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Abstract Introduction Oral submucosal fibrosis is a potentially life-threatening oral disease that significantly impacts physiological functions such as speech and swallowing while also diminishing the quality of life for patients. Currently, the mainstream treatment for oral submucosal fibrosis in clinical practice involves invasive glucocorticoid drugs such as injection therapy. However, this method often leads to intraoperative pain, anxiety, fear, and poor medical experience due to associated side effects. Methods There is an urgent need to actively explore new drugs and relatively noninvasive approaches for the treatment of oral submucosal fibrosis in order to enhance patients’ medical experience and compliance. This has become a focal point of attention in clinical research. After conducting an extensive literature search, it was discovered that curcumin, a natural polyphenolic compound, exhibits potent anti-tumor, anti-inflammatory, antioxidant, anti-metastatic and anti-angiogenic properties. Moreover, curcumin holds significant clinical potential in the prevention and treatment of various diseases such as oral submucosal fibrosis. Conclusion This review presents a comprehensive elaboration encompassing the action mechanisms, biological activity, potential applications, and clinical characteristics of curcumin in the management of oral submucosal fibrosis, aiming to provide diagnostic insights and novel therapeutic perspectives for its prevention and treatment.

Objective: To investigate the effects of cell passage number on the establishment of an oxidative stress model in human colon adenocarcinoma cells (Caco-2) caused by tert-butyl hydroperoxide (t-BHP). Methods: First, by applying various t-BHP concentrations (1, 2 and 3 mmol/L) to the F15 generation of Caco-2 cells for 1, 2, 3, 4, 5 and 6 hours, the content of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) in different treatment groups were measured to determine the basic conditions for constructing the oxidative stress model of Caco-2 cells. Then, based on the fundamental parameters, the effect of cell passage number (F14, F15, F18, F19 and F20) on the development of oxidative stress model was investigated using the content of 8-OHdG as an index. Results: When exposed to 1, 2 and 3 mmol/L of t-BHP for 3 to 6 hours, the oxidative stress model of Caco-2 cells from the F15 generation could be established steadily. The content of 8-OHdG in Caco-2 cells of the F14, F15 and F18 generations was significantly higher than that in control group (which had not been treated with t-BHP) after being exposed to 2.0 mmol/L t-BHP for 5 hours (P

Bacteria are the key group of micro-organisms during the fermentation of Paocai. This study applied the high-throughput sequencing technology to trace the dynamics of Paocai brine bacterial community structures at constant temperature (25 ℃) under airtight microcosm condition. The results showed that there were 10 phyla and 205 genera had been detected within 30 days after the experiment setup. Among them, there were 12 dominant genera which accounted for 94.7%~97.8% of the total OTUs. The sub-dominant were 13 genera and accounted for 2.1%~3.3%. The rare genera were 180 genera and accounted for 0.08%~2.7%. During the 1~7 days after the experiment setup, the community was relatively stable (phase A). From the 8~20 days, the sub-dominant and rare genera were continuously changing (phase B), and on the 8th day, the communities of sub-dominant and rare genera were acutely fluctuated. From 22~30 days, all of the genera changed obviously (phase C). Meanwhile, the Chao1, Ace indices were increasing during 1~30 days, in addition, the Shannon and Simpson indices reached the thresholds during phase C. Therefore, phase A and B, phase B and C had the similar communities, but not the phase A and C, while the pH during the three phases changed correspondingly. The results also showed that at 25 ℃, the dynamics of sub-dominant and rare genera were the key factor which caused the dynamic of the bacterial communities in Paocai brine during the 30 days experiment. In addition, the accumulated effect had been detected, the pH and the bacterial communities havd mutual influences. The optimal preservation time for the Paocai brine was one week under airtight condition at 25 ℃. The functional effects of rare genera from Paocai brine need pay more attentions on.

