Cell-surface antigens provide invaluable tools for the identification of cells and for the analysis of cell differentiation. In particular, stage-specific embryonic antigens that are developmentally regulated during early embryogenesis are widely used as markers to monitor the differentiation of both mouse and human embryonic stem (ES) cells and their malignant counterparts, embryonic carcinoma (EC) cells. However, there are notable differences in the expression patterns of some such markers between human and mouse ES/EC cells, and hitherto it has been unclear whether this indicates significant differences between human and mouse embryos, or whether ES/EC cells correspond to distinct cell types within the early embryos of each species. We now show that human ES cells are characterized by the expression of the cell-surface antigens, SSEA3, SSEA4, TRA-1-60, and TRA-1-81, and by the lack of SSEA1, and that inner cell mass cells of the human blastocyst express a similar antigen profile, in contrast to the corresponding cells of the mouse embryo.

Please cite this article as: D. Zhu, Y. Wang, M. Thomas, et al., Exosomes from adiposederived stem cells alleviate myocardial infarction via microRNA-31/FIH1/HIF-1α pathway,

Currently, the vapor pressure of crude oil is primarily controlled through Reid Vapor Pressure testing (ASTM D323-90) from both a commercial product and environmental air emissions standpoint. Environmental regulations do require a further estimation of the "True" crude oil vapor pressure from the Reid test results via a nomograph relationship contained in API 2517. The true vapor pressure of a given oil or fluid is of interest because it defines the point of vapor initiation (i.e., the boiling point or bubble point). The quantity of such oil vapors is of course directly related to product losses and environmental air emissions. However, the MITRE Corporation in support of the Strategic Petroleum Reserve Crude Oil Quality program has found the Reid test even in combination with the API 2517 adjustment for "True" vapor pressure to give 50% to even 300+% errors in the determination of a crude oil's actual true vapor pressure. MITRE therefore developed a test method and calculation algorithm that substantially improves the determination of a crude oil's "actual" true vapor pressure. The method involves use of a device to 1) analyze the composition of gas separating from a liquid oil stream at a known pressure and temperature, 2) measure the rate of gas and oil flow exiting the same gas/oil separator, and 3) use the described test data in an iterative calculation algorithm with industry- established gas/liquid equilibrium values to estimate the crude oil's vapor pressure within +/- 2% (or 0.3 psia). This test method provides a characterization of the oil's composition which allows prediction of vapor pressure and even air emissions quantification over the full temperature range of interest. In addition air toxics existing in the oil (H2S benzene, etc.) have been quantified to the 10 ppm level in the oil as well as in the evolved gases. Introduction The Strategic Petroleum Reserve (SPR), which maintains the nation's emergency supply of oil in the event of an international oil crisis, has developed several sites for underground storage of oil in salt-dome-leached caverns. The underground oil storage volumes are subject to natural gas intrusion and geothermal heating. Both gas and temperature rise can cause the vapor pressure of crude oil to increase to the point that oil vapors will be generated upon subsequent oil depressurization into atmospheric storage tanks. The SPR oil drawdown rates of over 1 million barrels per day (MMBD) per site and the SPR's unique storage system subject to gas and heat intrusion created a need for an accurate vapor pressure test method, since significant safety and environmental impacts are associated with evolved gas volumes of even less than 1 SCF/BBL for such large crude oil flowrates. Background At MimE's initial involvement in the SPR "gassy/hot" oil issue, there was a contradiction between Reid test results, which after adjustment by the API 2517 nomograph (Figure 1), indicated that the 'True" vapor pressure of the oil was less than atmospheric, and other tests conducted in the lab such as bubblepoint and gas/oil ratio tests which indicated that the oil's bubblepoint (or vapor pressure) was greater than atmospheric and that vapors were evolving from the oil when depressured to atmospheric pressure. Note that the vapor pressure of a liquid is defined as the point at which the liquid begins to form a vapor phase (bubbles) due to either a temperature increase or a pressure decrease. Since the vapor pressure of a liquid is closely associated with the initial formation of gas bubbles, the terms vapor pressure and bubblepoint are often used interchangeably.

Our previous study has revealed that exosomes from adipose-derived stem cells (ASCs) promote angiogenesis in subcutaneously transplanted gels by delivery of microRNA-31 (miR-31) which targets factor inhibiting hypoxia-inducible factor-1 (FIH1) in recipient cells. Here we hypothesized that ASC exosomes alleviate ischemic diseases through miR-31/FIH1/hypoxia-inducible factor-1α (HIF-1α) signaling pathway. Exosomes from ASCs were isolated by sequential centrifugations, and were characterized with nanoparticle tracking analysis, transmission electron microscopy, and immunoblotting analysis for exosomal markers. Results from laser imaging of ischemic mouse hindlimb revealed that exosomes enhanced the blood perfusion, and this enhancement was impaired when using miR-31-depleted exosomes. Immunohistochemistry analysis showed that administration of exosomes resulted in a higher arteriole density and larger CD31+ area in ischemic hindlimb than miR-31-delpleted exosomes. Similarly, knockdown of miR-31 in exosomes reduced the effects of the exosomes on increasing ventricular fraction shortening and CD31+ area, and on decreasing infarct size. Exosomes promoted endothelial cell migration and tube formation. These changes were attenuated when miR-31 was depleted in the exosomes or when FIH1 was overexpressed in the endothelial cells. Furthermore, the results from co-immunoprecipitation and luciferase reporter assay demonstrated that the effects of exosomes on elevating the binding of HIF-1α with co-activator p300 and enhancing HIF-1α activity were decreased when miR-31 was depleted in the exosomes or FIH1 was overexpressed. Our findings provide evidence that exosomes from ASCs promote angiogenesis in both mouse ischemic hindlimb and heart through transport of miR-31 which targets FIH1 and therefore triggers HIF-1α transcriptional activation.