| Perianal fistulae in Crohn's Disease: Current and future approaches to treatment.
October 17, 2009 at 6:35 am
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| | Perianal fistulae in Crohn's Disease: Current and future approaches to treatment. Inflamm Bowel Dis. 2009 Oct 15; Authors: Keshaw H, Foong KS, Forbes A, Day RM : Perianal fistulae are common in Crohn's disease but rarely heal without treatment. The main aim of treatment is to effectively close the fistula without affecting sphincter integrity and continence. Traditional surgical and medical approaches are not without their limitations and may result in either comorbidity, such as fecal incontinence, or incomplete healing of the fistulae. Over the last 2 decades these limitations have led to a paradigm shift toward the use of biomaterials, and more recently cell-based therapies, which have met with variable degrees of success. This review discusses the traditional and current methods of treatment, as well as emerging and possible alternative approaches that may improve fistula healing. Inflamm Bowel Dis 2009. PMID: 19834976 [PubMed - as supplied by publisher] |
| BIOLOGICAL RESTORATION OF CENTRAL NERVOUS SYSTEM ARCHITECTURE AND FUNCTION: PART 3-STEM CELL- AND CELL-BASED APPLICATIONS AND REALITIES IN THE BIOLOGICAL MANAGEMENT OF CENTRAL NERVOUS SYSTEM DISORDERS: TRAUMATIC, VASCULAR, AND EPILEPSY DISORDERS.
October 17, 2009 at 6:35 am
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| | BIOLOGICAL RESTORATION OF CENTRAL NERVOUS SYSTEM ARCHITECTURE AND FUNCTION: PART 3-STEM CELL- AND CELL-BASED APPLICATIONS AND REALITIES IN THE BIOLOGICAL MANAGEMENT OF CENTRAL NERVOUS SYSTEM DISORDERS: TRAUMATIC, VASCULAR, AND EPILEPSY DISORDERS. Neurosurgery. 2009 Nov;65(5):831-859 Authors: Farin A, Liu CY, Langmoen IA, Apuzzo ML STEM CELL THERAPY has emerged as a promising novel therapeutic endeavor for traumatic brain injury, spinal cord injury, stroke, and epilepsy in experimental studies. A few preliminary clinical trials have further supported its safety and early efficacy after transplantation into humans. Although not yet clinically available for central nervous system disorders, stem cell technology is expected to evolve into one of the most powerful tools in the biological management of complex central nervous system disorders, many of which currently have limited treatment modalities. The identification of stem cells, discovery of neurogenesis, and application of stem cells to treat central nervous system disorders represent a dramatic evolution and expansion of the neurosurgeon's capabilities into the neurorestoration and neuroregeneration realms. In Part 3 of a 5-part series on stem cells, we discuss the theory, experimental evidence, and clinical data pertaining to the use of stem cells for the treatment of traumatic, vascular, and epileptic disorders. PMID: 19834396 [PubMed - as supplied by publisher] |
| Matrix Metalloproteinase-3 Accelerates Wound Healing following Dental Pulp Injury.
October 17, 2009 at 6:35 am
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| | Matrix Metalloproteinase-3 Accelerates Wound Healing following Dental Pulp Injury. Am J Pathol. 2009 Oct 15; Authors: Zheng L, Amano K, Iohara K, Ito M, Imabayashi K, Into T, Matsushita K, Nakamura H, Nakashima M Matrix metalloproteinases (MMPs) are implicated in a wide range of physiological and pathological processes, including morphogenesis, wound healing, angiogenesis, inflammation, and cancer. Angiogenesis is essential for reparative dentin formation during pulp wound healing. The mechanism of angiogenesis, however, still remains unclear. We hypothesized that certain MMPs expressed during pulp wound healing may support recovery processes. To address this issue, a rat pulp injury model was established to investigate expression of MMPs during wound healing. Real-time RT-PCR analysis showed that expression MMP-3 and MMP-9 (albeit lower extent) was up-regulated at 24 and 12 hours after pulp injury, respectively, whereas expression of MMP-2 and MMP-14 was not changed. MMP-3 mRNA and protein were localized in endothelial cells and/or endothelial progenitor cells in injured pulp in vivo. In addition, MMP-3 enhanced proliferation, migration, and survival of human umbilical vein endothelial cells in vitro. Furthermore, the topical application of MMP-3 protein on the rat-injured pulp tissue in vivo induced angiogenesis and reparative dentin formation at significantly higher levels compared with controls at 24 and 72 hours after treatment, respectively. Inhibition of endogenous MMP-3 by N-Isobutyl-N-(4-methoxyphenylsulfonyl)-glycylhydroxamic acid resulted in untoward wound healing. These results provide suggestive evidence that MMP-3 released from endothelial cells and/or endothelial progenitor cells in injured pulp plays critical roles in angiogenesis and pulp wound healing. PMID: 19834065 [PubMed - as supplied by publisher] |
| Generation of functional ventricular heart muscle from mouse ventricular progenitor cells.