ObjectiveObese or overweight is a risk factor for some chronic diseases, and oxidative stress and inflammation may be one of the molecular mechanisms leading to the persistence of these chronic diseases. Discovering interventions to alleviate oxidative stress and inflammation in the overweight/obese population, is very important for public health and health education.MethodsA two-week panel intervention study (Run 0-Run 1-Run 2) was conducted. The subjects were 77 overweight/obese undergraduates attending Dali University, with a BMI>24 kg/m2. The physical indices measured at the end of each run included BMI, waist circumference, serum ROS, TNF-α, IL-1β and urinary 8-OHdG. Students were allocated to one of four intervention groups: No intervention (control); walking; taking vitamin C; and walking + taking vitamin C.ResultsThe results demonstrated (1) Walking significantly alleviated ROS levels, and this was consistent in Run 1 and Run 2; (2) During Run1, all three intervention modes reduced levels of 8-OHdG, but there was a statistically insignificant increase during Run 2; (3) No alleviating effects of the three intervention modes on TNF-α levels during Run 1 and Run 2 were observed; (4) The alleviating effects of the three intervention modes on IL-1β levels during Run 1 and Run 2 were clear.ConclusionWalking and taking vitamin C can reduce levels of ROS, 8-OHdG and IL-1β, but not TNF-α, in overweight/obese participants. These interventions may become potential preventive measures for the overweight against obese-induced oxidative stress and inflammation.

Heat input and ash residues are main components of vegetation fire disturbances. Understanding the distinct impacts of heat and ash on soil microorganisms is crucial to comprehend and predict the induced changes in soil ecosystem composition and dynamics following different types of fire disturbances. This study’s main goal was to track the dynamic shifts in the community of soil nematode-trapping fungi (NTF) following the separate disturbances of heat and ash by means of a specifically designed experiment conducted in the field. Four simulated fire treatments, one treatment reproducing natural burning, and one control treatment were taken into account. Every ten days following the disturbance, soil samples from each treatment were collected, and soil NTF and physicochemical characteristics were measured. The results showed that: (1) Heat drastically decreased the number of strains and heavily altered the NTF community, but it also encouraged the emergence of new NTF species. Instead, no overt changes were observed in the treatment that just experienced the addition of ash on the soil. (2) When compared to treatments that received only heat input, the lower strain count of NTF recovered more quickly in the natural burning treatment which was affected by both heat and ash input. These findings suggest that the disruptive effect of fire heat on soil NTF biomass may be counterbalanced by the emergence of new species and the repairing capabilities of new nutrients introduced by ash residue. In the future, both conventional and cutting-edge techniques should be considered in research designs to better understand the ecological role of fire disturbances occurring at different intensities, as well as the mechanisms that make soil ecosystems resilient to fire, in particular the role of new species.

Abstract Lack of health knowledge can be a main cause of barriers to early diagnosis and treatment, and it can also highlight the deficiencies in health education. Therefore, it is essential to understand the health knowledge needs of individuals and the related influencing factors in order to improve health education models. A total of 935 administrative staff (AS) were selected as study participants by convenience sampling in Yuxi City, China. An electronic questionnaire, comprising four parts—Health Knowledge Needs, Sociodemographic Characteristics, Health Psychology and Behavior, and Self-Reported Medical History—were used to collect data. Statistical analysis was conducted using an internal consistency test, Kruskal–Wallis test, principal component analysis, hierarchical clustering analysis, and binary logistic regression analysis, performed with SPSS version 19.0. The Health Knowledge Needs Questionnaire had a Cronbach’s α of 0.883 and a Guttman Split-Half coefficient of 0.907. The need rates for health knowledge exceeding 30% are as follows: Traditional Chinese Medicine, Hypertension, Weight Management, Dietary Nutrition and Food Hygiene, Hyperlipidemia, Gastrointestinal Diseases, Heart Diseases, and First Aid. Health knowledge needs were summarized into six dimensions: “Diseases with Low Health Knowledge Needs”, “Maternal and Child Health Care and Thyroid Diseases”, “Cardiovascular and Cerebrovascular Diseases and Malignancies”, “Health Preservation and First Aid”, “The Four Highs Syndrome”, and "Respiratory and Digestive Diseases”. Gender, self-rated economic pressure, family size, and self-reported number of diseases were identified as influencing factors of health knowledge needs (P

