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1.  EFFECT OF AT1 RECEPTOR BLOCKADE ON INTERMITTENT HYPOXIA-INDUCED ENDOTHELIAL DYSFUNCTION 
Chronic intermittent hypoxia (CIH) raises arterial pressure, impairs vasodilator responsiveness, and increases circulating angiotensin II (Ang II); however, the role of Ang II in CIH-induced vascular dysfunction is unknown. Rats were exposed to CIH or room air (NORM), and a subset of these animals was treated with losartan (Los) during the exposure period. After 28 days, vasodilatory responses to acetylcholine or nitroprusside were measured in isolated gracilis arteries. Superoxide levels and Ang II receptor protein expression were measured in saphenous arteries. After 28 days, arterial pressure was increased and acetylcholine-induced vasodilation was blunted in CIH vs. NORM, and this was prevented by Los. Responses to nitroprusside and superoxide levels did not differ between CIH and NORM. Expression of AT2R was decreased and the AT1R:AT2R ratio was increased in CIH vs. NORM, but this was unaffected by Los. These results indicate that the blood pressure elevation and endothelial dysfunction associated with CIH is dependent, at least in part, on RAS signaling.
doi:10.1016/j.resp.2012.05.025
PMCID: PMC3409315  PMID: 22728949
Intermittent hypoxia; Endothelial function; Angiotensin II
2.  Voltage-gated sodium channel expression and action potential generation in differentiated NG108-15 cells 
BMC Neuroscience  2012;13:129.
Background
The generation of action potential is required for stimulus-evoked neurotransmitter release in most neurons. Although various voltage-gated ion channels are involved in action potential production, the initiation of the action potential is mainly mediated by voltage-gated Na+ channels. In the present study, differentiation-induced changes of mRNA and protein expression of Na+ channels, Na+ currents, and cell membrane excitability were investigated in NG108-15 cells.
Results
Whole-cell patch-clamp results showed that differentiation (9 days) didn’t change cell membrane excitability, compared to undifferentiated state. But differentiation (21 days) induced the action potential generation in 45.5% of NG108-15 cells (25/55 cells). In 9-day-differentiated cells, Na+ currents were mildly increased, which was also found in 21-day differentiated cells without action potential. In 21-day differentiated cells with action potential, Na+ currents were significantly enhanced. Western blot data showed that the expression of Na+ channels was increased with differentiated-time dependent manner. Single-cell real-time PCR data demonstrated that the expression of Na+ channel mRNA was increased by 21 days of differentiation in NG108-15 cells. More importantly, the mRNA level of Na+ channels in cells with action potential was higher than that in cells without action potential.
Conclusion
Differentiation induces expression of voltage-gated Na+ channels and action potential generation in NG108-15 cells. A high level of the Na+ channel density is required for differentiation-triggered action potential generation.
doi:10.1186/1471-2202-13-129
PMCID: PMC3502467  PMID: 23095258
Action potential; Na+ channel; NG108-15 cell; Patch clamp; Single-cell real-time PCR; Western blot
3.  N-[(2S)-2-Chloro­propano­yl]glycine 
The title compound, C5H8ClNO3, was prepared by the nucleophilic substitution reaction of (2S)-2-chloro­propanoyl chloride with glycine. The acetate group forms a dihedral angle of 84.6 (1)° with the mean plane of the C—NH—C=O fragment. In the crystal, the molecules are linked by N—H⋯O and O—H⋯O hydrogen bonds, generating a three-dimensional network, which consolidates the crystal packing.
doi:10.1107/S1600536812036720
PMCID: PMC3435838  PMID: 22969684
4.  Diethyl 3,3′-(phenyl­methyl­ene)bis­(1H-indole-2-carboxyl­ate) 
In the title compound, C29H26N2O4, the benzene ring is twisted by 73.5 (5) and 84.9 (3)° with respect to the mean planes of the two indole ring systems; the mean planes of the indole ring systems are oriented at a dihedral angle of 82.0 (5)°. In the crystal, mol­ecules are linked by pairs of N—H⋯O hydrogen bonds into chains.
doi:10.1107/S1600536812036239
PMCID: PMC3435799  PMID: 22969645
5.  Mitochondria-Derived Superoxide Links to Tourniquet-Induced Apoptosis in Mouse Skeletal Muscle 
PLoS ONE  2012;7(8):e43410.
Our previous study has reported that superoxide mediates ischemia-reperfusion (IR)-induced necrosis in mouse skeletal muscle. However, it remains poorly understood whether IR induces apoptosis and what factors are involved in IR-induced apoptosis in skeletal muscle. Using a murine model of tourniquet-induced hindlimb IR, we investigated the relationship between mitochondrial dysfunction and apoptosis in skeletal muscle. Hindlimbs of C57/BL6 mice were subjected to 3 h ischemia and 4 h reperfusion via placement and release of a rubber tourniquet at the greater trochanter. Compared to sham treatment, tourniquet-induced IR significantly elevated mitochondria-derived superoxide production, activated opening of mitochondrial permeability transition pore (mPTP), and caused apoptosis in the gastrocnemius muscles. Pretreatment with a superoxide dismutase mimetic (tempol, 50 mg/kg) or a mitochondrial antioxidant (co-enzyme Q10, 50 mg/kg) not only decreased mitochondria-derived superoxide production, but also inhibited mPTP opening and apoptosis in the IR gastrocnemius muscles. Additionally, an inhibitor of mPTP (cyclosporine A, 50 mg/kg) also inhibited both mPTP opening and apoptosis in the IR gastrocnemius muscles. These results suggest that mitochondria-derived superoxide overproduction triggers the mPTP opening and subsequently causes apoptosis in tourniquet-induced hindlimb IR.
doi:10.1371/journal.pone.0043410
PMCID: PMC3422247  PMID: 22912870

Results 1-5 (5)