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NES1/KLK10 and hNIS gene therapy enhanced iodine-131 internal radiation in PC3 proliferation

Jiajia Hu, Wenbin Shen, Qian Qu, Xiaochun Fei, Ying Miao, Xinyun Huang, Jiajun Liu, Yingli Wu, Biao Li

《医学前沿（英文）》 2019年 第13卷 第6期   页码 646-657 doi: 10.1007/s11684-018-0643-y

摘要： gene is thought to be a tumor-suppressor gene. Our previous study found that overexpression of gene in PC3 cell line could slow down the tumor proliferation rate, associated with a mild decrease in expression. The decrease could increase the sensitivity of radiotherapy to tumors. Thus, we supposed to have an “enhanced firepower” effect by combining overexpressed gene therapy and I radiation therapy uptake by overexpressed hNIS protein. We found a weak endogenous expression of hNIS protein in PC3 cells and demonstrated that the low expression of hNIS protein in PC3 cells might be the reason for the low iodine uptake. By overexpressing in PC3, the radioactive iodine uptake ability was significantly increased. Results of and tumor proliferation experiments and F-fluorothymidine ( F-FLT) micro-positron emission tomography/computed tomography (micro-PET/CT) imaging showed that the combined gene therapy and I radiation therapy mediated by overexpressed hNIS protein had the best tumor proliferative inhibition effect. Immunohistochemistry showed an obvious decrease of expression and the lowest expression. These data suggest that via inhibition of expression, overexpressed might enhance the effect of radiation therapy of I uptake in overexpressed PC3 cells.

关键词： androgen-independent prostate cancer     normal epithelial cell-specific 1/kallikrein 10     sodium/iodide symporter     radiation therapy     proliferation    

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Genomic variations in the counterpart normal controls of lung squamous cell carcinomas

null

《医学前沿（英文）》 2018年 第12卷 第3期   页码 280-288 doi: 10.1007/s11684-017-0580-1

摘要：

Lung squamous cell carcinoma (LUSC) causes approximately 400 000 deaths each year worldwide. The occurrence of LUSC is attributed to exposure to cigarette smoke, which induces the development of numerous genomic abnormalities. However, few studies have investigated the genomic variations that occur only in normal tissues that have been similarly exposed to tobacco smoke as tumor tissues. In this study, we sequenced the whole genomes of three normal lung tissue samples and their paired adjacent squamous cell carcinomas. We then called genomic variations specific to the normal lung tissues through filtering the genomic sequence of the normal lung tissues against that of the paired tumors, the reference human genome, the dbSNP138 common germline variants, and the variations derived from sequencing artifacts. To expand these observations, the whole exome sequences of 478 counterpart normal controls (CNCs) and paired LUSCs of The Cancer Genome Atlas (TCGA) dataset were analyzed. Sixteen genomic variations were called in the three normal lung tissues. These variations were confirmed by Sanger capillary sequencing. A mean of 0.5661 exonic variations/Mb and 7.7887 altered genes per sample were identified in the CNC genome sequences of TCGA. In these CNCs, C:G→T:A transitions, which are the genomic signatures of tobacco carcinogen N-methyl-N-nitro-N-nitrosoguanidine, were the predominant nucleotide changes. Twenty five genes in CNCs had a variation rate that exceeded 2%, including ARSD (18.62%), MUC4 (8.79%), and RBMX (7.11%). CNC variations in CTAGE5 and USP17L7 were associated with the poor prognosis of patients with LUSC. Our results uncovered previously unreported genomic variations in CNCs, rather than LUSCs, that may be involved in the development of LUSC.

关键词： lung cancer     counterpart normal control     genomic variations    

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Epithelial-to-mesenchymal transition in cancer: complexity and opportunities

Yun Zhang, Robert A. Weinberg

《医学前沿（英文）》 2018年 第12卷 第4期   页码 361-373 doi: 10.1007/s11684-018-0656-6

摘要：

The cell-biological program termed the epithelial-to-mesenchymal transition (EMT) plays an important role in both development and cancer progression. Depending on the contextual signals and intracellular gene circuits of a particular cell, this program can drive fully epithelial cells to enter into a series of phenotypic states arrayed along the epithelial-mesenchymal phenotypic axis. These cell states display distinctive cellular characteristics, including stemness, invasiveness, drug-resistance and the ability to form metastases at distant organs, and thereby contribute to cancer metastasis and relapse. Currently we still lack a coherent overview of the molecular and biochemical mechanisms inducing cells to enter various states along the epithelial-mesenchymal phenotypic spectrum. An improved understanding of the dynamic and plastic nature of the EMT program has the potential to yield novel therapies targeting this cellular program that may aid in the management of high-grade malignancies.

