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1.
Khachatryan G.E. Mkrtchyan N.I. Simonyan N.V. Khachatryan T.V. Tatikyan S.Sh. 《World journal of microbiology & biotechnology》2000,16(4):393-395
Several strains of aerobic bacteria tolerant to some chemical toxins were isolated from the water of man-made Yerevan Lake and from the soil and air of different regions of the city of Yerevan. Some of these bacteria were capable of degrading 2,4,6-trinitrotoluene (TNT) during shake-flask fermentation in liquid medium. Two bacterial strains with good ability to degrade TNT were isolated. These strains showed visible morphological and physiological differences during growth on numerous elective media. The comparative ability of these strains to transform TNT was investigated. 相似文献
2.
Steve Horvath Abu NM Nazmul-Hossain Rodney PE Pollard Frans GM Kroese Arjan Vissink Cees GM Kallenberg Fred KL Spijkervet Hendrika Bootsma Sara A Michie Sven U Gorr Ammon B Peck Chaochao Cai Hui Zhou David TW Wong 《Arthritis research & therapy》2012,14(6):1-13
Bone tissue has an exceptional quality to regenerate to native tissue in response to injury. However, the fracture repair process requires mechanical stability or a viable biological microenvironment or both to ensure successful healing to native tissue. An improved understanding of the molecular and cellular events that occur during bone repair and remodeling has led to the development of biologic agents that can augment the biological microenvironment and enhance bone repair. Orthobiologics, including stem cells, osteoinductive growth factors, osteoconductive matrices, and anabolic agents, are available clinically for accelerating fracture repair and treatment of compromised bone repair situations like delayed unions and nonunions. Preclinical and clinical studies using biologic agents like recombinant bone morphogenetic proteins have demonstrated an efficacy similar or better than that of autologous bone graft in acute fracture healing. A lack of standardized outcome measures for comparison of biologic agents in clinical fracture repair trials, frequent off-label use, and a limited understanding of the biological activity of these agents at the bone repair site have limited their efficacy in clinical applications. 相似文献
3.
Milica D olovi GM Jankovi RB olovi Vesna M Martinovi-emeriki 《Cancer immunology, immunotherapy : CII》1998,15(4):286-288
A case of primary nonsecretory plasmacytoma of the spleen is reported. On laparotomy and splenectomy a 920 g spleen was removed,
measuring 16×14×6 cm. The cut surface of the entire spleen showed that the tumour occupied most of the splenic tissue. A bone
marrow aspirate and trephine, skeletal survey showed no signs of myeloma. Biopsy of the liver and regional lymph nodes was
normal. Immunocytochemistry of the splenic tumour showed positivity for pan-B and plasma cell markers. After splenectomy the
patient was treated with chemotherapy according to protocol VBCMP (M2). 相似文献
4.
Sebastian Dolff Daniel Quandt Benjamin Wilde Thorsten Feldkamp Fan Hua Xin Cai Christof Specker Andreas Kribben Cees GM Kallenberg Oliver Witzke 《Arthritis research & therapy》2010,12(4):R150
Introduction
There is growing evidence that interleukin 17 (IL-17) producing T cells are involved in the pathogenesis of systemic lupus erythematosus (SLE). Previous studies showed that increased percentages of T-cell subsets expressing the costimulatory molecules CD80 and CD134 are associated with disease activity and renal involvement in SLE. The aim of this study was to investigate the distribution and phenotypical characteristics of IL-17 producing T-cells in SLE, in particular in patients with lupus nephritis, with emphasis on the expression of CD80 and CD134. 相似文献5.
