R rats. Moreover, esculetin bond to SIRT3 and activated SIRT3/AMPK/mTOR signaling both in vitro and in vivo. Furthermore, esculetin treatment enhanced cell viability and SIRT3 silencing reversed the impacts of esculetin on autophagy, inflammation, oxidative stress and apoptosis in H/R cell model. Conclusion: In a word, esculetin activated SIRT3/AMPK/mTOR signaling and autophagy to protect against inflammation, oxidative stress and apoptosis in intestinal I/R injury.

Biological and immunological significance of DLL3 expression in different tumor tissues: a pan-cancer analysis.

OBJECTIVE: To evaluate the biological and immunological significance of DLL3 expression in different tumor tissues and provide insight into the role of DLL3 in tumor immunotherapy. MATERIAL AND METHODS: RNA expression and clinical data of The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) were acquired, and we employed couple of bioinformatics methods to investigate the potential biological and immunological role DLL3, including pan-cancer expression, survival analysis, GSVA and it's correlation with immune infiltration scores, tumor mutation burden, tumor microsatellite instability. RESULTS: The findings indicate that DLL3 is expressed in the majority of tumors but is only weakly prevalent in HNSC. In 18 different types of cancers, DLL3 expression was linked to TMB and MSI, whereas in KIRC, LIHC, and PAAD, DLL3 expression and TME were correlated. Additionally, DLL3 gene expression linked positively with M0 and M2 macrophage infiltration levels but negatively with the infiltration of most immune cells. And connection with DLL3 expression varied depending on the kind of T cell. Finally, the GSVA data suggested that DLL3 expression is often unfavorably correlated with most pathways. CONCLUSIONS: DLL3 can be used as a stand-alone prognostic factor for many tumor types, and that the level of its expression will have a different prognostic impact for various tumor types. DLL3 expression across numerous cancer types was related to TMB, MSI, and immune cell infiltration. The role of DLL3 in carcinogenesis may serve as a guide for the creation of future immunotherapies that are more individualized and precise.

Stepwise on-demand functionalization of multihydrosilanes enabled by a hydrogen-atom-transfer photocatalyst based on eosin Y.

Organosilanes are of vital importance for modern human society, having found widespread applications in functional materials, organic synthesis, drug discovery and life sciences. However, their preparation remains far from trivial, and on-demand synthesis of heteroleptic substituted silicon reagents is a formidable challenge. The generation of silyl radicals from hydrosilanes via direct hydrogen-atom-transfer (HAT) photocatalysis represents the most atom-, step-, redox- and catalyst-economic pathway for the activation of hydrosilanes. Here, in view of the green characteristics of neutral eosin Y (such as its abundance, low cost, metal-free nature, absorption of visible light and excellent selectivity), we show that using it as a direct HAT photocatalyst enables the stepwise custom functionalization of multihydrosilanes, giving access to fully substituted silicon compounds. By exploiting this strategy, we realize preferable hydrogen abstraction of Si-H bonds in the presence of active C-H bonds, diverse functionalization of hydrosilanes (for example, alkylation, vinylation, allylation, arylation, deuteration, oxidation and halogenation), and remarkably selective monofunctionalization of di- and trihydrosilanes.

Gastric collision tumor with diffuse large B-cell lymphoma and adenocarcinoma: A rare case report and literature review.

ABSTRACT: Gastric adenocarcinoma is a common malignant tumor of the digestive system. Primary diffuse large B-cell lymphoma (DLBCL) of the stomach is a common lymphoma originating from gastric submucosal lymphoid tissue, and the coexistence of DLBCL and adenocarcinoma is exceedingly rare. A 58-year-old woman came to our hospital for treatment because of a choking feeling after eating. During endoscopy, it was confirmed that multiple irregular ulcers were seen in the fundus and body of the stomach, and the surrounding mucosa was raised. The biopsy pathology showed poorly differentiated cancer, and the patient did not undergo immunohistochemical detection. A distal gastrectomy was performed. Pathological evaluation of resected specimens is as follows: gastric tubular adenocarcinoma and germinal center-type (GC)-DLBCL. No migration was found at the junction of the two tumors, forming a collision tumor. The patient received two cycles of Rituximab - Cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP) chemotherapy, and there is no recurrence at present. We report a case of primary gastric adenocarcinoma colliding with the GC-DLBCL. Clinicians and pathologists should pay attention to it to avoid missed diagnosis.

Update on the natural orifice transluminal endoscopic surgery for gallbladder preserving gallstones therapy: A review.