关键词： epithelial-to-mesenchymal transition     cancer     metastasis     cancer stem cell    

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Effect of IL-10 on formation of foam cell induced by ox-LDL

WANG Fei, DAI Yalei, XU Ting, XU Bo, WANG Kaifeng

《医学前沿（英文）》 2008年 第2卷 第3期   页码 298-302 doi: 10.1007/s11684-008-0057-3

摘要： Atherosclerosis is a chronic disease that causes various cardiovascular complications. It has been realized that cellular and humoral immunity plays crucial roles in atherogenic lesion formation. In this study the effects of lipopolysaccharide (LPS) and interleukin-10 (IL-10) on the formation of foam cells during the early stages of atherosclerosis have been investigated. Macrophage was induced by phorbol myristate acetate (PMA) treatment on THP-1 cells. The cells were further stimulated by ox-LDL, ox-LDL plus LPS, ox-LDL plus IL-10 and LPS. By using an oil red O staining technique, the formation of foam cells was evaluated by lipid granules formation in the cells. The ratio of foam cell formation was increased from (9.77 ± 1.70)% to (16.27 ± 2.27)% after 24 h stimulation with ox-LDL, and the increase was observed with incubating time. The foam cells were significantly increased in the presence of LPS in a dose-dependent manner. The maximum increase of about 40% was observed. However, the significant elevation by LPS was abrogated when IL-10 was added. These results indicated that IL-10 can effectively prevent the formation of foam cells induced by ox-LDL with or without LPS. This study demonstrates that ox-LDL can cause foam cell formation from macrophages . LPS can significantly accelerate this event. IL-10, an anti-inflammatory cytokine, can inhibit the effect of ox-LDL and LPS. These results indicate that inflammatory effects in blood vessels can speed up foam cell formation. The inhibitive effect of IL-10 is an important factor for delaying atherosclerosis processes.

关键词： inflammatory     presence     interleukin-10     dose-dependent     ox-LDL    

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Intestinal Epithelial Axin1 Deficiency Protects Against Colitis via Altered Gut Microbiota

Shari Garrett,Yongguo Zhang,Yinglin Xia,Jun Sun,

《工程（英文）》 doi: 10.1016/j.eng.2023.06.007

摘要： Intestinal homeostasis is maintained by specialized host cells and the gut microbiota. Wnt/β-catenin signaling is essential for gastrointestinal development and homeostasis, and its dysregulation has been implicated in inflammation and colorectal cancer. Axin1 negatively regulates activated Wnt/β-catenin signaling, but little is known regarding its role in regulating host–microbial interactions in health and disease. Here, we aim to demonstrate that intestinal Axin1 determines gut homeostasis and host response to inflammation. Axin1 expression was analyzed in human inflammatory bowel disease datasets. To explore the effects and mechanism of intestinal Axin1 in regulating intestinal homeostasis and colitis, we generated new mouse models with Axin1 conditional knockout in intestinal epithelial cell (IEC; Axin1ΔIEC) and Paneth cell (PC; Axin1ΔPC) to compare with control (Axin1LoxP; LoxP: locus of X-over, P1) mice. We found increased Axin1 expression in the colonic epithelium of human inflammatory bowel disease (IBD). Axin1ΔIEC mice exhibited altered goblet cell spatial distribution, PC morphology, reduced lysozyme expression, and enriched Akkermansia muciniphila (A. muciniphila). The absence of intestinal epithelial and PC Axin1 decreased susceptibility to dextran sulfate sodium-induced colitis in vivo. Axin1ΔIEC and Axin1ΔPC mice became more susceptible to dextran sulfate sodium (DSS)-colitis after cohousing with control mice. Treatment with A. muciniphila reduced DSS-colitis severity. Antibiotic treatment did not change the IEC proliferation in the Axin1Loxp mice. However, the intestinal proliferative cells in Axin1ΔIEC mice with antibiotic treatment were reduced compared with those in Axin1ΔIEC mice without treatment. These data suggest non-colitogenic effects driven by the gut microbiome. In conclusion, we found that the loss of intestinal Axin1 protects against colitis, likely driven by epithelial Axin1 and Axin1-associated A. muciniphila. Our study demonstrates a novel role of Axin1 in mediating intestinal homeostasis and the microbiota. Further mechanistic studies using specific Axin1 mutations elucidating how Axin1 modulates the microbiome and host inflammatory response will provide new therapeutic strategies for human IBD.