Abstract Background Dysfunction of CD8+ T cells in the tumor microenvironment (TME) contributes to tumor immune escape and immunotherapy tolerance. The effects of hormones such as leptin, steroid hormones, and glucocorticoids on T cell function have been reported previously. However, the mechanism underlying thyroid‐stimulating hormone (TSH)/thyroid‐stimulating hormone receptor (TSHR) signaling in CD8+ T cell exhaustion and tumor immune evasion remain poorly understood. This study was aimed at investigating the effects of TSH/TSHR signaling on the function of CD8+ T cells and immune evasion in colorectal cancer (CRC). Methods TSHR expression levels in CD8+ T cells were assessed with immunofluorescence and flow cytometry. Functional investigations involved manipulation of TSHR expression in cellular and mouse models to study its role in CD8+ T cells. Mechanistic insights were mainly gained through RNA‐sequencing, Western blotting, chromatin immunoprecipitation and luciferase activity assay. Immunofluorescence, flow cytometry and Western blotting were used to investigate the source of TSH and TSHR in CRC tissues. Results TSHR was highly expressed in cancer cells and CD8+ T cells in CRC tissues. TSH/TSHR signaling was identified as the intrinsic pathway promoting CD8+ T cell exhaustion. Conditional deletion of TSHR in CD8+ tumor‐infiltrating lymphocytes (TILs) improved effector differentiation and suppressed the expression of immune checkpoint receptors such as programmed cell death 1 (PD‐1) and hepatitis A virus cellular receptor 2 (HAVCR2 or TIM3) through the protein kinase A (PKA)/cAMP‐response element binding protein (CREB) signaling pathway. CRC cells secreted TSHR via exosomes to increase the TSHR level in CD8+ T cells, resulting in immunosuppression in the TME. Myeloid‐derived suppressor cells (MDSCs) was the main source of TSH within the TME. Low expression of TSHR in CRC was a predictor of immunotherapy response. Conclusions The present findings highlighted the role of endogenous TSH/TSHR signaling in CD8+ T cell exhaustion and immune evasion in CRC. TSHR may be suitable as a predictive and therapeutic biomarker in CRC immunotherapy.

Abstract Chimeric antigen receptor T (CAR-T) cell therapy has greatly improved the prognosis of relapsed and refractory patients with large B-cell lymphoma (LBCL). Early identification and intervention of patients who may respond poorly to CAR-T cell therapy will help to improve the efficacy. Ninety patients from a Chinese cohort who received CAR-T cell therapy and underwent 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) scans at the screening stage (median time to infusion 53.5 days, range 27–176 days), 1 month and 3 months after CAR-T cell infusion were analyzed, with RNA-sequencing conducted on 47 patients at the screening stage. Patients with maximum diameter of the largest lesion (Dmax)

Abstract Osteogenesis imperfecta (OI) is a disorder of low bone mass and increased fracture risk due to a range of genetic variants that prominently include mutations in genes encoding type I collagen. While it is well known that OI reflects defects in the activity of bone-forming osteoblasts, it is currently unclear whether OI also reflects defects in the many other cell types comprising bone, including defects in skeletal vascular endothelium or the skeletal stem cell populations that give rise to osteoblasts and whether correcting these broader defects could have therapeutic utility. Here, we find that numbers of skeletal stem cells (SSCs) and skeletal arterial endothelial cells (AECs) are augmented in Col1a2 oim/oim mice, a well-studied animal model of moderate to severe OI, suggesting that disruption of a vascular SSC niche is a feature of OI pathogenesis. Moreover, crossing Col1a2 oim/oim mice to mice lacking a negative regulator of skeletal angiogenesis and bone formation, Schnurri 3 (SHN3), not only corrected the SSC and AEC phenotypes but moreover robustly corrected the bone mass and spontaneous fracture phenotypes. As this finding suggested a strong therapeutic utility of SHN3 inhibition for the treatment of OI, a bone-targeting AAV was used to mediate Shn3 knockdown, rescuing the Col1a2 oim/oim phenotype and providing therapeutic proof-of-concept for targeting SHN3 for the treatment of OI. Overall, this work both provides proof-of-concept for inhibition of the SHN3 pathway and more broadly addressing defects in the stem/osteoprogenitor niche as is a strategy to treat OI.