Cholecystectomy remains the "gold standard" for the management of symptomatic gallstones. Minimally invasive laparoscopic cholecystectomy has been the treatment of choice for the past 3 decades. However, the technique of natural orifice transluminal endoscopic surgery cholecystolithotomy is evolving, with some experts advocating gallbladder stone removal without gallbladder excision in order to preserve gallbladder function and eliminate post-cholecystectomy syndromes, including complications of the surgical incision, bile duct injury, functional gastrointestinal, and psychological conditions, and possibly an increase in colon cancer. In addition, transluminal endoscopic cholecystolithotomy is an option for elderly patients who are not suitable candidates for open surgery and those who desire scar-free minimally invasive surgery with organ preservation. This article summarizes the established pure natural orifice transluminal endoscopic surgery gallbladder preserving gallstone removal techniques and highlights the pros and cons of different popular available endoscopic approaches to gallstone therapy and how flexible endoscopic surgery via the natural orifice is compared to the well-established cholecystectomy.

MiR-135a-5p suppresses breast cancer cell proliferation, migration, and invasion by regulating BAG3.

BACKGROUND: MicroRNAs (miRNAs) are involved in the progression of diverse human cancers. This work aimed to delve into how microRNA-135a-5p (miR-135a-5p) affects the biological behaviors of Breast Cancer (BC) cells. METHODS: Gene Expression Omnibus (GEO) datasets were used to analyze the expression differences of miR-135a-5p in cancer tissues of BC patients. Quantitative real-time PCR and western blot were conducted to detect miR-135a-5p and Bcl-2 Associated Athanogene (BAG3) expression levels in BC tissues and cells, respectively. The proliferation, migration, invasion, and cell cycle of BC cells were detected by cell counting kit-8 assay, BrdU assay, wound healing assay, transwell assay, and flow cytometry. The targeted relationship between miR-135a-5p and BAG3 mRNA 3'UTR predicted by bioinformatics was further testified by a dual-luciferase reporter gene assay. Pearson's correlation analysis was adopted to analyze the correlation between miR-135a-5p expression and BAG3 expression. The downstream pathways of BAG3 were analyzed by the LinkedOmics database. RESULTS: MiR-135a-5p was significantly down-regulated and BAG3 expression was significantly raised in BC tissues. MiR-135a-5p overexpression repressed the viability, migration and invasion of BC cells, and blocked cell cycle progression in G0/G1 phase while inhibiting miR-135a-5p worked oppositely. BAG3 was verified as a target of miR-135a-5p. Overexpression of BAG3 reversed the impacts of miR-135a-5p on the malignant biological behaviors of BC cells. The high expression of BAG3 was associated with the activation of the cell cycle, mTOR and TGF-ß signaling pathways. CONCLUSION: MiR-135a-5p regulates BAG3 to repress the growth, migration, invasion, and cell cycle progression of BC cells.

Predicting in-hospital mortality for MIMIC-III patients: A nomogram combined with SOFA score.

Predicting the mortality of patients provides a reference for doctors to judge their physical condition. This study aimed to construct a nomogram to improve the prediction accuracy of patients' mortality. Patients with severe diseases were screened from the Medical Information Mart for Intensive Care (MIMIC) III database; 70% of patients were randomly selected as the training set for the model establishment, while 30% were used as the test set. The least absolute shrinkage and selection operator (LASSO) regression method was used to filter variables and select predictors. A multivariable logistic regression fit was used to determine the association between in-hospital mortality and risk factors and to construct a nomogram. A total of 9276 patients were included. The area under the curve (AUC) for the clinical nomogram based on risk factors selected by LASSO and multivariable logistic regressions were 0.849 (95% confidence interval [CI]: 0.835-0.863) and 0.821 (95% CI: 0.795-0.846) in the training and test sets, respectively. Therefore, this nomogram might help predict the in-hospital mortality of patients admitted to the intensive care unit (ICU).

miR-129-5p Plays an Anticancer Role in Colon Cancer by Targeting RSF1.

This study aimed to investigate the inhibitory effect of miR-129-5p on colon cancer by targeting RSF1. For this purpose, real-time quantitative PCR was used to analyze whether the expression of miR-129-5p in colon cancer and adjacent normal tissues had an impact on the proliferation and apoptosis of cancer cells (CC). We evaluated the role of miR-129-5p by targeting RSF1 in colon cancer tissue in the experimental group. But in the control group, only miR-129-5p was considered as a protective factor. Finally, we retrospectively analyzed data of 56 cases of colon cancer patients admitted to our clinical department between January 2019 and December 2019. Twenty-eight cases were investigated through just miR-129-5p protective factors for cancer (group A). The other 28 cases were studied by miR-129-5p anti-cancer agent and a completed RSF1 carcinoma factors for cancer (group B). We evaluated the comparative analysis of the patient's age and gender, clinical indicators (including for the first time of hospitalization and postoperative hospital stay, three times of anal exhaust), and complications (including chills, vomiting, hypertension, diabetes). The results showed that miR-129-5p had a more substantial effect on the proliferation and apoptosis of CC by targeting RSF1.

