Lithium (Li) metal is a promising anode material for high‐energy density batteries. However, the unstable and static solid electrolyte interphase (SEI) can be destroyed by the dynamic Li ...plating/stripping behavior on the Li anode surface, leading to side reactions and Li dendrites growth. Herein, we design a smart Li polyacrylic acid (LiPAA) SEI layer high elasticity to address the dynamic Li plating/stripping processes by self‐adapting interface regulation, which is demonstrated by in situ AFM. With the high binding ability and excellent stability of the LiPAA polymer, the smart SEI can significantly reduce the side reactions and improve battery safety markedly. Stable cycling of 700 h is achieved in the LiPAA‐Li/LiPAA‐Li symmetrical cell. The innovative strategy of self‐adapting SEI design is broadly applicable, providing opportunities for use in Li metal anodes
Stretching exercises: A flexible lithium polyacrylic acid (LiPAA) solid electrolyte interphase (SEI) layer which is highly stretchable is designed to address the dynamic volume changes during Li plating/stripping on the Li anode surface in Li ion batteries. The LiPAA polymer SEI can significantly reduce the side reactions and improve the safety performance.
Defects have been found to enhance the electrocatalytic performance of NiFe‐LDH for oxygen evolution reaction (OER). Nevertheless, their specific configuration and the role played in regulating the ...surface reconstruction of electrocatalysts remain ambiguous. Herein, cationic vacancy defects are generated via aprotic‐solvent‐solvation‐induced leaking of metal cations from NiFe‐LDH nanosheets. DFT calculation and in situ Raman spectroscopic observation both reveal that the as‐generated cationic vacancy defects tend to exist as VM (M=Ni/Fe); under increasing applied voltage, they tend to assume the configuration VMOH, and eventually transform into VMOH‐H which is the most active yet most difficult to form thermodynamically. Meanwhile, with increasing voltage the surface crystalline Ni(OH)x in the NiFe‐LDH is gradually converted into disordered status; under sufficiently high voltage when oxygen bubbles start to evolve, local NiOOH species become appearing, which is the residual product from the formation of vacancy VMOH‐H. Thus, we demonstrate that the cationic defects evolve along with increasing applied voltage (VM → VMOH → VMOH‐H), and reveal the essential motif for the surface restructuration process of NiFe‐LDH (crystalline Ni(OH)x → disordered Ni(OH)x → NiOOH). Our work provides insight into defect‐induced surface restructuration behaviors of NiFe‐LDH as a typical precatalyst for efficient OER electrocatalysis.
Along with increasing voltage during the OER process, the structural evolution of cationic defects within NiFe‐LDH, where the simple vacancy VM changes to VMOH and then to the most reactive VMOH‐H, and the surface restructuration, where surface crystalline Ni(OH)x is converted to disordered Ni(OH)x and then to the surface local NiOOH species, are voltage‐regulated concurrent events defining the eventual catalytic performance of the precatalyst.
Background
The National Comprehensive Cancer Network's Rectal Cancer Guideline Panel recommends American Joint Committee of Cancer and College of American Pathologists (AJCC/CAP) tumor regression ...grading (TRG) system to evaluate pathologic response to neoadjuvant chemoradiotherapy for locally advanced rectal cancer (LARC). Yet, the clinical significance of the AJCC/CAP TRG system has not been fully defined.
Materials and Methods
This was a multicenter, retrospectively recruited, and prospectively maintained cohort study. Patients with LARC from one institution formed the discovery set, and cases from external independent institutions formed a validation set to verify the findings from discovery set. Overall survival (OS), disease‐free survival (DFS), local recurrence‐free survival (LRFS), and distant metastasis‐free survival (DMFS) were assessed by Kaplan‐Meier analysis, log‐rank test, and Cox regression model.
Results
The discovery set (940 cases) found, and the validation set (2,156 cases) further confirmed, that inferior AJCC/CAP TRG categories were closely /ccorrelated with unfavorable survival (OS, DFS, LRFS, and DMFS) and higher risk of disease progression (death, accumulative relapse, local recurrence, and distant metastasis) (all p < .05). Significantly, pairwise comparison revealed that any two of four TRG categories had the distinguished survival and risk of disease progression. After propensity score matching, AJCC/CAP TRG0 category (pathological complete response) patients treated with or without adjuvant chemotherapy displayed similar survival of OS, DFS, LRFS, and DMFS (all p > .05). For AJCC/CAP TRG1–3 cases, adjuvant chemotherapy treatment significantly improved 3‐year OS (90.2% vs. 84.6%, p < .001). Multivariate analysis demonstrated the AJCC/CAP TRG system was an independent prognostic surrogate.
Conclusion
AJCC/CAP TRG system, an accurate prognostic surrogate, appears ideal for further strategizing adjuvant chemotherapy for LARC.