Abstract Purpose This study aimed to examine the correlation between different dominant follicle proportions (DFPs) and outcomes of in-vitro fertilization or intracytoplasmic sperm injection (IVF/ICSI) among patients classified under POSEIDON Groups 3 and 4, who underwent gonadotropin-releasing hormone antagonist (GnRH-ant) protocols. Additionally, it sought to determine the optimal DFP threshold for trigger timing. Methods A retrospective analysis was performed on patients classified under POSEIDON Groups 3 (n = 593) and 4 (n = 563) who underwent GnRH-ant protocols for controlled ovarian hyperstimulation (COH) between 2016 and 2022. These patients were categorized into two groups based on their DFPs, defined as the ratio of ≥ 18-mm dominant follicles to ≥ 12-mm follicles on the trigger day (DFP ≤ 40% and DFP ≥ 40%). Statistical analyses, including restricted cubic spline (RCS) and multivariate logistic regression, were employed to assess the relationship between DFP and IVF/ICSI outcomes. Results Demographic characteristics of patients were similar across groups. In POSEIDON Groups 3 and 4, DFP > 40 was associated with a significant decrease in the number (No.) of oocytes retrieved, cleaved embryos, and available embryos. Moreover, following the GnRH-ant cycle, the clinical pregnancy and live birth rates in fresh embryo transfer (ET) were notably reduced in the DFP > 40 group compared with the DFP ≤ 40 group, whereas no significant differences were observed in the pregnancy outcomes of the first frozen-thawed embryo transfer (FET) between the groups. In POSEIDON Group 3, the cumulative clinical pregnancy rate (CCPR) and cumulative live birth rate (CLRB) were significantly higher in the DFP ≤ 40 subgroup than in the DFP > 40 subgroup, with a notable decrease in CLRB observed with increasing DFP levels. However, in POSEIDON Group 4, no significant differences in CCPR and CLRB were found between the groups. Logistic regression analysis identified age and the No. of oocytes retrieved as pivotal factors influencing CLRB in Group 4. Conclusion For patients in POSEIDON Group 3, maintaining a DFP ≤ 40 mm is crucial to achieve optimal laboratory and pregnancy outcomes by avoiding delayed triggering. However, for patients in POSEIDON Group 4, age remains a critical factor influencing CLRB regardless of DFP, although a higher No. of oocytes retrieved and available embryos with DFP ≤ 40 is beneficial.

Abstract Purpose To investigate the impact of antibiotic treatment for chronic endometritis (CE) on the pregnancy outcome of frozen-thawed embryo transfer (FET) cycles and the relevant clinical risk factors associated with CE. Methods A retrospective cohort analysis was conducted on 1352 patients who underwent hysteroscopy and diagnostic curettage at Nanjing Maternal and Child Health Hospital from July 2020 to December 2021. All patients underwent CD138 immunohistochemical (IHC) testing to diagnose CE, and a subset of them underwent FET after hysteroscopy. Patient histories were collected, and reproductive prognosis was followed up. Results Out of 1088 patients, 443 (40.7%) were diagnosed with CE. Univariate and multivariate binary logistic regression analyses revealed that parity ≥ 2, a history of ectopic pregnancy, moderate-to-severe dysmenorrhea, hydrosalpinx, endometrial polyps, a history of ≥ 2 uterine operations, and RIF were significantly associated with an elevated risk of CE (P 0.05). Conclusion Infertile patients with a history of parity ≥ 2, hydrosalpinx, a history of ectopic pregnancy, moderate-to-severe dysmenorrhea, endometrial polyps, a history of ≥ 2 uterine operations, and RIF are at an increased risk of CE; these patients should be recommended to undergo hysteroscopy combined with CD138 examination before embryo transfer. Antibiotic treatment can improve the reproductive outcomes of FET in patients with CE, especially those with RIF.

ObjectivesProgrammed death-ligand 1 (PD-L1) is the only Food and Drug Administration-approved biomarker for monitoring response to immune checkpoint inhibitor (ICI) therapy in patients with lung adenocarcinoma. Understanding the nuances of molecular phenotypes, clinical attributes, and PD-L1 expression levels in primary and metastatic lung adenocarcinoma may help predict response to therapy and assist in the clinical management of lung adenocarcinoma.MethodsA total of 235 primary and metastatic lesion specimens from patients with non-small cell lung cancer (NSCLC) an institution in Shandong, China were analyzed. PD-L1 expression was assessed by immunohistochemistry using the 22C3 antibody, and the molecular phenotype was determined by next-generation sequencing of 450 genes. The molecular phenotypes of the primary and metastatic lesions were compared.ResultsElevated PD-L1 expression was significantly associated with advanced and metastatic disease (P = 0.001). The distribution of PD-L1 expression varied based on the anatomical location, showing a higher frequency of elevated PD-L1 expression in distal metastases than in the primary tumor. Metastatic lesions exhibited a higher proportion of carcinogenic pathway gene alterations and a greater number of DNA damage-repair pathway gene alterations than the primary lesions. Notably, CDKN2A copy number deletions were more prevalent in metastatic lesions than in primary lesions. Clinical data stemming from research conducted at the Memorial Sloan Kettering Cancer Center revealed an association between the absence of CDKN2A expression and a poorer prognosis in stage I lung adenocarcinoma.ConclusionSamples of metastatic tumors exhibited a higher proportion of elevated PD-L1 expression, a greater number of pathway alterations, and a higher occurrence of CDKN2A copy number deletions than primary samples. This highlights the importance of reinforcing the clinical management and follow-up of patients with CDKN2A deficiency, particularly within the subset of stage I lung adenocarcinoma.

