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Relevant bibliographies by topics / Bone inhibition

Academic literature on the topic 'Bone inhibition'

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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Journal articles on the topic "Bone inhibition"

1

Ransjö, Maria, and Ulf H. Lerner. "Calcitonin causes a sustained inhibition of protein kinase C-stimulated bone resorption in contrast to the transient inhibition of parathyroid hormone-induced bone resorption." Acta Endocrinologica 123, no. 3 (September 1990): 251–56. http://dx.doi.org/10.1530/acta.0.1230251.

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Abstract. Calcitonin is a well known inhibitor of osteoclastic bone resorption, both in vivo and in vitro. However, it is also known that calcitonin has only a transient inhibitory effect on bone resorption. The mechanism for this so-called "escape from inhibition" phenomenon is not clear. In the present study, the inhibitory effect of calcitonin on phorbol ester-induced bone resorption was examined in cultured neonatal mouse calvaria. Bone resorption was assessed as the release of radioactivity from bones prelabelled in vivo with 45Ca. Two protein kinase C-activating phorbol esters, phorbol-12-myristate-13-acetate and phorbol-12,13-dibutyrate, both stimulated 45Ca release in 120-h cultures at a concentration of 10 nmol/l. Calcitonin (30 nmol/l) inhibited phorbol esterstimulated bone resorption without any "escape from inhibition". This was in contrast to the transient inhibitory effect of calcitonin on bone resorption stimulated by parathyroid hormone (10 nmol/l), prostaglandin E2 (2 μmol/l), and bradykinin (1 μmol/l). Our results suggest that activation of protein kinase C produces a sustained inhibitory effect of calcitonin on bone resorption.

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Zhou, Jiabao, Jennifer M. Down, Christopher N. George, Jessica Murphy, Diane V. Lefley, Claudia Tulotta, Marwa A. Alsharif, Michael Leach, and Penelope D. Ottewell. "Novel Methods of Targeting IL-1 Signalling for the Treatment of Breast Cancer Bone Metastasis." Cancers 14, no. 19 (October 1, 2022): 4816. http://dx.doi.org/10.3390/cancers14194816.

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Breast cancer bone metastasis is currently incurable. Evidence suggests that inhibiting IL-1 signalling with the IL1R antagonist, Anakinra, or the IL1β antibody, Canakinumab, prevents metastasis and almost eliminates breast cancer growth in the bone. However, these drugs increase primary tumour growth. We, therefore, investigated whether targeting other members of the IL-1 pathway (Caspase-1, IL1β or IRAK1) could reduce bone metastases without increasing tumour growth outside of the bone. Inhibition of IL-1 via MLX01 (IL1β secretion inhibitor), VRT043198/VX765 (Caspase-1 inhibitor), Pacritinib (IRAK1 inhibitor) or Anakinra (IL1R antagonist) on tumour cell viability, migration and invasion were assessed in mouse mammary E0771 and Py8119 cells in vitro and on primary tumour growth, spontaneous metastasis and metastatic outgrowth in vivo. In vitro, Inhibition of IL-1 signalling by MLX01, VRT043198 and Anakinra reduced migration of E0771 and Py8119 cells and reversed tumour-derived IL1β induced-increased invasion and migration towards bone cells. In vivo, VX765 and Anakinra significantly reduced spontaneous metastasis and metastatic outgrowth in the bone, whereas MLX01 reduced primary tumour growth and bone metastasis. Pacritinib had no effect on metastasis in vitro or in vivo. Targeting IL-1 signalling with small molecule inhibitors may provide a new therapeutic strategy for breast cancer bone metastasis.

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Deng, Jianhua, Jun Wu, and Yuchang Zhu. "Inhibition of MicroRNA-9 Improves Fracture Healing by Modulating the Bone Morphogenetic Protein-7 Pathway." Pharmacology 104, no. 5-6 (2019): 352–58. http://dx.doi.org/10.1159/000502402.

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We evaluated the effect of microRNA (miR)-9 inhibition on fracture healing in a rat model of femoral fracture. The rats were divided into sham, negative control and miR-9 inhibitor groups. The miR-9 inhibitor group received 30 pmol/mL inhibitor intrathecally for 8 consecutive weeks following surgery-induced femoral fracture. The effect of miR-9 inhibition on fracture healing was estimated by determining the bone mineral density (BMD) and by performing X-ray analysis of the fractured bone. The serum levels of markers of bone formation were estimated by enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction, and western blotting and immunohistochemical analysis were performed to assess the effect of miR-9 inhibition on fracture healing. The BMD at the fracture site was significantly higher in the miR-9 inhibitor group than in the negative control group. Inhibition of miR-9 blocked the fracture gap and resulted in new callus formation at the fracture site. The serum levels of osteocalcin and bone GLA protein were increased and that of alkaline phosphatase was decreased by inhibition of miR-9 compared to levels in the negative control. However, inhibition of miR-9 significantly increased the mRNA levels of runt-related transcription factor 2 (Runx2) and bone morphogenetic protein 7 (BMP-7) in the bone tissue at the fracture site compared to the negative control group; this result was confirmed by western blotting. In conclusion, miR-9 inhibition enhanced fracture healing by modulating the BMP-7/Runx2 signalling pathway in a rat model of femoral fracture.

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Banu, Jameela, Erika Varela, Ali N. Bahadur, Raheela Soomro, Nishu Kazi, and Gabriel Fernandes. "Inhibition of Bone Loss byCissus quadrangularisin Mice: A Preliminary Report." Journal of Osteoporosis 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/101206.

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Women drastically loose bone during and after menopause leading to osteoporosis, a disease characterized by low bone mass increasing the risk of fractures with minor trauma. Existing therapies mainly reduce bone resorption, however, all existing drugs have severe side effects. Recently, the focus is to identify alternative medicines that can prevent and treat osteoporosis with minimal or no side effects. We usedCissus quadrangularis(CQ), a medicinal herb, to determine its effects on bone loss after ovariectomy in C57BL/6 mice. Two-month old mice were either sham operated or ovariectomized and fed CQ diet. After eleven weeks, mice were sacrificed and the long bones scanned using pQCT andμCT. In the distal femoral metaphysis, femoral diaphysis, and proximal tibia, control mice had decreased cancellous and cortical bone, while CQ-fed mice showed no significant differences in the trabecular number, thickness, and connectivity density, between Sham and OVX mice, except for cortical bone mineral content in the proximal tibia. There were no changes in the bone at the tibio-fibular junction between groups. We conclude that CQ effectively inhibited bone loss in the cancellous and cortical bones of femur and proximal tibia in these mice.

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Vallet, Sonia, Kishan Patel, Nileshwari Vaghela, Mariateresa Fulciniti, Petter Veiby, Teru Hideshima, Samantha Pozzi, et al. "CCL3 Impairs Osteoblast Function Via Downregulation of Osteocalcin." Blood 114, no. 22 (November 20, 2009): 739. http://dx.doi.org/10.1182/blood.v114.22.739.739.

