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Specific Molecules (specific + molecule)
Selected AbstractsIntracellular signaling involved in macrophage adhesion and FBGC formation as mediated by ligand,substrate interactionJOURNAL OF BIOMEDICAL MATERIALS RESEARCH, Issue 4 2002Weiyuan John Kao Abstract Fibronectin and RGD- and/or PHSRN-containing oligopeptides were preadsorbed onto physicochemically distinct substrata: polyethyleneglycol-based networks or tissue culture polystyrene (TCPS). The role of selected signaling kinases (namely protein tyrosine kinases, protein serine/threonine kinases, PI3-kinase, Src, and MAPK) in the adhesion of human primary blood-derived macrophages and the formation of foreign-body giant cells (FBGC) on these modified substrata was investigated. The involvement of individual intracellular signaling molecules in mediating macrophage adhesion dynamically varied with the culture time, substrate, and ligand. For example, fibronectin on TCPS or networks involved similar signaling events for macrophage adhesion; however, fibronectin and G3RGDG6PHSRNG, but not peptides with other RGD and/or PHSRN orientations, mediated similar signaling events for macrophage adhesion on TCPS but mediated different signaling events on networks. Depending on the substrate, a specific molecule (i.e., Src, protein kinase C) within the protein tyrosine kinase or protein serine/threonine kinase family was either an antagonist or agonist in mediating FBGC formation. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 62: 478,487, 2002 [source] Advanced Optical Microscopy Course at the Canale GrandeIMAGING & MICROSCOPY (ELECTRONIC), Issue 1 2007Alberto Diaspro Biophysics is a molecular science rapidly moving to the nanoscale. It seeks to explain biological function in terms of the molecular structures and properties of specific molecules. The size of these molecules varies dramatically, from small fatty acids and sugars (,1 nm = 10,9 m), to macromolecules like proteins (5,10 nm), starches (bigger than 1,000 nm), and the enormously elongated DNA molecules. Much effort in biophysics is directed to determining the structure of specific biological molecules and of the larger structures into which they assemble. Some of this effort involves inventing new methods and building new instruments for monitoring these structures. [source] RANKL/OPG/TRAIL plasma levels and bone mass loss evaluation in antiretroviral naive HIV-1-positive menJOURNAL OF MEDICAL VIROLOGY, Issue 10 2007Davide Gibellini Abstract Osteopenia and osteoporosis are common in HIV-1-infected individuals and represent a challenge in clinical and therapeutic management. This report investigated osteopenia/osteoporosis in a group of 31 antiretroviral naive HIV-1-positive men and the role of specific molecules belonging to TNF and the TNF-receptor family in HIV-1-related bone mass loss. Osteoprotegerin (OPG), the receptor activator of NF-,b-ligand (RANKL), and the TNF-related apoptosis-inducing ligand (TRAIL) were significantly increased in the plasma of antiretroviral naive HIV-1-positive patients compared to a control group of healthy blood donors. In addition, TRAIL and RANKL plasma concentrations were positively correlated to HIV-1-RNA viral load. Measurement of bone mineral density in 20 out of 31 HIV-1-positive subjects disclosed osteopenia/osteoporosis in 40% of these patients. The antiretroviral naive HIV-1-positive subjects with low bone mineral density had a decreased plasma OPG/RANKL ratio and a plasma RANKL concentration >500 pg/ml. Together, these data indicate that plasma concentrations of specific factors involved in bone homeostasis were increased during HIV-1 infection and that RANKL and OPG/RANKL ratio deregulation may be involved in osteopenia/osteoporosis occurring in antiretroviral naive HIV-1 individuals. J. Med. Virol. 79:1446,1454, 2007. © Wiley-Liss, Inc. [source] Nanotechnology advances in controlled drug delivery systemsPHYSICA STATUS SOLIDI (C) - CURRENT TOPICS IN SOLID STATE PHYSICS, Issue 12 2008C. Kiparissides Abstract Nanotechnology advances in drug delivery deal with the development of synthetic nanometer sized targeted delivery systems for therapeutic agents of increased complexity, and biologically active drug products. Therapeutic systems in this class are up to a million times larger than classical drugs like aspirin. Being larger there is more scope for diversity and complexity, which makes their protection much more challenging and their delivery more difficult. Their increased complexity however, gives these systems the unique power to tackle more challenging diseases. Targeted delivery systems can have multiple functions, a key one being their ability to recognize specific molecules which can be located either on the membrane of target cells, or in specific compartments within the cell. A challenging objective of targeted drug delivery is the development of innovative multidisciplinary approaches for the design, synthesis and functionalization of novel nanocarriers for targeted delivery of protein/peptide (P/P) drugs via oral, pulmonary and nasal administration routes as well as the fabrication of "smart" miniaturized drug delivery devices able to release a variety of drugs on demand. (© 2008 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source] Atomic force microscopy: A powerful molecular toolkit in nanoproteomicsPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 24 2009Yves F. DufrêneArticle first published online: 7 OCT 200 Abstract Analysing microbial cell surface proteins is a challenging task in current microbial proteomic research, which has major implications for drug design, vaccine development, and microbial monitoring. In this context, atomic force microscopy (AFM) has recently emerged has a powerful characterization platform, providing valuable insights into the surface proteome of microbial cells. The aim of this article is to show how advanced AFM techniques, that all have in common functionalization of the AFM tip with specific molecules, can be used to answer pertinent questions related to surface-associated proteins, such as what is their spatial arrangement on the cell surface, and what are the forces driving their interaction with the environment? [source] Riding The Ciliate Cell Cycle,A Thirty-Five-Year Prospective,THE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 5 2001JAMES D. BERGER ABSTRACT. Studies of the ciliate cell cycle have moved from early examination of its biochemistry with heat-synchronized Tetra-hymena through descriptive studies of Paramecium using small synchronous cell samples. These studies described what happens during