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Cranial radiation therapy for the treatment of pediatric brain tumors results in changes to brain development that are detectable with magnetic resonance imaging. We have previously demonstrated similar structural changes in both humans and mice. The goal of the current study was to examine the role of inflammation in this response. Because neuroanatomic volume deficits in pediatric survivors are more pronounced in female patients, we also evaluated possible dependence on sex.Other studies have shown that male mice deficient in the C-C chemokine ligand 2 gene (Ccl2; previously Mcp-1) have a muted neuroinflammatory response after irradiation. We irradiated Ccl2Irradiation of WT mice resulted in a deficit in neuroanatomic growth with limited sex dependence. HOM and HET male mice were significantly protected from this radiation-induced damage, whereas HOM and HET female mice were not.Interventions aimed at mitigating the effects of cranial radiation therapy in pediatric cancer survivors by modulating inflammatory response will need to consider patient sex.

Genetic alterations in the cell cycle pathway are common in head and neck squamous cell carcinoma (HNSCC). We identified four novel HNSCC susceptibility loci (CDKN1C rs452338, CDK4 rs2072052, E2F2 rs3820028 and E2F2 rs2075993) through a two-stage matched case–control study. There was a combined effect among the four single nucleotide polymorphisms (SNPs), as the number of risk genotypes increased, the risk of HNSCC displayed an increasing trend (Ptrend < 0.001). And there were multiplicative interactions between rs452338 and rs2072052, rs2072052 and rs3820028, rs2072052 and rs2075993. Functional bioinformatics analysis and dual-luciferase reporter assay revealed that E2F2 rs2075993 T>C reduced the stability of E2F2 3’-UTR secondary structure and affected the binding of E2F2 to miR-940, which was up-regulated in HNSCC tumor tissues (P = 2.9e−8) and was correlated with poor overall survival of HNSCC (HR = 1.39, 95% CI = 1.02–1.90). In vitro assays, we discovered that the expression of miR-940 was regulated by METTL3, and miR-940 promoted the proliferation, migration and invasion, and inhibited the senescence and autophagy of tumor cells. In terms of mechanism, compared with rs2075993 allele T, we found that the protective variant rs2075993 allele C interfered with the translational inhibition of E2F2 by miR-940, resulting in increased expression of E2F2 protein, which further reduced the proliferation, migration, invasion, and increased the senescence of tumor cells.

Anti-tumor immunity through checkpoint inhibitors, specifically anti-programmed death 1 (PD-1)/programmed death ligand 1 (PD-L1) interaction, is a promising approach for cancer therapy. However, as early clinical trials indicate that colorectal cancers (CRCs) do not respond well to immune-checkpoint therapies, new effective immunotherapy approaches to CRC warrant further study. Simvastatin is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (CoA) reductase (HMGCR), the rate-limiting enzyme of the mevalonate (MVA) pathway for the cholesterol biosynthesis. However, little is known about the functions of simvastatin in the regulation of immune checkpoints or long noncoding RNA (lncRNA)-mediated immunoregulation in cancer. Here, we found that simvastatin inhibited PD-L1 expression and promoted anti-tumor immunity via suppressing the expression of lncRNA SNHG29. Interestingly, SNHG29 interacted with YAP and inhibited phosphorylation and ubiquitination-mediated protein degradation of YAP, thereby facilitating downregulation of PD-L1 transcriptionally. Patient-derived tumor xenograft (PDX) models and the clinicopathological analysis in samples from CRC patients further supported the role of the lncRNA SNHG29-mediated PD-L1 signaling axis in tumor microenvironment reprogramming. Collectively, our study uncovers simvastatin as a potential therapeutic drug for immunotherapy in CRC, which suppresses lncRNA SNHG29-mediated YAP activation and promotes anti-tumor immunity by inhibiting PD-L1 expression.

During faunal studies of psammophilic ciliates along the coast of Qingdao, China, several marine karyorelictean species were isolated. Among them, four species within the genus在对青岛潮间带的沙栖原生动物研究中，我们分离鉴定出四种核残迹纲纤毛虫，它们分别是褶皱海喙虫、长海喙虫（新种）、拟中华海喙虫（新种）和单泡海喙虫。褶皱海喙虫虽已被多次报道，但本研究首次揭示该种详细的形态学特征及系统进化地位。长海喙虫（新种）与其相近种最主要的区别在于皮层颗粒排布方式复杂，大核数量少，体型大。拟中华海喙虫（新种）与相近种最主要的区别是其具有14–17列体动基列，口内动基列由24–37对毛基粒构成。根据详细的形态学特征，本研究将亚种单泡褶皱海喙虫升级为种，即单泡海喙虫，并首次报道其详细的活体特征和纤毛图式。基于核糖体小亚基序列的系统演化关系分析揭示海喙虫与喙纤虫属形成姐妹枝, 共同构成单系发生的喙纤科。.