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Abstract Abstract 739 A common feature of bone disease in cancer is hyperactivity of osteoclasts (OC). However, osteoblast (OB) inhibition is critical to the development of osteolytic lesions. Tumor-OC interactions have been extensively studied, the mechanism of OB inhibition however still remains elusive. Several chemokines are upregulated in the multiple myeloma (MM)/bone microenvironment. CCL3 (MIP-1αa), in particular, mediates MM cell migration and stimulates OC differentiation, directly, by stimulating precursor cell fusion, and indirectly, by inducing OB secretion of RANKL. Here, we investigate whether CCL3 interferes with OB differentiation and activity. In vitro osteoblastogenesis consists of differentiation of alkaline phosphatase (ALP) positive cells, followed by secretion and mineralization of the extracellular matrix. We observed that ALP-positive cells express both CCL3 receptors, CCR1 and CCR5, late in differentiation (40% and 32%, respectively, isotype control 9%). No significant CCL3 secretion was detected in OB culture supernatant, suggesting that paracrine CCL3 may primarily affect matrix mineralization. Indeed, exogenous CCL3 (25 to 100 ng/ml) did not modify OB number, instead it decreased calcium deposition (10% decrease at 25ng/ml, 33% decrease at 50 and 100 ng/ml, p<0.05). We next assessed the expression levels of proteins critical to matrix formation and mineralization including osteopontin, bone-sialoprotein and osteocalcin. Osteopontin expression was not affected by CCL3, while both bone-sialoprotein and osteocalcin were downregulated. Importantly, either continuous exposure to CCL3 or 24h stimulation of mature OB impaired RNA expression of osteocalcin (30% to 80%) and bone-sialoprotein (26% to 60%) but not ALP, confirming that CCL3 interferes with OB function rather than formation. We also observed a correlation between osteocalcin expression by IHC on BM biopsies and CCL3 levels in BM serum of MM patients. These data suggest that MM-derived CCL3 interferes with bone mineralization by inhibiting osteocalcin expression. Using neutralizing antibodies against CCL3 we restored both osteocalcin and bone sialoprotein RNA expression levels in the presence of CCL3. Importantly, pretreatment with a small molecule CCR1 inhibitor, MLN3897 (Millennium Pharmaceuticals) completely abrogated the inhibition on osteocalcin and partially reversed bone-sialoprotein expression, suggesting CCR1 as the main mediator of CCL3 effects. We further verified these results in an in-vivo setting of MM bone disease, using the SCID-hu model. CB17 SCID mice bearing a human fetal bone implant were engrafted with CCL3-expressing INA6 MM cells and treated orally with MLN3897 for a total of 49 doses. After 4 weeks of treatment the bones were harvested and stained for TRAP activity, hematoxylin-eosin and osteocalcin. The number of OC/400x field was significantly reduced in the treated group (2.7 vs 1.9, p<0.05), thus confirming in vivo the anti-osteoclastogenic effect of CCR1 inhibition. Moreover, in the presence of INA6 MM cells osteocalcin levels were downregulated compared to non-injected bones and treatment with the CCR1 inhibitor partially restored osteocalcin expression. These results suggest a new role for the CCL3/CCR1 pathway in the development of osteolytic lesions in MM, as inhibitor of OB function other than OC growth factor. Targeting this pathway represents a promising strategy for the treatment of bone disease. Disclosures: Veiby: Millennium Pharmaceuticals: Employment. Anderson:Millennium: Research Funding. Raje:Astrazeneca, Novartis, Celgene: Research Funding.

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Wada, Teiji. "RANKL inhibition in bone metastases." Folia Pharmacologica Japonica 141, no. 1 (2013): 22–26. http://dx.doi.org/10.1254/fpj.141.22.

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Takayanagi, Hiroshi. "RANKL inhibition -Bone and beyond-." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): SY42–1. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_sy42-1.

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Momenzadeh, Mahnaz, Maryam Khosravian, and Bhaskar VKS Lakkakula. "Potential of renin-angiotensin system inhibition to improve metabolic bone disorders." Journal of Nephropharmacology 10, no. 2 (October 17, 2020): e16-e16. http://dx.doi.org/10.34172/npj.2021.16.

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Metabolic bone disorder is an abnormality of bones indicated by reduced bone mass and high risk of fractures. Several lines of evidence have demonstrated that the local bone tissue renin-angiotensin system (RAS) is directly involved in bone metabolism and influences the bone health. This review aimed to assess the role of RAS in bone metabolism and comparative effectiveness of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) in reducing the bone fractures. In summary, the clinical trials, in vivo studies, and functional - pharmacological experiments suggested that the RAS regulates bone marrow metabolism and influences the bone health. Hence, it warrants further investigation on the role of ACEIs and ARBs in reducing risk fractures.

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Fraser, Christopher C., Kumiko Nagashima, Vito Sasseville, Jim Deeds, Alice McDonald, Chris Simpson, and Yajun Xu. "Selective Rapid B-Cell Depletion In Vivo by Pharmacologic IKK2 Inhibition." Blood 104, no. 11 (November 16, 2004): 2481. http://dx.doi.org/10.1182/blood.v104.11.2481.2481.

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Abstract Studies using genetically deficient mice have revealed that members of the NF-kB family play key roles in B-cell development. IKK2 which activates NF-kB by targeting degradation of IkB, is also required for B-cell development. We have studied the role of IKK2 in hematopoiesis using a chemical specific inhibitor (ML120B). Mice given daily oral dosing of ML120B for 4 days had severe B-cell depletion in spleen and bone marrow. B-cells at all stages (pro-B, pre-B, immature and mature B) were depleted 10 fold in the bone marrow while granulocyte numbers were largely unaffected. IKK2 inhibition in vivo showed selective sensitivity of B-cell progenitors (4 fold decrease) in the marrow compared to myeloid progenitors which were unaffected at an equivalent dose. Foci of cells with an apoptotic morphology were visible in bone marrow and spleen within 6 hours of a single oral dose. Apoptotic cells detected by labeling fragmented DNA were increased within splenic follicles (6 fold) and bone marrow. Also an increase in B220+ / annexin V+ cells and a decrease in pre-B (B220+/IgM−) cells in the marrow were observed. RNA expression studies in the marrow 6 hours after a single oral dose revealed a decrease in IL-7 and increased GM-CSF expression. Image analysis of B220 in spleens within 18 hours of a single dose of an IKK inhibitor revealed decreased follicle size. In order to evaluate hematopoietic progenitor sensitivity to NF-kB inhibition, dose responses to ML120B, panepoxydone (PPD) and proteasome inhibitor Lactacystin (Lcyst) were evaluated in B-cell and myeloid bone marrow colony assays. Inhibitors PPD and Lcyst were more effective at inhibiting B-cell colony growth than myeloid colony growth. In summary, pharmacologic inhibition of IKK2 results in a rapid induction of apoptosis with preferential depletion of B-cells and retention of myeloid cells and progenitors within the bone marrow.

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Kaipatur, N. R., M. Murshed, and M. D. McKee. "Matrix Gla Protein Inhibition of Tooth Mineralization." Journal of Dental Research 87, no. 9 (September 2008): 839–44. http://dx.doi.org/10.1177/154405910808700907.

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Extracellular matrix (ECM) mineralization is regulated by mineral ion availability, proteins, and other molecular determinants. To investigate protein regulation of mineralization in tooth dentin and cementum, and in alveolar bone, we expressed matrix Gla protein (MGP) ectopically in bones and teeth in mice, using an osteoblast/odontoblast-specific 2.3-kb Col1a1 promoter. Mandibles were analyzed by radiography, micro-computed tomography, light microscopy, histomorphometry, and transmission electron microscopy. While bone and tooth ECMs were established in the Col1a1-Mgp mice, extensive hypomineralization was observed, with values of unmineralized ECM from four- to eight-fold higher in dentin and alveolar bone when compared with that in wild-type tissues. Mineralization was virtually absent in tooth root dentin and cellular cementum, while crown dentin showed “breakthrough” areas of mineralization. Acellular cementum was lacking in Col1a1-Mgp teeth, and unmineralized osteodentin formed within the pulp. These results strengthen the view that bone and tooth mineralization is critically regulated by mineralization inhibitors.

