Literatura académica sobre el tema "Hematopoietic growth factors Therapeutic use"
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Artículos de revistas sobre el tema "Hematopoietic growth factors Therapeutic use"
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Costa, John J. "The therapeutic use of hematopoietic growth factors". Journal of Allergy and Clinical Immunology 101, n.º 1 (enero de 1998): 1–6. http://dx.doi.org/10.1016/s0091-6749(98)70185-x.
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Sola, Martha y Robert D. Christensen. "Use of Hematopoietic Growth Factors in the Neonatal Intensive Care Unit". Journal of Intensive Care Medicine 12, n.º 4 (julio de 1997): 187–205. http://dx.doi.org/10.1177/088506669701200403.
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Recombinant hematopoietic growth factors have emerged as valuable treatments for a variety of medical conditions. Recently, their applications have reached the neonatal intensive care unit, where they offer new therapeutic options for problems as common as anemia of prematurity, or as catastrophic as neonatal sepsis. When facing bacterial infection, it is known that newborn infants are capable of increasing their serum G-CSF concentrations. However, their response does not reach the concentrations that adults are able to achieve, and frequently neutropenia complicates the picture of neonatal sepsis. Although Phase III clinical trials are still in progress, published animal studies, case reports, and Phase I trials suggest that neonates with a variety of neutropenias experience a rapid elevation in their blood neutrophil concentration following administration of rG-CSF, without significant adverse effects. Although many factors contribute to the development of the “anemia of prematurity,” one of the major factors is the inability of preterm infants to generate an erythropoietin (Epo) response appropriate to their degree of anemia. On the basis of this fact, administration of rEpo to preterm neonates to treat or to prevent the anemia of prematurity has been the subject of multiple clinical studies, and it is now clear that rEpo administration to this population can indeed result in lower transfusion requirements, with only occasional and mild adverse effects. Neonatal thrombocytopenia is also a frequent clinical problem, which in most patients develops without a clear underlying cause. Recent studies, quantifying circulating megakaryocyte progenitors in the peripheral blood of thrombocytopenic neonates, suggest that impaired megakaryocytopoiesis may be the main underlying mechanism of many cases of thrombocytopenia. On the basis of this finding, it is tempting to speculate that recombinant thrombopoietin, the newly discovered physiological stimulator of platelet production, will be of clinical relevance in the treatment of thrombocytopenic neonates.
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Bossi, Paolo, Cristina Gurizzan, Luigi Lorini, Pierluigi di Mauro, Chiara Sardini y Marco Merlano. "Not all hematopoietic growth factors are created equal: should we gain information for their use with immunotherapy?" Journal for ImmunoTherapy of Cancer 9, n.º 8 (agosto de 2021): e003154. http://dx.doi.org/10.1136/jitc-2021-003154.
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Myeloid growth factors, either granulocyte colony-stimulating factor (CSF) or granulocyte-macrophage CSF, are widely used to reduce the incidence and severity of chemotherapy-induced neutropenia by prophylactic or therapeutic administration. However, their activity in the novel therapeutic regimens, which often rely on the association between immunotherapy and chemotherapy, has not been thoroughly characterized yet. This paper presents some of the preclinical and clinical research regarding the putative interplay between myeloid growth factors and the immune system, advocating further studies to elucidate their potential positive or negative consequences on the outcomes when administered with immunotherapeutic agents.
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Bridges, Sandra H., Margaret I. Johnston y John J. McGowan. "Immunosuppression and HIV Infection: A Therapeutic Challenge". Canadian Journal of Infectious Diseases 3, suppl b (1992): 55–59. http://dx.doi.org/10.1155/1992/740587.
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The optimal use of biological response modifiers (BRMs) in human immunodeficiency virus (HIV)-related disease depends on knowledge of the molecular basis of the immune deficiencies and dysregulations that occur during the course of the infection; evidence for the role of viral products and cytokines in the suppression of immune function is discussed. Immunebased therapies are currently being explored alone and in combination with drugs targeted to HIV and associated opportunistic infections and malignancies. These therapies include hematopoietic growth factors for the management of drug toxicities, cytokines, antigen- and cell-based therapies, and synthetic immunomodulators. The entry of additional BRMs into clinical trials for HIV-disease can be facilitated by well-designed preclinical studies that address special problems related to the disease. including the need for concomitant therapy for the spectrum of disease manifestations encountered.
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Siena, Salvatore, Roberta Schiavo, Paolo Pedrazzoli y Carmelo Carlo-Stella. "Therapeutic Relevance of CD34 Cell Dose in Blood Cell Transplantation for Cancer Therapy". Journal of Clinical Oncology 18, n.º 6 (13 de marzo de 2000): 1360–77. http://dx.doi.org/10.1200/jco.2000.18.6.1360.
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PURPOSE: To review recent advances in peripheral-blood progenitor-cell (PBPC) transplantation in order to define the optimal cell dose required for autologous and allogeneic transplantation. MATERIALS AND METHODS: A search of MEDLINE was conducted to identify relevant publications. Their bibliographies were also used to identify further articles and abstracts for critical review. RESULTS: The CD34+ cell content of a graft is regarded as an accurate predictor of engraftment success. Postchemotherapy autologous PBPC transplantation with ≥ 5 × 106 CD34+ cells/kg body weight leads to more rapid engraftment than does transplantation of lower cell doses. Further increases in transplant cell dose further accelerate platelet but not neutrophil engraftment. Evidence that long-term hematopoietic recovery may be more accurately predicted by the subpopulation of primitive progenitors transplanted suggests that the content of CD34+CD33− and long-term culture-initiating cells in cell collection samples may be important for predicting successful engraftment, particularly in patients with poor mobilization. Allogeneic transplantation has been limited by concerns regarding graft-versus-host disease and the use of hematopoietic growth factors in donors. The risk of graft rejection and engraftment failure after HLA-mismatched allogeneic transplantation may be overcome by intensive chemoradiotherapy and the infusion of large numbers of T cell–depleted hematopoietic stem cells. CONCLUSION: An optimal cell dose of ≥ 8 × 106 CD34+ cells/kg seems to be recommended for autologous PBPC transplantation. This dose facilitates the administration of scheduled chemotherapy on time and reduces the demand for other supportive therapies. A combination of growth factors may enable patients with poor mobilization to achieve a collection sufficient to allow transplantation. The optimum PBPC dose for allogeneic transplantation remains to be defined.
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Zhao, Q., X. Song, T. Waldschmidt, E. Fisher y AM Krieg. "Oligonucleotide uptake in human hematopoietic cells is increased in leukemia and is related to cellular activation". Blood 88, n.º 5 (1 de septiembre de 1996): 1788–95. http://dx.doi.org/10.1182/blood.v88.5.1788.1788.
