In recent years, researchers have made some breakthroughs on human embryonic stem cells, in particular, on reprogramming differentiated cell (such as human skin fibroblast) into human embryonic stem cell. Induced pluripotent stem cells could be generated from human skin fibroblasts by inducting into four transcription factors known as OCT3/4, SOX2, C-MYC and KLF4. This approach enables better understanding the pathogenesis of diseases from the perspective of genetic component and promising in the treatment of related diseases. This article introduces the latest advancement of those researches.

As a powerful intervention to protect ischemic tissues,ischemic preconditioning (IPC) has been a hot spot due to its greatly potential clinical values throughout the past decades.From the triggers and cell-membrane receptors to intracellular signal molecules and mitochondrial signal chains,we inquire in this review the common points and relativities on the signaling transduction of IPC by conferring the cardio-and neuro-protection mechanisms of IPC.

Protein kinase C pathway is an important intracellular signal transduction pathway.A growing number of evidences showes that activation of PKC influences endothelial cell permeability.In this review,we briefly summarize the effects and regulating pathways of protein kinase C in modulation of vascular endothelium permeability.

Endogenous carbon monoxide (CO) is proposed to be an intracellular signaling molecule. As a new gaseous messenger, CO shares with nitric oxide (NO) the ability of modulating neuroendocrine function and inducing vasorelaxation, mainly by stimulating soluble guanylate cyclase and regulating the level of cGMP. This review emphasized the endogenous source of CO and the interaction of CO- and NO-generating systems. It also discussed the biological effects of CO and the underlying mechanisms.

Theincreasedmicrovascularpermeabilityappearsmainlyinvenuleduringinflammation , shock ,andburns .Endothelialcellsplayanimportantroleinvenulepermeabilityenhancement.Therearetwo kindsofpathwayformacromoleculeextravasation .Oneisparacellularpathwayandanotheristranscellular pathway ,whicharerelatedtotheformationofendothelialgaportranscellularopeningsseperately .Thealter ationofintercellularrelatedprotein ,suchasoccludin ,claudin ,zonaoccludens (ZO) ,junctionaladhesion molecule (JAM) ,VE -cadherin ,catenin ,integrin ,etc ,andthealterationofendothelialcytoskeleton ,such asrearrangementofactinfilament,formationofstressfiberandfocaladhesion ,etc ,involveinthepathogenesis ofincreasedmicrovascularpermeability . [

Objective To gain a higher quality of pathophysiology experiment teaching of students studying abroad.Methods To improve greatly in knowing the characteristics of students studying abroad,preparation before class, teaching method and effect judgement.Results We have a conspicuous improvement in the quality and effect of pathophysiology experiment teaching. Conclusions To gain a higher quality of pathophysiology experiment teaching of students studying abroad,we should improve greatly in knowing the characteristics of students studying abroad,preparation before class,teaching method and effect judgement.

[ ABSTRACT] Myosin light chain kinase ( MLCK) activates the regulatory light chain of myosin II, and the phos-phorylated myosin light chain leads to actomyosin contractile activity, as well as the cell contraction and increasing intercel-lular gap, which finally results in endothelial barrier dysfunction.MLCK-dependent hyperpermeability occurs in response to multiple cell signaling molecules and signaling pathways, including Ca2+, Src, PKC, NO, cGMP and mitogen activated protein kinases ( MAPK) .In this review, different mechanisms of endothelial hyperpermeability mediated by MLCK are discussed.

AIM: To investigate whether small GTPase RhoA's downstream effector Rho kinase mediates burn serum-induced endothelial hyperpermeability. METHODS: Primary cultured rat dermal microvascular endothelial cells (DMECs) were exposed to serum isolated from burned or sham burn rats for 6 hours and 8 hours, respectively, and did or didn't pretreated or post-treated with Y-27632 (30 ?mol/L), a specific inhibitor of Rho kinase. ECs were then prepared for routine scanning electron microscopy observation, or stained with rhodamine-phalloidin for F-actin visualization. Permeability to FITC-albumin was evaluated using EC monolayers. RESULTS: Stimulation with 15% burn serum for 6 h changed the ultrastructure on cellular surface of DMECs with appearance of ripple marks instead of microvillus. The small protuberances at cellular lateral were shorten and the gaps were seen between adjacent cells. Post-treatment of Y-27632 reversed the changes of ultrastructure on the cellular surface. Burn serum induced a striking reorganization of actin cytoskeleton with a weakening of fluorescent intensity of the peripheral filament bands and formation of the long and thick stress fibers, lamellipodia and filopodia. The stress fibers were diminished by pretreatment or post-treatment of Y-27632. But lamellipodia and filopodia were not influenced by pretreatment or post-treatment of Y-27632. Pre-treatment of Y-27632 also attenuated significantly the increase in EC monolayer permeability stimulated by burn serum for 6 h. However, post-treatment of Y-27632 could not attenuated burn serum-induced endothelial hyperpermeability response although their Pa values were lower than simple burn serum group's. CONCLUSION: These findings indicate that Rho kinase is involved in the mediation of burn serum-induced endothelial actin cytoskeleton reorganization and early stage of barrier dysfunction. [

AIM: To study the effect of microelement powder (MP) on membrane potential of vascular endothelial and smooth muscle cells of rats in order to elucidate the mechanism of microcirculation improvement by MP. METHODS: Cultured pulmonary vascular endothelial cells (EC) and aortic smooth muscle cells (SMC) of rats and detecting the changes of cellular membrane potentials by using potential-sensitive fluorescent probe and laser jet confocal microscope. RESULTS: MP hyperpolarized SMCs significantly. Glybenclamide (2 μmol/L), a blocker of KATP channel, which had no effect on membrane potential of SMCs, reversed the hyperpolarization of MP completely; MP hyperpolarized ECs slightly, but the effect was unaffected by glybenclamide. CONCLUSION: MP hyperpolarizes SMCs by activating KATP channels and leads to dilation of microvessels and improvement of microcirculation.

AIM: To study the effect of cGMP-dependent protein kinase (PKG) on the pathogenesis of burn shock. METHODS: Confluent endothelial cells were disintegrated and centrifugated to obtain cell lysates after being treated with 10% burn serum or PKG activator 8-Br-cGMP. PKG activity of lysates was measured with radioactive isotope label method in a reaction system of phosphorylation of specific substrate H2B by PKG, and the shape and the distribution of intracellular filamentous actin were detected by specific fluorescence staining. For the control study, the PKG specific inhibitor KT5823 were used to pretreat the endothelial cells before the administration of burn serum or PKG activator 8-Br-cGMP. RESULTS: Exposures to burn serum and 8-Br-cGMP led to a rapid time-dependent increase in endothelial PKG activity and the polar distribution of intracellular filamentous actin, and preincubation with KT5823 abolished those effects. CONCLUSIONS: The results suggest that burn serum induces PKG activation and the stress variety of filamentous actin in the vascular endothelial cells, which probably contributes to the endothelial hyperpermeability after burn shock. [