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Dissertations / Theses on the topic "Bone inhibition"

1

Hussein, Hayam. "Cathepsin K Inhibition In Bone And Bone Marrow In Horses." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1449218489.

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Bui, Lynn. "Inhibition of System Xc⁻ Reduces Cancer-Induced Bone Pain." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/321599.

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The most common cancer types have a high likelihood of metastasizing to the bone and can cause cancer-induced bone pain (CIBP). Current therapeutic options do not offer proper management and thus CIBP can severely affect a patient's quality of life. Dysregulation of the excitatory neurotransmitter, glutamate, may be involved in the complex and multifaceted mechanisms of CIBP. Because glutamatergic signaling promotes pain, a local rise in glutamate in the bone-tumor microenvironment may contribute to CIBP. Glutamate levels are regulated in part by the cystine/glutamate antiporter, system xc⁻. System xc⁻ is known to be expressed by many different cancer cell types. It functions by transporting cystine into cells and in return releasing glutamate into the extracellular space. Elevated glutamate levels driven by the upregulated expression of this antiporter may contribute to CIBP. Here we demonstrate that system xc⁻ is expressed on a spontaneously occurring murine mammary tumor cell line (66.1) and that treatment of these cells with the established inhibitor and anti-inflammatory agent, sulfasalazine, decreases glutamate secretion in a time and dose-dependent manner. Furthermore, in a novel model of breast CIBP, systemic sulfasalazine treatment not only reduces glutamate levels within the femur, but also significantly attenuates CIBP behaviors. Studies utilized 66.1 cells implanted into the femur intramedullary space of immunocompetent mice. Measurements of spontaneous and evoked pain were made 7 and 10 days post cancer cell inoculation. Systemic administration of sulfasalazine for 4 days (on days 7-10) significantly reduced spontaneous pain-related behaviors and glutamate in femur extrudate as compared to vehicle treated controls. In summary, we demonstrate that pharmacological inhibition of the system xc⁻ transporter attenuates CIBP related behaviors in mice. These data support a role for system xc⁻ in CIBP and validate it as an analgesic target. Further research is warranted to evaluate the potential repurposing of sulfasalazine as an antinociceptive agent for patients with CIBP.

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Pappalardo, Angela. "Defining the role of γδ cells in bone loss associated with chronic inflammation." Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=203414.

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The extensive infiltration of immune cells in the joints of patients affected by rheumatoid arthritis (RA), and the subsequent production of pro-inflammatory cytokines triggers bone erosion through the extensive stimulation of bone resorbing osteoclasts (OCs). The activity of γδ T cells has been implicated to influence the onset and severity of the disease pathology in murine models of human RA. With this study the effects of γδ T cells for influencing OC differentiation and resorptive activity were assessed in vitro. Activated γδ T cells exerted inhibitory effects on OC differentiation and resorptive activity, these effects were mediated by the release of soluble factors, since similar inhibitory effects were obtained using conditioned medium (CM) from activated γδ T cells. The primary mediator of such effects was determined to be IFN, since neutralisation markedly restored OC differentiation and resorptive activity. γδ T cell proliferation, activation and survival following culture with autologous mature OCs were assessed by flow cytometry. Interestingly, OCs and OC-derived CM induced activation of γδ T cells as determined by the expression of the early activation marker CD69. A mediator of this stimulatory effect on T cells was found to be TNF, since neutralisation of TNFα decreased the stimulatory effect of OCs on CD69 expression. Consistently, OCs, but not OC-derived CM, increased the proliferation of IL-2-stimulated γδ T cells and also supported the survival of resting γδ T cells. This study provides new insights into the in vitro interactions between human γδ T cells and OCs, moreover it defines osteoclasts as immune competent cells capable of influencing the activation status and the viability of T lymphocytes, and provide evidence for a novel stimulatory effect of OCs on γδ T cells.

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Al-Masri, Maher. "Limitations of bone formation in oral implantology : inhibition of osteoblast functions by gingival tissues." Thesis, Queen Mary, University of London, 2010. http://qmro.qmul.ac.uk/xmlui/handle/123456789/356.

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Clinical observation suggest that bone formation is influenced by the environmental niche where it takes place and specifically that soft connective tissues may inhibit the bone healing process. The aim of the studies described in this thesis is to test the hypothesis that fibroblasts inhibit the differentiation and function of osteoblasts in vitro. To address this aim the ability of fibroblasts and their supernatants to inhibit osteoblast differentiation was investigated. In addition, the inhibitory effects of gingival and periodontal ligament fibroblasts were compared. Next Bone Morphogenetic Proteins (BMPs) and their antagonists were tested for their ability to modulate the activity of fibroblast supernatants. Finally the effects of fibroblast supernatants on osteoblast chemotactic responses were investigated. Primary fibroblasts were isolated from rat gingivae, skin, oral mucosa and periodontal ligament (PDL) using explant cultures. Primary osteoblast cultures were established by enzymatic digestion of neonatal rat calvariae. In other experiments the osteoblastic cell line ROS 17/2.8 was used. Osteoblast differentiation was assessed by measuring alkaline phosphatase (ALP). In co-culture experiments using 3-D collagen gels and diffusion chamber inserts fibroblasts strongly inhibited osteoblast differentiation. Furthermore conditioned medium from superficial connective tissues fibroblasts consistently inhibited osteoblast differentiation (greater than 50% inhibition of ALP expression. In contrast, PDL cells strongly stimulated ALP expression (greater than 100% increase). Stimulation of ROS 17/2.8 cells with BMP-2 increased ALP expression (more than 3 fold increase with 10ng/ml BMP-2), and this effect could be completely blocked by the BMP-antagonist 100ng/ml noggin. Similarly conditioned media from gingival, oral mucosal and skin fibroblasts totally suppressed the effects of BMP-2. In contrast, PDL conditioned media stimulated ALP expression in additively with BMP-2, and his effect could also be blocked by noggin. Using a micro-well Boyden Chamber both PDGF and BMP-2 caused a dose-dependent increase in chemotaxis. However fibroblast conditioned medium totally blocked the chemotactic effects on BMP-2, but had no effect on PDGF-induced chemotaxis. Overall these studies demonstrate that fibroblasts from superficial connective tissues (gingival, oral mucosa and skin) can inhibit osteoblast function by secretion of BMPantagonists and that superficial connective tissues and PDL are distinct in respect to their role in bone healing. Further studies are needed to identify the specific molecular identity of this inhibitory activity and to extend these observations to an in vitro model. However in the longer term it is proposed that information on the regional expression of BMP inhibitors may lead to novel therapeutic interventions to promote bone growth in periodontal and implant related bone regeneration procedures.

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Sukhtankar, Devki, Alec Okun, Anupama Chandramouli, Mark Nelson, Todd Vanderah, Anne Cress, Frank Porreca, and Tamara King. "Inhibition of p38-MAPK signaling pathway attenuates breast cancer induced bone pain and disease progression in a murine model of cancer-induced bone pain." BioMed Central, 2011. http://hdl.handle.net/10150/610213.