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Abstract The use of antisense oligonucleotides as tools for modulating gene expression represents a novel strategy for designing drugs to treat a variety of diseases. Several factors, including cellular uptake and internalization of the oligonucleotides, are important parameters in determining the effectiveness of antisense agents such as therapeutic drugs. We have studied oligonucleotides uptake in normal and leukemic human hematopoietic cells, such as peripheral blood, bone marrow (BM), and HL-60 cell line; and have found that, in normal human blood and BM, myeloid cells and B cells preferably took up more oligonucleotides than T cells. There was no marked difference in oligonucleotide uptake between CD4+ helper T cells and CD8+ cytolytic T cells. Leukemic cells had greater oligonucleotide uptake than their normal counterparts. Furthermore, oligonucleotide uptake was closely related to cell activation status and can be modulated by growth factors or inhibitors. These studies provide a basis for using oligonucleotides as therapeutic drugs both in vitro and in vivo.
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Zhao, Q., X. Song, T. Waldschmidt, E. Fisher y AM Krieg. "Oligonucleotide uptake in human hematopoietic cells is increased in leukemia and is related to cellular activation". Blood 88, n.º 5 (1 de septiembre de 1996): 1788–95. http://dx.doi.org/10.1182/blood.v88.5.1788.bloodjournal8851788.
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The use of antisense oligonucleotides as tools for modulating gene expression represents a novel strategy for designing drugs to treat a variety of diseases. Several factors, including cellular uptake and internalization of the oligonucleotides, are important parameters in determining the effectiveness of antisense agents such as therapeutic drugs. We have studied oligonucleotides uptake in normal and leukemic human hematopoietic cells, such as peripheral blood, bone marrow (BM), and HL-60 cell line; and have found that, in normal human blood and BM, myeloid cells and B cells preferably took up more oligonucleotides than T cells. There was no marked difference in oligonucleotide uptake between CD4+ helper T cells and CD8+ cytolytic T cells. Leukemic cells had greater oligonucleotide uptake than their normal counterparts. Furthermore, oligonucleotide uptake was closely related to cell activation status and can be modulated by growth factors or inhibitors. These studies provide a basis for using oligonucleotides as therapeutic drugs both in vitro and in vivo.
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Thaker, Hatim y Arun K. Sharma. "Engaging Stem Cells for Customized Tendon Regeneration". Stem Cells International 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/309187.
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The need for a consistent therapeutic approach to tendon injury repair is long overdue. Patients with tendon microtears or full ruptures are eligible for a wide range of invasive and non invasive interventions, often subjectively decided by the physician. Surgery produces the best outcomes, and while studies have been conducted to optimize graft constructs and to track outcomes, the data from these studies have been inconclusive on the whole. What has been established is a clear understanding of healthy tendon architecture and the inherent process of healing. With this knowledge, tissue regeneration efforts have achieved immense progress in scaffold design, cell line selection, and, more recently, the appropriate use of cytokines and growth factors. This paper evaluates the plasticity of bone-marrow-derived stem cells and the elasticity of recently developed biomaterials towards tendon regeneration efforts. Mesenchymal stem cells (MSCs), hematopoietic progenitor cells, and poly(1,8-octanediol co-citrate) scaffolds (POC) are discussed in the context of established grafting strategies. With POC scaffolds to cradle the growth of MSCs and hematopoietic progenitor cells, developing a fibroelastic network guided by cytokines and growth factors may contribute towards consistent graft constructs, enhanced functionality, and better patient outcomes.
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Mohindru, Mani, Perry Pahanish, Efstratios Katsoulidis, Robert Collins, Thomas Rogers, Tony Navas, Linda Higgins, Leonidas Platanias y Amit Verma. "Novel P38 MAP Kinase Inhibitor and Anti-P38 RNA Interference as Potential Therapeutic Approaches in Myelodysplastic Syndromes." Blood 104, n.º 11 (16 de noviembre de 2004): 470. http://dx.doi.org/10.1182/blood.v104.11.470.470.
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Abstract Cytokines such as TNF α, IFN γ and others have been implicated in the pathogenesis of ineffective hematopoiesis in MDS and are thought to lead to the high rate of apoptosis in hematopoietic progenitors. The p38 Mitogen Activated Protein Kinase (MAPK) is an evolutionary conserved enzyme that is involved in many cellular processes including stress signaling. We have previously shown that the p38 MAP kinase is strongly activated by IFNs, TNF α, TGF β and other inhibitory cytokines in normal primary hematopoietic progenitors and plays an important role in the negative regulation of normal hematopoiesis. In the present study, we determined the role of the p38 MAPK in the pathogenesis of MDS evaluated its inhibition as a potential therapeutic strategy in this disease. p38 MAPK inhibition was achieved by the use of a novel p38 inhibitor - SD-282, a specific inhibitor of p38α MAP kinase. SD-282 performs very similarly in animal and cell models to a p38 inhibitor now in the clinic. We also transfected primary hematopoietic cells with flurescent labeled siRNAs against p38 and successfully downregulated the levels of the protein. Using these approaches, we demonstrate that pharmacological inhibition of the p38 MAPK can reverse the growth inhibitory effects of TNF α and IFN γ on erythroid and myeloid colony formation. This reversal of TNF α mediated inhibition correlates with significant reduction of apoptosis seen in human hematopoeitic progenitors pretreated with p38 inhibitor SD-282. Having established the importance of p38 MAPK in cytokine mediated inhibition of normal hematopoiesis, we performed colony forming assays with bone marrow CD34+ cells from 8 patients with MDS in the presence of either pharmacologic or siRNA based inhibitors of p38. All patients had refractory cytopenias with multilineage dysplasia. Our data indicates that SD-282 treatment strongly enhances both erythroid and myeloid colony formation in MDS CD34+ bone marrow cells in vitro. This increase was not observed when these progenitors were grown in the presence of negative controls - SB 202474 and the MEK inhibitor PD 98059. Similarly, an increase in hematopoietic colony formation, though of a lesser magnitude was seen when MDS bone marrow progenitors were transfected with siRNAs against p38 MAPK. To further determine the role of cytokines in the pathogenesis of MDS, we also used bone marrow derived sera from the same MDS patients. Our studies show exposure to patient derived sera led to the phosphorylation/activation of p38 MAPK in normal hematopoietic progenitors when compared to sera from healthy volunteers. Our studies also demonstrate that bone marrow derived sera from MDS patients can inhibit erythroid and myeloid colony formation of normal hematopoietic progenitors. This inhibition can be reversed by blocking p38 MAPK using SD-282, other p38 inhibitors and siRNAs. This finding confirms the role of marrow cytokine /serum factors in the ineffective hematopoiesis seen in MDS and suggests the importance of p38 MAPK activation in this phenomenon. Thus our studies show the p38 MAPK may be a common effector of inhibitory cytokine signaling in normal and MDS hematopoietic cells. These results provide a strong rationale for using p38 inhibition as a novel treatment strategy for MDS. Supported by Harris Methodist Foundation Grant, VISN-17 New Investigator Grant and VA Research Corp Grant to AV.
