Research progress in tumor angiogenesis and drug resistance in breast cancer.

Angiogenesis is considered a hallmark pathophysiological process in tumor development. Aberrant vasculature resulting from tumor angiogenesis plays a critical role in the development of resistance to breast cancer treatments, via exacerbation of tumor hypoxia, decreased effective drug concentrations within tumors, and immune-related mechanisms. Antiangiogenic therapy can counteract these breast cancer resistance factors by promoting tumor vascular normalization. The combination of antiangiogenic therapy with chemotherapy, targeted therapy, or immunotherapy has emerged as a promising approach for overcoming drug resistance in breast cancer. This review examines the mechanisms associated with angiogenesis and the interactions among tumor angiogenesis, the hypoxic tumor microenvironment, drug distribution, and immune mechanisms in breast cancer. Furthermore, this review provides a comprehensive summary of specific antiangiogenic drugs, and relevant studies assessing the reversal of drug resistance in breast cancer. The potential mechanisms underlying these interventions are discussed, and prospects for the clinical application of antiangiogenic therapy to overcome breast cancer treatment resistance are highlighted.

Muscone abrogates breast cancer progression through tumor angiogenic suppression via VEGF/PI3K/Akt/MAPK signaling pathways.

BACKGROUND: Angiogenesis strongly reflects poor breast cancer outcome and an important contributor to breast cancer (BC) metastasis; therefore, anti-angiogenic intervention is a potential tool for cancer treatment. However, currently used antibodies against vascular endothelial growth factor A (VEGFA) or inhibitors that target the VEGFA receptor are not effective due to weak penetration and low efficiency. Herein, we assessed the anti-BC angiogenic role of muscone, a natural bioactive musk constituent, and explored possible anti-cancer mechanisms of this compound. METHODS: CCK-8, EdU, scratch and Transwell assessments were employed to detect the muscone-mediated regulation of breast cancer (BC) and human umbilical vein endothelial cells (HUVECs) proliferation and migration. Tube formation, matrigel plug assay and zebrafish assay were employed for assessment of regulation of tumor angiogenesis by muscone. In vivo xenograft mouse model was constructed to compare microvessel density (MVD), vascular leakage, vascular maturation and function in muscone-treated or untreated mice. RNA sequencing was performed for gene screening, and Western blot verified the effect of the VEGFA-VEGFR2 pathway on BC angiogenic inhibition by muscone. RESULTS: Based on our findings, muscone suppressed BC progression via tumor angiogenic inhibition in cellular and animal models. Functionally, muscone inhibited BC cell proliferation and migration as well as tumor cell-conditioned medium-based endothelial cell proliferation and migration. Muscone exhibited a strong suppressive influence on tumor vasculature in cellular and animal models. It abrogated tumor cell growth in a xenograft BC mouse model and minimized tumor microvessel density and hypoxia, and increased vascular wall cell coverage and perfusion. Regarding the mechanism of action, we found that muscone suppressed phosphorylation of members of the VEGF/PI3K/Akt/MAPK axis, and it worked synergistically with a VEGFR2 inhibitor, an Akt inhibitor, and a MAPK inhibitor to further inhibit tube formation. CONCLUSION: Overall, our results demonstrate that muscone may proficiently suppress tumor angiogenesis via modulation of the VEGF/PI3K/Akt/MAPK axis, facilitating its candidacy as a natural small molecule drug for BC treatment.

The crosstalk between benign thyroid disease and breast cancer: A single center study.

This study aims to investigate the relationship between benign thyroid disease and breast cancer. The clinical study includes a total of 600 participants, divided into 2 groups: the control group (N = 300), which consists of individuals from the checkup population during the same periods, and the experimental group (N = 300), which consists of patients with breast cancer. General data of the participants, including age, tumor diameter, tumor staging, pathological classification, lymph node metastasis, and classification of benign thyroid disease, were collected and analyzed. The levels of TT3, TT4, FT3, FT4, TSH, TPOAb, and TgAb in blood samples from the experimental and control groups were determined using a radioimmune method. The levels of TPOAb, TgAb, and TSH in the experimental group were significantly higher than those in the control group, while the levels of TT3, TT4, FT3, and FT4 in the experimental group were significantly lower. The general data of the participants contributed to the appropriate sample size and allocation. Furthermore, benign thyroid disease contributes to the development of breast cancer by regulating the levels of TT3, TT4, FT3, FT4, TSH, TPOAb, and TgAb.