October 17, 2009 at 6:35 am
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| | Generation of functional ventricular heart muscle from mouse ventricular progenitor cells. Science. 2009 Oct 16;326(5951):426-9 Authors: Domian IJ, Chiravuri M, van der Meer P, Feinberg AW, Shi X, Shao Y, Wu SM, Parker KK, Chien KR The mammalian heart is formed from distinct sets of first and second heart field (FHF and SHF, respectively) progenitors. Although multipotent progenitors have previously been shown to give rise to cardiomyocytes, smooth muscle, and endothelial cells, the mechanism governing the generation of large numbers of differentiated progeny remains poorly understood. We have employed a two-colored fluorescent reporter system to isolate FHF and SHF progenitors from developing mouse embryos and embryonic stem cells. Genome-wide profiling of coding and noncoding transcripts revealed distinct molecular signatures of these progenitor populations. We further identify a committed ventricular progenitor cell in the Islet 1 lineage that is capable of limited in vitro expansion, differentiation, and assembly into functional ventricular muscle tissue, representing a combination of tissue engineering and stem cell biology. PMID: 19833966 [PubMed - in process] |
| Ly6d marks the earliest stage of B-cell specification and identifies the branchpoint between B-cell and T-cell development.
October 17, 2009 at 6:35 am
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| | Ly6d marks the earliest stage of B-cell specification and identifies the branchpoint between B-cell and T-cell development. Genes Dev. 2009 Oct 15;23(20):2376-81 Authors: Inlay MA, Bhattacharya D, Sahoo D, Serwold T, Seita J, Karsunky H, Plevritis SK, Dill DL, Weissman IL Common lymphoid progenitors (CLPs) clonally produce both B- and T-cell lineages, but have little myeloid potential in vivo. However, some studies claim that the upstream lymphoid-primed multipotent progenitor (LMPP) is the thymic seeding population, and suggest that CLPs are primarily B-cell-restricted. To identify surface proteins that distinguish functional CLPs from B-cell progenitors, we used a new computational method of Mining Developmentally Regulated Genes (MiDReG). We identified Ly6d, which divides CLPs into two distinct populations: one that retains full in vivo lymphoid potential and produces more thymocytes at early timepoints than LMPP, and another that behaves essentially as a B-cell progenitor. PMID: 19833765 [PubMed - in process] |
| Dimeric integrin alpha5beta1 ligands confer morphological and differentiation responses to murine embryonic stem cells.
October 17, 2009 at 6:35 am
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| | Dimeric integrin alpha5beta1 ligands confer morphological and differentiation responses to murine embryonic stem cells. Biochem Biophys Res Commun. 2009 Oct 12; Authors: Singh MD, Kreiner M, McKimmie CS, Holt S, Walle CF, Graham GJ We present the first report utilizing, and showing the functional relevance of, self-assembling polyvalent ligands specific for integrin alpha5beta1 in murine embryonic stem (mES) cell adhesion. Di, tri and tetrameric 9(th)-10(th) type III fibronectin domains (FIII9'10) were used to generate clustered integrin alpha5beta1 ligand surfaces for mES cell culture. Compared to gelatin, FIII9'10 (monomer), FIII9'10-trimer and -tetramer, the FIII9'10-dimer supported the highest number of mES cell colonies. No evidence of domain unfolding upon surface adsorption was found. Colonies appeared disperse with a spread cell morphology unless subdued back to a tight morphology with increasing concentrations of leukemia inhibitory factor (LIF). In the presence of LIF, mES cells adherent to the FIII9'10-dimer showed transient upregulation of Oct-4, the mesodermal transcription factor, Brachyury, and the ectodermal marker, Nestin. However, dual upregulation of Nanog maintained the mES cells in a pluripotent state, confirmed by alkaline phosphatase staining. Therefore, the behavior of mES cells adherent to dimeric integrin alpha5beta1 ligands is a largely morphological phenomenon conferring pro-differentiation signals towards mesodermal and ectodermal lineages. This work will be of interest to cell and tissue engineering groups aiming to control ES cell behavior through integrin ligand presentation and synthetic substrates. PMID: 19833095 [PubMed - as supplied by publisher] |
| Pharmacotherapy of the overactive bladder.