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Or, Reuven, Sigal Grisaro, Batia Ronit Avni, Igor Resnick, Lilyan Dari, David Shoshani, Dalia Bracha, Nurit Beilin, Limor Lior y Michael Y. Shapira. "Correction of Post-Transplant Hematopoiesis by Novel Use of Mesenchymal-Like Placental Expanded Cells (PLX) Administered Intra-Muscular". Blood 120, n.º 21 (16 de noviembre de 2012): 4133. http://dx.doi.org/10.1182/blood.v120.21.4133.4133.
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Abstract Abstract 4133 Post autologous or allogeneic stem cell transplantation hematopoietic dysfunction is a common phenomenon caused by multiple factors. Complicating the treatment of this condition is the fact that additional reserves of stem cells for autologous transplantation is usually unavailable and the use of allogeneic stem cells, if available, may be associated with transplant related complications, including graft versus host disease. Furthermore, the addition of donor cells may be ineffective because the underlying disease may also damage the supplemented stem cells. Prolonged pancytopenia in cases not responding to hematopoietic growth factors is a major life threatening condition. Bone marrow derived mesenchymal stem cells (MSC) are multi-potent cell that are being clinically explored as immune modulators and inducers of stem cell plasticity. Placental-expanded (PLX) cells are mesenchymal-like adherent stromal cells derived from the full term placenta. The cells are expanded in a bioreactor system, which provides a three dimensional microenvironment for cell growth. This system enables full control over the manufacturing process, large-scale growth of these cells and batch-to-batch consistency. PLX cells are immune privileged and suitable for allogeneic administration without HLA-Matching. Additionally, PLX cells are known to secrete a wide range of anti-inflammatory cytokines as well as various growth factors. Three patients suffered from severe and long-standing pancytopenia with associated complications after receiving hematopoietic stem cell transplantations (two allogeneic and one autologous). They were treated on a compassionated basis with intra-muscular (IM) injections of PLX cells in an attempt to enhance hematopoiesis. The first case was a 7 year-old girl that suffered from severe aplastic anemia and underwent two un-manipulated allogeneic stem cell transplantations from two different unrelated donors. The second patient was a 55 year-old woman that suffered from non-Hodgkin lymphoma and sustained an autologous stem cell transplantation. The third patient was a 45 year-old male with AML that underwent an allogeneic, un-manipulated transplant from an unrelated source. On days 74, 46, 144 post-transplant respectively for each patient, PLX cells were injected IM at a dose of 600×106 cells per adult and 160×106cell per child, divided in two administrations one week apart. No local or systemic side effects were observed. All three patients had impressive clinical improvement, which enabled them to be discharged from the hospital. The first 2 patients responded 4 and 9 days respectively after the second PLX cell administration, with improvement of tri-linage hematopoiesis. The third patient became significantly less transfusion dependent. PLX cell's immunomodulatory properties and cytokine secretory potential might be involved in the bone marrow regeneration capacity seen in these patients. The endocrine mode of action following the IM administration of PLX cells is a new and simple concept for cell therapy. Future clinical trials are needed to investigate the potential of PLX cells to enhance and shorten bone marrow engraftment following autologous or allogeneic bone marrow transplantation. Disclosures: Shoshani: Pluristem Therapeutics Inc., Haifa, Israel: Employment. Bracha:Pluristem Therapeutics Inc., Haifa, Israel: Employment. Beilin:Pluristem Therapeutics Inc., Haifa, Israel: Employment. Lior:Pluristem Therapeutics Inc., Haifa, Israel: Employment.
Tesis sobre el tema "Hematopoietic growth factors Therapeutic use"
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Ang, Main-fong y 洪明楓. "Ex vivo expansion of hematopoietic stem cells: preclinical studies and clinical application". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B3122815X.
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Haylock, David Norman. "Ex vivo expansion of human haemopoietic progenitor cells". Title page, abstract and contents only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phh4181.pdf.
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"December 2001." Includes bibliographical references (leaves 178-225) Focuses on the ex vivo growth of human haemopoietic progenitor cells with the objective of defining culture conditions for generating myeloid post-progenitor cells for therapy
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Hercus, Timothy Robert. "Structure-junction studies on human granulocyte-macrophage colony-stimulating factor /". Title page, table of contents and summary only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09phh539.pdf.
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Korpelainen, Eija. "Interleukin -3 receptor expression and function in now-hemopoietic cells /". Title page, contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09PH/09phk84.pdf.
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Ng, Hoi-man y 伍凱敏. "Regulation of vascular endothelial growth factor by ginsenoside RG1 inhuman endothelial cells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43955915.
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"The effects of hematopoietic growth factors and tanshinone IIA on neuro-protection". Thesis, 2005. http://library.cuhk.edu.hk/record=b6073980.
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Neonatal hypoxic-ischemic encephalopathy (HIE) is a common clinical problem. Tanshinone IIA is a compound purified from the Chinese herb Danshen ( Radix Salviae Miltiorrhiza Bge). Thrombopoietin (TPO) and Erythropoietin (Epo) are hematopoietic growth factors. The effects of tanshinone IIA, EPO and TPO on hypoxia-ischemia brain injury were investigated in this study, using in vitro model of neural cell culture and an in vivo model of hypoxic-ischemic brain damage.Our observation provided the first evidence showing the expression of functional TPO receptor c-mpl in central nervous system. It revealed that novel agents TPO, EPO and tanshinone IIA have neuroprotection effects against brain injury induced by hypoxia-ischemia in neonatal rats, and these agents could be developed for clinical applications.