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BACKGROUND:Mechanisms driving cancer-induced bone pain are poorly understood. A central factor implicated to be a key player in the process of tumorigenesis, osteoclastogenesis and nociception is p38 MAPK. We determined the role of p38 MAPK in a mouse model of breast cancer induced bone pain in which mixed osteolytic and osteoblastic remodeling occurs.RESULTS:In cancer-treated mice, acute as well as chronic inhibition of p38 MAPK with SB203580 blocked flinching and guarding behaviors in a dose-dependent manner whereas no effect on thresholds to tactile stimuli was observed. Radiographic analyses of bones demonstrated that chronic inhibition of p38 MAPK reduced bone loss and incidence of spontaneous fracture in cancer-treated mice. Histological analysis of bones collected from mice treated with the p38 MAPK inhibitor showed complete absence of osteoblastic growth in the intramedullary space as well as significantly reduced tumor burden.CONCLUSIONS:Blockade of non-evoked pain behaviors but not hypersensitivity suggests differences in the underlying mechanisms of specific components of the pain syndrome and a possibility to individualize aspects of pain management. While it is not known whether the role of p38 MAPK signaling can be expanded to other cancers, the data suggest a need for understanding molecular mechanisms and cellular events that initiate and maintain cancer-induced bone pain for effective management for both ongoing pain as well as breakthrough pain.

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Yoshioka, Yumiko. "Differential effects of inhibition of bone morphogenetic protein (BMP) signalling on T-cell activation and differentiation." Kyoto University, 2012. http://hdl.handle.net/2433/157448.

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Wickman, Sanna. "Aromatase inhibition in boys with delayed puberty effects on growth, maturation, bone, serum lipids, and insulin." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/wickman/.

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Dai, Rongchen. "Development of an osteoclast-targeted cathespin K inhibitor for postmenopausal osteoporosis : in vitro evaluation and pharmacokinetic profile." HKBU Institutional Repository, 2020. https://repository.hkbu.edu.hk/etd_oa/840.

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Background: Postmenopausal osteoporosis which results in a reduction of bone quality and bone density is one of the most prevalent diseases affecting people around the world. Cathepsin K (CatK) is one of the most potent proteases in lysosomal cysteine proteases family, of which main function is to mediate bone resorption. Currently, the Odanacatib (ODN) developed by Merck & Co. is the only Phase III CatK inhibitor candidate with high efficacy in treating postmenopausal osteoporosis. Unfortunately, the development of ODN was finally terminated due to the cardio-cerebrovascular adverse effects. In order to enhance the specificity of ODN to osteoclasts for suppression of bone resorption in postmenopausal osteoporosis, we have previously designed and synthesized (D-Asp8)-ODN conjugate by linking ODN with a promising osteoclast-targeted moiety D-Asp8. The data showed that D-Asp8 could facilitate the conjugated ODN specifically approaching osteoclasts, with reduced distribution in non-bone tissues, to inhibit the functional CatK activity within bone tissues in healthy rats. In this thesis, we hypothesized that the in vitro antiresorptive effects of (D-Asp8)-ODN conjugate were comparable with that of ODN. On the other hand, we also developed a QQQ-LC/MS method for quantitation of (D-Asp8)-ODN conjugate in plasma, which will be a valuable tool to support further pre-clinical studies. Aim: (1) To compare the antiresorptive effect between (D-Asp8)-ODN conjugate and ODN in vitro. (2) To develop and validate a practicable method for pharmacokinetic profile of (D-Asp8)-ODN conjugate in rats. Materials and Methods: The cytotoxic effect of (D-Asp8)-ODN conjugate and ODN were evaluated and compared by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The effect of (D-Asp8)-ODN conjugate and ODN on Receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclasts formation and osteoclast function-related genes were evaluated and compared by Tartrate-resistant acid phosphatase (TRAP) staining and quantitative real time polymerase chain reaction (qRT-PCR). The effect of (D-Asp8)-ODN conjugate and ODN on osteoclast bone resorption activities were evaluated and compared by bone resorption pit assay. Moreover, the pharmacokinetic profile of (D-Asp8)-ODN conjugate in rat plasma was determined by using triple quadrupole liquid chromatography-mass spectrometry (QQQ-LC/MS) system. Result: The cytotoxicity of (D-Asp8)-ODN conjugate was significantly lower than that of ODN on the murine macrophage RAW 264.7 cell line. (D-Asp8)-ODN conjugate had no effect on RANKL-induced osteoclast formation, which was comparable with that of ODN. (D-Asp8)-ODN conjugate had no effect on the mRNA level of CTSK, but it could upregulate the mRNA levels of ACP5 and OSCAR, which was comparable with that of ODN. (D-Asp8)-ODN conjugate inhibited osteoclast bone resorption activity, which was comparable with that of ODN. The newly established QQQ-LC/MS protocol had good precision and accuracy for detecting (D-Asp8)-ODN conjugate in rat plasma. Finally, the pharmacokinetic profile of (D-Asp8)-ODN conjugate in rat plasma was determined. Following subcutaneous administration, the time to reach maximum concentration (Tmax) was 1.0 h, the antibiotics area under the concentration time-curves from time zero to infinity (AUC0-∞) was found to be 27.78 ug·mL-1·h and the terminal half-life (t½) was 1.4 h. Conclusion: (D-Asp8)-ODN conjugate had no effect on RANKL-induced osteoclast formation, which was comparable with ODN. The antiresorptive effect of (D-Asp8)-ODN conjugate was comparable with that of ODN. On the other hand, a new QQQ-LC/MS protocol has been established for the pharmacokinetic profile of (D-Asp8)-ODN conjugate in rat.

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Nolan, Kristof T. "Insights into the Molecular Determinants Required for DAN-family Mediated Inhibition of BMP Signaling." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1468335666.

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Albishi, Waleed. "Inhibition of fibroblast growth factor receptor 3 (FGFR3) signalling to accelerate bone formation during distraction osteogenesis of mice tibiae." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121465.

