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Search Results: 1 - 10 of 1386 matches for " Proliferation "
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Use of Platelet-Rich Plasma for Collagen Matrixes Revitalization with Human Fibroblast  [PDF]
Maxim Sergeevich Makarov, Natalya Valerjevna Borovkova, Olga Ivanovna Konushko, Valery Borisovich Khvatov
Journal of Biosciences and Medicines (JBM) , 2015, DOI: 10.4236/jbm.2015.310011
Abstract: We studied in vitro attachment, proliferation and survival of сadaver skin fibroblasts in collagen bands, dermal matrix and cancellous demineralized bone, enriched with platelet components. It was shown, that PRP enhanced revitalization of collagen grafts, especially followed by components of activated or freezed platelets. Fibroblasts had the best rate of proliferative activity in response to 150 pg platelet derived growth factor (PDGF), released from 100 million platelets with granules and measured for 100 × 103 cultivated cells. The use of platelet-derived material could increase fibroblast proliferation activity for 1.5-3 times in all types of collagen transplants without damage or decay of cell’s biological value.
The Influence of Caldesmon Suppression on Proliferation and Motilities of Vascular Smooth Muscle Cells  [PDF]
Bin Gao, Qifeng Jiang
Journal of Biomedical Science and Engineering (JBiSE) , 2016, DOI: 10.4236/jbise.2016.99038
Abstract: Migration of vascular smooth muscle cells (VSMCs) from the media to intima constitutes a critical step in the development of proliferative vascular diseases. To elucidate the regulatory mechanism of VSMCs motility, the roles of caldesmon (CaD) were investigated previously. CaD is an actin-binding protein dynamically regulating cytoskeleton structure. In this study, the potential role of CaD in mediating proliferation and motility of VSMCs were discussed. First, structural effect of CaD on cytoskeleton integrity was analyzed with CaD knock-down; second, the proliferation of VSMCs was measured in CaD knock-down and control cells; third, the specific role of CaD on VSMCs motilities was evaluated with in vitro migration and invasion assays. We found that CaD is an integral component to maintain cytoskeleton integrity of VSMCs. Our data indicated that CaD suppression does not show significant influence on VSMCs proliferation, but negatively modulates the motilities of VSMCs, and CaD depletion would significantly facilitate migration and invasion of VSMCs.
Relative Proliferation of Gullies on Three Geological Sediments: The Influence of Soil Consistency Limits and Shear Strength  [PDF]
Louis A. Oparaku, Raphael T. Iwar, Joseph E. Edeh
Journal of Environmental Protection (JEP) , 2018, DOI: 10.4236/jep.2018.91003
Abstract: This study was carried out to evaluate the influence of soil consistency limits and shear strength on the relative proliferation of gullies on three geological sediments, namely: the Upper Coal Measures (UCM), the Ajalli Sandstones (AS), and the Lower Coal Measures (LCM), which has been ranked as AS > UCM > LCM. Soil samples were collected from a depth range of 60 - 90 cm of sampling pits dug at a selected location on each of these texturally homogenous and unique formations. These were analysed for consistency limits and shear strength using standard methods and procedures. Results showed that the plasticity index (PI) of the UCM (PIUCM) was 24.49%; PIAS, 5.89%; and PILCM, 44.85%. The shear strength (S) of the UCM (SUCM) was 314.74 KN/m2; SAS, 196.23 KN/m2; and SLCM, 321.72 KN/m2. The results of the study show that rankings of the respective contributions of these two geotechnical properties to the vulnerability of the sediments to gully (soil) erosion follow the same order of proliferation of gullies on the plateau landscape: AS > UCM > LCM. Hence, consistency limits and shear strength parameters partly influence and explain the relative proliferation of gullies on the three formations. Further studies are required to determine other soil factors of gully erosion in the area in order to evolve appropriate management strategies for these sediments.
2D Numerical Simulation of Liver Cell Proliferation with Angiogenesis for Hepatic Lobule Formation  [PDF]
Katsuya Nagayama, Hiroto Tanaka, Yuki Oshiumi, Nana Shirakigawa, Hiroyuki Ijima
Journal of Biosciences and Medicines (JBM) , 2016, DOI: 10.4236/jbm.2016.43007

The liver has the ability to reform and regenerate in our body. However, the mechanisms of reformation or regeneration of the liver have not been elucidated. In this study, we propose an analysis model using a Particle Model to elucidate the mechanism of liver formation. The object of analysis is a hepatic lobule, which is the basic component of the liver. First, a 2-dimensional cell proliferation around one blood vessel was modeled. Second, angiogenesis was added and considered. And finally, the model was applied to the hepatic lobule and the 2D formation of the hepatic lobule was revealed. We used experimentally derived parameters such as diffusivity, oxygen concentration, and oxygen consumption of a cell. The model will be expected to facilitate in developing tissue-engineered liver using regenerative medicine technology.

