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Search Results: 1 - 10 of 176657 matches for " YANG Hai-li "
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南极超微细菌ANT52(Alteromonas stellipolaris)外膜蛋白和脂多糖的提取物对黑鲷的免疫活性研究

WANG Hai-Li,YANG Ji-Fang,

海洋与湖沼 , 2009,
Abstract: The immunity competence of Acanthopagrus schlegeli was studied by injecting with crude outer membrane protein (OMP) and lippolysacchride (LPS) extracted from Antarctic ultramicrobacteria ANT52 (Alteromonas stellipolaris) in different combinations. Four parameters: the phagocytic activity of leucocytes in blood, and the activities of lysozme, antibacteria, and phenoloxidase in serum of immunized fish, being used to represent the non-specific immunogenicity, were determined in 1, 7, 14, 21, 28, and 35 days after the injection. The results showed that the four parameters rose significantly during the experimental period (P<0.05). These parameters of single OMP or LPS treatment group were greater than those injected with OMP+LPS combination treatment group; and reached peak value in 28 days post vaccination. It indicates that immunization with OMP and LPS of ANT52 could stimulate and enhance the function of non-specific immunity of A. schlegeli. Future studies are needed to understand the mechanism of the immunity competence.
Estrification of Acetic Acid with Isoamyl Alcohol over Expandable Graphite Catalyst
Xiu-Yan Pang,Pu Lv,Yi-Shuang Yang,Hai-Li Ren
Journal of Chemistry , 2008, DOI: 10.1155/2008/941953
Research Progress in Photodynamic Therapy for Peri-implantitis.

杨海丽, 邹海啸, 宋莉
YANG Hai-li
, ZOU Hai-xiao, SONG Li

- , 2018, DOI: 10.13701/j.cnki.kqyxyj.2018.05.002
Abstract: 摘要 种植体周围炎是牙种植术后常见的并发症之一,是造成种植体松动、脱落的主要原因。它是一种以厌氧微生物感染为主的疾病,其治疗手段包括非手术和手术治疗,但均存在一些缺陷和不足。20世纪90年代以来,光动力疗法(photodynamic therapy, PDT)为种植体周围炎的治疗提供新的选择,日益受到广大牙周科医师的青睐。本文对目前PDT治疗种植体周围炎的进展进行综述,旨在为临床医生采用PDT治疗种植体周围炎提供参考
Combination of Taxanes, Cisplatin and Fluorouracil as Induction Chemotherapy for Locally Advanced Head and Neck Cancer: A Meta-Analysis
Hao Qin, Jie Luo, Yuan-Ping Zhu, Hai-Li Xie, Wei-Qiang Yang, Wen-Bin Lei
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0051526
Abstract: Background Some investigations have suggested that induction chemotherapy with a combination of taxanes, cisplatin and fluorouracil (TPF) is effective in locally advanced head and neck cancer. However, other trials have indicated that TPF does not improve outcomes. The objective of this study was to compare the efficacy and safety of TPF with a cisplatin and fluorouracil (PF) regimen through a meta-analysis. Methods Four randomized clinical trials were identified, which included 1,552 patients with locally advanced head and neck cancer who underwent induction chemotherapy with either a TPF or PF protocol. The outcomes included the 3-year survival rate, overall response rate and different types of adverse events. Risk ratios (RRs) and their 95% confidence intervals (CIs) were pooled using RevMan 5.1 software. Results The 3-year survival rate (51.0% vs. 42.4%; p = 0.002), 3-year progression-free survival rate (35.9% vs. 27.2%; p = 0.007) and overall response to chemotherapy (72.9% vs. 62.1%; p<0.00001) of the patients in the TPF group was statistically superior to those in the PF group. In terms of toxicities, the incidence of febrile neutropenia (7.0% vs. 3.2%; p = 0.001) and alopecia (10.8% vs. 1.1%; p<0.00001) was higher in the TPF group. Conclusion The TPF induction chemotherapy regimen leads to a significant survival advantage with acceptable toxicity rates for patients with locally advanced head and neck cancer compared with the PF regimen.
Effect and Mechanism of Propranolol on Proliferation, Migration, and Angiogenesis of Human Melanoma A375 cells