关键词： Axin1     Bacteria     Microbiome inflammation     Inflammatory bowel disease     Immunity     Microbiome     Paneth cells     Akkermansia muciniphila     Wnt    

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Innate immune checkpoint Siglec10 in cancers: mining of comprehensive omics data and validation in patient

《医学前沿（英文）》 2022年 第16卷 第4期   页码 596-609 doi: 10.1007/s11684-021-0868-z

摘要： Sialic acid binding Ig-like lectin 10 (Siglec10) is a member of innate immune checkpoints that inhibits the activation of immune cells through the interaction with its ligand CD24 on tumor cells. Here, by analyzing public databases containing 64 517 patients of 33 cancer types, we found that the expression of Siglec10 was altered in 18 types of cancers and was associated with the clinical outcomes of 11 cancer types. In particular, Siglec10 was upregulated in patients with kidney renal clear cell carcinoma (KIRC) and was inversely associated with the prognosis of the patients. In 131 KIRC patients of our settings, Siglec10 was elevated in the tumor tissues of 83 (63.4%) patients compared with that in their counterpart normal kidney tissues. Moreover, higher level of Siglec10 was associated with advanced disease (stages III and IV) and worse prognosis. Silencing of CD24 in KIRC cells significantly increased the number of Siglec10-expressing macrophages phagocytosing KIRC cells. In addition, luciferase activity assays suggested that Siglec10 was a potential target of the transcription factors c-FOS and GATA1, which were identified by data mining. These results demonstrate that Siglec10 may have important oncogenic functions in KIRC, and represents a novel target for the development of immunotherapies.

关键词： innate immune checkpoint     Siglec10     kidney renal clear cell carcinoma    

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基于表位定向细胞库筛选高亲和力PD-1突变体诱骗分子 Article

刘昊, 乔春霞, 胡乃静, 王志宏, 王晶, 冯健男, 沈倍奋, 马远方, 罗龙龙

《工程（英文）》 2021年 第7卷 第11期   页码 1557-1565 doi: 10.1016/j.eng.2020.11.011

摘要：

抗程序性细胞死亡蛋白-1（programmed cell death protein-1,PD-1）/程序性细胞死亡配体-1（programmed cell death ligand-1, PD-L1）单克隆抗体的免疫疗法已成为治疗肺癌、肠癌和黑色素瘤等多种癌症的常规方法。PD-1/PD-L1信号通路在肿瘤微环境中可抑制T细胞活化，使其成为一个热门的抗癌靶点。野生型（wild type, WT）PD-1胞外结构域由于亲和力低而难以阻断PD-1/PD-L1复合物的形成。在MC38转基因小鼠模型中，463可有效逆转PD-1对T细胞活化的抑制作用，而且10 mg·kg−1的463突变体蛋白对肿瘤生长的抑制率约为75%，与同等剂量下更有趣的是，低剂量的463（2 mg·kg−1）显示出比10 mg·kg−1的野生型PD-1更好的抑瘤效果

关键词： 诱饵程序性细胞死亡蛋白-1     程序性细胞死亡配体-1     哺乳动物细胞文库     表位定向    

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Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP

Lihui WANG, Lianhong LI, Shen LV, Shujun FAN, Li ZHAN, Bo WANG, Zhong ZHANG

《医学前沿（英文）》 2009年 第3卷 第2期   页码 164-170 doi: 10.1007/s11684-009-0038-1

摘要： The invasion and metastasis of breast cancer are supposed to involve several stages in which epithelial-mesenchymal transition (EMT) is regarded as the mechanistic basis for the behavior of cancer cells. A series of factors related to EMT are apparently involved in such process. The current study aimed to investigate the contributions of EMT and related factors in lymph node metastasis of breast cancer. The expressions of E-cadherin (E-Cad), N-cadherin (N-Cad), vascular endothelial cell growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), cyclooxygenase-2 (COX-2), and CD34 were examined in 74 cases of breast cancer, including 39 cases with lymph node metastasis and 35 cases without lymph node metastasis by immunohistochemistry. Multivariable Cox proportional hazards model was used to analyze the patients’ prognosis. The expressions of N-Cad, VEGF, MMP-9, and COX-2 in cases with lymph node metastasis were significantly higher than those without lymph node metastasis ( <0.05), while the E-Cad level was inversely related to status of lymph node metastasis ( <0.05). The metastasis rate of lymph node in the cases with EMT (lower E-Cad expression and higher N-Cad expression) was 78.3%, while that without EMT (higher E-Cad expression and lower N-Cad expression) was 11.1%. There was a statistical difference in the expression of COX-2 protein between histological grade I and grade II or III, respectively ( <0.05). In the cases with higher grade, the expression of E-Cad was decreased, while that of N-Cad was increased. Higher microvascular density (MVD) was also found to be significantly associated with lymphatic metastasis ( <0.05), and the cases with higher MVD had shorter survival time. This study indicates that EMT and expressions of VEGF, MMP-9 and COX-2, and MVD value are strongly correlated with lymph node metastasis in breast cancer.

