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[의학]Tissue engineering_tissue dynamics

Tissue engineering ch.3 tissue dynamics박 종 혁IntroductionAll tissue Dynamic characteristic replacement and production rates of cell Ex) bone marrow, small intestine, epidermis (a few days) vs. Liver cell (one year) Describe the different dynamic states of tissue3.1 Dynamic states of tissueThree dynamic states of tissues Tissue homeostasis : the normal steady-state function of tissue (tissues adapt to the physiological need) Tissue repair : wound healing process Tissue formation : developmental biology morphogenesis (key concern in cellular therapy)3.2 Homeostasis in highly prolific tissueProlific tissues Have stem cell  source of all the types of differentiated cells in tissues Tissues Highly organized pattern of stem cell replication and differentiation to mature progeny 3.2.1 Bone marrow 3.2.2 Villi in the small intestine 3.2.3 Skin3.2.1 Bone marrowThe boy's most dynamic tissue (2~3days)3.2.2 Villi in the small intestineAbsorb nutrients and digestion Epithelial cell layer turns over every 5 days (body's 2nd dynamic tissue) Crypt  the site of epithelial cell production, about 20 stem cells in crypt3.2.3 SkinSeparated by a basal lamina  Dermis, Epidermis Cell must leave the basal lamina  divide and differentiation (prickel cell, granular cell) Turn over rate  a few weeks ( body's 3rd dynamic tissue) varies with the region of the body 10~12 basal cells  epidemal progenitor cellconsist of fibroblastdifferentiating keratino-cytes3.3 Tissue repairWhen tissue damaged Induced healing response : vary with age Fetal : rapidly and restoration of scarless tissue Postnatal : slow and lead to scar 3.3.1 sequence of events that underlie wound healing 3.3.2 engineering wound healing 3.3.3 fetal wound healing3.3.1 sequence of events that underlie wound healingA : adhesion of platelets secrete substance recruit more platelets to thrombus B : release of agent from the platelets  cause vasodilatation and permeability Clotting cascade : cleavage of fibrinogen  fibrin plug fibrin plug : hold the tissue together and form a provisional matrix matrix : play a role recruitment of inflammatory cell and migration of fibroblast and epidermal cellC : neutrophiles and marcrophages : phagocytose cellular debris combat invading microorganism provide the source of chemo-attractents and mitogen  stimulate fibroblast and endothelial cell proliferation D : granulation tissue formation consist of fibroblast, macrophage, collagen, hyaluronic acid contraction of myofibroblast shrinking the size of woundsequence of events that underlie wound healingThe last stage : resolution of the scar (take many months) ex: healing of cartilage matrix remodeling the coordinated synthesis degradation of connective-tissue protein3.3.2 engineering wound healingWound healing can modified with tissue engineering strategies Porous template (skin) Composed of collagen1, chondroitin6-sulfate Delay wound contracture Promote dermal regenerationthe optimal pore size for the wound area to decrease by 50% 20~120um Fibroblast migration through the template Very small size : fibroblast can not penetrate Large size : surface area available for cell adhesion decline Delay of Fibroblast migration  wound contracture and scar formation  wound healingThe degradation rate of the template (optimal)  normal wound-healing rateThe formation of “tissue analogs” By cell-contracted ECM gel Depend on cell density : cell number ↑contraction↑ ECM ↑degree and contraction ↓3.3.3 fetal wound healingstrategies to improve adult wound healing3.4 tissue dynamics as interacting cellular-fate processesThe dynamic stats of tissue function are complex process Involve interplaying among many different cell typesQuizTissue 의 3가지 dynamic stats은? Adult wound healing과 fetal wound healing의 과정에서 나타나는 차이점은? Tissue dynamic을 유발하는 Cellular-fate processes 5가지는?{nameOfApplication=Show}

의/약학| 2007.07.23| 18페이지| 2,000원| 조회(257)

tissue, Dynamic, States, Homeostasis, repair

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New artificial nerve conduits made with photocrosslinked hyaluronic acid for peripheral nerve regeneration