To investigate the effect of TPO, EPO and tanshinone IIA on in-vivo neural protection, a neonatal rat model of hypoxic-ischemic brain damage was established. Our results demonstrated significant and sustained brain injury in the hypoxic-ischemic and vehicle-treated group, measured by the reduction in relative weights of the ipsilateral (right) to the contralateral (left) brain at 1 and 3 weeks post-surgery, compared with those of sham-operated animals. At 3 weeks post-surgery, the hypoxic-ischemic animals had decreased cortical neuron density quantified by neuron-specific enolase (NSE) staining, and compromised sensorimotor functions in response to the postural reflex test. Treatment with TPO, EPO and tanshinone IIA significantly reduced the severity of brain injury, as indicated by the significantly increased ipsilateral brain weight and neuron density. Recoveries of sensorimotor functions (p < 0.05) and histopathology were also observed in animals that received TPO, EPO and tanshinone IIA. The plasma of tanshinone IIA-treated animals exhibited higher antioxidant activities (oxygen radical absorbance capacity assay) than those from vehicle-treated rats.
TPO and TPO receptor (c-mpl) mRNA was identified in human cerebral hemispheres, cerebellum, mouse neural progenitor cell line C17.2 and four neuroblastoma cell lines (SK-N-MC, MHH-NB-11, SK-N-AS and SH-SY-5Y) using RT-PCR methods. TPO proteins were detected in human cerebrospinal fluid (CSF) and plasma by ELISA. Furthermore, TPO receptor c-mpl was confirmed in human cerebral hemispheres, hippocampus, cerebellum, brainstem and spinal cord using immunohistostaining. TPO had a stimulating effect on the growth of neural progenitor cell C17.2 in culture via the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway as demonstrated by Western blot. The anti-apoptotic effects of TPO, EPO on C17.2 cells were demonstrated by staining with Annexin-V and PI. EPO exerted a protective effect against SHSY-5Y cell damage induced by NMDA (N-methyl-d-aspartate), as demonstrated by the MTT and LDH assay. The anti-oxidative property of tanshinone IIA was studied in the C17.2 cell line. Tanshinone IIA increased the viability of these cells subjected to 2,2'-azobis (2-amidino propane hydrochloride) (AAPH)-induced oxidative stress.
by Xia Wen-Jie.
"May 2005."
Advisers: Kwok-Pui Fung, Tai-Fai Fok.
Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0126.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2005.
Includes bibliographical references (p. 126-146).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
School code: 1307.
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Hunt, Benjamin Matthew. "Recovery of transforming growth factor-[beta]2 from Whey Growth Factor Extract with immunoaffinity techniques / by Benjamin Matthew Hunt". 2000. http://hdl.handle.net/2440/19851.
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Includes errata on last 3 leaves.Includes bibliographical references (leaves 232-246).
xix, 246 leaves : ill. (some col.) ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
Describes attempts to develop an immunoaffinity process for commercial-scale purification of TGF-[beta]2 from Whey Growth Factor Extract
Thesis (Ph.D.)--Adelaide University, Dept. of Chemical Engineering, 2001
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Sekhejane, Palesa Rose. "Effect of low level laser irradiation on expression of cytokines and growth factors involved in wound healing". Thesis, 2010. http://hdl.handle.net/10210/3121.
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M. Tech.Phototobiomodulation (PBM), also known as low level laser therapy (LLLT) or photobiostimulation, is a non-invasive form of therapy that utilizes low intensity laser light or irradiation to provide healing. However, in order for healing to be successful certain laser parameters need to be taken into consideration i.e. fluence (dosage), wavelength and power density. Laser therapy has been used for various medical applications and fields. Multiple cytokines and growth factors are involved in wound healing including Interleukin (IL)-1, IL-6 and Tumour Necrosis Factor alpha (TNF- a). In diseased state(s) such as diabetes mellitus (DM) or psoriasis, these growth factors or cytokines are either found elevated or decreased depending on various factors and for abnormally prolonged periods. However, inflammatory cytokines are usually elevated. Phototherapy has been reported to accelerate wound healing, attenuate pain and cease inflammation. However, the effect of phototherapy on cytokine modulation has not been explored extensively, especially under various stress mechanisms. Furthermore, the pathway that laser irradiation induces on modulated pro-inflammatory cytokines has not been clearly elucidated as scientists typically report on the up- or down-regulated expression of cytokines. Numerous authors have reported on the efficacy of laser irradiation to enhance the rate of wound healing and proliferation in normal and diabetic cells or tissue; however, literature that has demonstrated the latter on hypoxic insulted cells is inadequate. In this study hypoxic insult was induced as it is one of the factors that usually prolong the healing process in diabetic wounds. Prior to commencing with the main study, a pilot study was done to exclude the effect of osmotic pressure on cells grown in media containing additional glucose, and thus simulating a diabetic model iv in vitro. Mannitol was used as a control since it is not absorbed by the cells. The study involved four groups namely: normal, normal wounded, mannitol wounded and diabetic wounded cells with each group having a non-irradiated control. Mannitol wounded and diabetic wounded cells had a final concentration of 30 mM mannitol and glucose respectively. A wavelength of 636 nm at a fluence of 5 J/cm2 was used on day 1; experiments were repeated four times and all tests were done in duplicate. Cellular responses (Trypan Blue, adenosine triphosphate (ATP) and lactate dehydrogenase (LDH)) and morphological changes were assessed after 1 h incubation post-irradiation in both irradiated and non-irradiated cultures.
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Martin, Holly René. "Mechanism of Transformation and Therapeutic Targets for Hematological Neoplasms Harboring Oncogenic KIT Mutation". Thesis, 2014. http://hdl.handle.net/1805/5503.
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Indiana University-Purdue University Indianapolis (IUPUI)Gain-of-function mutations in the KIT receptor tyrosine kinase have been associated with highly malignant human neoplasms. In particular, an acquired somatic mutation at codon 816 in the second catalytic domain of KIT involving an aspartic acid to valine substitution is found in patients with systemic mastocytosis (SM) and acute myeloid leukemia (AML). The presence of this mutation in SM and AML is associated with poor prognosis and overall survival. This mutation changes the conformation of the KIT receptor resulting in altered substrate recognition and constitutive tyrosine autophosphorylation leading to constitutive ligand independent growth. As there are currently no efficacious therapeutic agents against this mutation, this study sought to define novel therapeutic targets that contribute to aberrant signaling downstream from KITD816V that promote transformation of primary hematopoietic stem/progenitor cells in diseases such as AML and SM. This study shows that oncogenic KITD814V (murine homolog) induced myeloproliferative neoplasms (MPN) occurs in the absence of ligand stimulation, and that intracellular tyrosines are important for KITD814V-induced MPN. Among the seven intracellular tyrosines examined, tyrosine 719 alone has a unique role in regulating KITD814V-induced proliferation and survival. Residue tyrosine 719 is vital for activation of the regulatory subunit of phosphatidylinositol 3-kinase (PI3K), p85α, downstream from KITD814V. Downstream effectors of the PI3K signaling pathway, in of leukemic cells bearing KITD814V with an allosteric inhibitor of Pak or its genetic inactivation results in growth repression due to enhanced apoptosis. To assess the role of Rac GEFs in KITD814V induced transformation, EHop-016, an inhibitor of Rac, was used to specifically target Vav1, and found to be a potent inhibitor of human and murine leukemic cell growth. In vivo, the inhibition of Vav or Rac or Pak delayed the onset of MPN and rescued the associated pathology in mice. These studies provide insight on mechanisms and potential novel therapeutic targets for hematological malignancies harboring an oncogenic KIT mutation.