The enhancer of zeste homolog 2 (EZH2) and its highly related homolog EZH1 are considered to be epigenetic silencing factors, and they play key roles in the growth and differentiation of cells as the core components of polycomb repressive complex 2 (PRC2). EZH1 and EZH2 are known to have a role in human malignancies, and alterations in these two genes have been implicated in transformation of human malignancies. Inhibition of EZH1/2 has been shown to result in tumor regression in humans and has been studied and evaluated in the preclinical setting and in multiple clinical trials at various levels. Our work thus contributes to the understanding of the relationship between regulatory molecules associated with EZH1/2 proteins and tumor progression, and may provide new insights for mechanism-based EZH1/2-targeted therapy in tumors.

Background Cranial radiation therapy (CRT) is a mainstay of treatment for malignant pediatric brain tumors and high-risk leukemia. Although CRT improves survival, it has been shown to disrupt normal brain development and result in cognitive impairments in cancer survivors. Animal studies suggest that there is potential to promote brain recovery after injury using metformin. Our aim was to evaluate whether metformin can restore brain volume outcomes in a mouse model of CRT. Methods C57BL/6J mice were irradiated with a whole-brain radiation dose of 7 Gy during infancy. Two weeks of metformin treatment started either on the day of or 3 days after irradiation. In vivo magnetic resonance imaging was performed prior to irradiation and at 3 subsequent time points to evaluate the effects of radiation and metformin on brain development. Results Widespread volume loss in the irradiated brain appeared within 1 week of irradiation with limited subsequent recovery in volume outcomes. In many structures, metformin administration starting on the day of irradiation exacerbated radiation-induced injury, particularly in male mice. Metformin treatment starting 3 days after irradiation improved brain volume outcomes in subcortical regions, the olfactory bulbs, and structures of the brainstem and cerebellum. Conclusions Our results show that metformin treatment has the potential to improve neuroanatomical outcomes after CRT. However, both timing of metformin administration and subject sex affect structure outcomes, and metformin may also be deleterious. Our results highlight important considerations in determining the potential benefits of metformin treatment after CRT and emphasize the need for caution in repurposing metformin in clinical studies.

Herein, we report a nickel-catalyzed three-component coupling of butadiene, aldimines, and arylboronic acids to form synthetically important homoallylic amines. The starting materials are stable an...

We herein report a Ni-catalyzed three-component coupling of 1,3-butadiene, carbonyl compounds, and arylboronic acids as a general synthetic approach to 1,4-disubstituted homoallylic alcohols, an important class of compounds, which have previously not been straightforward to access. The reaction occurs efficiently using a Ni(cod)2 catalyst without any external base and ligand at ambient temperature and allows a highly regioselective and trans-selective 1,4-dicarbofunctionalization of feedstock butadiene in a single operation. This simple and practical protocol could apply to a comprehensive scope of substrates. The neutral conditions show extraordinary tolerance for even highly base-sensitive functional groups.

To explore the effects of nicotinamide (NAM) on the growth, biofilm formation and exopolysaccharides (EPS) production ofThe minimum inhibitory concentration (MIC) of NAM onThe MIC of NAM onUnder the influence of NAM at certain concenrations, the growth, biofilm formation, and EPS synthesis of

Professor总结张善忱先生在针灸领域主要临床经验与治学思想。先生注重理论探究，著有《针灸甲乙经腧穴重辑》一书，并发表系列文章考证和阐释腧穴之命名；认为临床之参悟须以理论为指导，强调整体综合辨证，树立人体为一有机整体以及与自然相适应等整体观念，加以综合诊断方能有效施治；主张从简取穴，辨虚实而定补泻，针法精炼而合法度，注重加强针下辨气以应之；同时，亦特别重视灸法在临床中的研究与应用，使之与针法相辅相成，两者相宜以成佳效。.