Implications for Practice
The National Comprehensive Cancer Network recommends the American Joint Committee of Cancer and College of American Pathologists (AJCC/CAP) tumor regression grading (TRG) four‐category system to evaluate the pathologic response to neoadjuvant treatment for patients with locally advanced rectal cancer; however, the clinical significance of the AJCC/CAP TRG system has not yet been clearly addressed. This study found, for the first time, that any two of four AJCC/CAP TRG categories had the distinguished long‐term survival outcome. Importantly, adjuvant chemotherapy may improve the 3‐year overall survival for AJCC/CAP TRG1–3 category patients but not for AJCC/CAP TRG0 category patients. Thus, AJCC/CAP TRG system, an accurate surrogate of long‐term survival outcome, is useful in guiding adjuvant chemotherapy management for rectal cancer.
The aim of this large cohort study was to define the clinical significance of the AJCC/CAP tumor regression grading system for locally advanced rectal cancer, which could potentially be used to select the patients who would benefit from more intensive adjuvant chemotherapy as well as to protect patients from excessive treatment.
Although tobacco smoking has been reported as a risk factor for liver cancer, few studies have specifically explored the association among Chinese females and the potential interaction between ...smoking and other risk factors. A population‐based case–control study was conducted and 2,011 liver cancer cases and 7,933 healthy controls were enrolled in Jiangsu, China from 2003 to 2010. Epidemiological data were collected, and serum hepatitis B surface antigen (HBsAg) and anti‐HCV antibody were measured. Unconditional logistic regression was used to examine association and potential interaction, while semi‐Bayes (SB) method was employed to make estimates more conservative. The prevalence of serum HBsAg positivity was 43.2% among cases and 6.5% among controls. The adjusted odds ratios (OR) for ever smoking were 1.62 (95% confidence interval CI: 1.33–1.96) among male and 0.82 (95% CI: 0.53–1.26) among female. Age at first cigarette, duration of smoking and pack‐years of smoking were all significantly associated with liver cancer among men. Compared to HBsAg‐negative never smokers, the adjusted ORs were 1.25 (95% CI: 1.03–1.52) for HBsAg‐negative ever smokers, 7.66 (95% CI: 6.05–9.71) for HBsAg‐positive never smokers, and 15.68 (95% CI: 12.06–20.39) for HBsAg‐positive ever smokers. These different odds ratios indicated super‐additive (RERI: 7.77, 95% CI: 3.81–11.73) and super‐multiplicative interactions (ROR: 1.64, 95% CI: 1.17–2.30) between hepatitis B virus (HBV) infection and tobacco smoking. Most associations and interactions detected remained statistically significant after SB adjustments. Tobacco smoking and HBV infection positively interact in the development of liver cancer.
What's new?
Tobacco smoking is a major risk factor for various cancer types, including liver cancer. Half of new liver cancer cases reported annually worldwide occur in China, where the prevalence of smoking and hepatitis B virus (HBV) infection are high. Here, associations between tobacco smoking and liver cancer and interactions between smoking and other risk factors were examined in a Chinese population. Significant interactions were detected between smoking and HBV infection. Analyses by gender indicated that associations between smoking and liver cancer existed primarily among men, who were more likely than women to have been ever smokers or current smokers.
Background & Aims
The potential interaction between family history of liver cancer and HBV infection on liver cancer has not been fully examined.
Methods
We conducted a population‐based case‐control ...study composed of 2011 liver cancer cases and 7933 controls in Jiangsu province, China from 2003 to 2010. Data on major risk or protective factors were collected and HBV/HCV sero‐markers were assayed using blood samples. Semi‐Bayes (SB) adjustments were applied to provide posterior estimates.
Results
Both family history of liver cancer (adjusted odds ratios OR: 4.32, 95% confidence intervals CI: 3.25‐5.73) and hepatitis B surface antigen (HBsAg) positivity (adjusted OR: 9.94, 95% CI: 8.33‐11.87) were strongly associated with liver cancer development. For individuals with different combinations of serological markers, the adjusted ORs were 8.45 (95% CI: 5.16‐13.82) for HBsAg‐ and HBcAb‐positive; 7.57 (95% CI: 4.87‐11.77) for HBsAg‐, HBeAg‐ and HBcAb‐positive; and 3.62 (95% CI: 2.47‐5.31) for HBsAg‐, HBeAb‐ and HBcAb‐positive, compared to all negatives in HBV serological markers. One log increase in HBV DNA level was associated with 17% increased risk (adjusted OR: 1.17, 95% CI: 1.03‐1.32). The SB‐adjusted OR of HBV‐positive individuals with family history of liver cancer was 41.34 (95% posterior interval PI: 23.69‐72.12) compared with those HBV‐negative without family history. Relative excess risk due to additive interaction, the attributable proportion and synergy index were 73.13, 0.87 and 8.04 respectively. Adjusted ratio of OR for multiplicative interaction was 2.84 (95% CI: 1.41‐5.75).