the cell cycle and provided some initial insights into control, especially the idea that there was a point at which cells became committed to division. This early work was followed by an analytical phase in which the same small sample techniques, combined with gene mutations, were used to tease apart some major features of the regulation of cell growth kinetics, including regulation of macronuclear DNA content and regulation of cell size, the control of timing of initiation of macronuclear DNA synthesis, and the control of commitment to division in Paramecium. The availability of new molecular genetic approaches and new means of manipulating cells en masse made it possible to map out some of the basic features of the molecular biology of cell cycle regulation in ciliates. The challenge before us is to move beyond the ,me-too-ism' of validating the presence of basic molecular regulative machinery underlying the cell cycle in ciliates to a deeper analysis of the role of specific molecules in processes unique to ciliates or to analysis of the role of regulatory molecules in the control of cell process that can be uniquely well studied in ciliates. [source] Clinical Implications of Advances in the Basic Science of Liver Repair and RegenerationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 9 2009S. J. Karp Recent advances in our understanding of the basic mechanisms that control liver regeneration and repair will produce the next generation of therapies for human liver disease. Insights gained from large-scale genetic analysis are producing a new framework within which to plan interventions. Identification of specific molecules that drive regeneration will increase the options for live-donor liver transplantation, and help treat patients with small-for-size syndrome or large tumors who would otherwise have inadequate residual mass after resection. In a complementary fashion, breakthroughs in the ability to manipulate various cell types to adopt the hepatocyte or cholangiocyte phenotype promise to revolutionize therapy for acute liver failure and metabolic liver disease. Finally, elucidating the complex interactions of liver cells with each other and various matrix components during the response to injury is essential for fabricating a liver replacement device. This focused review will discuss how a variety of important scientific advances are likely to impact the treatment of specific types of liver disease. [source] Modulation of synaptic plasticity by stress and antidepressantsBIPOLAR DISORDERS, Issue 3 2002Maurizio Popoli Recent preclinical and clinical studies have shown that mechanisms underlying neuronal plasticity and survival are involved in both the outcome of stressful experiences and the action of antidepressants. Whereas most antidepressants predominantly affect the brain levels of monoamine neurotransmitters, it is increasingly appreciated that they also modulate neurotransmission at synapses using the neurotransmitter glutamate (the most abundant in the brain). In the hippocampus, a main area of the limbic system involved in cognitive functions as well as attention and affect, specific molecules enriched at glutamatergic synapses mediate major changes in synaptic plasticity induced by stress paradigms or antidepressant treatments. We analyze here the modifications induced by stress or antidepressants in the strength of synaptic transmission in hippocampus, and the molecular modifications induced by antidepressants in two main mediators of synaptic plasticity: the N -methyl- D -aspartate (NMDA) receptor complex for glutamate and the Ca2+/calmodulin-dependent protein kinase II (CaM kinase II). Both stress and antidepressants induce alterations in long-term potentiation of hippocampal glutamatergic synapses, which may be partly accounted for by the influence of environmental or drug-induced stimulation of monoaminergic pathways projecting to the hippocampus. In the course of antidepressant treatments significant changes have been described in both the NMDA receptor and CaM kinase II, which may account for the physiological changes observed. A central role in these synaptic changes is exerted by brain-derived neurotrophic factor (BDNF), which modulates both synaptic plasticity and its molecular mediators, as well as inducing morphological synaptic changes. The role of these molecular effectors in synaptic plasticity is discussed in relation to the action of antidepressants and the search for new molecular targets of drug action in the therapy of mood disorders. [source] Recent advances in the molecular pathology of soft tissue sarcoma: Implications for diagnosis, patient prognosis, and molecular target therapy in the futureCANCER SCIENCE, Issue 2 2009Yoshinao Oda In the present paper, recent advances in the molecular pathology of soft tissue sarcomas (STS) and the implications for their prognostic value are reviewed, and the potential targets of molecular therapy are discussed. According to the molecular genetic aspect, STS are divided into two groups: chromosome translocation-associated sarcomas and sarcomas without specific translocation. In the former group, specific fusion transcripts, such as SS18,SSX, EWS,FLI1, and PAX3,FKHR, could be detected in synovial sarcoma, Ewing's sarcoma and primitive neuroectodermal tumor, and alveolar rhabdomyosarcoma, respectively. The direct or indirect interactions between these fusion transcripts and cell cycle regulators have been elucidated by several investigators. Therefore, these fusion transcripts are promising candidates as molecular targets. As evaluated in carcinomas, alterations of several tumor-suppressor genes and adhesion molecules and overexpression of growth factors and their receptors have been extensively assessed in STS. In mixed-type STS, epidermal growth factor receptor overexpression was associated with decreased overall survival, suggesting the beneficial role of epidermal growth factor receptor inhibitors in STS. In malignant rhabdoid tumor and epithelioid sarcoma, frequent alteration of the SMARCB1/INI1tumor-suppressor gene and the loss of its protein have been demonstrated, indicating that this molecule could be an effective target of these sarcomas. In sarcomas with epithelioid differentiation, such as synovial sarcoma and epithelioid sarcoma, overexpression of dysadherin, which downregulates E-cadherin expression, was a poor prognostic factor. In conclusion, further studies are necessary to search for effective and specific molecules for the inhibition of tumor growth in each type of STS, especially in sarcomas without specific translocation. (Cancer Sci 2009; 100: 200,208) [source] | |||||||||||||