Diffusive modelling of glioma evolution: a review  [PDF]
Alexandros Roniotis, Kostas Marias, Vangelis Sakkalis, Michalis Zervakis
Journal of Biomedical Science and Engineering (JBiSE) , 2010, DOI: 10.4236/jbise.2010.35070
Abstract: Gliomas, the most aggressive form of brain cancer, are known for their widespread invasion into the tissue near the tumor lesion. Exponential models, which have been widely used in other types of cancers, cannot be used for the simulation of tumor growth, due to the diffusive behavior of glioma. Diffusive models that have been proposed in the last two decades seem to better approximate the expansion of gliomas. This paper covers the history of glioma diffusive modelling, starting from the simplified initial model in 90s and describing how this have been enriched to take into account heterogenous brain tissue, anisotropic migration of glioma cells and adjustable proliferation rates. Especially, adjustable proliferation rates are very important for modelling therapy plans and personalising therapy to different patients.
Similar effects of mouse and human pub gene on proliferation and embryoid bodies formation in mouse embryonic stem cells in vitro  [PDF]
Ekaterina Novosadova, Nella Khaydarova, Ekaterina Manuilova, Elena Arsenyeva, Andrey Lebedev, Vyacheslav Tarantul, Igor Grivennikov
Stem Cell Discovery (SCD) , 2012, DOI: 10.4236/scd.2012.22012
Abstract: Previously we have demonstrated that pub gene modulates expression of PU.1 transcription factor and plays an important role in differentiation of embryonic stem cells not only at early stages (during formation of embryoid bodies), but also during differentiation into ectodermal, mesodermal and endodermal derivatives in vitro. We have compared the influence of elevated expression of two homological genes mpub and hpub of mouse and human respectively on early stages of differentiation of murine embryonic stem cells. Overexpression of both genes caused an increase in the number of formed embryoid bodies but did not alter the proliferative activity of transfected embryonic stem cells. It was also observed that expression of mpub and hpub led to decreased expression of pu.1 mRNA.
Immunohistochemical Expression of Ki-67, PCNA, pRb, p16, p53, Bcl-2 and Bax in Esophageal Adenocarcinoma and Barrett’s Associated Dysplasia  [PDF]
Andrey Iskrenov Kotzev, Margarita Angelova Kamenova, Alexander Petrov Tcherveniakov
Journal of Cancer Therapy (JCT) , 2012, DOI: 10.4236/jct.2012.36143
Abstract: Background: Esophageal adenocarcinoma (EAC) has an extremely poor prognosis. There is a need to characterize the molecular alterations in the carcinogenesis of EAC in order to improve the diagnosis and treatment. Materials and Methods: We used 7 markers to explore the changes in the cell cycle, proliferation and apoptosis in patients with EAC and Barrett’s esophagus (BE)-associated dysplasia. The protein expression of Ki-67, PCNA, pRb, p16, p53, Bcl-2 and Bax was evaluated by immunohistochemistry in archival tissue samples, collected from 15 patients with EAC and 5 patients with BE-associated dysplasia. We analyzed also lymph-node, omentum and liver metastases from the primary esophageal tumors. Results: Ki-67, PCNA, pRb, p16, p53, Bcl-2 and Bax expression was observed in 100%, 87%, 60%, 40%, 100%, 7% and 93% of tumor samples, and in 100%, 80%, 0%, 80%, 80%, 20% and 100% of dysplasia samples, respectively. Significant difference in the expression of the markers between EAC and BE-associated dysplasia was detected for pRb (p = 0.006). Ki-67 expression was associated with clinicopathological parameter T (p = 0.012; V = 0.585). Ninefold higher risk to develop EAC was established for the patient with strong p53 expression, than the lacking p53 patient. Patients with strong p53 expression survived 6.8 months longer than the patients with weak p53 expression and 8.6 months longer than the patients with moderate p53 expression. No correlation was found between the expression of the other markers and prognosis. Conclusion: The results suggest that Ki-67, PCNA, pRb, p16, p53 and Bax participate in the pathogenesis of EAC, whereas Bcl-2 does not play essential role in EAC and BE-associated dysplasia. The balance between cell proliferation and apoptosis is lost in EAC and BE-associated dysplasia. Abnormal p53 protein expression has predictive and prognostic value in EAC. Larger prospective studies are needed to confirm these findings.
The Role of CYLD in Blocking Oncogenic Cell Signaling in Melanoma  [PDF]
Hengning Ke, Ramin Massoumi
Journal of Cancer Therapy (JCT) , 2013, DOI: 10.4236/jct.2013.46A1005