Integrative landscape analysis of prognostic model biomarkers and immunogenomics of disulfidptosis-related genes in breast cancer based on LASSO and WGCNA analyses.

BACKGROUND: Disulfidptosis is a novel type of programmed cell death. However, the value of disulfidptosis-related genes (DRGs) in the prediction of breast cancer prognosis is unclear. METHODS: RNA-seq data of 1231 patients, together with information on patient clinical characteristics and prognosis, were downloaded from TCGA. DRGs were identified between cancerous and non-cancerous tissues. The LASSO algorithm was used to assign half of the samples to the training set. Risk scores were used for construction of a prognostic model for risk stratification and prognosis prediction, and the clinical applicability was examined using a line diagram. The relationships between risk scores, immune cell infiltration, molecular subtypes, and responses to immunotherapy and chemotherapy were examined. RESULTS: We identified and obtained four DRG-related prognostic lncRNAs (AC009097.2, AC133552.5, YTHDF3-AS1, and AC084824.5), which were used for establishing the risk model. Longer survival was associated with low risk. The DRG-associated lncRNAs were found to independently predict patient prognosis. The AUCs under the ROCs for one-, three-, and 5-year survival in the training cohort were 0.720, 0.687, and 0.692, respectively. The model showed that the high-risk patients had reduced overall survival as well as high tumor mutation burdens. Furthermore, high-risk patients showed increased sensitivity to therapeutic drugs, including docetaxel, paclitaxel, and oxaliplatin. CONCLUSION: The risk score model was effective for predicting both prognosis and sensitivity to therapeutic drugs, suggesting its possible usefulness for the management of patients with breast cancer.

Molecular mechanisms of immunotherapy resistance in triple-negative breast cancer.

The emergence of immunotherapy has profoundly changed the treatment model for triple-negative breast cancer (TNBC). But the heterogeneity of this disease resulted in significant differences in immunotherapy efficacy, and only some patients are able to benefit from this therapeutic modality. With the recent explosion in studies on the mechanism of cancer immunotherapy drug resistance, this article will focus on the processes of the immune response; summarize the immune evasion mechanisms in TNBC into three categories: loss of tumor-specific antigen, antigen presentation deficiency, and failure to initiate an immune response; together with the aberrant activation of a series of immune-critical signaling pathways, we will discuss how these activities jointly shape the immunosuppressive landscape within the tumor microenvironment. This review will attempt to elucidate the molecular mechanism of drug resistance in TNBC, identify potential targets that may assist in reversing drug resistance, and lay a foundation for research on identifying biomarkers for predicting immune efficacy and selection of breast cancer populations that may benefit from immunotherapy.

OTUD1 chemosensitizes triple-negative breast cancer to doxorubicin by modulating P16 expression.

Chemotherapy remains a critical component of triple-negative breast cancer (TNBC) treatment; however, patients often develop resistance to chemotherapeutic agents. Accumulating evidence indicates that deubiquitylases (DUBs) play pivotal roles in regulating cell proliferation, differentiation, apoptosis, and tumorigenesis. Deubiquitylase OTUD1 is considered a tumor suppressor in various cancers, yet its role in doxorubicin sensitivity in breast cancer patients remains inadequately understood. In this study, we investigated the expression levels and prognostic role of OTUD1 in breast cancer. Our findings demonstrated that OTUD1 was downregulated in TNBC, and lower OTUD1 expression levels were correlated with poor prognosis. We utilized the CCK-8 cell viability assay, flow cytometric analysis, and a TNBC mouse xenograft model to examine the influence of OTUD1 on doxorubicin (DOX) chemotherapy sensitivity in vitro and in vivo. Western blot and immunohistochemistry were employed to explore the correlation between OTUD1 and P16. Our results indicated that upregulation of OTUD1 expression inhibits TNBC cell proliferation and enhances its sensitivity to doxorubicin. Additionally, rescue experiments confirmed that the chemosensitizing effect of OTUD1 overexpression could be reversed by the inhibition of P16. Therefore, our findings reveal that OTUD1 sensitizes TNBC cells to DOX by upregulating P16 expression, suggesting a potential new diagnostic biomarker and therapeutic target for the future treatment of TNBC.