Immune-related gene signature associates with immune landscape and predicts prognosis accurately in patients with skin cutaneous melanoma.

Skin cutaneous melanoma (SKCM) is the skin cancer that causes the highest number of deaths worldwide. There is growing evidence that the tumour immune microenvironment is associated with cancer prognosis, however, there is little research on the role of immune status in melanoma prognosis. In this study, data on patients with Skin cutaneous melanoma were downloaded from the GEO, TCGA, and GTEx databases. Genes associated with the immune pathway were screened from published papers and lncRNAs associated with them were identified. We performed immune microenvironment and functional enrichment analyses. The analysis was followed by applying univariate/multivariate Cox regression algorithms to finally identify three lncRNAs associated with the immune pathway for the construction of prognostic prediction models (CXCL10, RXRG, and SCG2). This stepwise downscaling method, which finally screens out prognostic factors and key genes and then uses them to build a risk model, has excellent predictive power. According to analyses of the model's reliability, it was able to differentiate the prognostic value and continued existence of Skin cutaneous melanoma patient populations more effectively. This study is an analysis of the immune pathway that leads lncRNAs in Skin cutaneous melanoma in an effort to open up new treatment avenues for Skin cutaneous melanoma.

MiR-135a-5p suppresses breast cancer cell proliferation, migration, and invasion by regulating BAG3

Abstract Background MicroRNAs (miRNAs) are involved in the progression of diverse human cancers. This work aimed to delve into how microRNA-135a-5p (miR-135a-5p) affects the biological behaviors of Breast Cancer (BC) cells. Methods Gene Expression Omnibus (GEO) datasets were used to analyze the expression differences of miR-135a-5p in cancer tissues of BC patients. Quantitative real-time PCR and western blot were conducted to detect miR-135a-5p and Bcl-2 Associated Athanogene (BAG3) expression levels in BC tissues and cells, respectively. The proliferation, migration, invasion, and cell cycle of BC cells were detected by cell counting kit-8 assay, BrdU assay, wound healing assay, transwell assay, and flow cytometry. The targeted relationship between miR-135a-5p and BAG3 mRNA 3′UTR predicted by bioinformatics was further testified by a dual-luciferase reporter gene assay. Pearson's correlation analysis was adopted to analyze the correlation between miR-135a-5p expression and BAG3 expression. The downstream pathways of BAG3 were analyzed by the LinkedOmics database. Results MiR-135a-5p was significantly down-regulated and BAG3 expression was significantly raised in BC tissues. MiR-135a-5p overexpression repressed the viability, migration and invasion of BC cells, and blocked cell cycle progression in G0/G1 phase while inhibiting miR-135a-5p worked oppositely. BAG3 was verified as a target of miR-135a-5p. Overexpression of BAG3 reversed the impacts of miR-135a-5p on the malignant biological behaviors of BC cells. The high expression of BAG3 was associated with the activation of the cell cycle, mTOR and TGF-β signaling pathways. Conclusion MiR-135a-5p regulates BAG3 to repress the growth, migration, invasion, and cell cycle progression of BC cells.

Ultrasound Image Features under Deep Learning in Breast Conservation Surgery for Breast Cancer.

This study was to analyze the effect of the combined application of deep learning technology and ultrasound imaging on the effect of breast-conserving surgery for breast cancer. A deep label distribution learning (LDL) model was designed, and the semiautomatic segmentation algorithm based on the region growing and active contour technology (RA) and the segmentation model based on optimized nearest neighbors (ON) were introduced for comparison. The designed algorithm was applied to the breast-conserving surgery of breast cancer patients. According to the difference in intraoperative guidance methods, 102 female patients with early breast cancer were divided into three groups: 34 cases in W1 group (ultrasound guidance based on deep learning segmentation model), 34 cases in W2 group (ultrasound guidance), and 34 cases in W3 group (palpation guidance). The results revealed that the tumor area segmented by the LDL algorithm constructed in this study was closer to the real tumor area; the segmentation accuracy (AC), Jaccard, and true-positive (TP) values of the LDL algorithm were obviously greater than those of the RA and ON algorithms, while the false-positive (FP) value was significantly lower in contrast to the RA and ON algorithms, showing statistically observable differences (P < 0.05); the actual resection volume of the patients in the W1 group was the closest to the ideal resection volume, which was much smaller in contrast to that of the patients in the W2 and W3 groups, showing statistical differences (P < 0.05); the positive margins of the patients in the W1 group were statistically lower than those in the W2 and W3 groups (P < 0.05). In addition, 1 patient in the W1 group was not satisfied with the cosmetic effect, 3 patients in the W2 group were not satisfied with the cosmetic effect, and 9 patients in the W3 group were not satisfied with the cosmetic effect. Finally, it was found that the ultrasound image based on the deep LDL model effectively improved the AC of tumor resection and negative margins, reduced the probability of normal tissue being removed, and improved the postoperative cosmetic effect of breast.