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Rodrigues, Maria Inês Moreira Patrício. "New roles of Rab GTPases on eye diseases: targeting VEGF secretion". Doctoral thesis, 2012. http://hdl.handle.net/10362/10533.
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RESUMO: A retina é composta, entre outras estruturas, pelo epitélio pigmentar da retina (EPR)e pela coróide. A região central da retina denomina-se mácula, e é a zona mais afetada na degenerescência macular relacionada com a idade, a forma mais comum de degenerescência da retina. Nesta doença, a secreção de fatores de crescimento pelo EPR é afetada, nomeadamente a do fator de crescimento vascular endotelial (VEGF), e pouco se sabe ainda sobre os mecanismos moleculares conducentes a esta condição. A família de proteínas Rab GTPases está envolvida nas vias intracelulares de sinalização e tráfego membranares, essenciais na transdução de sinais extracelulares em respostas biológicas. A
sua crucial importância nestes mecanismos levou-nos a considerar o seu potencial
envolvimento nas vias de secreção do VEGF, e a questionar-nos se teriam algum papel
regulador sobre as mesmas. O principal objetivo deste trabalho é identificar Rab GTPases importantes para as vias de secreção e endocitose do VEGF no EPR. Essa identificação ajudará a esclarecer a patogénese da degenerescência macular da retina, e poderá servir para uma procura mais direcionada de novos agentes terapêuticos. A caracterização de dois
modelos in vitro do EPR, células primárias isoladas de murganho e a linha celular B6-RPE07,levou-nos a concluir que são ambos semelhantes. Contudo, a linha celular foi escolhida como protótipo do EPR por permitir o acesso a um número ilimitado de células. No decurso deste trabalho, desenvolvemos e caracterizámos uma biblioteca de ferramentas moleculares que nos permitiram reduzir os níveis proteicos das proteínas Rab GTPases, com base na tecnologia de ácido ribonucleico (ARN) de interferência. O papel das proteínas Rab GTPases na secreção do VEGF no EPR foi estudado com base no silenciamento de apenas uma proteína, ou combinando várias, segundo a sua localização e funções intracelulares descritas. Este trabalho permitiu-nos concluir que as proteínas Rab GTPases são importantes intervenientes no processo de secreção de VEGF pelo EPR, e confirmar dados anteriores que relatam o envolvimento de algumas Rab GTPases endocíticas no processo. Propomos ainda
um novo modelo para a interação destas proteínas no EPR, e sugerimos que a Rab10 e a
Rab14 atuam negativamente sobre a Rab8, controlando o seu funcionamento. Os nossos
resultados evidenciam a importância das proteínas Rab GTPases na secreção do VEGF pelas células do EPR, e servem de base a futuros estudos que melhor procurem compreender este mecanismo e de que modo a sua alteração se relaciona com a degenerescência da retina.--------ABSTRACT: Retinal pigment epithelium (RPE) and choroid are components of the mammalian retina, of which the central region is called macula. The most common form of retinaldegeneration, age-related macular degeneration (AMD), involves primarily deregulation of
growth factors secretion by the RPE. Very little is known about the molecular mechanisms that lead to impairment of RPE’s homeostatic intracellular processes, namely the secretion of vascular endothelial growth factor (VEGF). Rab GTPases’ family regulates membrane targeting and traffic, being essential in the transduction of signal pathways. Given Rab proteins’ role in intracellular trafficking, we propose to identify key regulatory Rab proteins
involved in either the secretory or the recycling pathways of VEGF in RPE. Understanding how Rab proteins’ function disruption could lead to retinal and choroidal pathology would ultimately contribute to find new therapeutic agents. Here, we characterized two mouse RPE
in vitro cell models, primary cells and B6-RPE07 cell line, and concluded that both display important epithelial features as the RPE presents in vivo. Considering unlimited cell number and results reproducibility, we chose B6-RPE07 cells to further study Rab proteins’ function.
To scrutinize the consequences of Rab proteins’ absence or diminished levels, we have developed novel molecular tools to achieve silencing of these key proteins using miRNA technology. We further addressed the effect of Rab proteins’ absence on VEGF secretion by performing an extensive screening where different Rab proteins were silenced, both individually and in multiple combinations considering their cellular/ compartment location.
We conclude that Rab GTPases are important intervenients in VEGF secretion by RPE cells,
confirming endocytic Rab proteins’ role in regulation of VEGF biology. We also propose a
novel model for Rab proteins’ interaction in RPE. Our results suggest that Rab10 and Rab14
might influence Rab8 in a negative feedback mechanism, important for controlling VEGF
secretion. Our achievements’ unravel Rab proteins’ role in VEGF secretion by RPE cells and are the basis for future studies to better understand RPE molecular secretory machinery.
Libros sobre el tema "Hematopoietic growth factors Therapeutic use"
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C, Dale David y SpringerLink (Online service), eds. Hematopoietic Growth Factors in Oncology. Boston, MA: Springer Science+Business Media, LLC, 2011.
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L, Spivak Jerry, Drohan William y Dooley Douglas, eds. Hematopoietic growth factors in transfusion medicine: Proceedings of the XXth Annual Scientific Symposium of the American Red Cross, held in Bethesda, Maryland, May 10-11, 1989. New York: Wiley-Liss, 1990.
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J, Quesenberry Peter, Asano Shigetaka 1943- y Saito Kazuhisa 1922-, eds. Hematopoietic growth factors: Molecular biology to clinical applications of rG-CSF : proceedings of a satellite symposium of the Sixth International Congress of Mucosal Immunology, Tokyo, July 22, 1990. Amsterdam: Excerpta Medica, 1991.
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Th, Smit Sibinga C., Das P. C y Fratantoni Joseph C, eds. Alternative approaches to human blood resources in clinical practice: Proceedings of the Twenty-Second International Symposium on Blood Transfusion, Groningen 1997. Dordrecht: Kluwer Academic, 1998.