Traditionally the rubble-built structures are constructed manually with low efficiency and long time consuming. It is studied in this research that the rubble-built structures are constructed with models according to designed profile. Firstly, the natural stones are piled up inside the model and then filled with self-compacting mortar into the inter-space of the stones at certain flow rate, and at last the models are removed after the mortar get hardened, so as to form the rubble-built structures with fast and mechanical construction process. The water and cement-sand mixture ratio for this construction process shall satisfy high flowability for flowing into the gaps of stones and also ensure the compressive strength of the structure. An indoor triangle box filling test is carried out to prove that the designed mixture ratio for filling the rubble-built structure is feasible and to determine the optimized mortar proportioning ratio.

Amyloid β-protein(Aβ) deposition in the brain is directly responsible for neuronal mitochondrial damage of Alzheimer's disease(AD) patients. Mitophagy, which removes damaged mitochondria, is a vital mode of neuron protection. Ginsenoside Rg_1(Rg_1), with neuroprotective effect, has displayed promising potential for AD treatment. However, the mechanism underlying the neuroprotective effect of Rg_1 has not been fully elucidated. The present study investigated the effects of ginsenoside Rg_(1 )on the autophagy of PC12 cells injured by Aβ_(25-35) to gain insight into the neuroprotective mechanism of Rg_1. The autophagy inducer rapamycin and the autophagy inhi-bitor chloroquine were used to verify the correlation between the neuroprotective effect of Rg_1 and autophagy. The results showed that Rg_1 enhanced the viability and increased the mitochondrial membrane potential of Aβ-injured PC12 cells, while these changes were blocked by chloroquine. Furthermore, Rg_(1 )treatment increased the LC3Ⅱ/Ⅰ protein ratio, promoted the depletion of p62 protein, up-regulated the protein levels of PINK1 and parkin, and reduced the amount of autophagy adaptor OPTN, which indicated the enhancement of autophagy. After the silencing of PINK1, a key regulatory site of mitophagy, Rg_1 could not increase the expression of PINK1 and parkin or the amount of NDP52, whereas it can still increase the LC3Ⅱ/Ⅰ protein ratio and promote the depletion of OPTN protein which indicated the enhancement of autophagy. Collectively, the results of this study imply that Rg_1 can promote autophagy of PC12 cells injured by Aβ, and may reduce Aβ-induced mitochondrial damage by promoting PINK1-dependent mitophagy, which may be one of the key mechanisms of its neuroprotective effect.

To investigate the pollution characteristics and sources of nitrated polycyclic aromatic hydrocarbons (NPAHs) in Guangdong-Hong Kong-Macao Greater Bay Area (GBA), 44 ambient air samples were collected using the active sampling method, which were then determined via gas chromatography-triple quadrupole tandem mass spectrometry. The main results showed that filters, polyurethane foam, and XAD-2 resin were the essential materials for sampling NPAHs in ambient air in order to characterize the pollution status accurately. The levels of

To explore the effect of polystyrene (PS) and PS-polyvinylpyrrolidone (PVP) electrospun materials on the adhesion ability ofPS and PS-PVP electrospun materials were prepared with stainless steel needles in high-voltage electric field. The growth and adhesion ofSEM images showed that both PS and PS-PVP can be used to form electrospun fibers with a diameter of 0.2 μm. SEM images and CFU counts of the biofilm at 24 h and 48 h showed that there was a smaller amount ofPS and PS-PVP electrospun materials can be used to reduce the adhesion ability of

BackgroundChronic obstructive pulmonary disease (COPD) is one of the most common pulmonary diseases. There is evidence to suggest that dysbiosis of pulmonary microbiota participates in COPD development. Yifei Sanjie Formula (YS) is widely used to treat diseases in respiratory systems, yet its mechanisms are little known. MethodsIn the present study, the efficacy of YS was evaluated by analyzing its effects on the severity of pulmonary pathological damage, pulmonary function, pro-inflammation cytokines, the activation of NLRP3/caspase-1/IL-1β signaling pathway, and changes of lung microbiota. ResultsYS improved animal behaviors, prevented declines in pulmonary ventilatory function and lung injury in a rat model of COPD. Administration of YS significantly suppressed the release of proinflammatory cytokines and collagen deposition and downregulated NLRP3/caspase-1/IL-1β signaling in vivo. YS changed the relative abundance of specific pulmonary microbiota and modulated bacterial flora in the rat model. Conclusions These results suggest that the effects of YS involved lung microbes and anti-inflammatory mechanisms.