Kinesin family member 3C (KIF3C) is a novel non-small cell lung cancer (NSCLC) oncogene whose expression is modulated by microRNA-150-5p (miR-150-5p) and microRNA-186-3p (miR-186-3p).

This study is aimed at investigating the biological function of kinesin family member 3 C (KIF3C) in non-small cell lung cancer (NSCLC) progression and its upstream regulatory mechanism. Quantitative real-time PCR, Western blot and immunohistochemistry were adopted to examine microRNA-150-5p (miR-150-5p), microRNA-186-3p (miR-186-3p) and kinesin family member 3 C (KIF3C) expression levels. NSCLC cell proliferation, migration, and invasion were detected through cell counting kit-8 (CCK-8) assay, EdU assay, and Transwell assay. The metastasis of NSCLC cells was evaluated utilizing a pulmonary metastasis model in nude mice in vivo. The targeted relationship among KIF3C 3'UTR, miR-186-3p, and miR-150-5p were verified by dual-luciferase reporter gene assays. It was confirmed that in NSCLC tissues and cells, KIF3C expression level was increased and KIF3C overexpression promoted NSCLC cell proliferation and metastasis. Additionally, miR-150-5p and miR-186-3p directly targeted KIF3C to repress its expression. Our data suggest that KIF3C, which is negatively regulated by miR-150-5p and miR-186-3p, is an oncogenic factor in NSCLC progression.

Bromine radical as a visible-light-mediated polarity-reversal catalyst.

Polarity-reversal catalysts enable otherwise sluggish or completely ineffective reactions which are characterized by unfavorable polar effects between radicals and substrates. We herein disclose that when irradiated by visible light, bromine can behave as a polarity-reversal catalyst. Hydroacylation of vinyl arenes, a three-component cascade transformation and deuteration of aldehydes were each achieved in a metal-free manner without initiators by using inexpensive N-bromosuccinimide as the precatalyst. Light is essential to generate and maintain the active bromine radical during the reaction process. Another key to success is that HBr can behave as an effective hydrogen donor to turn over the catalytic cycles.

Geoarchaeological evidence of the AD 1642 Yellow River flood that destroyed Kaifeng, a former capital of dynastic China.

Rising global temperatures will increase the number of extreme weather events, creating new challenges for cities around the world. Archaeological research on the destruction and subsequent reoccupation of ancient cities has the potential to reveal geological and social dynamics that have historically contributed to making urban settings resilient to these extreme weather events. Using a combination of archaeological and geological methods, we examine how extreme flood events at Kaifeng, a former capital of dynastic China, have shaped the city's urban resilience. Specifically, we focus on an extreme Yellow River flood event in AD 1642 that historical records suggest killed around 300,000 people living in Kaifeng. Our recent archaeological excavations have discovered compelling geological and archaeological evidence that corroborates these documents, revealing that the AD 1642 Yellow River flood destroyed Kaifeng's inner city, entombing the city and its inhabitants within meters of silt and clay. We argue that the AD 1642 flood was extraordinarily catastrophic because Kaifeng's city walls only partly collapsed, entrapping most of the flood waters within the city. Both the geology of the Yellow River floods as well as the socio-political context of Kaifeng shaped the city's resilience to extreme flood events.

Fibulin-5 contributes to colorectal cancer cell apoptosis via the ROS/MAPK and Akt signal pathways by downregulating transient receptor potential cation channel subfamily V member 1.