A Review of Extracellular Vesicles in COVID-19 Diagnosis, Treatment, and Prevention.

The 2019 novel coronavirus disease (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is ongoing, and has necessitated scientific efforts in disease diagnosis, treatment, and prevention. Interestingly, extracellular vesicles (EVs) have been crucial in these developments. EVs are a collection of various nanovesicles which are delimited by a lipid bilayer. They are enriched in proteins, nucleic acids, lipids, and metabolites, and naturally released from different cells. Their natural material transport properties, inherent long-term recycling ability, excellent biocompatibility, editable targeting, and inheritance of parental cell properties make EVs one of the most promising next-generation drug delivery nanocarriers and active biologics. During the COVID-19 pandemic, many efforts have been made to exploit the payload of natural EVs for the treatment of COVID-19. Furthermore, strategies that use engineered EVs to manufacture vaccines and neutralization traps have produced excellent efficacy in animal experiments and clinical trials. Here, the recent literature on the application of EVs in COVID-19 diagnosis, treatment, damage repair, and prevention is reviewed. And the therapeutic value, application strategies, safety, and biotoxicity in the production and clinical applications of EV agents for COVID-19 treatment, as well as inspiration for using EVs to block and eliminate novel viruses are discussed.

A Review of Gut Microbiota-Derived Metabolites in Tumor Progression and Cancer Therapy.

Gut microbiota-derived metabolites are key hubs connecting the gut microbiome and cancer progression, primarily by remodeling the tumor microenvironment and regulating key signaling pathways in cancer cells and multiple immune cells. The use of microbial metabolites in radiotherapy and chemotherapy mitigates the severe side effects from treatment and improves the efficacy of treatment. Immunotherapy combined with microbial metabolites effectively activates the immune system to kill tumors and overcomes drug resistance. Consequently, various novel strategies have been developed to modulate microbial metabolites. Manipulation of genes involved in microbial metabolism using synthetic biology approaches directly affects levels of microbial metabolites, while fecal microbial transplantation and phage strategies affect levels of microbial metabolites by altering the composition of the microbiome. However, some microbial metabolites harbor paradoxical functions depending on the context (e.g., type of cancer). Furthermore, the metabolic effects of microorganisms on certain anticancer drugs such as irinotecan and gemcitabine, render the drugs ineffective or exacerbate their adverse effects. Therefore, a personalized and comprehensive consideration of the patient's condition is required when employing microbial metabolites to treat cancer. The purpose of this review is to summarize the correlation between gut microbiota-derived metabolites and cancer, and to provide fresh ideas for future scientific research.

Necroptosis-Related LncRNAs Signature and Subtypes for Predicting Prognosis and Revealing the Immune Microenvironment in Breast Cancer.