Abstract Importance The first meta-analysis focused only on gonadotropin-releasing hormone (GnRH) antagonists, which helped determine the effect of delay trigger on pregnancy outcomes. Objective To evaluate the impact of delay trigger compared with standard trigger in normal responders undergoing GnRH antagonist protocol in improving pregnancy outcomes. Methods Studies published before April 2023 in PubMed, EMBASE, Cochrane Library, Web of Science, CNKI, Wanfang, VIP and CBM databases were searched. Randomized controlled trials (RCTs) and cohort studies conducted in normal responders reporting the efficacy of delay trigger using GnRH antagonist protocol were included. Data were combined to calculate mean differences (MD) for continuous variables and odd ratios (OR) for categorical variables with their corresponding 95% confidence intervals (CIs). Heterogeneity was assessed using Cochran’s Q test. Results Endpoints, including clinical pregnancy rate (CPR), live birth rate (LBR), the number of oocyte retrievals and embryos, and fertilization rate, were analyzed. Six (6) clinical studies (4 RCTs and 2 cohort studies) with 1,360 subjects were included. The pooled results showed that the number of oocyte retrievals (MD: 1.20, 95% CI: 1.10, 1.30, p

Abstract The Ciona intestinalis voltage-sensing phosphatase (Ci-VSP) is a membrane protein containing a voltage-sensing domain (VSD) that is homologous to VSDs from voltage-gated ion channels responsible for cellular excitability. Previously published crystal structures of Ci-VSD in putative resting and active conformations suggested a helical-screw voltage sensing mechanism in which the S4 helix translocates and rotates to enable exchange of salt-bridge partners, but the microscopic details of the transition between the resting and active conformations remained unknown. Here, by combining extensive molecular dynamics simulations with a recently developed computational framework based on dynamical operators, we elucidate the microscopic mechanism of the resting-active transition at physiological membrane potential. Sparse regression reveals a small set of coordinates that distinguish intermediates that are hidden from electrophysiological measurements. The intermediates arise from a noncanonical helical-screw mechanism in which translocation, rotation, and side-chain movement of the S4 helix are only loosely coupled. These results provide insights into existing experimental and computational findings on voltage sensing and suggest ways of further probing its mechanism.

Abstract Objectives To establish a predictive model for sepsis after percutaneous nephrolithotomy (PCNL) using machine learning to identify high-risk patients and enable early diagnosis and intervention by urologists. Methods A retrospective study including 694 patients who underwent PCNL was performed. A predictive model for sepsis using machine learning was constructed based on 22 preoperative and intraoperative parameters. Results Sepsis occurred in 45 of 694 patients, including 16 males (35.6%) and 29 females (64.4%). Data were randomly segregated into an 80% training set and a 20% validation set via 100-fold Monte Carlo cross-validation. The variables included in this study were highly independent. The model achieved good predictive power for postoperative sepsis (AUC = 0.89, 87.8% sensitivity, 86.9% specificity, and 87.4% accuracy). The top 10 variables that contributed to the model prediction were preoperative midstream urine bacterial culture, sex, days of preoperative antibiotic use, urinary nitrite, preoperative blood white blood cell (WBC), renal pyogenesis, staghorn stones, history of ipsilateral urologic surgery, cumulative stone diameters, and renal anatomic malformation. Conclusion Our predictive model is suitable for sepsis estimation after PCNL and could effectively reduce the incidence of sepsis through early intervention.

Synthetic aperture radar tomography (TomoSAR) can acquire high resolution in height direction by forming a large synthetic aperture along the tomographic direction. Compressed sensing (CS) is widely utilized in TomoSAR imaging to reduce the costs of data sensing. Nevertheless, traditional CS-based algorithms are limited to computational complexity and the nontrivial parameters' tuning. To address such problems, an efficient unfolded deep shrinkage-thresholding network is proposed for TomoSAR imaging in this article. The proposed method adopts convolutional neural network module to learn a generalized nonlinear sparse transformation operator, showing great benefits in exploring the optimal prior. Besides, the hyperparameters of the optimization framework are learned by end-to-end learning mechanism instead of manual-defined, which obviously improves the efficiency of imaging process. Inspired by residual network, the residual learning is introduced to reconstruction blocks of the proposed imaging network, improving the robustness of the network. In addition, the training dataset is constructed from point cloud data based on TomoSAR imaging principles, enhancing the network's ability to extract structural information. Finally, extensive simulation and measured experimental results show the effectiveness of the proposed method, obtaining high-quality imaging results while maintaining high computational efficiency.