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Distraction osteogenesis (DO) is a surgical technique widely used for the treatment of limb length discrepancies, limb deformities, long bone nonunions, and bone loss. The technique involves performing an osteotomy and then gradually distracting the two bone segments with an external fixator. This generates new bone within the distracted gap. Although very successful, one of the limitations of this technique is the long period of time the external fixator needs to be kept on, until the newly formed bone in the distracted zone consolidates. This prolonged process may lead to numerous social, psychological, and medical complications. Recent studies from our laboratory showed that the absence of signalling through the fibroblast growth factor receptor 3 (FGFR3) in DO leads to an increase in bone formation in mice deficient for FGFR3. Thus, we hypothesize that exogenous blocking of the FGFR3 pathway in wild-type mice may be efficacious in promoting bone formation in DO. We thus planned to block this pathway using the small molecule inhibitor, PD173074 or using anti-FGFR3 antibodies. In this study, we used 2-month old wild-type C57BL/6 mice divided in 5 groups. The mice have undergone a surgical osteotomy and installation of an external fixator (distraction apparatus). Following a 5-day latency period, distraction (0.2 mm/12 hours for 12 days) was initiated. The animals were sacrificed at day 33 post-surgery (mid consolidation). Micro-computed tomography (μCT) of the wild-type control group tibiae (not treated) was compared to the tibiae of mice receiving one of three increasing doses of small molecule inhibitors and mice receiving a blocking dose of anti-FGFR3 antibodies. Our results showed a trend towards increased bone volume in mice receiving the higher doses of the small molecule inhibitor as compared to those of the untreated wild-type mice. This dose ranging experiment represents a critical study in this translational research effort to accelerate bone formation in DO.
L'ostéogénèse par distraction (Distraction Osteogenesis, DO) est une technique chirurgicale largement utilisée pour le traitement des anomalies de la longueur des membres, des malformations, des fractures non-union, et de la perte osseuse suivant un traumatisme. La technique consiste à effectuer une ostéotomie puis à éloigner progressivement les deux segments osseux à l'aide d'un fixateur externe. Du nouveau tissu osseux se forme progressivement dans l'espace créé par la traction. Bien que montrant un taux de succès élevé, un des désavantages de cette technique est la longue période de temps où le fixateur externe doit être maintenu en place afin que l'os nouvellement formé se consolide. Cette période prolongée peut entraîner de nombreuses complications d'ordre social, psychologique ou médical. Des résultats récents de notre laboratoire montrent que l'absence de signalisation par le récepteur 3 des facteurs de croissance fibroblastiques (Fibroblast Growth Factor Receptor 3, FGFR3) au cours de la DO conduit à une augmentation de la formation osseuse chez les souris déficientes en FGFR3. Nous avons donc émis l'hypothèse que le blocage de la voie signalétique FGFR3 chez des souris de type sauvage pourrait être efficace afin d'augmenter la formation osseuse au cours de la DO. Afin de bloquer cette voie signalétique, nous avons utilisé un inhibiteur synthétique, PD173074, ou des anticorps anti-FGFR3. Des souris C57Bl/6 de type sauvage agée de 2 mois et divisée en 5 groupes. Les souris ont subi une ostéotomiechirurgicale et l'installation du fixateur externe (appareil de distraction). Après une période de récupération de 5 jours, la distraction a été amorcée (0,2 mm/12 heures pendant 12 jours). Les animaux ont été sacrifiés au jour 33 post-chirurgie (mi-consolidation). À l'aide de la tomographie haute résolution assistée par ordinateur (micro-computedtomography, μCT), nous avons comparé la formation osseuse dans l'espace créé par la traction entre le groupe contrôle (recevant seulement le véhicule) et les groupes traités avec une des trois doses croissantes d'inhibiteur ou avec l'anticorps anti-FGFR3. Nos résultats montrent une tendance dose-dépendante à l'augmentation de la formation osseuse chez les souris recevant l'inhibiteur, par rapport aux souris non traitées. Cette étude pilote est un jalon important dans la recherche translationnellevisant à accélérer la formation osseuse au cours de l'ostéogénèse par distraction.

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Books on the topic "Bone inhibition"

1

Gevorgyan, Artur. Radiation-induced craniofacial bone growth inhibition: Investigation of the mechanisms and radioprotection in vitro. 2007.

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Ruabens, Robert D. The Management of Bone Metastases and Hypercalcaemia by Osteoclast Inhibition: An International Symposium Held During the 5th European Conference on. Hogrefe & Huber Pub, 1990.

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Maria, Bijvoet Olav Leonardus, Lipton Allan, and International Cancer Congress (15th : 1990 : Hamburg, Germany), eds. Osteoclast inhibition in the management of malignancy-related bone disorders: An international symposium held during the 15th International Cancer Congress, Hamburg, Germany, August 1990. Seattle: Hogrefe & Huber, 1993.

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P, Halloran Bernard, and Ames Research Center, eds. The role of 1,25-Dihydroxyvitamin D in the inhibition of bone formation induced by skeletal unloading. [Moffett Field, Calif.?: National Aeronautics and Space Administration, Ames Research Center?, 1985.

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P, Halloran Bernard, and Ames Research Center, eds. The role of 1,25-Dihydroxyvitamin D in the inhibition of bone formation induced by skeletal unloading. [Moffett Field, Calif.?: National Aeronautics and Space Administration, Ames Research Center?, 1985.

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P, Halloran Bernard, and Ames Research Center, eds. The role of 1,25-Dihydroxyvitamin D in the inhibition of bone formation induced by skeletal unloading. [Moffett Field, Calif.?: National Aeronautics and Space Administration, Ames Research Center?, 1985.

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D, Rubens R., and European Conference on Clinical Oncology (5th : 1989 : London, England), eds. The Management of bone metastases and hypercalcaemia by osteoclast inhibition: An international symposium held during the 5th European Conference on Clinical Oncology (ECCO 5), London, September 1989. Toronto: Hogrefe & Huber, 1990.

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Figueiredo, Camille, and Georg Schett. Assessment of joint and bone structure in PsA patients: Using high-resolution computed tomography. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0019.

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Psoriatic arthritis (PsA) is associated with a distinct pattern of bone pathology, which influences the clinical picture of the disease. High-resolution computed tomography (CT) has contributed to understanding structural bone changes in PsA. Periarticular bone erosions in PsA are characterized by periosteal responses around the cortical break, distinguishing them from bone erosions in rheumatoid arthritis. Furthermore, a large number of enthesophytes can be found in CT studies of joints of PsA patients and in psoriasis patients without clinical arthritis. This latter observation supports the idea that articular changes start in psoriasis before joint disease commences. Moreover, enthesophytes are not influenced by methotrexate treatment and tumour necrosis factor inhibition. Finally, studies of systemic bone loss by high-resolution CT revealed significant alterations of the bone architecture in PsA but not in patients with skin disease only. In summary, CT has made valuable contributions in understanding the structural bone changes in PsA.

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Bijvoet, O. L. M. Osteoclast Inhibition in the Management of Malignancy-Related Bone Disorders: An International Symposium Held During the 15th International Cancer Co. Hogrefe & Huber Pub, 1992.

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Healey, John H., and David McKeown. Orthopaedic surgery in the palliation of cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0125.

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Metastatic spread of cancer to bone is frequent and causes pain, disability, and functional limitation. New understanding of the homing method of cancer cells to bone and the mechanism of cancer production of pain raise possible new treatment strategies. Non-surgical treatments such as chemotherapy and hormone therapy are effective in early disease. Bisphosphonates and inhibition of osteoprotegerin prevent progression of bone lesions and avoid pain, radiation, and surgery. Radiotherapy arrests disease and relieves pain in many cases. Surgery is needed when the bone is weak or fractured. It effectively relieves pain and preserves function. It usually requires replacing or bypassing the deficient bone with site-specific reconstructive surgery. Surgery should be selected based on projections of patient survival. New tools to make these projections have been validated and are now available. New targeted drug therapies appear to be changing metastatic bone disease into a more chronic condition. This will alter the management of local disease in many histological subtypes of metastatic cancers.

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Book chapters on the topic "Bone inhibition"

1

Franck, H., F. van Valen, E. Keck, and H. L. Krüskemper. "Inhibition of Protein Synthesis and Amino Acid Transport by Dihydrotestosterone and 17ß-Estradiol in Chick Osteoblasts." In Generalized Bone Diseases, 87–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-73346-8_10.

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Yasui, Hiroshi, Teru Hideshima, and Kenneth C. Anderson. "Inhibition of TGF-β Signaling in Multiple Myeloma and Its Bone Marrow Microenvironment." In Transforming Growth Factor-β in Cancer Therapy, Volume II, 219–27. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-293-9_15.