关键词： epithelial-mesenchymal transition     vascular endothelial cell growth factor     matrix metalloproteinase-9     cyclooxygenase-2     higher microvascular density     breast cancer    

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以“功能”储备补足“资源”储备——甲醇战略储备替代1/10~1/5的石油战略储备

金涌,陈丙珍

《中国工程科学》 2008年 第10卷 第11期   页码 4-6

摘要： 对于中国而言，这就需要战略储备石油3×107~9×107 t，这需要一个长时间段和大量资金注入才能完成。

关键词： 功能储备     战略石油储备     甲醇    

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车用燃料电池电堆比功率提升的技术途径探讨

侯明,邵志刚,衣宝廉

《中国工程科学》 2019年 第21卷 第3期   页码 84-91 doi: 10.15302/J-SSCAE-2019.03.002

摘要：

燃料电池车作为新能源汽车的一种，以其续驶里程长、动力性能高、燃料加注快、兼容可再生能源等特点，得到愈来愈广泛的重视。燃料电池堆是燃料电池汽车的核心，其比功率是反应燃料电池堆技术水平的重要指标，掌握高比功率燃料电池电堆技术可以降低电堆硬件数量，从而也会使电堆成本得到大幅降低。国际上先进的燃料电池堆由于具有高的比功率使其在车辆有限空间能提供较大功率，满足了车辆动力需求；然而，国内目前电堆比功率相比国际先进水平还有一定差距，针对这一问题，本文从高活性催化剂、增强复合质子交换膜、高扰动流场、导电耐腐蚀薄金属双极板、电堆组装与一致性等多方面，探讨了提高燃料电池电堆比功率的技术途径，基于理论与实践积累分析了燃料电池活化极化、欧姆极化及传质极化与材料、部件、组装的关联性，为进一步提高燃料电池堆性能与比功率提供方向性参考。

关键词： 燃料电池车     燃料电池电堆     性能     比功率    

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Application of StrucGP in medical immunology: site-specific -glycoproteomic analysis of macrophages

《医学前沿（英文）》 2023年 第17卷 第2期   页码 304-316 doi: 10.1007/s11684-022-0964-8

摘要： The structure of N-glycans on specific proteins can regulate innate and adaptive immunity via sensing environmental signals. Meanwhile, the structural diversity of N-glycans poses analytical challenges that limit the exploration of specific glycosylation functions. In this work, we used THP-1-derived macrophages as examples to show the vast potential of a N-glycan structural interpretation tool StrucGP in N-glycoproteomic analysis. The intact glycopeptides of macrophages were enriched and analyzed using mass spectrometry (MS)-based glycoproteomic approaches, followed by the large-scale mapping of site-specific glycan structures via StrucGP. Results revealed that bisected GlcNAc, core fucosylated, and sialylated glycans (e.g., HexNAc4Hex5Fuc1Neu5Ac1, N4H5F1S1) were increased in M1 and M2 macrophages, especially in the latter. The findings indicated that these structures may be closely related to macrophage polarization. In addition, a high level of glycosylated PD-L1 was observed in M1 macrophages, and the LacNAc moiety was detected at Asn-192 and Asn-200 of PD-L1, and Asn-200 contained Lewis epitopes. The precision structural interpretation of site-specific glycans and subsequent intervention of target glycoproteins and related glycosyltransferases are of great value for the development of new diagnostic and therapeutic approaches for different diseases.