Fibulin-5, a multifunctional extracellular matrix (ECM) protein, is secreted into the ECM, regulating metastasis and invasion in many malignant tumors. However, its role in colorectal cancer (CRC) has not been reported. In this study, we detected the expression of fibulin-5 in 56 CRC patients and eight CRC cell lines, revealing that fibulin-5 was expressed lower in CRC tumor tissues than in peritumor tissues. Furthermore, our study verified that fibulin-5 promoted cell apoptosis and reactive oxygen species (ROS) production by inhibiting transient receptor potential cation channel subfamily V member 1 (TRPV1) in CRC cells. Moreover, NAC (the scavenger of ROS), SB203580 (the inhibitor of p38), PD98059 (the inhibitor of ERK), and SC79 (the activator of Akt) were used to uncover that fibulin-5 induced apoptosis through the ROS/mitogen-activated protein kinase and Akt signal pathways by downregulating TRPV1. Together, these results suggest that fibulin-5 might serve as a novel drug target for the treatment of CRC patients.

miR-130a-3p inhibits invasion of breast cancer MCF-7 cells through HGF/MET pathway / 中国肿瘤生物治疗杂志

@# Objective: To explore the molecular mechanism of miR-130a-3p regulating epithelial mesenchymal transition (EMT) to affect the invasion and metastasis of breast cancer cells through HGF/MET pathway. Methods: A total of 22 pairs of cancer tissues and adjacent normal tissues from breast cancer patients, who were admitted to Affiliated Hospital of Chengde Medical College from January 2018 to October 2018, were collected for this study; in addition, breast cancer cell lines (MCF-7, MDA-MB-231 and MDA-MB453) and normal breast epithelial cells MCF10A were obtained from the Institute of Basic Sciences, Chengde Medical College. And then, the expression of miR-130a-3p in tissues and cell lines were detected by qRT-PCR. The experiment cells were divided into control group, miR-130a-3p mimics group, miR-130a-3p inhibitor group, PHA665752 (a small-molecule MET inhibitor) transfection group and PHA665752+miR-130a-3p inhibitor co-transfection group. CCK-8 assay and Transwell assay were performed to detect the proliferation, invasion and migration of MCF-7 cells, respectively. The expressions of EMT and HGF/MET signaling pathway related proteins in MCF-7 cells were detected by WB. In addition, the targeted relationship between miR-130a-3p and MET was verified by Dual luciferase reporter gene assay. Results: miR-130a-3p was down-regulated in breast cancer tissues and cell lines. Over-expression of miR130a-3p could suppress the proliferation, invasion, migration and EMT of MCF-7 cells, while knockdown of miR-130a-3p had the opposite results. The results of Dual luciferase reporter gene assay indicated that miR-130a-3p targetedly down-regulated the expression of MET, and miR-130a-3p negatively regulated the expression of HGF/MET signaling pathway. Further experiments confirmed that miR-130a-3p inhibited the proliferation, invasion, migration and EMT of MCF-7 cells by blocking HGF/MET signaling pathway. Conclusion: miR-130a-3p suppresses the EMT of MCF-7 cells via blocking HGF/MET signaling pathway, thereby repressing the invasion and metastasis of MCF-7 cells.

Visible-Light-Mediated Metal-Free Hydrosilylation of Alkenes through Selective Hydrogen Atom Transfer for Si-H Activation.

Although there has been significant progress in the development of transition-metal-catalyzed hydrosilylations of alkenes over the past several decades, metal-free hydrosilylation is still rare and highly desirable. Herein, we report a convenient visible-light-driven metal-free hydrosilylation of both electron-deficient and electron-rich alkenes that proceeds through selective hydrogen atom transfer for Si-H activation. The synergistic combination of the organophotoredox catalyst 4CzIPN with quinuclidin-3-yl acetate enabled the hydrosilylation of electron-deficient alkenes by selective Si-H activation while the hydrosilylation of electron-rich alkenes was achieved by merging photoredox and polarity-reversal catalysis.

Metal-free direct alkylation of unfunctionalized allylic/benzylic sp3 C-H bonds via photoredox induced radical cation deprotonation.

Despite notable recent efforts, a catalytic and convenient strategy for the direct alkylation of unactivated allylic or benzylic sp3 C-H bonds remains a formidable challenge facing the synthesis community. We herein report an unprecedented allylic/benzylic alkylation using only an organo-photoredox catalyst, which enables coupling of a broad scope of alkenes/arenes and electron-deficient alkenes in an atom- and redox-economic manner. A photoredox induced alkene/arene radical cation deprotonation is proposed to smoothly generate the key allylic and benzylic radical intermediates. It represents the first C-C bond formation via radical cation deprotonation under visible light conditions. The resulting products can be easily scaled up and directly converted to γ,δ-unsaturated or α,ß-diaryl-acids, -esters, -amides, -pyrazoles, -isoxazoles, as well as lactones, which enables this mild and selective sp3 C-H alkylation to rapidly access complex bioactive molecules.