邹海啸, 杨海丽, 赵怡芳, 宋莉
ZOU Hai-xiao
, YANG Hai-li, ZHAO Yi-fang, SONG Li

- , 2018, DOI: 10.13701/j.cnki.kqyxyj.2018.02.008
Abstract: 摘要 目的:探讨普萘洛尔对人黑色素瘤A375细胞增殖、迁移和促血管生成能力的影响和机制。方法:将1、5、10、20 μmol/L普萘洛尔作用于体外培养的A375细胞,MTT法检测普萘洛尔对A375细胞增殖能力的影响;细胞划痕实验测定普萘洛尔对A375细胞的迁移能力的影响;小管形成实验评估普萘洛尔对A375细胞促血管生成能力的影响;RT-PCR和 Western bolt分别检测普萘洛尔对A375细胞VEGF、MMP-9、CXCR4 mRNA 和蛋白表达的影响。结果:与对照组相比,普萘洛尔对A375细胞的增殖能力无显著性抑制,呈浓度依赖性抑制A375细胞的迁移能力和促血管生成能力,并且可显著性下调A375细胞中VEGF、MMP-9、CXCR4 mRNA 和蛋白的表达(P<0.01) 。结论:普萘洛尔可能通过下调VEGF、MMP-9和CXCR4的表达发挥抑制A375细胞的迁移和促血管生成能力的作用
Aggressive Fibromatosis in Infratemporal Fossa: Three Cases Report.

邹海啸, 杨海丽, 刘明军, 宋莉
ZOU Hai-xiao
, YANG Hai-li, LIU Ming-jun, SONG Li

- , 2018, DOI: 10.13701/j.cnki.kqyxyj.2018.05.027
Abstract: 摘要 目的:报道颞下窝侵袭性纤维瘤病的临床表现、病理特征、治疗方式及预后。方法:回顾3例颞下窝侵袭性纤维瘤病的临床资料并复习文献。结果:颞下窝的侵袭性纤维瘤病以浸润性生长、局部易复发及无远处转移为特点,临床症状为疼痛、张口困难,治疗以手术切除为主。结论:颞下窝侵袭性纤维瘤常无法完整切除,术后需补充放疗
2 株南极海洋寡营养细菌(Alteromonas stellipolaris)脂多糖对三疣梭子蟹(Portunus trituberculatus) 非特异性免疫活性的影响

YANG Ji-Fang,GUO Lu-Yun,CHEN Fu-Sheng,WANG Hai-Li,

海洋与湖沼 , 2011,
Abstract: The indices of non-specific immunity were measured in 3, 6, 9, 12 days after Portunus trituberculatus was treated with lipopolysaccharides (LPS) extracted from two Antarctic ultramicro-bacteria Alteromonas stellipolaris, AT52 and AT82. The results showed those LPS were able to improve the activities of anti-bacteria, lysozme (LSZ), phenoloxidase (PO), superoxide dismutase (SOD), and peroxidase (POD) significantly (P<0.05). A variety of enzyme activities reached maximum levels at different days, and AT82 LPS injection group was found better than those of AT52 LPS injection group. Our studies suggested LPS of Antarctic ultramicro-bacteria is a desirable potential immunologic stimulant for P. trituberculatus to fight for bacterial diseases. Future studies are needed to understand the mechanism of the immunity response and the best dosage for these LPS.