关键词： macrophage     glycoproteome     glycopeptides     N-glycan structures     PD-L1    

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Annexin A2-S100A10 heterotetramer is upregulated by PML/RARα fusion protein and promotes plasminogen-dependent

null

《医学前沿（英文）》 2017年 第11卷 第3期   页码 410-422 doi: 10.1007/s11684-017-0527-6

摘要：

Aberrant expression of annexin A2-S100A10 heterotetramer (AIIt) associated with PML/RARα fusion protein causes lethal hyperfibrinolysis in acute promyelocytic leukemia (APL), but the mechanism is unclear. To facilitate the investigation of regulatory association between ANXA2 and promyelocytic leukemia/retinoic acid receptor a (PML/RARα) fusion protein, this work was performed to determine the transcription start site of ANXA2 promoter with rapid amplification of 5′-cDNA ends analysis. Zinc-induced U937/PR9 cells expressed PML/RARα fusion protein, and resultant increases in ANXA2 transcripts and translational expressions of both ANXA2 and S100A10, while S100A10 transcripts remained constitutive. The transactivation of ANXA2 promoter by PML/RARα fusion protein was 3.29±0.13 fold higher than that by control pSG5 vector or wild-type RARα. The overexpression of ANXA2 in U937 transfected with full-length ANXA2 cDNA was associated with increased S100A10 subunit, although S100A10 transcripts remained constitutive. The tPA-dependent initial rate of plasmin generation (IRPG) in zinc-treated U937/PR9 increased by 2.13-fold, and cell invasiveness increased by 27.6%. Antibodies against ANXA2, S100A10, or combination of both all remarkably inhibited the IRPG and invasiveness in U937/PR9 and NB4. Treatment of zinc-induced U937/PR9 or circulating APL blasts with all-trans retinoic acid (ATRA) significantly reduced cell surface ANXA2 and S100A10 and associated reductions in IRPG and invasiveness. Thus, PML/RARα fusion protein transactivated the ANXA2 promoter to upregulate ANXA2 and accumulate S100A10. Increased AIIt promoted IRPG and invasiveness, both of which were partly abolished by antibodies against ANXA2 and S100A10 or by ATRA.

关键词： annexin A2-S100A10 heterotetramer     PML/RARα fusion protein     plasmin     cell invasion     acute promyelocytic leukemia    

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Comparison of human nasal epithelial cells grown as explant outgrowth cultures or dissociated tissue

null

《医学前沿（英文）》 2013年 第7卷 第4期   页码 486-491 doi: 10.1007/s11684-013-0287-x

摘要：

The purpose of this study was to compare cell growth characteristics, ciliated cell differentiation, and function of human nasal epithelial cells established as explant outgrowth cultures or dissociated tissue cultures. Human nasal mucosa of the uncinate process was obtained by endoscopy and epithelial cell cultures were established by explant outgrowth or dissociated tissue culture methods. Epithelial cell growth characteristics were observed by inverted phase contrast microscopy. Ciliated cell differentiation was detected by β-tubulin IV and ZO-1 immunocytochemistry. Basal and ATP-stimulated ciliary beat frequency (CBF) was measured using a high-speed digital microscopic imaging system. Both the explant and dissociated tissue cultures established as monolayers with tight junctions and differentiated cell composition, with both types of cultures comprising ciliated and non-ciliated epithelial cells. Fibroblasts were also frequently found in explant cultures but rarely seen in dissociated tissue cultures. In both culture systems, the highest ciliated cell density appeared at 7th–10th culture day and declined with time, with the lifespan of ciliated cells ranging from 14 to 21 days. Overall, 10% of the cells in explant cultures and 20% of the cells in the dissociated tissue cultures were ciliated. These two cultures demonstrated similar ciliary beat frequency values at baseline (7.78±1.99 Hz and 7.91±2.52 Hz, respectively) and reacted equivalently following stimulation with 100 μM ATP. The results of this study indicate that both the explant outgrowth and dissociated tissue culture techniques are suitable for growing well-differentiated nasal ciliated and non-ciliated cells, which have growth characteristics and ciliary activity similar to those of nasal epithelial cells in vivo.

关键词： ciliated cells     ciliary beat frequency     dissociated tissue culture     explant culture     nasal epithelial cells    

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Soluble triggering receptor expressed on myeloid cell-1 (sTREM-1): a potential biomarker for the diagnosis