Conventional 3-D synthetic aperture radar (SAR) sparse imaging algorithms suffer from degradation in weakly sparse scenes due to their reliance on inherent sparsity. In addition, they are constrained by high computational complexity and parametric tuning. To address these problems, we propose a novel 3-D SAR enhanced imaging network based on swin transformer dubbed SEIS-Net. The proposed algorithm consists of two cascaded stages. The first one focuses on estimating the missing measurement elements by constructing a Unet based on the swin transformer. The second stage aims to recover a high-quality image from the estimated echo matrix. The proposed imaging network is theoretically derived from fast iterative shrinkage-thresholding algorithm optimization framework, where the network weights can be learned from an end-to-end training procedure. Finally, simulations and real-measured experiments are carried out. Both visual and quantitative results demonstrate the superiority of the proposed SEIS-Net over the current state-of-the-art algorithms in reconstructing 3-D images from sparsely sampled echoes.

Abstract Regulatory T cells (Tregs) are a key determinant for the immunosuppressive and premetastatic niche for cancer progression after surgery resection. However, the precise mechanisms regulating Tregs function during surgical stress-facilitated cancer metastasis remain unknown. This study aims to unravel the mechanisms and explore potential strategies for preventing surgical stress-induced metastasis by targeting NEDD8. Using a surgical stress mouse model, we found that surgical stress results in the increased expression of NEDD8 in Tregs. NEDD8 depletion abrogates postoperative lung metastasis of colon cancer cells by inhibiting Treg immunosuppression and thereby partially recovering CD8+T cell and NK cell-mediated anti-tumor immunity. Furthermore, Treg mitophagy and mitochondrial respiration exacerbated in surgically stressed mice were attenuated by NEDD8 depletion. Our observations suggest that cancer progression may result from surgery-induced enhancement of NEDD8 expression and the subsequent immunosuppressive function of Tregs. More importantly, depleting or inhibiting NEDD8 can be an efficient strategy to reduce cancer metastasis after surgery resection by regulating the function of Tregs.

Abstract Background Endostar is a strong angiogenesis inhibitor that is effective in treating non-small cell lung cancer (NSCLC), but the effect of Endostar in the treatment of patients with EGFR-TKI-resistant NSCLC remains unclear. We evaluated the clinical efficacy and safety of Endostar in EGFR-mutant NSCLC patients resistant to EGFR inhibition treatment. Methods From January 1, 2016 to June 30, 2018, 68 patients were selected from the 4 institutions for the study. Patients with NSCLC received Endostar plus chemotherapy every 21-day cycle. Chemotherapy types included platinum-containing dual drugs and platinum-free single drugs. Endostar was administered by intermittent intravenous infusion or continuous microinfusion pump infusion. The overall response rate (ORR), disease control rate (DCR) and adverse events were analyzed. Survival of patients was also evaluated. Results For all patients, the median progression-free survival (PFS) was 2.8 months, and the median overall survival (OS) was 14.2 months. PFS and OS in the Endostar pump continuous group were better than those in the Endostar intravenous infusion group. The disease control rate (DCR) was 79.4%. A total of 28 (41.2%) patients experienced varying grades of adverse events during treatment. No treatment-associated deaths were observed. The grade 3 treatment-emergent adverse events (TEAEs) were myelosuppression, weakness, and nausea/vomiting. Conclusions Endostar was effective and well tolerated in advanced NSCLC patients. Endostar treatment showed promising survival results in EGFR-mutant NSCLC patients.

DNA is highly vulnerable to spontaneous and environmental timely damage in living cells. DNA damage may cause genetic instability and increase cancer risk if the damages are not repaired timely and efficiently. Human cells possess several DNA damage response (DDR) mechanisms to protect the integrity of their genome. Clarification of the mechanisms underlying the DNA damage response following lethal damage will facilitate the identification of therapeutic targets for cancers. Histone post-translational modifications (PTMs) have been indicated to play different roles in the repair of DNA damage. In this context, histone PTMs regulate recruitment of downstream effectors, and facilitate appropriate repair response. This review outlines the current understanding of different histone PTMs in response to DNA damage repair, besides, enumerates the role of new type PTMs such as histone succinylation and crotonylation in regulating DNA damage repair processes.