Purpose: Necroptosis is a mode of programmed cell death that overcomes apoptotic resistance. We aimed to construct a steady necroptosis-related signature and identify subtypes for prognostic and immunotherapy sensitivity prediction. Methods: Necroptosis-related prognostic lncRNAs were selected by co-expression analysis, and were used to construct a linear stepwise regression model via univariate and multivariate Cox regression, along with least absolute shrinkage and selection operator (LASSO). Quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to measure the gene expression levels of lncRNAs included in the model. Based on the riskScore calculated, we separated patients into high- and low-risk groups. Afterwards, we performed CIBERSORT and the single-sample gene set enrichment analysis (ssGSEA) method to explore immune infiltration status. Furthermore, we investigated the relationships between the signature and immune landscape, genomic integrity, clinical characteristics, drug sensitivity, and immunotherapy efficacy. Results: We constructed a robust necroptosis-related 22-lncRNA model, serving as an independent prognostic factor for breast cancer (BRCA). The low-risk group seemed to be the immune-activated type. Meanwhile, it showed that the higher the tumor mutation burden (TMB), the higher the riskScore. PD-L1-CTLA4 combined immunotherapy seemed to be a promising treatment strategy. Lastly, patients were assigned to 4 clusters to better discern the heterogeneity among patients. Conclusions: The necroptosis-related lncRNA signature and molecular clusters indicated superior predictive performance in prognosis and the immune microenvironment, which may also provide guidance to drug regimens for immunotherapy and provide novel insights into precision medicine.

Identification of Ferroptosis-Related Prognostic Signature and Subtypes Related to the Immune Microenvironment for Breast Cancer Patients Receiving Neoadjuvant Chemotherapy.

Purpose: To identify molecular clusters associated with ferroptosis and to develop a ferroptosis-related signature for providing novel potential targets for the recurrence-free survival and treatment of breast cancer. Methods: Ferroptosis-related gene (FRG) signature was constructed by univariate and multivariate Cox regression and least absolute shrinkage and selection operator (LASSO). Receiver operating characteristic curves, Kaplan-Meier survival analysis, principal component analysis, and univariate and multivariate Cox regression analyses in the training and test cohorts were used to evaluate the application of this signature. Quantitative reverse transcriptase-PCR (qRT-PCR) was employed to detect the expression of FRGs in the model. Furthermore, the correlations between the signature and immune microenvironment, somatic mutation, and chemotherapeutic drugs sensitivity were explored. Results: Internal and external validations affirmed that relapse-free survival differed significantly between the high-risk and low-risk groups. Univariate and multivariate Cox regression analyses indicated that the riskScore was an independent prognostic factor for BRCA. The areas under the curve (AUCs) for predicting 1-, 2-, and 3-year survival in the training and test cohorts were satisfactory. Significant differences were also found in the immune microenvironment and IC50 of chemotherapeutic drugs between different risk groups. Furthermore, we divided patients into three clusters based on 18 FRGs to ameliorate the situation of immunotherapy failure in BRCA. Conclusions: The FRG signature functions as a robust prognostic predictor of the immune microenvironment and therapeutic response, with great potential to guide individualized treatment strategies in the future.

Predicting Axillary Response in Hormone Receptor-Positive Breast Cancer after Neoadjuvant Chemotherapy Using Real-World Data.

Purpose: To develop a scoring system for hormone receptor-positive (HR+) breast cancer patients who are expected to achieve axillary pathological complete response (pCR) after neoadjuvant chemotherapy (NAC). To confirm the correlation between axillary status and survival rate in HR+ breast cancer after NAC. Methods: Women from the Shanghai Jiao Tong University Breast Cancer Database (SJTU-BCDB) who underwent NAC for cT1-4N1-3M0 primary HR+ breast cancer between 2009 and 2018 were included in the study. In this case, patient follow up was performed until 2022 for those with complete data before and after NAC. The main outcome measures were the axillary pCR rate, overall survival (OS), and disease-free survival (DFS). The patients were randomly assigned to a test set (n = 175) and a validation set (n = 68) in a 7 : 3 ratio. A prediction risk score was then developed based on the odds ratios from the multivariate analysis of the test set (n = 175) before being validated in the validation set (n = 68). Finally, the Kaplan-Meier curves were used to explore the survival on this score system. Results: From the database, 243 women were included, and the median follow-up period was 47.5 months (95% confidence interval: 41.9-53.1). The axillary pCR rate was 18.9% (46 of 243), with the independent predictors of residual positive axillary lymph nodes (LNs) being lymphovascular invasion (LVI), breast conserving surgery (BCS), Ki67 < 14%, HER2 negativity, positive lymph nodes in ultrasound (US) before surgery, and stage III histological grade (All, P < 0.05). Using the above predictors of the model, the receiver operating characteristic (ROC) curve was used for calibration and inspection, with values for the test and validation sets being 0.847 (P < 0.001; 95% CI: 0.769, 0.925) and 0.813 (P < 0.001; 95% CI: 0.741, 0.885), respectively. The total risk score ranged from 0 to 6 for the multivariate analysis, and from this range, a risk score of 0-2 was defined as a low-risk group, while scores of 3-6 were defined as the high-risk one. By constructing the survival curve, it was found that the 5-year OS rates for the low-risk and high-risk groups were 89.0% and 84.2% (P = 0.236). Similarly, the 5-year DFS rates for the low-risk and high-risk groups were 80% and 68.5% (P = 0.048), respectively. In addition, axillary pathological stages were significantly correlated with the overall survival (OS) and disease-free survival (DFS) (All, P < 0.05). Conclusion: The prediction model showed good performance for HR + breast cancer. LVI, BCS, low Ki-67, HER2 negativity, suspected positive LNs before surgery, and stage III histological grade were all risk factors for residual positive axillary LNs. However, unlike pathological stages, achieving pCR in the axillary LNs does not affect the survival status.