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Dworkin, Chaim R. The use of growth factors in cancer therapy. [Bethesda, Md.?]: U.S. DHHS, PHS, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1993.
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Van de Water, Thomas R. y Koszer Samuel, eds. Clinical applications of neurotrophic factors. Philadelphia: Lippincott-Raven, 1997.
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Krul, Kenneth G. Emerging cancer therapies. Waltham, MA: Decision Resources, 1994.
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Sherbet, G. V. Growth factors and their receptors in cell differentiation, cancer and cancer therapy. London: Elsevier, 2011.
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Bengt, Westermark, Betsholtz Christer y Hökfelt Bernt, eds. Growth factors in health and disease: Basic and clinical aspects : proceedings of the 4th Nordisk Insulin Symposium "Growth Factors in Health and Disease," Copenhagen, Denmark, 18-20 June 1990. Amsterdam: New York :Excerpta Medica, 1990.
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Anti-VEGF. Basel: Karger, 2010.
Buscar texto completoCapítulos de libros sobre el tema "Hematopoietic growth factors Therapeutic use"
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Nimer, Stephen D. y Richard E. Champlin. "Therapeutic use of hematopoietic growth factors in bone marrow transplantation". En Cancer Treatment and Research, 141–64. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1493-6_9.
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Seipelt, G. "Clinical Use of Hematopoietic Growth Factors". En Antibiotics and Chemotherapy, 94–105. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000059319.
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Mininberg, Eric D. y Frankie Ann Holmes. "Use of Granulocyte Growth Factors in Breast Cancer". En Hematopoietic Growth Factors in Oncology, 285–309. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-747-5_15.
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Foote, MaryAnn. "Use of Hematopoietic Growth Factors in AIDS-Related Malignancies". En Hematopoietic Growth Factors in Oncology, 357–71. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-747-5_18.
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Lichtin, Alan E. "Clinical Practice Guidelines for the Use of Erythroid-Stimulating Agents: ASCO, EORTC, NCCN". En Hematopoietic Growth Factors in Oncology, 239–48. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7073-2_14.
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Finke, Jürgen y Roland Mertelsmann. "Use of Recombinant Growth Factors after Hematopoietic Cell Transplantation". En Thomas’ Hematopoietic Cell Transplantation, 480–91. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118416426.ch43.
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Fox, Richard M. "Commentary on the ASCO and ESMO Evidence-Based Clinical Practice Guidelines for the Use of Hematopoietic Colony-Stimulating Factors". En Hematopoietic Growth Factors in Oncology, 211–17. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-747-5_10.
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Demetri, George D. "Evidence-Based Use of Hematopoietic Cytokines in Clinical Oncology". En Clinical Applications of Cytokines and Growth Factors, 137–49. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5013-6_6.
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Jendiroba, David B., Benjamin Lichtiger y Emil J. Freireich. "The Use of Hematopoietic Growth Factors for Recruitment of Leukocytes for Transfusion". En Clinical Applications of Cytokines and Growth Factors, 178–85. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5013-6_9.
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Vose, J. M., E. C. Reed, P. J. Bierman y J. O. Armitage. "Autologous Bone Marrow Transplantation for Lymphoid Malignancies: The Use of Hematopoietic Growth Factors". En Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 201–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78350-0_34.
Texto completoActas de conferencias sobre el tema "Hematopoietic growth factors Therapeutic use"
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Barminko, Jeffrey, Jean Pierre Dolle, Rene Schloss, Martin Grumet y Martin L. Yarmush. "Encapsulated Mesenchymal Stem Cells for Central Nervous System Repair". En ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19712.
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Mesenchymal stromal cells (MSC) have long been regarded as a cell source with the potential to provide therapies for various different tissue pathologies. They were originally identified for their ability to adhere to tissue culture plastic and gained favor due to their tremendous ability to propagate[1]. It was this finding as well as their ability to differentiate into lineages of mesoderm which have long made MSC a potential tool for autologous cellular replacement therapies [2, 3]. More recently, their cyto-protective role has been realized and been implicated in the benefit achieved in treating various different tissue pathologies. MSC have been found to secrete several different cytokines and growth factors in vitro. Furthermore, these factors can be modulated based on the environment MSC are exposed to. MSC have shown therapeutic benefits in models of GVHD, myocardial infarction, fulminant hepatic failure, central nervous system trauma and others, without any apparent cellular replacement. These advances propelled MSC to the fore front of potential cellular therapies and many are seeking to take advantage of their tissue protective properties. However, several draw backs in current methods of MSC implantation limit the ability to carry out safe and controlled clinical trials. Limitation with current MSC implantation approaches include; 1) directly transplanted MSCs exposed to the complex injury environment may be affected themselves early in the treatment processes, 2) MSC may also migrate to undesired tissue locations and 3) may differentiate into undesired end stage cells. These issues severally limit the translatability of MSC treatments in clinical settings; they make controlling experiments very difficult. There becomes a need to develop engineered methods for delivering these cells in a controlled manner. In order to circumvent these potential problems, we propose to use an alginate microencapsulation system as a vehicle for MSC delivery taking advantage of the soluble factors MSC provide.
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Nagy, Diána. "Possibilities of Digitalization and Service Design in the Development of Patient Adherence". En New Horizons in Business and Management Studies. Conference Proceedings. Corvinus University of Budapest, 2021. http://dx.doi.org/10.14267/978-963-503-867-1_05.
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In parallel with the development of modern health systems and the growth of the welfare state, diseases have shifted towards chronic diseases. Today, instead of rapid-onset infections, most resources are focused on the long-term treatment of mostly lifelong chronic conditions. The condition for the effective use of therapies is to take the specified dose with the prescribed frequency and for the required period of time. If these parameters are met, we can talk about patient collaboration or adherence. For certain diseases and treatments, adherence is critically low. In the case of complex preparations to be taken several times a day, or diseases that do not cause serious, noticeable complaints, the initial number of patients treated is reduced to a fraction within a short time. As a result, economic harm is perceived not only by the patient but also by all those involved in the health care system, including pharmaceutical companies. However, the factors influencing patient collaboration vary widely. In order to achieve high adherence, the goal is to develop health services that coordinate the actors involved, the infrastructure, the communication, the material components to improve the user experience. As a user-centered methodology, service design can play a prominent role in the design of therapeutic services, contributing to the reduction of uncertainties in innovation processes. In my study, I assess the digital toolkit of patient education in Hungarian society. The aim is to explore digital tools and technologies that can contribute to the development of health awareness and education so that both science and the pharmaceutical and technology companies that exploit it can apply the results of research.