박종혁Introductionbiodegradable tubular conduits frontier of nerve repair surgery An ideal biodegradable conduit maintain its structural integrity nano-structured porous scaffold with pore large surface area permitting cell adhesion and infiltration subsequent tissue ingrowth during nerve regenerative processbioresorbable materials polyglycolic acid, collagens, chitosan, poly L-lactic acid and polycaprolactone (not efficient nerve regeneration) new artificial nerve conduits made with hyaluronic acid (HA) Facilitate a pathway for cellular and axonal ingrowth during peripheral nerve regeneration identifying viability of disseminated Schwann cells and neuron cells into HA conduits in vitro leading to a cell adhesive HA conduit for the peripheral nerve regenerationMaterials and methodsFabrication of HA conduits dissolved in water at a concentration of 4.0 wt% Pure solution into PDMS mold exposed to ultraviolet (UV) light (280 nm, 20 J/cm2), −20◦C for 15 min.Cell preparation Schwann cell (from dorsal root ganglia) Neurosphere (from the hippocampus) In vitro cell culture studies Into the photocrosslinked HA conduits + 0.8% collagen gel was filled with Schwann cells (1.0×104) + neurosphere (1.0×104) separately Culture for 3weeks SEM analysisResultsHA tubular conduit inner diameter of 1.2 mm After 3-week experimental periods  maintained the size and  shape of the original architecture of the tubeSEM micrographs of Schwann cellsCulture for 1 weekCulture for 3 weeksSEM micrographs of NeurospheresCulture for 1 weekCulture for 3 weeksDiscussionHA nerve conduit have several advantages for axonal regeneration implicated in wound healing and tissue repair organized the ECM into a hydrated open lattice  creating a more open matrix with better alignment of fibrin and stimulating the cellular ingrowth  axonal ingrowth synaptogenesis and angiogenesis degraded by hyaluronidase resorbable through multiple metabolic pathwaysThe in vitro cell culture on 3D porous scaffold support of cell differentiation and neurite outgrowth feasibility of using the HA conduit  better cell adhesion and differentiation  leading to axonal regeneration in peripheral nerve reconstruction Further study maintain the structure at suturing keep their structure for the nerve regeneration periods with elasticity for the fixation to the nerve stump suitable design for artificial nerve conduit clinically{nameOfApplication=Show}

의/약학| 2007.07.23| 10페이지| 2,000원| 조회(426)

HA, regeneration, conduits, nerve, periphera..

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[의학]effect of hyaluronic acid on peripheral nerve scarring and regeneration in rat

20070319 박종혁IntroductionPeripheral nerve surgery Several factors are responsible for incomplete recovery Scar formation inevitable sequel of peripheral nerve surgery mechanical barrier to axonal regeneration tethering of nerves to adjacent tissue preventing nerve mobility causing traction injuryReducing scar formation improve the outcome after peripheral nerve repair Reducing scar formation pharmacologic agents Aprotinin (antibody to TGFb) Human amniotic fluid positive effects in experimental study  not apply in clinical field wrapping of nerves with vein, muscle, fat  inconsistentObjective of this study Investigate the effects of HA (1000KDa) on peripheral nerve scarring and regeneration after nerve surgery Hyaluronic acid (HA) reduce the extent of scar formation inhibiting lymphocyte migration proliferation chemotaxis granulocyte pagocytosis and degranulation macrophage motilityMATERIALS AND METHODSRat sciatic nerve length and ease of dissection sharply transected with a scalpel approximately 10 mm Forty-eight nerves were randomly divided into two group The experimental group (n = 24) absorbable gelatin sponge soaked with 0.3 ml HA The control group (n = 24) absorbable gelatin sponge soaked with 0.3 ml saline around the repair site Twenty-four nerves from each group (12 nerves at 4 weeks, and 12 at 12 weeks)ResultMacroscopic StudyIn the nerve adherence category significantly lower scores were found in nerves treated with HA than nerves treated with saline at 4 and 12 weeks after surgery HA prevents perineural adhesion formation without impairment of the wound-healing process.Histologic StudyEpineural connective-tissue thickening stained with Masson trichrome for collagen which appears dark  epineural scar tissue clearly minimal in the HA-treated group The mean thickness of connective tissue surrounding the nerve HA : 0.29 ± 0.03 ㎛ Saline: 0.33 ± 0.03 ㎛The mean axon and fiber diameter in nerve Treated with HA was significantly larger than in nerves treated with saline No significant difference in axon count  table 3Longitudinal sections taken at repair site at week 12 A: Good organization was observed in nerves treated with HA B: Poor organization was seen in nerves treated with salineElectrophysiologic Studies Mean conduction velocities of nerves across the suture site HA : 0.82 ± 0.08 m/sec saline : 0.76 ±0.04 m/sec Gastrocnemius Muscle Weight HA: 0.69± 0.02g Saline: 0.65 ± 0.04 g muscle weight  degree of muscle innervation. HA enhances the peripheral nerve regeneration processDISCUSSIONApplication of HA significantly reduces extraneural and epineural scar formation, resulting in enhancement of peripheral nerve regeneration HA organized the ECM into a hydrated open lattice  facilitating the migration of regenerating axonsThe MW and the concentration of the HA critical to its potential beneficial effects Low concentration and low MW  stimulating effect on granulocyte function high-concentration and high MW  inhibit the movements and phagocytosis of granulocytes Ex) 100KDa, 1000KDa  inhibition of granulocyte function HA create a scaffold around the nerve repair site prevent fibrous ingrowth from surrounding tissuesConclusionTopical application of HA enhanced the nerve regeneration by preventing perineural scar formation Benefit in combination with microsurgical nerve repair techniques in human Further studies need to clarify what doses of HA should be used, and what the toxicity might be.{nameOfApplication=Show}