Integrated Analysis of ceRNA Network Reveals Prognostic and Metastasis Associated Biomarkers in Breast Cancer.

BACKGROUND: Breast cancer is a malignancy and lethal tumor in women. Metastasis of breast cancer is one of the causes of poor prognosis. Increasing evidences have suggested that the competing endogenous RNAs (ceRNAs) were associated with the metastasis of breast cancer. Nonetheless, potential roles of ceRNAs in regulating the metastasis of breast cancer remain unclear. METHODS: The RNA expression (3 levels) and follow-up data of breast cancer and noncancerous tissue samples were downloaded from the Cancer Genome Atlas (TCGA). Differentially expressed and metastasis associated RNAs were identified for functional analysis and constructing the metastasis associated ceRNA network by comprehensively bioinformatic analysis. The Kaplan-Meier (K-M) survival curve was utilized to screen the prognostic RNAs in metastasis associated ceRNA network. Moreover, we further identified the metastasis associated biomarkers with operating characteristic (ROC) curve. Ultimately, the data of Cancer Cell Line Encyclopedia (CCLE, https://portals.broadinstitute.org/ccle) website were selected to obtained the reliable metastasis associated biomarkers. RESULTS: 1005 mRNAs, 22 miRNAs and 164 lncRNAs were screened as differentially expressed and metastasis associated RNAs. The results of GO function and KEGG pathway enrichment analysis showed that these RNAs are mainly associated with the metabolic processes and stress responses. Next, a metastasis associated ceRNA (including 104 mRNAs, 19 miRNAs, and 16 lncRNAs) network was established, and 12 RNAs were found to be related to the overall survival (OS) of patients. In addition, 3 RNAs (hsa-miR-105-5p, BCAR1, and PANX2) were identified to serve as reliable metastasis associated biomarkers. Eventually, the results of mechanism analysis suggested that BCAR1 might promote the metastasis of breast cancer by facilitating Rap 1 signaling pathway. CONCLUSION: In the present research, we identified 3 RNAs (hsa-miR-105-5p, BCAR1 and PANX2) might associated with prognosis and metastasis of breast cancer, which might be provide a new perspective for metastasis of breast cancer and contributed to the treatment of breast cancer.

Hyperglycemia and Chemoresistance in Breast Cancer: From Cellular Mechanisms to Treatment Response.

Female breast cancer is a complex, multifactorial disease. Studies have shown that hyperglycemia is one of the most important contributing factors to increasing the risk of breast cancer that also has a major impact on the efficacy of chemotherapy. At the cellular level, hyperglycemia can promote the proliferation, invasion, and migration of breast cancer cells and can also induce anti-apoptotic responses to enhance the chemoresistance of tumors via abnormal glucose metabolism. In this article, we focus on the latest progress in defining the mechanisms of chemotherapy resistance in hyperglycemic patients including the abnormal behaviors of cancer cells in the hyperglycemic microenvironment and the impact of abnormal glucose metabolism on key signaling pathways. To better understand the advantages and challenges of breast cancer treatments, we explore the causes of drug resistance in hyperglycemic patients that may help to better inform the development of effective treatments.