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Kanzaki, Hiroyuki, Xiaozhe Han, Yukiko Asami, Maiko Suzuki, Toshihisa Kawai, and Martin Taubman. "Inhibition of T-Cell-Mediated and Infection-Induced Periodontal Bone Resorption by TACE Blockade." In Interface Oral Health Science 2011, 173–75. Tokyo: Springer Japan, 2012. http://dx.doi.org/10.1007/978-4-431-54070-0_45.

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Vinci, G., J. P. Vernant, C. Cordonnier, A. Henri, H. Rochant, J. Breton-Gorius, and W. Vainchenker. "In vitro Inhibition of Hematopoiesis by T3, HNK1, T8, DR Positive T Cells after Bone Marrow Transplantation." In 11th Annual meeting of the EBMT, 69. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-662-40457-7_49.

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Schneider, Katharina S., Christina J. Thomas, and Olaf Groß. "Inflammasome Activation and Inhibition in Primary Murine Bone Marrow-Derived Cells, and Assays for IL-1α, IL-1β, and Caspase-1." In Methods in Molecular Biology, 117–35. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-523-1_10.

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Niculescu, Rodica, John F. Renz, and George F. Kalf. "Benzene-Induced Bone Marrow Cell Depression Caused by Inhibition of the Conversion of Pre-Interleukins-1α and -1β to Active Cytokines by Hydroquinone, a Biological Reactive Metabolite of Benzene." In Advances in Experimental Medicine and Biology, 329–37. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9480-9_40.

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Kirthi, Arivarasan Vishnu, and Loganathan Karthik. "Inhibition of Mosquito Vectors of Malaria and Filariasis Using Marine Microorganisms and Their Associated Compounds." In Microbial Control of Vector-Borne Diseases, 27–36. Boca Raton : Taylor & Francis, 2018.: CRC Press, 2018. http://dx.doi.org/10.1201/b22203-3.

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Alpaslan, Ece, Hilal Yazici, Negar Golshan, Katherine S. Ziemer, and Thomas J. Webster. "Dextran Coated Cerium Oxide Nanoparticles for Inhibiting Bone Cancer Cell Functions." In Ceramic Transactions Series, 187–96. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781119190134.ch17.

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Fang, J., J. W. Stern, S. Shusterman, K. Alcorn, G. Pierson, R. Barr, B. Pawel, L. Diller, J. M. Maris, and S. A. Grupp. "Angiogenesis Inhibitor TNP-470 During Bone Marrow Transplant and in Minimal Residual Disease." In Transplantation in Hematology and Oncology II, 283–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55774-3_34.

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Endo, Tatsuo, Tamami Hoshino, Hiromi Sasazaki, Etsuko Miura, and Masashi Komatsu. "Improvement of the Dentin Bond System by Reducing the Oxygen Inhibition Effect on Curing of Resin-Based Bond Materials." In Interface Oral Health Science 2011, 257–59. Tokyo: Springer Japan, 2012. http://dx.doi.org/10.1007/978-4-431-54070-0_74.

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Conference papers on the topic "Bone inhibition"

1

Ghura, H., C. Zoeller, and I. Nakchbandi. "Pharmacologic inhibition of fibronectin accumulation suppresses bone metastasis growth." In OSTEOLOGIE 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680008.

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Qin, Yi-Xian, and Hoyan Lam. "Bone Formation and Inhibition of Bone Loss by Dynamic Muscle Stimulation With Altered Interstitial Fluid Pressure." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176607.

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Tissue-level mechanisms and functions, including bone strain and muscle, are the potential key players in bone physiology and adaptation [1,2,3]. However, the mechanisms are not yet fully understood. Exercise such as muscle contraction appears to increase blood flow to the skeletal tissues, i.e., bone and muscle. These evidences imply that bone fluid flow induced by muscle dynamics may be an important role in regulating fluid flow through coupling of muscle and bone via microvascular system.

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3

Adam, S., N. Simon, U. Steffen, F. Andes, D. Müller, S. Culemann, D. Andreev, et al. "P148 JAK-inhibition by baricitinib and tofacitinib ameliorates pathological bone loss." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.131.

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Qin, Yi-Xian, Tamara Kaplan, and Hoyan Lam. "Anabolic Fluid Flow as Dependent on It Dose and Frequency in Bone Formation and Inhibition of Bone Loss." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61388.

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Anabolic response of bone to interstitial fluid flow is strongly dependent on the dynamic components of the fluid pressure, implying that fluid flow is a critical regulatory component to bone mass and morphology. While the fluid stimulus can be potentially applied for therapeutic in promoting turnover, the hypothesis of fluid induced bone adaptation was evaluated in an avian ulna model using varied flow rates and magnitudes. Total of 12 one-year old male avian animals was used in this study. A sinusoidal fluid pressure was applied to the experimental ulna 10 min/day for 4 weeks. Three experimental groups of loading were performed at 1 and 30 Hz of fluid loading. The results reveal an increase of 22.7%±7.2 in trabecular volume for group of 30 Hz, 76mmHg loading, while it had only 0.5 % increase at 1Hz, 76 mmHg loading. Under physiologic fluid pressure, a higher flow rate of stimuli generates much higher remodeling response than a lower rate of loading. This implies that bone turnover may be sensitive to the dynamic components of fluid flow, thereby initiating the adaptive response.

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Placek, L., A. W. Wren, A. Coughlan, and M. R. Towler. "Gallium Containing Glass Polyalkenoate Bone Cements: Ion Release and E. coli Inhibition." In 2013 39th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2013. http://dx.doi.org/10.1109/nebec.2013.99.

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6

Penninger, Charles L., Andre´s Tovar, Glen L. Niebur, and John E. Renaud. "Signaling Pathways for Bone Resorption Predicted as a Hybrid Cellular Automaton Process." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-39358.

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The bone remodeling process provides for various functions such as mineral homeostasis, damage repair, and adaptation to mechanical loading. At present, a clear link between the mechanical stimulation of bones and the biochemical response is not fully understood. Computational simulations can provide a means to test hypotheses and gain insight into processes that are difficult to examine experimentally. The objective of this work is to predict the effect of damage and strain as the stimulus for regulating the cellular signaling activity of remodeling. In this study, potential signaling pathways that mediate this cellular activity were incorporated in a hybrid cellular automaton (HCA) algorithm. Biological rules were implemented in this model to control recruitment, differentiation, and activation of osteoclasts. Prominent processes for describing recruitment and inhibition of the bone cells, as reported from experimental studies, are utilized. This work focuses on the resorption of a damaged site on a trabecular strut.

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7

Joiner, Danese M., Ethan L. H. Daley, and Steven A. Goldstein. "The Effects of the Inhibition of Connexin 43 on Pre-Osteoblasts and Their Response to Mechanical Stimulation." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192700.

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It is well established that bone can adapt to the demands of daily mechanical usage. Mechanical loading can result in bone formation depending on the magnitude, duration, and frequency. Unloading, which can occur during bed rest, micro-gravity exposure and a variety of clinical conditions, can result in bone resorption. In vitro studies have demonstrated that osteoblasts and osteocytes respond to mechanical stimulation, especially oscillatory fluid shear stress. Mechano-responses have included increases in inter- and intra-cellular communication through gap junctions and soluble factors such as nitric oxide and prostaglandin E2 [1]. Bone cell gap junctions are primarily comprised of connexin 43 (Cx43). Mice lacking Cx43 have an osteopenic phenotype and when subjected to cyclic 4 pt. bending loads have an increased tibia bone marrow area [2, 3]. These observations may represent altered cell signaling. To investigate the role of Cx43 in cell signaling and bone mechanotransduction the Cx43 gene was silenced in MC3T3-E1 pre-osteoblast cells subjected to oscillatory fluid shear stress.