Metastasis is the primary cause of cancer-related mortality in colorectal cancer (CRC) patients. How to improve therapeutic options for patients with metastatic CRC is the core question for CRC treatment. However, the complexity and diversity of stromal context of the tumor microenvironment (TME) in liver metastases of CRC have not been fully understood, and the influence of stromal cells on response to chemotherapy is unclear. Here we performed an in-depth analysis of the transcriptional landscape of primary CRC, matched liver metastases and blood at single-cell resolution, and a systematic examination of transcriptional changes and phenotypic alterations of the TME in response to preoperative chemotherapy (PC). Based on 111,292 single-cell transcriptomes, our study reveals that TME of treatment-naïve tumors is characterized by the higher abundance of less-activated B cells and higher heterogeneity of tumor-associated macrophages (TAMs). By contrast, in tumors treated with PC, we found activation of B cells, lower diversity of TAMs with immature and less activated phenotype, lower abundance of both dysfunctional T cells and ECM-remodeling cancer-associated fibroblasts, and an accumulation of myofibroblasts. Our study provides a foundation for future investigation of the cellular mechanisms underlying liver metastasis of CRC and its response to PC, and opens up new possibilities for the development of therapeutic strategies for CRC.

The tumor suppressor p53 is an important regulator of cell fate response after DNA damage. Cell fate response following metabolic stresses has also been linked to p53-dependent pathways. In this study, we asked if 5′-adenosine monophosphate-activated protein kinase (AMPK), the master sensor of cellular energy balance, played a role in p53-dependent apoptosis of neural progenitor cells (NPCs) in the hippocampus after irradiation. Adult mice with targeted disruption of p53 or prkaa2 (gene that encodes AMPKα) in the brain were used to determine the role of p53 and AMPK, respectively, in radiation-induced apoptosis of NPCs in the hippocampus. The p53-dependent apoptosis of NPCs was associated with an increase in phospho-AMPK expression in the dentate gyrus at 8 hours after irradiation. Activation of AMPK was seen in granule neurons and subgranular NPCs. Compared with wildtype mice, apoptosis of NPCs was significantly attenuated in AMPK deficient (nestinCre: prkaa2fl/fl) mice after irradiation. AMPK deficiency did not however alter p53 activation in NPCs after irradiation. We conclude that AMPK may regulate apoptosis of hippocampal NPCs after irradiation. These findings suggest that cellular metabolism may play a role in determining cell fate response such as apoptosis after DNA damage in NPCs.

The ring-opening reaction of imidazo[1,5-a]quinolines under photoredox conditions has been described. With Eosin Y as the organophotoredox catalyst, synthetically useful and medicinally important imides were obtained in moderate to excellent yields under mild reaction conditions.

It is expected that BiFeO3-based materials will have both ferroelectricity and ferromagnetism. (1-y)BiFe(1-x)MnxO3-yBaTiO3 system was prepared using solid state reaction method. The goal of this study is to uncover the impacts of Mn doping and BaTiO3 content on the crystal structure, magnetism and ferroelectric properties. By forming a solid solution with BaTiO3, stable perovskite BiFeO3 was achieved. The rhombohedrally distorted (1-y)BiFe(1-x)MnxO3-yBaTiO3 showed weak ferromagnetism due to the composition of BaTiO3 and the doping of Mn ion. 0.8BiFe0.9Mn0.1O3-0.2BaTiO3 and 0.7BiFe0.9Mn0.1O3-0.3BaTiO3 ceramics exhibited typical P-E hysteresis loops.

5'-Adenosine monophosphate-activated protein kinase (AMPK), a key regulator of cellular energy homeostasis, plays a role in cell fate determination. Whether AMPK regulates hippocampal neuronal development remains unclear. Hippocampal neurogenesis is abrogated after DNA damage. Here, we asked whether AMPK regulates adult hippocampal neurogenesis and its inhibition following irradiation. Adult Cre-lox mice deficient in AMPK in brain, and wild-type mice were used in a birth-dating study using bromodeoxyuridine to evaluate hippocampal neurogenesis. There was no evidence of AMPK or phospho-AMPK immunoreactivity in hippocampus. Increase in p-AMPK but not AMPK expression was observed in granule neurons and subgranular neuroprogenitor cells (NPCs) in the dentate gyrus within 24 hours and persisted up to 9 weeks after irradiation. AMPK deficiency in Cre-lox mice did not alter neuroblast and newborn neuron numbers but resulted in decreased newborn and proliferating NPCs. Inhibition of neurogenesis was observed after irradiation regardless of genotypes. In Cre-lox mice, there was further loss of newborn early NPCs and neuroblasts but not newborn neurons after irradiation compared with wild-type mice. These results are consistent with differential negative effect of AMPK on hippocampal neuronal development and its inhibition after irradiation.