October 17, 2009 at 6:35 am
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| | Pharmacotherapy of the overactive bladder. Discov Med. 2009 Oct;8(42):118-24 Authors: Andersson KE Lower urinary tract symptoms (LUTS), the overactive bladder syndrome (OAB), and detrusor overactivity (DO) are all conditions that can have major effects on quality of life and social functioning. Antimuscarinic drugs are first-line treatment -- they often have good initial response rates, but adverse effects and decreasing efficacy cause long-term compliance problems, and alternatives are needed. The recognition of the functional contribution of the urothelium, the spontaneous myocyte activity during bladder filling, and the diversity of nerve transmitters involved has sparked interest in both peripheral and central modulation of LUTS/OAB/DO pathophysiology. There may be several new possibilities to treat LUTS/OAB/DO. For example, beta(3)-adrenoceptor (AR) agonists (mirabegron), phosphodiesterase type 5 inhibitors (sildenafil, tadalafil, vardenafil), combinations (alpha(1)-AR antagonist + antimuscarinic), and drugs with a central mode of action (tramadol, gabapentin) all have positive proof of concept documented in randomized, controlled trials. Which of these therapeutic principles will be developed to become clinically useful treatments remain to be established. PMID: 19833057 [PubMed - in process] |
| Effect of Bioactive Glasses on Angiogenesis: In-vitro and In-vivo Evidence. A Review.
October 17, 2009 at 6:35 am
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| | Effect of Bioactive Glasses on Angiogenesis: In-vitro and In-vivo Evidence. A Review. Tissue Eng Part B Rev. 2009 Oct 15; Authors: Gorustovich A, Roether J, Boccaccini AR The incorporation of bioactive glass into bone tissue engineering scaffolds can be widely beneficial based on emerging evidence in the literature about the angiogenic potential of this material, in particular the composition 45S5 Bioglass(R). The present paper reviews the literature discussing in vitro studies which have demonstrated that increases in angiogenic indicators have been achieved through both direct and indirect contact of relevant cells with 45S5 Bioglass(R) particles or with their dissolution products. A few available in vivo studies confirming the ability of bioactive glass, incorporated into scaffolds, to stimulate neovascularization are also discussed. Suggestions for further research are given, highlighting the need for specific investigations designed to assess the effect of particular ion dissolution products from bioactive glasses and their relative concentration on angiogenesis both in-vitro and in-vivo. PMID: 19831556 [PubMed - as supplied by publisher] |
| Effects of cyclic flexure on endothelial permeability and apoptosis in arterial segments perfused ex vivo.
October 17, 2009 at 6:35 am
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| | Effects of cyclic flexure on endothelial permeability and apoptosis in arterial segments perfused ex vivo. J Biomech Eng. 2009 Oct;131(10):101005 Authors: Van Epps JS, Chew DW, Vorp DA Certain arteries (e.g., coronary, femoral, etc.) are exposed to cyclic flexure due to their tethering to surrounding tissue beds. It is believed that such stimuli result in a spatially variable biomechanical stress distribution, which has been implicated as a key modulator of remodeling associated with atherosclerotic lesion localization. In this study we utilized a combined ex vivo experimental/computational methodology to address the hypothesis that local variations in shear and mural stress associated with cyclic flexure influence the distribution of early markers of atherogenesis. Bilateral porcine femoral arteries were surgically harvested and perfused ex vivo under pulsatile arterial conditions. One of the paired vessels was exposed to cyclic flexure (0-0.7 cm(-1)) at 1 Hz for 12 h. During the last hour, the perfusate was supplemented with Evan's blue dye-labeled albumin. A custom tissue processing protocol was used to determine the spatial distribution of endothelial permeability, apoptosis, and proliferation. Finite element and computational fluid dynamics techniques were used to determine the mural and shear stress distributions, respectively, for each perfused segment. Biological data obtained experimentally and mechanical stress data estimated computationally were combined in an experiment-specific manner using multiple linear regression analyses. Arterial segments exposed to cyclic flexure had significant increases in intimal and medial apoptosis (3.42+/-1.02 fold, p=0.029) with concomitant increases in permeability (1.14+/-0.04 fold, p=0.026). Regression analyses revealed specific mural stress measures including circumferential stress at systole, and longitudinal pulse stress were quantitatively correlated with the distribution of permeability and apoptosis. The results demonstrated that local variation in mechanical stress in arterial segments subjected to cyclic flexure indeed influence the extent and spatial distribution of the early atherogenic markers. In addition, the importance of including mural stresses in the investigation of vascular mechanopathobiology was highlighted. Specific example results were used to describe a potential mechanism by which systemic risk factors can lead to a heterogeneous disease. PMID: 19831475 [PubMed - in process] | | | 
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