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8

Liu, Sijin, Robert H. Goldstein, Ellen M. Scepansky, and Michael Rosenblatt. "Abstract A63: Inhibition of ROCK signaling prevents breast cancer metastasis to human bone." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-a63.

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Sousa, Sofia, Evelyne Gineyts, Sandra Geraci, Martine Croset, and Philippe Clézardin. "Abstract 29: RANK-RANKL signaling inhibition delays early breast cancer bone metastasis formation." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-29.

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Hu, M., R. Yeh, M. Lien, and Y. X. Qin. "In Vivo Mesenchymal Stem Cell Proliferation in Response to Dynamic Fluid Flow Stimulation." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80586.

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Osteoporosis is a debilitating disease characterized as decreased bone mass and structural deterioration of bone tissue. Osteoporotic bone tissue turns itself into altered structure, which leads to weaker bones that are more susceptible for fractures. While often happening in elderly, long-term bed-rest patients, e.g. spinal cord injury, and astronauts who participate in long-duration spaceflights, osteoporosis has been considered as a major public health thread and causes great medical cost impacts to the society. Mechanobiology and novel stimulation on regulating bone health have long been recognized. Loading induced bone fluid flow, as a critical mechanotransductive promoter, has been demonstrated to regulate cellular signaling, osteogenesis, and bone adaptation [4]. As one of the factors that mediate bone fluid flow, intromedullary pressure (ImP) creates a pressure gradient that further influence the magnitude of mechanotransductory signals [5]. As for a potential translational development of ImP, our group has recently introduced a novel, non-invasive dynamic hydraulic stimulation (DHS) on bone structural enhancement. Its promising effects on inhibition of disuse bone loss has been shown with 2 Hz loading through a 4-week hindlimb suspension rat study followed by microCT analysis. At the cellular level, mesenchymal stem cells (MSCs) are defined by their self-renewal ability and that to potentially differentiate into the cells that form tissues such as bone [1]. To further elucidate the cellular effects of DHS and its potential mechanism on bone quality enhancement, the objective of this study was to measure MSC quantification in response to the in vivo mechanical signals driven by DHS.

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Reports on the topic "Bone inhibition"

1

Schaffler, Mitchell B., and Robert D. Boyd. Influence of Bone Remodeling Inhibition on the Development of Experimental Stress Fractures. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada437496.

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Schaffler, Mitchell B., and Robert D. Boyd. Influence of Bone Remodeling Inhibition on the Development of Experimental Stress Fractures. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada374061.

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Boyd, Robert D., and Mitchell B. Schaffler. Influence of Bone Remodeling Inhibition on the Development of Experimental Stress Fractures. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada392895.

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Schaffler, Mitchell B. Influence of Bone Remodeling Inhibition on the Development of Experimental Stress Fractures. Fort Belvoir, VA: Defense Technical Information Center, November 2005. http://dx.doi.org/10.21236/ada471385.

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Ganju, Ramesh K. Receptor for Advanced Glycation End Products (RAGE) as a Novel Target for Inhibiting Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada592353.

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Ehrlich, Marcelo, John S. Parker, and Terence S. Dermody. Development of a Plasmid-Based Reverse Genetics System for the Bluetongue and Epizootic Hemorrhagic Disease Viruses to Allow a Comparative Characterization of the Function of the NS3 Viroporin in Viral Egress. United States Department of Agriculture, September 2013. http://dx.doi.org/10.32747/2013.7699840.bard.

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Project Title: "Development of a plasmid-based reverse genetics system for the Bluetongue and Epizootic Hemorrhagic Disease viruses to allow comparative characterization of the function of the NS3 viroporin in viral egress". Project details: No - IS-4192-09; Participants – Ehrlich M. (Tel Aviv University), Parker J.S. (Cornell University), DermodyT.S. (Vanderbilt University); Period - 2009-2013. Orbiviruses are insect-borne infectious agents of ruminants that cause diseases with considerable economical impact in Israel and the United States. The recent outbreaks of BTV in Europe and of Epizootic Hemorrhagic Disease Virus (EHDV) in Israel, underscore the need for: (i) a better comprehension of the infection process of orbiviruses, (ii) the identification of unique vs. common traits among different orbiviruses, (iii) the development of novel diagnosis and treatment techniques and approaches; all aimed at the achievement of more effective control and treatment measures. It is the context of these broad goals that the present project was carried out. To fulfill our long-term goal of identifying specific viral determinants of virulence, growth, and transmission of the orbiviruses, we proposed to: (i) develop reverse genetics systems for BTV and EHDV2-Ibaraki; and (ii) identify the molecular determinants of the NS3 nonstructural protein related to viroporin/viral egress activities. The first objective was pursued with a two-pronged approach: (i) development of a plasmid-based reverse genetics system for BTV-17, and (ii) development of an "in-vitro" transcription-based reverse genetics system for EHDV2-Ibaraki. Both approaches encountered technical problems that hampered their achievement. However, dissection of the possible causes of the failure to achieve viral spread of EHDV2-Ibaraki, following the transfection of in-vitro transcribed genomic segments of the virus, revealed a novel characteristic of EHDV2-Ibaraki infection: an uncharacteristically low fold increase in titer upon infection of different cell models. To address the function and regulation of NS3 we employed the following approaches: (i) development (together with Anima Cell Metrology) of a novel technique (based on the transfection of fluorescently-labeledtRNAs) that allows for the detection of the levels of synthesis of individual viral proteins (i.e. NS3) in single cells; (ii) development of a siRNA-mediated knockdown approach for the reduction in levels of expression of NS3 in EHDV2-Ibaraki infected cells; (iii) biochemical and microscopy-based analysis of the localization, levels and post-translational modifications of NS3 in infected cells. In addition, we identified the altered regulation and spatial compartmentalization of protein synthesis in cells infected with EHDV2-Ibaraki or the mammalian reovirus. In EHDV2-Ibaraki-infected cells such altered regulation in protein synthesis occurs in the context of a cell stress reponse that includes the induction of apoptosis, autophagy and activation of the stressrelated kinase c-Jun N-terminal Kinase (JNK). Interestingly, inhibition of such stress-related cellular processes diminishes the production of infectious virions, suggesting that EHDV usurps these responses for the benefit of efficient infection. Taken together, while the present project fell short of the generation of novel reverse genetics systems for orbiviruses, the development of novel experimental approaches and techniques, and their employment in the analysis of EHDV-infected cells, yielded novel insights in the interactions of orbiviruses with mammalian cells.

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Dickman, Martin B., and Oded Yarden. Genetic and chemical intervention in ROS signaling pathways affecting development and pathogenicity of Sclerotinia sclerotiorum. United States Department of Agriculture, July 2015. http://dx.doi.org/10.32747/2015.7699866.bard.