We herein report a Ni-catalyzed three-component coupling of 1,3-butadiene, carbonyl compounds, and arylboronic acids as a general synthetic approach to 1,4-disubstituted homoallylic alcohols, an important class of compounds, which have previously not been straightforward to access. The reaction occurs efficiently using a Ni(cod)

A rare photoluminescent nitroxide pyridine bisphosphonate-based metal–organic framework, [Eu4(L)3(H2O)6]n (1) [H4L = 2,6-bis(phosphonomethyl)pyridine 1-oxide], was prepared under hydrothermal conditions and has a 3D supramolecular structure built from phosphonate linkers bridging Eu3+. It was characterized by single-crystal X-ray diffraction (SXRD), powder X-ray diffraction (PXRD), thermogravimetric analyses (TGAs), etc. The luminescence spectra of 1 show the strong characteristic luminescence of Eu3+ ions, and 1 shows high water stability, thermal stability, and chemical stability. Furthermore, luminescence studies have shown that 1 can be used as a fluorescent probe for detecting trace amounts of Cr(VI) ions and acetone in water samples with excellent sensitivity, great selectivity, and reproducibility. The detection limits are as low as 0.61 μM, 0.63 μM, and 0.0066 vol% for Cr2O72-, CrO42-, and acetone, respectively. The fluorescence quenching of 1 by Cr(VI) ions and acetone may be due to spectral overlap and absorption competition. This is the first example of a Eu-based pyridine phosphonate fluorescence sensor for simultaneous detection of Cr(VI) ions and acetone.

To study the antibacterial effect of berberine combined with amylmetacresol onBoth dilution method and live bacteria CFU were used to determine the minimum inhibitory concentration (MIC) of berberine and amylmetacresol onThe MIC of berberine was 512 μg/mL, and the MIC of amylmetacresol was 0.023 3%. 512 μg/mL berberine and 0.002 33% amylmetacresol had a weak killing effect on planktonicBerberine and amylmetacresol had synergism against

Metastasis is the primary cause of cancer-related mortality in colorectal cancer (CRC) patients. How to improve therapeutic options for patients with metastatic CRC (mCRC) is the core question for CRC treatment. However, the complexity and diversity of stromal context of the tumor microenvironment (TME) in liver metastases of CRC is not fully understood, and its influence on response to chemotherapy is unclear. Here we provide an in-depth analysis of transcriptional landscape of primary CRC, matched liver metastases and blood at single-cell resolution, and perform a systematic examination of transcriptional changes and phenotypic alteration of the TME in response to preoperative chemotherapy (PC). Based on 111,292 single-cell transcriptomes, our study reveal that TME of treatment-naïve tumors is characterized by higher abundance of less-activated B cells and higher heterogeneity of tumor-associated macrophages (TAMs). By contrast, in tumors treated with preoperative chemotherapy, we find reprogramming of B cell activation, lower diversity of TAMs with immature and less activated phenotype, lower abundance of both dysfunctional T cells and ECM-remodeling cancer-associated fibroblasts (CAFs), an accumulation of myofibroblast. Our study may provide a foundation to investigate the cellular mechanisms underlying liver metastasis of CRC and response to preoperative chemotherapy, and open up new possibilities for predicting and guiding therapeutic responsiveness.