The IRENA lncRNA converts chemotherapy-polarized tumor-suppressing macrophages to tumor-promoting phenotypes in breast cancer.

Although chemotherapy can stimulate antitumor immunity by inducing interferon (IFN) response, the functional role of tumor-associated macrophages in this scenario remains unclear. Here, we found that IFN-activated proinflammatory macrophages after neoadjuvant chemotherapy enhanced antitumor immunity but promoted cancer chemoresistance. Mechanistically, IFN induced expression of cytoplasmic long noncoding RNA IFN-responsive nuclear factor-κB activator (IRENA) in macrophages, which triggered nuclear factor-κB signaling via dimerizing protein kinase R and subsequently increased production of protumor inflammatory cytokines. By constructing macrophage-conditional IRENA-knockout mice, we found that targeting IRENA in IFN-activated macrophages abrogated their protumor effects, while retaining their capacity to enhance antitumor immunity. Clinically, IRENA expression in post-chemotherapy macrophages was associated with poor patient survival. These findings indicate that lncRNA can determine the dichotomy of inflammatory cells on cancer progression and antitumor immunity and suggest that targeting IRENA is an effective therapeutic strategy to reversing tumor-promoting inflammation.

The Breast Cancer Stem Cells Traits and Drug Resistance.

Drug resistance is a major challenge in breast cancer (BC) treatment at present. Accumulating studies indicate that breast cancer stem cells (BCSCs) are responsible for the BC drugs resistance, causing relapse and metastasis in BC patients. Thus, BCSCs elimination could reverse drug resistance and improve drug efficacy to benefit BC patients. Consequently, mastering the knowledge on the proliferation, resistance mechanisms, and separation of BCSCs in BC therapy is extremely helpful for BCSCs-targeted therapeutic strategies. Herein, we summarize the principal BCSCs surface markers and signaling pathways, and list the BCSCs-related drug resistance mechanisms in chemotherapy (CT), endocrine therapy (ET), and targeted therapy (TT), and display therapeutic strategies for targeting BCSCs to reverse drug resistance in BC. Even more importantly, more attention should be paid to studies on BCSC-targeted strategies to overcome the drug resistant dilemma of clinical therapies in the future.

LncRNA POU3F3 promotes proliferation and inhibits apoptosis of cancer cells in triple-negative breast cancer by inactivating caspase 9.

It has been reported that lncRNA POU3F3 was upregulated in esophageal squamous-cell carcinomas, indicating its role as an oncogene in this disease. However, the mechanism of its function and its involvement in other malignancies is unknown. In the present study we found that expression levels of lncRNA POU3F3 were higher in tumor tissues than in adjacent healthy tissues of triple negative breast cancer (TNBC) patients and were significantly and inversely correlated with levels of cleaved caspase 9 only in tumor tissues. In addition, plasma levels of lncRNA POU3F3 were higher in TNBC patients than in healthy controls and were significantly and inversely correlated with levels of cleaved caspase 9 only in TNBC patients. In addition, treatment of exogenous Cleaved Caspase-9 significantly attenuated the effects of lncRNA POU3F3 overexpression on cancer cell proliferation and apoptosis. lncRNA POU3F3 may promote proliferation and inhibit apoptosis of cancer cells in triple-negative breast cancer.

Cation Dynamics Governed Thermal Properties of Lead Halide Perovskite Nanowires.