의/약학| 2007.03.20| 15페이지| 2,000원| 조회(415)

scar formation, hyaluronic acid, nerve reg..

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A painful factor

20061218 박종혁IntroductionNeuropathic pain chronic pain condition with limited treatment options caused by damage to the nerves that transmit sensory information Allodynia pain in response to stimuli that are not normally painful Research on neuropathic pain focus on injury-induced changes in sensory nerves secondary changes in the spinal cord neuronsIntroductionRecent work nerve injury also activates immune-like scavenger cells — microglia — in the spinal cord resulting neuropathic painMicroglia disrupt the inhibitory control of key spinal-cord pain neurons BDNF mediates this signaling between microglia and neurons. lamina I region injury-induced alterations in neurons in the spinal cord  link to neuropathic pain pain pathways to the brainThe action of the neurotransmitters glycine and GABA dampen neuronal excitability Released from 'inhibitory' neurons bind to receptors on the surface membrane of target neurons The GABA and glycine receptors ion channels open when activated, allowing anions (chloride) to flow down into the neuron influx of anions makes the neuron's membrane more negative (hyperpolarized)Hyperpolarization acts to limit neuronal activity  inhibiting the lamina I pain pathway. Nerve injury reduces the levels of the potassium-chloride co-transporter(KCC2) in the membranes of spinal-cord neurons  intracellular chloride concentration increasesThe anions flooding out of the neuron neuron's membrane potential more positive (depolarized) inhibitory transmitters GABA and glycine  no longer able to suppress signaling in the lamina I pain pathwayThe development of allodynia following nerve injury Require for Increased synthesis and activation of the ATP receptor P2X4 on microglia ATP-stimulated microglia positively shifted the in lamina I neuronsHow do activated microglia communicate with lamina I neurons? BDNF  brain-derived neurotrophic factor secreted by microglia involved in chronic pain Produced allodynia induced change in the anion gradient enabling GABA to depolarize the lamina I neuronsBDNF released in the spinal cord neurons during pain processing required for the development of neuropathic pain BDNF–TrkB signaling was prevented  spinal slices from nerve-damaged animals did not show the typical depolarizing shift in Eanion. When spinal BDNF–TrkB signaling was blocked  ATP-stimulated microglia can not produce allodynia BDNF-deficient microglia did not cause allodyniaBDNF a crucial mediator of microglial–neuronal signaling during neuropathic pain disrupting BDNF signaling was able to reverse established allodyniaThe several remaining questions. Where does the ATP that stimulates microglia come from? What signaling pathway leads to the release of BDNF from microglia? How does BDNF–TrkB signaling alter Eanion in lamina I neurons? How dose TrkB receptors activated on other spinal cells that then influence lamina I neurons?{nameOfApplication=Show}

의/약학| 2007.02.21| 12페이지| 2,000원| 조회(295)

GABA, pain factor, microglia

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Inhibition of Nogo: A key strategy to increase regeneration, plasticity and functional recovery of the lesioned central nervous system