Conclusions
Super‐additive and super‐multiplicative interactions may exist between family history of liver cancer and HBV infection on the development of liver cancer.
Eukaryotic cells maintain mitochondrial integrity through mitophagy, an autophagic process by which dysfunctional mitochondria are selectively sequestered into double-layered membrane structures, ...termed phagophores, and delivered to lysosomes for degradation. Here we show that small fragments of parkin-labelled mitochondria at omegasome-marked sites are engulfed by autophagic membranes one at a time. Using a light-activation scheme to impair long mitochondrial tubules, we demonstrate that sites undergoing bit-by-bit mitophagy display preferential ubiquitination, and are situated where parkin-labelled mitochondrial tubules and endoplasmic reticulum intersect. Our observations suggest contact regions between the endoplasmic reticulum and impaired mitochondria are initiation sites for local LC3 recruitment and mitochondrial remodelling that support bit-by-bit, parkin-mediated mitophagy. These results help in understanding how cells manage to fit large and morphologically heterogeneous mitochondria into micron-sized autophagic membranes during mitophagy.
Lysosomes are the major degradative compartments within cells, harbouring a wide variety of hydrolytic enzymes within their lumen. Release of lysosomal hydrolases from lysosomes into the cell ...cytoplasm results in cell death. Here we report that damaged lysosomes undergo autophagic turnover. Using a light-induced lysosome impairing scheme that can be controlled spatially and temporally within a cell, we show that damaged lysosomes are selectively ubiquitinated, recruit autophagic proteins and are eventually incorporated into autolysosomes for degradation. We propose that autophagic removal of lysosomes, which we term lysophagy, is a surveillance mechanism that alleviates cells from the adverse effects of lysosomal damage. We envision our method to induce lysosomal damage will enable detailed molecular studies of the lysophagy pathway in the future.
To investigate the associations between dietary fatty acids and cholesterol consumption and stomach cancer (SC), we analyzed data from a population-based case-control study with a total of 1900 SC ...cases and 6532 controls. Dietary data and other risk or protective factors were collected by face-to-face interviews in Jiangsu Province, China, from 2003 to 2010. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multiple unconditional logistic regression models and an energy-adjusted method. The joint associations between dietary factors and known risk factors on SC were examined. We observed positive associations between dietary saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and total cholesterol and the development of SC, comparing the highest versus lowest quarters. Increased intakes of dietary SFAs (
-trend = 0.005; aOR, 1.11; 95% CI, 1.01-1.22 with a 7 g/day increase as a continuous variable) and total cholesterol (
-trend < 0.001; aOR, 1.13; 95% CI, 1.06-1.22 with a 250 mg/day increase as a continuous variable) were monotonically associated with elevated odds of developing SC. Our results indicate that dietary SFAs, MUFAs, and total cholesterol are associated with stomach cancer, which might provide a potential dietary intervention for stomach cancer prevention.
Aim
The programmed death 1/programmed death 1 ligand (PD‐1/PD‐L1) pathway can decrease the immune clearance effects of antigen‐presenting cells and T lymphocytes to promote immune evasion of cervical ...cancer cells. However, the effects of this pathway on cervical intraepithelial neoplasia (CIN) progression and squamous cell carcinoma (SCC) metastasis are not clear. We herein investigated whether human papillomavirus infection could affect PD‐1 and PD‐L1 expression in CIN, and whether their expression is associated with CIN progression and SCC metastasis.
Methods
We collected paraffin‐embedded samples from two cohorts of patients: (i) CIN samples from cohort I (40 women who tested positive or negative for high‐risk human papillomavirus HR‐HPV with grades 0, I, and II–III CIN); and (ii) paired primary and metastatic tumor samples from cohort II (20 SCC patients with or without metastasis). Immunohistochemistry was used to detect expressions of PD‐L1 in tumor cells and PD‐1 in tumor‐associated macrophages and tumor‐infiltrating lymphocytes. We also measured P16INK4a expression and interferon‐γ levels in the cervical tissues.
Results
The most common HPV type seen in both cohorts of patients was HPV16, followed by HPV18. Increase in PD‐L1 and PD‐1 expression was positively correlated with HPV‐positivity, increase in CIN grade, and tumor metastasis. Furthermore, upregulation of the PD‐1/PD‐L1 pathway was associated with decreased expression of the pro‐inflammatory cytokine, interferon‐γ and increased expression of P16INK4a.
Conclusion
Expression of PD‐L1 and PD‐1 could be used as clinical prognostic biomarkers for evaluating CIN and cervical cancer because of its positive correlation with CIN progression and tumor metastasis.
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