BACKGROUND The spinal cord is one of the central nervous system. Spinal cord injury (SCI) will cause loss of physical function and dysfunction below the injury site, causing them to lose sensation and mobility, thereby reducing the quality of life of patients. Although regular rehabilitation management can reduce its severity, the current effective treatment methods are limited to the treatment of secondary injuries to SCI. The purpose of treatment should not only include the restoration of the histology of the lesion, but also should focus on the restoration of sensory and mobility and. The key to effective treatment is to reduce secondary injuries. RhoA inhibitor can improve the pathophysiological changes related to secondary injury and promote the recovery of activity ability, so it may become a clinical drug for the treatment of SCI. This article systematically analyzed the effects of RhoA inhibitors on the promotion of axon regeneration and the recovery of mobility and compared the therapeutic effects of different inhibitors on SCI and their effects on physical function recovery. METHODS We used a meta-analysis to systematically evaluate the effects of Rho inhibitors on SCI treatment and the recovery of body function. RESULTS 21 articles (738 animals) were identified in the literatures search. Studies were selected if they reported the therapeutic effects of RhoA/ROCK inhibitors (BA-210, EGCG, β-elemene, C3-exoenzmye, LINGO-1-Fc, Ibuprofen, SiRhoA, iRhoA + FK506, Fasudil, p21Cip1/WAF1, HA-1007, Y-27,632 and C3bot154-182). We measure the functional recovery by BBB and BMS scores. The random effect model of weighted mean difference (WMD, 95 % confidence interval) was used to analyze the effects. The WMD of the forest graph was 2.277; 95 % CI: 1.705∼2.849, P < 0.001, suggesting that RhoA inhibitors can effectively treat SCI. In addition to EGCG, all the other agents also showed the effects on the activity recovery post-SCI (P < 0.05). CONCLUSION β-elemene, LINGO-1-Fc, Ibuprofen, SiRhoA, RhoA + FK506, Fasudil, p21Cip1/WAF1 and Y-27,632 have similar effects to BA-210, they can promote axon germination and nerve fiber regeneration after thoracic spinal cord injury and reduce the formation of syringomyelia and protect white matter, thereby improving locomotor recovery. RhoA inhibitors have great potential to restore motor function and provide a new trend for the treatment of SCI.

BACKGROUND Through observing the changes of indexes of the intestinal mucosal barrier and intestinal flora in rats, we explored the mechanism by which Hetiao Jianpi Decoction (HTJPD) treats antibiotic-associated diarrhea (AAD) by repairing intestinal mucosal injury and regulating intestinal flora. MATERIAL AND METHODS Samples of colon tissues were collected for HE staining. Enzyme-linked immunosorbent assay (ELISA) was used to assess levels of diamine oxidase (DAO) and D-lactic acid in rat plasma and the expression of secretory immunoglobulin A (SIgA) in colon tissue. We assessed the abundance of intestinal contents by high-throughput sequencing of the 16S rRNA gene. RESULTS Compared with the Model group, the muscle layer and intestinal mucosal edema were improved, and the continuity was restored; the levels of DAO and D-lactic acid in plasma decreased, and the SIgA level were increased in the HTJPD group. The structure of the intestinal flora changed, as indicated by increased levels of certain beneficial bacteria (Verrucomicrobia, Actinobacteria, CF231, and Akkermansia), decreased levels of pathogenic bacteria (Spirochaetes and Treponema), and increased species diversity. CONCLUSIONS By improving the permeability and immune function of the intestinal mucosa, Hetiao Jianpi decoction prevented the occurrence of AAD by repairing the intestinal mucosal damage and regulating the structure and diversity of intestinal flora.

This paper proposed a disturbance rejection control method based on linear quadratic (LQ) for nonminimum-phase discrete-time systems with unmatched signals. By introducing a new cost function that considers the influences of disturbance on the input signal, we apply the novel control method to hypersonic flight vehicle (HFV) system to solve the problem of turbulence compensation. A two-component control input is generated through systematic derivation of finite-time LQ optimal control law, improving the stability, output regulation capability, and robustness of the HFV system. Comparison analysis under different control schemes in simulation study shows the effectiveness of the proposed method.

Comparing to classical Grignard-type carbonyl additions, transfer hydrogenative C–C bond-forming reactions using alcohols as carbonyl precursors have shown remarkable advantages from the perspective of atom economy, step economy and redox economy. The significant drawbacks of conventional method, such as the use of multi-step reactions, the premetalated reagents, and stoichiometric oxidants and reductants, can be avoided by using hydrogen transfer processes. Moreover, the development of reactions employing earth-abundant and eco-friendly base metal as catalysts is an important objective in modern sustainable chemistry. In this review, we summarized recent advances in base metal-catalyzed C–C coupling of alcohols under hydrogen transfer conditions.

Reported is a highly enantioselective copper-catalyzed Markovnikov protoboration of unactivated terminal alkenes. A variety of simple and abundant feedstock α-olefins bearing a diverse array of functional groups and heterocyclic substituents can be used as substrates, and the reaction proceeds under mild reaction conditions at ambient temperature to provide expedient access to enantioenriched alkylboronic esters in good regioselectivity and with excellent enantiocontrol. Critical to the success of the protocol was the development and application of a novel, sterically hindered N-heterocyclic carbene, (R,R,R,R)-ANIPE, as the ligand for copper.