Changlin Cao, Jingxian Gu, Jingyao Zhang

《医学前沿（英文）》 2017年 第11卷 第2期   页码 169-177 doi: 10.1007/s11684-017-0505-z

摘要： Sensitive and useful biomarkers for the diagnosis and prognosis of infectious diseases have been widely developed. An example of these biomarkers is triggering receptor expressed on myeloid cell-1 (TREM-1), which is a cell surface receptor expressed on monocytes/macrophages and neutrophils. TREM-1 amplifies inflammation by activating the TREM-1/DAP12 pathway. This pathway is triggered by the interaction of TREM-1 with ligands or stimulation by bacterial lipopolysaccharide. Consequently, pro-inflammatory cytokines and chemokines are secreted. Soluble TREM-1 (sTREM-1) is a special form of TREM-1 that can be directly tested in human body fluids and well-known biomarker for infectious diseases. sTREM-1 level can be potentially used for the early diagnosis and prognosis prediction of some infectious diseases, including infectious pleural effusion, lung infections, sepsis, bacterial meningitis, viral infections (e.g., Crimean Congo hemorrhagic fever and dengue fever), fungal infections (e.g., infection), and burn-related infections. sTREM-1 is a more sensitive and specific biomarker than traditional indices, such as C-reactive protein and procalcitonin levels, for these infectious diseases. Therefore, sTREM-1 is a feasible biomarker for the targeted therapy and rapid and early diagnosis of infectious diseases.

关键词： soluble triggering receptor expressed on myeloid cells-1     infectious diseases     diagnosis and prognosis     biomarker    

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Combined gemcitabine and CHK1 inhibitor treatment induces apoptosis resistance in cancer stem cell-likecells enriched with tumor spheroids from a non-small cell lung cancer cell line

null

《医学前沿（英文）》 2013年 第7卷 第4期   页码 462-476 doi: 10.1007/s11684-013-0270-6

摘要：

Evaluating the effects of novel drugs on appropriate tumor models has become crucial for developing more effective therapies that target highly tumorigenic and drug-resistant cancer stem cell (CSC) populations. In this study, we demonstrate that a subset of cancer cells with CSC properties may be enriched into tumor spheroids under stem cell conditions from a non-small cell lung cancer cell line. Treating these CSC-like cells with gemcitabine alone and a combination of gemcitabine and the novel CHK1 inhibitor PF-00477736 revealed that PF-00477736 enhances the anti-proliferative effect of gemcitabine against both the parental and the CSC-like cell populations. However, the CSC-like cells exhibited resistance to gemcitabine-induced apoptosis. Collectively, the spheroid-forming CSC-like cells may serve as a model system for understanding the mechanism underlying the drug resistance of CSCs and for guiding the development of better therapies that can inhibit tumor growth and eradicate CSCs.

关键词： drug resistance     cancer stem cell     checkpoint kinase 1 (CHK1)     PF-00477736     lung cancer     tumorigenicity    

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标题 作者 时间 类型 操作

NES1/KLK10 and hNIS gene therapy enhanced iodine-131 internal radiation in PC3 proliferation

Jiajia Hu, Wenbin Shen, Qian Qu, Xiaochun Fei, Ying Miao, Xinyun Huang, Jiajun Liu, Yingli Wu, Biao Li

期刊论文

Genomic variations in the counterpart normal controls of lung squamous cell carcinomas

null

期刊论文

Epithelial-to-mesenchymal transition in cancer: complexity and opportunities

Yun Zhang, Robert A. Weinberg

期刊论文

Effect of IL-10 on formation of foam cell induced by ox-LDL

WANG Fei, DAI Yalei, XU Ting, XU Bo, WANG Kaifeng

期刊论文

Intestinal Epithelial Axin1 Deficiency Protects Against Colitis via Altered Gut Microbiota

Shari Garrett,Yongguo Zhang,Yinglin Xia,Jun Sun,

期刊论文

Innate immune checkpoint Siglec10 in cancers: mining of comprehensive omics data and validation in patient

期刊论文

基于表位定向细胞库筛选高亲和力PD-1突变体诱骗分子

刘昊, 乔春霞, 胡乃静, 王志宏, 王晶, 冯健男, 沈倍奋, 马远方, 罗龙龙

期刊论文

Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP

Lihui WANG, Lianhong LI, Shen LV, Shujun FAN, Li ZHAN, Bo WANG, Zhong ZHANG

期刊论文

以“功能”储备补足“资源”储备——甲醇战略储备替代1/10~1/5的石油战略储备

金涌,陈丙珍

期刊论文

车用燃料电池电堆比功率提升的技术途径探讨

侯明,邵志刚,衣宝廉

期刊论文

Application of StrucGP in medical immunology: site-specific -glycoproteomic analysis of macrophages

期刊论文

Annexin A2-S100A10 heterotetramer is upregulated by PML/RARα fusion protein and promotes plasminogen-dependent

null

期刊论文

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