HE Chun-yang,ZHOU Hai-li,YU Zhang-tao,ZHANG Qing-tao,

资源科学 , 2002,
Abstract: Regional land use/cover change has gained increasing concerns within land use/cover research literatures. Regional land use/cover information processing supported by "3S" technology is becoming the precondition of further quantitative research of regional land use/cover. From the perspective of information flow and method, a notional scheme of regional land use/cover information processing is developed in this paper, firstly. And then relevant methods of the scheme is introduced and summarized, aimed at offering help for current research of regional land use/cover change.
Fibrillization of Human Tau Is Accelerated by Exposure to Lead via Interaction with His-330 and His-362
Hai-Li Zhu, Sheng-Rong Meng, Jun-Bao Fan, Jie Chen, Yi Liang
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0025020
Abstract: Background Neurofibrillary tangles, mainly consisted of bundles of filaments formed by the microtubule-associated protein Tau, are a hallmark of Alzheimer disease. Lead is a potent neurotoxin for human being especially for the developing children, and Pb2+ at high concentrations is found in the brains of patients with Alzheimer disease. However, it has not been reported so far whether Pb2+ plays a role in the pathology of Alzheimer disease through interaction with human Tau protein and thereby mediates Tau filament formation. In this study, we have investigated the effect of Pb2+ on fibril formation of recombinant human Tau fragment Tau244–372 and its mutants at physiological pH. Methodology/Principal Findings As revealed by thioflavin T and 8-anilino-1-naphthalene sulfonic acid fluorescence, the addition of 5–40 μM Pb2+ significantly accelerates the exposure of hydrophobic region and filament formation of wild-type Tau244–372 on the investigated time scale. As evidenced by circular dichroism and Fourier transform infrared spectroscopy, fibrils formed by wild-type Tau244–372 in the presence of 5–40 μM Pb2+ contain more β-sheet structure than the same amount of fibrils formed by the protein in the absence of Pb2+. However, unlike wild-type Tau244–372, the presence of 5–40 μM Pb2+ has no obvious effects on fibrillization kinetics of single mutants H330A and H362A and double mutant H330A/H362A, and fibrils formed by such mutants in the absence and in the presence of Pb2+ contain similar amounts of β-sheet structure. The results from isothermal titration calorimetry show that one Pb2+ binds to one Tau monomer via interaction with His-330 and His-362, with sub-micromolar affinity. Conclusions/Significance We demonstrate for the first time that the fibrillization of human Tau protein is accelerated by exposure to lead via interaction with His-330 and His-362. Our results suggest the possible involvement of Pb2+ in the pathogenesis of Alzheimer disease and provide critical insights into the mechanism of lead toxicity.
Involvement of lysophosphatidic acid in bone cancer pain by potentiation of TRPV1 via PKC? pathway in dorsal root ganglion neurons
Hai-Li Pan, Yu-Qiu Zhang, Zhi-Qi Zhao
Molecular Pain , 2010, DOI: 10.1186/1744-8069-6-85
Abstract: Bone cancer was established by injection of mammary gland carcinoma cells into the rat tibia. Following the development of bone cancer pain, the TRPV1 expression and capsaicin-evoked currents were up-regulated in rat DRG neurons at L4-6 segments. Immunohistochemistry staining revealed a high co-localization of LPA1 with TRPV1 in DRG neurons. In isolated DRG neurons, whole-cell patch recording showed that capsaicin-induced currents were potentiated by LPA in a dose-dependent manner. The potentiation was blocked by either LPA1 antagonist, protein kinase C (PKC) inhibitor or PKC? inhibitor, but not by protein kinase A (PKA) inhibitor or Rho inhibitor. In the behavioral tests, both mechanical allodynia and thermal hyperalgesia in bone cancer rats were attenuated by LPA1 antagonist.LPA potentiates TRPV1 current via a PKC?-dependent pathway in DRG neurons of rats with bone cancer, which may be a novel peripheral mechanism underlying the induction of bone cancer pain.Pain is the first clinical symptom of cancer in a large population of cancer patients, particularly in advanced or terminal cancer patients [1], which strongly impacts the patients' quality of life. Tumor-derived, inflammatory, and neuropathic factors may simultaneously contribute to cancer pain such as bone cancer pain [2].Lysophosphatidic acid (LPA) is a lipid metabolite released after tissue injury, which induces diverse cellular responses including proliferation, adhesion, migration, morphogenesis, differentiation and survival [3]. Increasing evidence shows that LPA is a key mediator in cancer development including cancer cell proliferation, survival and migration [4-7]. There is a high concentration of LPA in ascitic fluid and plasma of cancer patients. Released by activated blood platelets [8], LPA promotes progression of bone metastases by inducing secretion of tumor-derived cytokine (IL-6 and IL-8) in breast and ovarian cancer cells [9,10]. Additionally, lines of study have revealed that LPA may also b
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