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Devi, Pinki, Ganapathi Bhat y Harish S. Ahuja. "To Predict Success of Postapheresis Yield and Post–Autologous Transplant Engraftment Based on Preapheresis Peripheral Blood CD34+ Cell Counts: An Indian Scenario–Based Study". En Annual Conference of Indian Society of Medical and Paediatric Oncology (ISMPO). Thieme Medical and Scientific Publishers Pvt. Ltd., 2021. http://dx.doi.org/10.1055/s-0041-1735370.
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Abstract Introduction The use of hematopoietic stem cells for autologous and allogeneic transplantation has increased in the recent past significantly, due to introduction of newer chemotherapeutic drugs, immunological techniques, and better stem cell technology. Among the bone marrow and peripheral blood stem cells, collection of the latter being more convenient to the patient and associated with faster granulocyte and platelet engraftment has been known as preferred method for mobilization. Peripheral blood stem cells can be extracted from the autologous or allogeneic donor. Mobilization of the stem cells for autologous stem cell transplant is traditionally done using growth factors alone or in combination with chemotherapy, with or without an additional mobilizing agent. A significant number of hematological malignancy patients are poor mobilizers, (i.e., they are unable to achieve the minimal target cell dose during their first round of mobilization).Therefore, a prediction for a successful stem cell mobilization ideally should be made before initiating any apheresis procedure to spare those with a low rate of success from the risks associated with apheresis procedure. Preapheresis CD34 cell count can predict postapheresis yield and hence, can help to reduce the collection sessions. Reduction of apheresis sessions decreases the discomfort, inconvenience, time, and monetary expenses. Objectives This study was aimed to analyze preapheresis and postapheresis CD34+ cell counts. Materials and Methods Patients of any age and gender with diagnosis of hematological malignancies admitted for autologous stem cell transplantation for hematological malignancies (including Hodgkin lymphoma, non-Hodgkin lymphoma, and multiple myeloma) and germ cell tumors in our institute from July 2008 to July 2016 were included in the study. The post-GCSF CBC, preapheresis CBC, CD34+ cell counts, and postapheresis CBC, CD34+ cell counts, mononuclear cell counts to predict the outcome of amount of yield. The effect on engraftment will be measured according to the defining criteria of achieving a sustained peripheral blood neutrophil count of >500 × 106/L (Wolff 2002) and a platelet count of more than >20 × 109/L (Teltschik et al. 2016) independent of platelet transfusion for at least 7 days. Collection of stem cells was done using apheresis machine (COBE SPECTRA). Complete peripheral blood counts using automated analyzers. Peripheral blood CD34 + cell counts and postapheresis CD34+ cell count using BD FACS CANTO II flow cytometer. To calculate postapheresis yield, the related CD34 count measured by flow cytometer was multiplied by the apheresis product volume and divided by the recipient’s body weight (kg). Number of CD34+ cells collected = (CD34 cell concentration in final product) × (final product volume). Results A total of 100 patients who underwent a total of 320 apheresis sessions were included in the study. There were 78 males and 22 females. We also found a significant correlation between preapheresis CD34 + cell count and postapheresis CD34 percentage on days 1, 2, and 3 of the apheresis sessions. In our study, to obtain more than 1.31 × 106 cells (median = 1.04, range: 0.15–4.70), an absolute count of pre apheresis CD34 + cells ≥14 cells would be necessary. A target of CD34 + cells ≥ 2 × 106/kg was obtained in majority of patients if a concentration of ≥25 CD34 + cells was present in postapheresis collection. Conclusion Compiling our results with the previous published data, we conclude that there is a strong correlation between preapheresis absolute CD34 + cell counts and postapheresis CD34 + cell count. Our study also suggests that the minimum absolute cell count of >10 cells/μL is required, to achieve a target of >2–5 × 106 cells for postapheresis yield.
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Arora, Rahul D. "Definition, etiopathogenesis, management and role of flouroquinolone prophylaxis in prevention of spontaneous bacterial peritonitis complicating malignant ascites". En 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685345.
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Background: Malignancy related ascites encompasses multiple etiologies which include peritoneal carcinomatosis, hepatic synthetic dysfunction due to parenchymal involvement by the tumour, transcoeloemic metastasis and chylous ascites due to lymphatic obstruction. Primary Cancer type, liver metastasis and serum albumin have been listed as independent prognostic markers in malignant ascites. Spontaneous Bacterial Peritonitis is usually seen as a complication of decompensated chronic liver disease due to translocation of bacteria or haematogenous dissemination from a distant focus of infection. The combination of a positive peritoneal fluid culture and an ascitic fluid neutrophil count >250 cells/mm3 and no evidence of intra-abdominal source of infection; or 2) culture negative neutrocytic ascites: the combination of negative peritoneal fluid bacterial culture and neutrophil count >500 cells/mm3, without antibiotics within 7 days with no obvious source of infection are used to define spontaneous bacterialperitonitis. Ciprofloxacin prophylaxis has been proposed as a prophylaxis to reduce the incidence and prevent the recurrence of spontaneous bacterial peritonitis. Materials and Methods: A web search of indexed literature was carried out articles containing information on spontaneous bacterial peritonitis in the setting of malignancy or malignancy related ascites or malignant ascites. Articles that carried relevant information about etiopathogenesis, management and translational research in the context of malignant ascites were also included. Results: A total of 32 articles were analysed and about half of them included in the discussion to answer the research question. Discussion: Inflammatory cytokines released by tumor and immune cells compromise the mesothelial cell layer that lines the peritoneal cavity, exposing the underlying extracellular matrix to which cancer cells readily attach leading to formation of spheroids which imparts resistance to anoikis, apoptosis and chemotherapeutics leading to efficient feed forward progressive cycle of seeding and growth of peritoneal metastasis. Intraperitoneal metastasis can cause peritoneal dysfunction, adhesions and malignant ascites. Epithelial mesenchymal transistion and myofibroblastic transformation occur in the mesothelial cells in response to pathological stimuli. Vascular endothelial growth factor is an important mitogen for endothelial cells and plays an important role in increasing capillary vascular permeability. In preclinical studies systemic administration of VEGF Trap which acts as a decoy receptor for VEGF has shown to decrease the formation of ascites fluid and prevent tumour dissemination. Epithelial ovarian cancer cells have developed various mechanisms to evade immune surveillance like development of surface microvesicles which contain CD 95 ligand leading to apoptosis of immune cells. Higher levels of osteoproteogerin, IL 10 and leptin in the ascitic fluid have been associated with a poor prognosis in malignant ascites. Tethered bowel sign and presence of fluid in the omental bursa on CT have been shown to distinguish between malignant ascites and Cirrhotic ascites with accuracy. Immunological approaches to management of malignant ascites include use of intraperitoneal triamcinolone, interferon, long acting synthetic corticosteroids and the trifoliate antibody catumaxomab. VEGF Inhihibitors like octreotide and long acting depot preparations of lanreotide have also been shown to be feasible therapeutic options. Anti androgenic agents and PARP inhibitors have also been proposed as management options. Spontaneous bacterial peritonitis in the setting of malignancy in the absence of hepatic dysfunction has been reported to have a poorer prognosis than SBP in the setting of decompensated liver disease. Monomicrobial and polymicrobial bacterascites have been proposed in the absence of an elevated neutrophil ascitic fluid count that does not meet the diagnostic criteria. Extensive liver metastasis where the diseased liver can be expected to behave like a cirrhotic liver and gastrointestinal bleeding (on the basis of an isolated case report) have been considered as risk factors for the development of SBP in malignant ascites. In a case series of 8 patients with malignancy related ascites Patients with total ascitic fluid concentration of less than 1 gm per litre were found to be at risk for Spontaneous bacterial peritonitis and warrant flouroquinolone prophylaxis. Conclusion: Spontaneous Bacterial Peritonitis complicating malignant ascites is questionable entity. Good quality Audits and Randomised control trials are warranted to in this domain to enable the definition of incidence, antecedent complications, management and prophylaxis to ensure applicability of translational research to the clinical domain.