Vandegriff KD Malavalli A Mkrtchyan GM Spann SN Baker DA Winslow RM 《Bioconjugate chemistry》2008,19(11):2163-2170
Hemospan is an acellular hemoglobin-based oxygen therapeutic in clinical trials in Europe and the United States. The product is prepared by site-specific conjugation of maleimide-activated poly(ethylene) glycol (PEG, MW approximately 5500) to human oxyhemoglobin through maleimidation reactions either (1) directly to reactive Cys thiols or (2) at surface Lys groups following thiolation using 2-iminothiolane. The thiolation/maleimidation reactions lead to the addition of approximately 8 PEGs per hemoglobin tetramer. Identification of PEG modified globins by SDS-PAGE and MALDI-TOF reveals a small percentage of protein migrating at the position for unmodified globin chains and the remaining as separate bands representing globin chains conjugated with 1 to 4 PEGs per chain. Identification of PEG modification sites on individual alpha and beta globins was made using reverse-phase HPLC, showing a series of alpha globins conjugated with 0 to 3 PEGs and a series of beta globins conjugated with 0 to 4 PEGs per globin. Mass analysis of tryptic peptides from hemoglobin thiolated and maleimidated with N-ethyl maleimide showed the same potential sites of modification regardless of thiolation reaction ratio, with seven sites identified on beta globins at beta8, beta17, beta59, beta66, beta93, beta95, and beta132 and three sites identified on alpha globins at alpha7, alpha16, and alpha40. 相似文献
6.
H JMP Verhagen D C de Leeuw M GM Roemer F Denkers W Pouwels A Rutten P H Celie G J Ossenkoppele G J Schuurhuis L Smit 《Cell death & disease》2014,5(6):e1300
Despite high remission rates after chemotherapy, only 30–40% of acute myeloid leukemia (AML) patients survive 5 years after diagnosis. This extremely poor prognosis of AML is mainly caused by treatment failure due to chemotherapy resistance. Chemotherapy resistance can be caused by various features including activation of alternative signaling pathways, evasion of cell death or activation of receptor tyrosine kinases such as the insulin growth factor-1 receptor (IGF-1R). Here we have studied the role of the insulin-like growth factor-binding protein-7 (IGFBP7), a tumor suppressor and part of the IGF-1R axis, in AML. We report that IGFBP7 sensitizes AML cells to chemotherapy-induced cell death. Moreover, overexpression of IGFBP7 as well as addition of recombinant human IGFBP7 is able to reduce the survival of AML cells by the induction of a G2 cell cycle arrest and apoptosis. This effect is mainly independent from IGF-1R activation, activated Akt and activated Erk. Importantly, AML patients with high IGFBP7 expression have a better outcome than patients with low IGFBP7 expression, indicating a positive role for IGFBP7 in treatment and outcome of AML. Together, this suggests that the combination of IGFBP7 and chemotherapy might potentially overcome conventional AML drug resistance and thus might improve AML patient survival.Only 30–40% of acute myeloid leukemia (AML) patients survive 5 years after diagnosis.1 This extremely poor prognosis is mainly caused by treatment failure due to chemotherapy resistance. This resistance is often a multifactorial phenomenon that can include enhanced expression or activation of receptor tyrosine kinases such as the insulin growth factor-1 receptor (IGF-1R).2, 3 The IGF-1R stimulates proliferation, protects cells from apoptosis and has been implicated in the development and maintenance of various cancers.4, 5 Several oncogenes require an intact IGF-1R pathway for their transforming activity6 and moreover, disruption or inhibition of IGF-1R activity has been shown to inhibit the growth and motility of a wide range of cancer cells in vitro and in mouse models.4, 5 IGF-1Rs are membrane receptors and binding of their ligand, the insulin-like growth factor-1 (IGF-1), results in receptor phosphorylation and activation of MAPK and PI3K/Akt signaling.4 Importantly, IGF-1, normally produced by the liver and bone marrow stromal cells, can stimulate the proliferation of cancer cells in vitro and genetic manipulations that reduce IGF-1 signaling can lead to decreased tumor growth.7, 8In hematological malignancies, a role for IGF-1 signaling has been demonstrated in multiple myeloma (MM) where it stimulates growth and potently mediates survival.9 Several anti-IGF-1R