20070115 박종혁IntroductionInjured nerve cells and nerve fibres of the CNS Have regenerative ability (can be restricted or boosted) The specific regeneration and growth inhibitory proteins of the adult CNS Nogo-A MAG (myelin associated glycoprotein) OMgp (oligodendrocyte and myelin glycoprotein) Nogo protein Nogo-A, Nogo-B, Nogo-C Focus on Nogo-ANogo-A and its interaction partnersNogo-A inhibitory for growing neurites and cell migration Nogo-66 region interact with different subunits of a receptor complex common to all isoforms of Nogo inhibits neurite outgrowth NiG unique to Nogo-A inhibitory domainsNgR GPI anchoring  located on the surface of neurons Receptor complex has an affinity for MAG and Omgp Signaling mechanism Nogo-A, MAG, OMgp interact with receptor complex Intracellular Ca ↑ RhoA pathway activation  regulator of cytoskeletonRhoA signaling pathway  regulate to cytoskeletonLead to growth cone collapseSpinal cord injuryAfter mechanical damage spinal cord leads to local inflammation and secondary tissue damage The glial scar formed after CNS injury impediment to axonal regeneration consists of astrocytes, inflammatory cell, connective tissue Act as a mechanical barrier for growing axons Chondroitin-sulfate proteoglycans  inhibit growing axons CSPG in astrocytes  increase following CNS injury Chondroitinase  remove CSPG  enhance sprouting of axonThe presence of specific glial cell types in CNS Astrocytes Oligodendrocytes Microglial cells The most apparent difference between the regeneration permissive PNS and the non-regenerating CNS Nogo-A MAG OMgp Proteoglycans brevican and versican V2 Semaphorins 4D and 5A Ephrin B3StrategyBlocking myelinassociated inhibitors Blocking signalling partners such as NgR or RhoA Applying growth stimulating neurotrophic factors Dissolving the scar with chondroitinase Implanting bridges across the lesion site with stem cellEffects of inactivation of Nogo-A on regeneration and axonal sprouting in vivoNogo-A NgR blocking reagent lead to increase regeneration and functional recovery of corticospinal axon Applied directly after the time of lesion or 1wk post-injuryFunctional recovery after spinal cord injury and Nogo-A inactivationFunctional recovery formation of new functional and meaningful connections and circuits Beam (analyze proper limb placement), swimming, food pellet grasping (forelimb reaching)  an intact CST and rubrospinal tract Anti-Nogo-A treatment  complete restoration of skilled forelimb useNogo antibodies in ischaemic stroke and traumatic brain injuryDegree of recovery depends on the size of the lesion and the age Adult brain  certain self-recovery Inactivation of the Nogo/NgR system  enhance the capacity In the immature CNS After brain injury  rearrangements of remaining fibre systems and regeneration of lesioned fibres The adult brain decrease regenerative potential Nogo-A antibody or NgR blocking peptide  functional recovery in adult rats after cerebral ischaemiaStroke In human, immediately treatment impossible Delayed Nogo-A neutralization after stroke  functional recovery Ex) 24 hours after stroke in adult rat recovery of skilled forelimb movements and CST remodeling Nogo-A function-blocking NgR fragment (7days after stroke) functional recoveryOutlookNogo-A blocking treatment Relevant for human spinal cord injury, stroke, traumatic brain injury Future therapies Combine growth-promoting treatment Enhancing regeneration and plasticity Decrease or bridge the glial scar Specific rehabilitation program to strengthen the newly formed connectionTerminologyTraumatic brain injury (외상성 뇌 손상) 교통사고나 산업재해 등에 의한 뇌 손상으로서 주로 폐쇄성 뇌손상이며 다양한 신체적, 신경 해동학적인 장애를 나타냄. Stroke(뇌졸증)과 비교해보면 TBI환자는 신경 손상 부위가 일부 살아있어 뇌의 plasticity가 뇌졸증 환자보다 좋다. Neuroglial cell 신경의 기능을 보조해주는 세포, 영양분등을 neuron에 공급하는 역할을 하며, 종류로는 oligodendrocyte, astrocyte, microglial cell이 존재 한다. Corticospinal track (pyramidal track) Cerebral cortex와 spinal cord를 연결하는 axon의 massive 한 집합으로 motor axon을 많이 포함 한다. Reticulospinal track 뇌에서 처음으로 spinal cord로 하행하는 신경로 Vestibulospinal track 평형감각과 관련된 신경로 Tectospinal track 시각과 관련된 신경로 Rubrospinal track 사지의 운동에 관여하는 신경로{nameOfApplication=Show}

의/약학| 2007.02.21| 14페이지| 2,000원| 조회(358)

Spinal Cord Injury, 신경 재생, nogo proteins

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