Metal halide perovskite (MHP) nanowires such as hybrid organic-inorganic CH3NH3PbX3 (X = Cl, Br, I) have drawn significant attention as promising building blocks for high-performance solar cells, light-emitting devices, and semiconductor lasers. However, the physics of thermal transport in MHP nanowires is still elusive even though it is highly relevant to the device thermal stability and optoelectronic performance. Through combined experimental measurements and theoretical analyses, here we disclose the underlying mechanisms governing thermal transport in three different kinds of lead halide perovskite nanowires (CH3NH3PbI3, CH3NH3PbBr3 and CsPbBr3). It is shown that the thermal conductivity of CH3NH3PbBr3 nanowires is significantly suppressed as compared to that of CsPbBr3 nanowires, which is attributed to the cation dynamic disorder. Furthermore, we observed different temperature-dependent thermal conductivities of hybrid perovskites CH3NH3PbBr3 and CH3NH3PbI3, which can be attributed to accelerated cation dynamics in CH3NH3PbBr3 at low temperature and the combined effects of lower phonon group velocity and higher Umklapp scattering rate in CH3NH3PbI3 at high temperature. These data and understanding should shed light on the design of high-performance MHP based thermal and optoelectronic devices.

Tuning Transpiration by Interfacial Solar Absorber-Leaf Engineering.

Plant transpiration, a process of water movement through a plant and its evaporation from aerial parts especially leaves, consumes a large component of the total continental precipitation (≈48%) and significantly influences global water distribution and climate. To date, various chemical and/or biological explorations have been made to tune the transpiration but with uncertain environmental risks. In recent years, interfacial solar steam/vapor generation is attracting a lot of attention for achieving high energy transfer efficiency. Various optical and thermal designs at the solar absorber-water interface for potential applications in water purification, seawater desalination, and power generation appear. In this work, the concept of interfacial solar vapor generation is extended to tunable plant transpiration by showing for the first time that the transpiration efficiency can also be enhanced or suppressed through engineering the solar absorber-leaf interface. By tuning the solar absorption of membrane in direct touch with green leaf, surface temperature of green leaf will change accordingly because of photothermal effect, thus the transpiration efficiency as well as temperature and relative humidity in the surrounding environment will be tuned. This tunable transpiration by interfacial absorber-leaf engineering can open an alternative avenue to regulate local atmospheric temperature, humidity, and eventually hydrologic cycle.

Scalable Production of the Silicon-Tin Yin-Yang Hybrid Structure with Graphene Coating for High Performance Lithium-Ion Battery Anodes.

Alloy anodes possessed of high theoretical capacity show great potential for next-generation advanced lithium-ion battery. Even though huge volume change during lithium insertion and extraction leads to severe problems, such as pulverization and an unstable solid-electrolyte interphase (SEI), various nanostructures including nanoparticles, nanowires, and porous networks can address related challenges to improve electrochemical performance. However, the complex and expensive fabrication process hinders the widespread application of nanostructured alloy anodes, which generate an urgent demand of low-cost and scalable processes to fabricate building blocks with fine controls of size, morphology, and porosity. Here, we demonstrate a scalable and low-cost process to produce a porous yin-yang hybrid composite anode with graphene coating through high energy ball-milling and selective chemical etching. With void space to buffer the expansion, the produced functional electrodes demonstrate stable cycling performance of 910 mAh g-1 over 600 cycles at a rate of 0.5C for Si-graphene "yin" particles and 750 mAh g-1 over 300 cycles at 0.2C for Sn-graphene "yang" particles. Therefore, we open up a new approach to fabricate alloy anode materials at low-cost, low-energy consumption, and large scale. This type of porous silicon or tin composite with graphene coating can also potentially play a significant role in thermoelectrics and optoelectronics applications.

Poly(dimethylsiloxane) Thin Film as a Stable Interfacial Layer for High-Performance Lithium-Metal Battery Anodes.

A modified poly(dimethylsiloxane) film with nanopores, fabricated through a scalable and low-cost process, can serve as a protective layer for improving lithium-metal anodes. This film can suppress Li-dendrite formation because of its chemical inertness and mechanical properties. Stable cycling over 200 cycles with an averaged CE of 94.5% is demonstrated at 0.5 mA cm-2 .