strategies have been shown to inhibit MM growth.10, 11 In AML, expression of the IGF-1R and IGF-1 was detected in AML cell lines and primary AML blasts and stimulation with IGF-1 can promote the growth of AML cells.12, 13, 14 In addition, neutralizing IGF-1R antibodies and the tyrosine kinase inhibitors (TKIs) NVP-AEW541 and NVP-ADW742, have been shown to inhibit proliferation and to induce apoptosis.15, 16In addition to its mitogenic and anti-apoptotic roles, directly influencing tumor development, IGF-1R appears to be a critical determinant of response to numerous anti-cancer therapies, including TKIs and chemotherapy.2, 3, 17, 18, 19, 20, 21, 22 In AML, activated IGF-1R signaling has been linked to cytarabine resistance, a drug included in every AML treatment schedule.17 Notably, in several cancer cell lines, a small subpopulation of drug-tolerant cancer cells exists that maintains their viability, after treatment with a lethal drug dose, via engagement of the IGF-1R.18The activity of the IGF-1R is tightly controlled at multiple levels, including their processing, endocytosis, trafficking and availability of its ligands.4 Ligand bioavailability is partly controlled by the family of secreted insulin-like growth factor-binding protein (IGFBP1 to IGFBP6), which can bind to IGFs therewith regulating the interaction of these ligands to their receptors. However, as IGFBPs are able to induce IGF-dependent and IGF-independent effects, the results of several studies on their role in cancer cell survival appeared to be controversial and complex.23, 24 In addition to IGFBPs, various IGFBP-related proteins have been identified.23, 25 One of these is the IGFB-related protein 1, also known as insulin-like growth factor-binding protein-7 (IGFBP7). IGFBP7 has 30% homology to IGFBP1 to IGFBP6 in its N-terminal domain and functions predominantly as a tumor suppressor.23, 24, 25, 26 In contrast to IGFBP1 to IGFBP6, which bind to the IGFs,23 IGFBP7 is a secreted protein that can directly bind to the IGF-1R and thereby inhibits its activity.27 The abundance of IGFBP7 is inversely correlated with tumor progression in hepatocellular carcinoma.28 Importantly, decreased expression of IGFBP7 has been associated with therapy resistance29, 30 and increasing IGFBP7 levels can inhibit melanoma and breast cancer growth.31, 32 IGFBP7 was originally identified as being involved in Raf-mediated apoptosis and senescence33 and also has been shown to induce senescence in mesenchymal stromal cells.34We established that IGFBP7 induces a cell cycle block and apoptosis in AML cells and cooperates with chemotherapy in the induction of leukemia cell death. AML patients with low IGFBP7 expression have a worse outcome than patients with high IGFBP7 expression, indicating that AML patients might benefit from a combination therapy consisting of chemotherapy and IGFBP7. Our results define IGFBP7 as a focus to enhance chemotherapy efficacy and improve AML patient survival. 相似文献
7.
Catherine Ronin Herman van Halbeek Johannah GM Mutsaers Johannes F G Vliegenthart 《Glycoconjugate journal》1987,4(3):247-254
The lipid-linked precursor ofN-type glycoprotein oligosaccharides was isolated from porcine thyroid microsomes after in cubation with UDP[3H] Glucose. The carbohydrate was released from dolichol pyrophosphate by mild acid hydrolysis, purified by gel filtration and characterized by 500-MHz1H-NMR spectroscopy in combination with enzymatic degradation. The parent oligosaccharide was found to be Glc3Man9Glc-NAc2. The three glucose residues are present in the linear sequence Glcα1-2Glα1-3 Glc, the latter being α(1-3)-linked to one of the mannose residues. In order to establish the branch location of the triglucosyl unit, the parent compound was digested with jack-bean α-mannosidase. The oligosaccharide product was purified by gel filtration, and identified by1H-NMR as Glc3Man5GlcNAc2 lacking the mannose residues A, D2, B and D3. Therefore, the structure of the precursor oligosaccharide is as follows: $$begin{gathered} c b a D_1 C 4 hfill Glcalpha 1 - 2Glcalpha 1 - 3Glcalpha 1 - 3Manalpha 1 - 2Manalpha 1 - 2Manalpha 1 hfill 3 swarrow 3 2 1 hfill Manalpha 1 - 2Manalpha 1 Manbeta 1 - 4GlcNAcbeta 1 - 4GlcNAc hfill D_{2 } A 3 6 hfill Manalpha 1 hfill 6 hfill Manalpha 1 - 2Manalpha 1 nwarrow 4 hfill D_3 B hfill end{gathered} $$ 相似文献
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