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Sequential Differentiation of Human Bone Marrow Stromal Cells for Bone Regeneration
Eva Johanna Huebner,Nestor Torio Padron,David Kubosch,Guenter Finkenzeller,Norbert P. Suedkamp,Philipp Niemeyer 한국조직공학과 재생의학회 2015 조직공학과 재생의학 Vol.12 No.5
In this study we hypothesized that as a simulation of endochondral bone formation, bone marrow stromal cell (BMSC) provide a sequential chondro-osteogenic differentiation potential. A chondrogenic priming of BMSC leads to a spontaneous three-dimensional cell formation. BMSC were chondrogenically differentiated prior to an osteogenic stimulation. Duration of cell culture was 28 days, whereas in group A BMSC were chondrogenically differentiated for 1 day, followed by an osteogenic differentiation for 27 days. In group B BMSC were chondrogenically differentiated for 14 days prior to an osteogenic differentiation of 14 days and group C BMSC were differentiated chondrogenically for 28 days serving as a chondrogenic control group. Chondrogenic priming induced a spontaneous three-dimensional cell formation. To survey the stability of the osteogenic phenotype in the absence of an osteogenic stimulus, investigations were performed in vivo in a specially adapted chorioallantoic membrane model of fertilized White Leghorn eggs. Histology and real time polymerase chain reaction revealed a higher amount of osteogenic extracellular matrix synthesis and significant higher expressions of osteogenic marker genes in group B after 14 days of chondrogenic and 14 days of osteogenic stimulation. Matrix calcification in vivo in the absence of an osteogenic stimulus could be demonstrated. The results of the present study support the theory of a sequential differentiation potential of BMSC. A chondrogenic priming of BMSC stimulated into the osteogenic lineage result in a stable osteogenic phenotype in a scaffold-free, three-dimensional tissue engineering application.
A Novel Model for Studying Baculovirus Infection Process
Christoph Lindeberger,Lukas Pflug,Holger Huebner,BUCHHOLZHANS RAINER 한국생물공학회 2012 Biotechnology and Bioprocess Engineering Vol.17 No.1
In this paper, a new Ansatz for modelling the Baculovirus infection cycle is presented. The base of this model is the cell cycle distribution at the time of infection. It is possible to calculate the growth of the culture and the initiation of virus processing by considering cell cycle distribution. By taking into account the length of the viral genome and the polymerase activity, it is possible to calculate the virus production rate, which underlies a logistic growth. In the present work, a new hypothesis explaining the accelerated death rates of infected cells has been introduced. This assumption provides the possibilities of performing calculation without any fixed time intervals. The simulation was tested by comparing experimental data with the model prediction. Therefore, cell cycle distributions over the culture time and the growth behaviour of infected and non-infected insect cells were measured. A model, Baculovirus coding for GFP was employed for the present investigation, as it allows tracking the infection and determining the effectiveness of the infection, which is highly dependent on the cell density at the time of infection (TOI). Furthermore, the new model is is taken to simulate data gained from literature about virus release and adsorption. The new assumptions make the model more independent to fit into different cultivation systems.
Picosecond Spin Seebeck Effect
Kimling, Johannes,Choi, Gyung-Min,Brangham, Jack T.,Matalla-Wagner, Tristan,Huebner, Torsten,Kuschel, Timo,Yang, Fengyuan,Cahill, David G. American Physical Society 2017 Physical Review Letters Vol.118 No.5
<P>We report time-resolved magneto-optic Kerr effect measurements of the longitudinal spin Seebeck effect in normal metal/Y3Fe5O12 bilayers driven by an interfacial temperature difference between electrons and magnons. The measured time evolution of spin accumulation induced by laser excitation indicates transfer of angular momentum across normal metal/Y3Fe5O12 interfaces on a picosecond time scale, too short for contributions from a bulk temperature gradient in an yttrium iron garnet. The product of spin-mixing conductance and the interfacial spin Seebeck coefficient determined is of the order of 10(8) Am-2K-1.</P>
Suh, Sung-Suk,Yoo, Ji Young,Cui, Ri,Kaur, Balveen,Huebner, Kay,Lee, Taek-Kyun,Aqeilan, Rami I.,Croce, Carlo M. Public Library of Science 2014 PLoS genetics Vol.10 No.10
<P>Metastasis is the principal cause of cancer death and occurs through multiple, complex processes that involve the concerted action of many genes. A number of studies have indicated that the Fragile Histidine Triad (<I>FHIT</I>) gene product, FHIT, functions as a tumor suppressor in a variety of common human cancers. Although there are suggestions of a role for FHIT loss in progression of various cancers, a role for such loss in metastasis has not been defined. Here, via <I>in vivo</I> and <I>in vitro</I> assays, we reveal that the enforced expression of FHIT significantly suppresses metastasis, accompanied by inhibition of the epithelial-mesenchymal transition (EMT), a process involved in metastasis through coordinate modulation of EMT-related genes. Specifically, miR-30c, a FHIT-upregulated microRNA, contributes to FHIT function in suppression of EMT and metastasis by directly targeting metastasis genes Metadherin (<I>MTDH</I>), High-mobility group AT—hook 2 (<I>HMGA2</I>), and the mesenchymal markers, Vimentin (<I>VIM</I>) and Fibronectin (<I>FN1</I>), in human lung cancer. Finally, we demonstrate that the expression pattern of FHIT and miR-30c is inversely correlated with that of MTDH and HMGA2 in normal tissue, non-metastatic and metastatic tumors, serving as a potential biomarker for metastasis in lung cancer.</P><P><B>Author Summary</B></P><P>Although Fragile Histidine Triad (<I>FHIT</I>) is known as a potential tumor suppressor gene in terms of tumor initiation and progression, the role of FHIT in the metastatic process is not well characterized. Here it is shown that FHIT reduces the motility and invasiveness of lung cancer cells <I>in vitro</I> and ability to metastasize <I>in vivo</I>, at least partially through the miR-30c-mediated suppression of EMT, a critical process during tumor metastasis. This study provides new insights into the role of FHIT and a FHIT-activated miRNA, miR-30c, as crucial modulators in lung metastasis.</P>