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Abstract: The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotior11111. The focus in this project was on the elucidation of the signaling events and environmental cues involved in the regulation of these processes, utilizing and continuously developing tools our research groups have established and/or adapted for analysis of S. sclerotiorum, Our stated objectives: To take advantage of the recent conceptual (ROS/PPs signaling) and technical (amenability of S. sclerotiorumto manipulations coupled with chemical genomics and next generation sequencing) developments to address and extend our fundamental and potentially applicable knowledge of the following questions concerning the involvement of REDOX signaling and protein dephosphorylation in the regulation of hyphal/sclerotial development and pathogenicity of S. sclerotiorum: (i) How do defects in genes involved in ROS signaling affect S. sclerotiorumdevelopment and pathogenicity? (ii) In what manner do phosphotyrosinephosphatases affect S. sclerotiorumdevelopment and pathogenicity and how are they linked with ROS and other signaling pathways? And (iii) What is the nature of activity of newly identified compounds that affect S. sclerotiori,111 growth? What are the fungal targets and do they interfere with ROS signaling? We have met a significant portion of the specific goals set in our research project. Much of our work has been published. Briefly. we can summarize that: (a) Silencing of SsNox1(NADPHoxidase) expression indicated a central role for this enzyme in both virulence and pathogenic development, while inactivation of the SsNox2 gene resulted in limited sclerotial development, but the organism remained fully pathogenic. (b) A catalase gene (Scatl), whose expression was highly induced during host infection is involved in hyphal growth, branching, sclerotia formation and infection. (c) Protein tyrosine phosphatase l (ptpl) is required for sclerotial development and is involved in fungal infection. (d) Deletion of a superoxidedismutase gene (Sssodl) significantly reduced in virulence on both tomato and tobacco plants yet pathogenicity was mostly restored following supplementation with oxalate. (e) We have participated in comparative genome sequence analysis of S. sclerotiorumand B. cinerea. (f) S. sclerotiorumexhibits a potential switch between biotrophic and necrotrophic lifestyles (g) During plant microbe interactions cell death can occur in both resistant and susceptible events. Non pathogenic fungal mutants S. sclerotior111n also cause a cell death but with opposing results. We investigated PCD in more detail and showed that, although PCD occurs in both circumstances they exhibit distinctly different features. The mutants trigger a restricted cell death phenotype in the host that unexpectedly exhibits markers associated with the plant hypersensitive (resistant) response. Using electron and fluorescence microscopy, chemical effectors and reverse genetics, we have established that this restricted cell death is autophagic. Inhibition of autophagy rescued the non-pathogenic mutant phenotype. These findings indicate that autophagy is a defense response in this interaction Thus the control of cell death, dictated by the plant (autophagy) סr the fungus (apoptosis), is decisive to the outcome of certain plant microbe interactions. In addition to the time and efforts invested towards reaching the specific goals mentioned, both Pls have initiated utilizing (as stated as an objective in our proposal) state of the art RNA-seq tools in order to harness this technology for the study of S. sclerotiorum. The Pls have met twice (in Israel and in the US), in order to discuss .נחd coordinate the research efforts. This included a working visit at the US Pls laboratory for performing RNA-seq experiments and data analysis as well as working on a joint publication (now published). The work we have performed expands our understanding of the fundamental biology (developmental and pathogenic) of S. sclerotioז111וז. Furthermore, based on our results we have now reached the conclusion that this fungus is not a bona fide necrotroph, but can also display a biotrophic lifestyle at the early phases of infection. The data obtained can eventually serve .נ basis of rational intervention with the disease cycle of this pathogen.

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Manulis, Shulamit, Christine D. Smart, Isaac Barash, Guido Sessa, and Harvey C. Hoch. Molecular Interactions of Clavibacter michiganensis subsp. michiganensis with Tomato. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7697113.bard.

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Clavibacter michiganensis subsp. michiganensis (Cmm), the causal agent of bacterial wilt and canker of tomato, is the most destructive bacterial disease of tomato causing substantial economic losses in Israel, the U.S.A. and worldwide. The molecular strategies that allow Cmm, a Gram-positive bacterium, to develop a successful infection in tomato plants are largely unknown. The goal of the project was to elucidate the molecular interactions between Cmmand tomato. The first objective was to analyze gene expression profiles of susceptible tomato plants infected with pathogenic and endophytic Cmmstrains. Microarray analysis identified 122 genes that were differentially expressed during early stages of infection. Cmm activated typical basal defense responses in the host including induction of defense-related genes, production of scavenging of free oxygen radicals, enhanced protein turnover and hormone synthesis. Proteomic investigation of the Cmm-tomato interaction was performed with Multi-Dimensional Protein Identification Technology (MudPIT) and mass spectroscopy. A wide range of enzymes secreted by Cmm382, including cell-wall degrading enzymes and a large group of serine proteases from different families were identified in the xylem sap of infected tomato. Based on proteomic results, the expression pattern of selected bacterial virulence genes and plant defense genes were examined by qRT-PCR. Expression of the plasmid-borne cellulase (celA), serine protease (pat-1) and serine proteases residing on the chp/tomA pathogenicity island (chpCandppaA), were significantly induced within 96 hr after inoculation. Transcription of chromosomal genes involved in cell wall degradation (i.e., pelA1, celB, xysA and xysB) was also induced in early infection stages. The second objective was to identify by VIGS technology host genes affecting Cmm multiplication and appearance of disease symptoms in plant. VIGS screening showed that out of 160 tomato genes, which could be involved in defense-related signaling, suppression of 14 genes led to increase host susceptibility. Noteworthy are the genes Snakin-2 (inhibitor of Cmm growth) and extensin-like protein (ELP) involved in cell wall fortification. To further test the significance of Snakin -2 and ELP in resistance towards Cmm, transgenic tomato plants over-expressing the two genes were generated. These plants showed partial resistance to Cmm resulting in a significant delay of the wilt symptoms and reduction in size of canker lesion compared to control. Furthermore, colonization of the transgenic plants was significantly lower. The third objective was to assess the involvement of ethylene (ET), jasmonate (JA) and salicylic acid (SA) in Cmm infection. Microarray and proteomic studies showed the induction of enzymes involved in ET and JA biosynthesis. Cmm promoted ET production 8 days after inoculation and SIACO, a key enzyme of ET biosynthesis, was upregulated. Inoculation of the tomato mutants Never ripe (Nr) impaired in ET perception and transgenic plants with reduced ET synthesis significantly delayed wilt symptoms as compared to the wild-type plants. The retarded wilting in Nr plants was shown to be a specific effect of ET insensitivity and was not due to altered expression of defense related genes, reduced bacterial population or decrease in ethylene biosynthesis . In contrast, infection of various tomato mutants impaired in JA biosynthesis (e.g., def1, acx1) and JA insensitive mutant (jai1) yielded unequivocal results. The fourth objective was to determine the role of cell wall degrading enzymes produced by Cmm in xylem colonization and symptoms development. A significance increase (2 to 7 fold) in expression of cellulases (CelA, CelB), pectate lyases (PelA1, PelA2), polygalacturonase and xylanases (XylA, XylB) was detected by qRT-PCR and by proteomic analysis of the xylem sap. However, with the exception of CelA, whose inactivation led to reduced wilt symptoms, inactivation of any of the other cell wall degrading enzymes did not lead to reduced virulence. Results achieved emphasized the complexity involved in Cmm-tomato interactions. Nevertheless they provide the basis for additional research which will unravel the mechanism of Cmm pathogenicity and formulating disease control measures.

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