Dysregulation of components of the ubiqutin system has been linked to many diseases including melanoma. This is vital since the post-translational modification of different proteins via direct ubiquitin attachment is an important process for various cellular processes. CYLD is a tumor suppressor gene and deubiquitinating enzyme, which can remove polyubiquitin chains from their specific substrate and interfere with different signaling pathways. CYLD is frequently downregulated or even lost in melanoma cell lines or tissues compared to melanocytes. Down-regulation of CYLD leads to sustained oncogenic signaling that promotes melanoma progression and metastasis. In this review, we summarize the recent insights into the mechanisms which are responsible for the down-regulation of CYLD levels in melanoma and the signaling interactions of the CYLD gene product in melanoma. We argue that these recent insights into CYLD function invite the development of novel molecular strategies for melanoma prevention and treatment.

Promotive Effects of Yokukansan, a Traditional Japanese Medicine, on Proliferation and Differentiation of Cultured Mouse Cortical Oligodendrocytes  [PDF]
Toshiyuki Ueki, Yasushi Ikarashi, Zenji Kawakami, Kazushige Mizoguchi, Yoshio Kase
Pharmacology & Pharmacy (PP) , 2014, DOI: 10.4236/pp.2014.57077

Effects of yokukansan, a traditional Japanese medicine, on proliferation and differentiation of oligodendrocytes were examined using purified mouse cortical oligodendrocyte precursor cells (OPCs). OPCs were cultured for four days, and proliferation was evaluated by counting A2B5 (a specific antibody to OPC)-reactive cells on the second day of cell culture. Differentiation from OPC to oligodendrocyte was evaluated by counting O4 (a specific antibody to detect differentiated cells in various stages)-reactive cells on the fourth day of culture. The effects of yokukansan (final concentration: 100 or 200 μg/ml) on proliferation and differentiation were examined by adding it to the medium for four days. Yokukansan increased not only the number of A2B5-positive cells on the second day but also the number of O4-positive cells on the fourth day compared to those in the corresponding controls. A WST-8 assay was used to identify active components from seven components of Uncaria Hook (UH), one of the constituent galenicals of yokukansan. Geissoschizine methyl ether (GM: 0.1 - 3.0 μM) was identified by this screening assay and increased the number of A2B5-positive cells on the second day and O4-positive cells on the fourth day as yokukansan did. These results suggest that yokukansan promotes the proliferation and differentiation of oligodendrocytes, and also that GM contained in UH is one of active components responsible for this effect of yokukansan.

Repair Mechanisms in Articular Cartilage—A Porcine in Vitro Study  [PDF]
Peter Storgaard Skagen, Hanne Aagaard Kruse, Thomas Horn
Microscopy Research (MR) , 2014, DOI: 10.4236/mr.2014.24009
Abstract: Explants are excellent systems for studying homeostasis in cartilage. The systems are very useful in pharmacological studies involving OA-treatment and in studies of repair mechanisms during injury to hyaline cartilage. The purpose of this study was to evaluate the reparative processes occurring in a young age porcine cartilage explant model examining tissue by Light (LM) and Transmission Electron Microscopy (TEM). Explants of articular cartilage were dissected from the femoral condyles of immature one-year-old pigs and cultured in DMEM/F12 medium with FCS (stimulated explant) or in medium without FCS (control explant) for up to 4 weeks. After 1 - 4 weeks of culture with FCS, LM showed migration and proliferation of chondrocytes in cartilage close to the injured surface differentiating two areas: proliferative zone and necrotic zone. The chondrocytes present in the necrotic zone showed a polarization towards the injured surface. After budding through the injured surface, the chondrocytes formed repair tissue in an interface repair zone and in outer repair tissue. TEM showed chondrocytes in expanded lacunae involving the proliferative zone. The pericellular matrix of the expanded lacunae was partly dissolved, indicating release of matrix-degrading enzymes during proliferation and remodeling. Migratory chondrocytes were identified in oval lacunae close to the injured surface. The pericellular matrix of these oval lacunae was significantly dissolved and immunohistochemistry demonstrated strong staining with a polyclonale collagenase antibody around these units, suggesting release of matrix-degrad- ing collagenase contributing to chondrocyte mobility. We describe an explant model comprising two different repair systems in immature articular cartilage. This model provides us with new reference points that are important in understanding the repair mechanisms.
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