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Yuan, Yuan y Diana-Andra Borca-Tasciuc. "The Influence of Coating and Agglomeration on Specific Absorption Rate of Iron Oxide Nanoparticles". En ASME 2011 9th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2011. http://dx.doi.org/10.1115/icnmm2011-58217.
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Magnetic nanofluids can be remotely heated by alternating magnetic field and have significant potential for cancer hyperthermia therapy. The heat generated by magnetic nanoparticles is typically quantified by the specific absorption rate (SAR), which represents the thermal power per unit mass of magnetic material generated in the presence of an alternating magnetic field. During hyperthermia treatment, heat dosage of tumor tissue correlates with slowing tumor growth. The therapeutic ratios of cancer can be increased with the use of biofunctionalized magnetic nanoparticles that have higher SAR for modest amplitudes of magnetic field[1]. Hence, understanding the factors that control the heat generation of magnetic nanoparticle suspensions is important to design fluids with optimized biocompatibility and functionality. In all biomedical applications, the nanoparticles must be coated on the surface to prevent their agglomeration [2], enhance biocompatibility and allow targeting to a specific area. Existing studies have shown that the SAR of nanoparticles may change in the presence of functional coating[3–5]. However, while these studies show that the coating may affect the heat generation rate, there is a limited understanding on the mechanisms that cause that changes of SAR. Hence, it is important to carry out a systematic investigation of nanoparticles similar in size but with different organic coating relevant to biomedical applications to obtain a more complete picture of the mechanisms contributing to changes in SAR. In this work, we present a review of our efforts in this area. Specifically, in our studies we are investigating the correlation between the magnetic and physical properties of commercially available nanoparticles systems and their heat generation rate. The susceptibility and SAR of suspensions of coated and uncoated iron oxide nanoparticles of similar particle size are measured. The coatings selected are highly relevant to biomedical applications and include amine and carboxyl functionalization as well as bioaffine ligands such as protein and biotin. The particle and cluster size was determined from transmission electron microscope (TEM), X-Ray diffraction (XRD) and Dynamic light scattering (DLS). TEM and DLS studies suggested that clusters exist in samples. A summary of all morphological properties together with pH of each suspension is shown in Table.1. The AC magnetic susceptibility of the suspensions was measured as a function of frequency with an in-house made apparatus. Finally SAR was determined by heating the suspension in a commercial induction system and measuring the temperature rise as function of time with a fiber optic sensor. Following these measurements, the SAR values were predicted in two ways: 1) based on measured AC susceptibility and 2) based on particle physical and magnetic properties, starting from Debye model for susceptibility. The normalized predicted and experimental SAR values for all samples are also shown in Table 1. From Table 1, it was found that pH may influence aggregation as described in Ref [6], which indicated that at pH about 2 nanoparticles are highly charged preventing their aggregation while in pH in 6–10 suspensions aggregations are more significant. Normalized SAR of nanoparticle system with aggregations seems to be not related to concentration, different from the well dispersed system[7]. The carboxyl coated sample has smallest diameter and show the lowest SAR, as reported in Ref[8]. The results of suspensions of uncoated iron oxide nanoparticles as well as particles coated with amine groups show that normalized experimental SAR (NSARE) agrees relatively well with calculated SAR using experimental susceptibility (NSARC_χ″E); poor agreement was found when experimental susceptibility was substituted with calculated one (NSART_χ″C) using Debye model, which is developed for non-interacting magnetic particles. These results suggest that the coating do not have a direct effect on SAR. On the other hand, agglomeration, which was present in both samples, may lead to dipolar interaction between nanoparticles and enhancement in magnetic properties and SAR. For carboxyl coated sample which has negligible clustering, showed no temperature increase and zero imaginary part of susceptibility. Therefore, good agreement between Debye-model based predictions of SAR and experimental results were obtained in this sample. However, unexpected results were obtained for bioaffine ligands coated sample, where the experimental SAR values are higher than the SAR values determined based on experimental susceptibility. Protein coated sample, which has the larger clusters among the two samples, has a heat generation rate is 6 times higher than the prediction. Meanwhile, the biotin coated sample which has relatively smaller clusters show only a small increase in heat generation rate. A possible explanation for these results is the loss of superparamagnetic character and an opening in hysteresis loop at test frequency for suspensions with large clusters, which may increase the dissipated power above that produced by the relaxation heat losses [9]. Above results show that coating had little effect on SAR. On the other hand, aggregations and clusters may significantly affect SAR, possibly due to dipolar interaction between nanoparticles in suspensions with relatively small clusters or loss of superparmagnetic characters when very large clusters are present.
Informes sobre el tema "Hematopoietic growth factors Therapeutic use"
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Sytkowski, Arthur J. Development of Hematopoietic Growth Factors for Use in Military Personnel. Fort Belvoir, VA: Defense Technical Information Center, julio de 1991. http://dx.doi.org/10.21236/ada242475.
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Sytkowski, Arthur J. Development of Hematopoietic Growth Factors for Use in Military Personnel. Fort Belvoir, VA: Defense Technical Information Center, agosto de 1990. http://dx.doi.org/10.21236/ada238603.
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