Charge Injection and Dielectric Characteristics of Polyethylene Terephthalate Based on Semiconductor Electrodes.

Employing a novel semiconductor electrode in comparison with the traditional semiconductor electrode made of polyethylene/ethylene-vinyl-acetate copolymer/carbon-black (PE/EVA/CB) composite, characteristic charge carriers are injected into polyethylene terephthalate (PET) as a polymer dielectric paradigm, which will be captured by specific deep traps of electrons and holes. Combined with thermal stimulation current (TSC) experiments and first-principles electronic-state calculations, the injected charges from the novel electrode are characterized, and the corresponding dielectric behavior is elucidated through DC conductance, electrical breakdown and dielectric spectrum tests. TSC experiments with novel and traditional semiconductor electrodes can distinguish the trapping characteristics between hole and electron traps in polymer dielectrics. The observable discrepancy in space charge-limited conductance and the stable dielectric breakdown strength demonstrate that the electron injection into PET film specimen is restricted by using the novel semiconductor electrode. Attributed to the favorable suppression on the inevitable electron injections from metal electrodes, adopting novel i-electrode can avoid the evident abatement of dipole orientation polarization caused by space charge clamp, but will engender the accessional high-frequency dielectric loss from dielectric relaxations of interface charges at i-electrodes.

Activation of transient receptor potential vanilloid 1 protects the heart against apoptosis in ischemia/reperfusion injury through upregulating the PI3K/Akt signaling pathway.

Transient receptor potential vanilloid 1 (TRPV1) is a nonselective cation channel and a molecular integrator of noxious stimuli. TRPV1 activation confers cardiac protection against ischemia/reperfusion (I/R) injury. The present study aimed to investigate whether the cardioprotective effects of TRPV1 were associated with the inhibition of apoptosis via the phosphatidylinositol 3­kinase (PI3K)/protein kinase B (Akt) and extracellular signal­regulated protein kinase 1/2 (ERK1/2) signaling pathways. Briefly, the hearts of TRPV1 knockout (TRPV1­/­) or wild­type (WT) mice were isolated and subjected to 30 min of ischemia followed by 60 min of reperfusion in a Langendorff apparatus in the presence or absence of the PI3K inhibitor, LY294002. At the end of reperfusion, infarct size was measured using 2,3,5­triphenyltetrazolium chloride staining and myocardial apoptosis was assessed by terminal deoxynucleotidyl transferase­mediated dUTP nick­end labeling (TUNEL) staining. The expression levels of B­cell lymphoma 2 (Bcl­2), Bcl­2­associated X protein (Bax), and phosphorylated Akt and ERK1/2 were determined by western blot analysis. There was a significant increase in the extent of infarction and the percentage of TUNEL­positive cells, and a decrease in the Bcl­2/Bax ratio, and Akt and ERK1/2 phosphorylation in TRPV1­/­ hearts. In addition, treatment with LY294002 increased infarct size and the percentage of TUNEL­positive cells, and reduced Bcl­2/Bax expression and Akt phosphorylation in WT hearts, but not in TRPV1­/­ hearts, following I/R. Taken together, these data suggested that TRPV1 serves a protective role against myocardial apoptosis during I/R via the PI3K/Akt signaling pathway. In conclusion, activating TRPV1 may be considered a potential approach to protect the heart against I/R injury.

ROS activates JNK-mediated autophagy to counteract apoptosis in mouse mesenchymal stem cells in vitro.

AIM: Transplantation of mesenchymal stem cells (MSCs) for the treatment of diabetic erectile dysfunction (ED) is hampered by apoptosis of the transplanted cells. In diabetic ED, there is increased oxidative stress and decreased NO in the corpora cavernosa, and reactive oxygen species (ROS) induce apoptosis of the transplanted cells. In this study we examined whether and how autophagy was involved in ROS-induced apoptosis of MSCs. METHODS: Mouse C3H10 MSCs were treated with H2O2 to simulate the high oxidative condition in diabetic ED. Cell viability was measured using MTT assay. Apoptosis was analyzed by flow cytometry. Apoptosis- and autophagy-related proteins were detected with Western blot assays. Intracellular autophagosome accumulation was studied using transmission electron microscopy. RESULTS: Treatment of MSCs with H2O2 (50-400 µmol/L) inhibited the cell viability in concentration- and time-dependent manners. Furthermore, H2O2 (300 µmol/L) induced apoptosis, as well as activated autophagy in MSCs. Pretreatment with lysosome inhibitor chloroquine (10 µmol/L) or PI3K inhibitor 3-methyladenine (5 mmol/L) significantly enhanced H2O2-induced cell death. Pretreatment with JNK inhibitor SP600125 (10 µmol/L) abrogated H2O2-induced accumulation of LC3-II, and attenuated H2O2-induced reduction of Bcl-2 levels in MSCs. CONCLUSION: ROS induce autophagy to counteract apoptosis in MSCs by activation of JNK. Thus, augmentation of autophagy may reduce apoptosis, prolonging MSC survival and improving MSC-based therapeutic efficacy for diabetic ED.

[Clinical analysis for the treatment of 63 cases of orbital tumors in Xinjiang].

OBJECTIVE: To analyse the clinical features, histopathological classifications, treatments and prognosis of orbital tumors in Xinjiang. METHODS: The authors retrospectively analyse 63 patients (64 eyes) with orbital tumors, including all nationalities which had been received and treated in ophthalmic department of the PLA 474th Hospital during 2005 to 2009. RESULTS: The nationality composition in our cases was 37 Han, 16 Uygur (16 eyes), 4 Hui, 3 Mongol, and 3 Kazak. Our data mainly consisted of benign tumor., in which, the majority were the vascular tumors, and then were cysts, inflammatory pseudotumor, neurogenic tumors, mixed tumors of lacrimal gland, lipoma and hydatid. The malignant tumors mainly consisted of rhabdomyosarcoma and adenocarcinoma of lacrimal gland, then was non-Hodgkin lymphoma. The operation methods we selected were approaching by orbital skin or anterior skin incision, lateral orbitotomy and approaching by outer canthus incision plus lower fornical conjunctiva incision. The severe postoperative complication was impaired vision, and 2 patients with inflammatory pseudotumor had recrudesced. CONCLUSIONS: There is no difference on the types and morbidity situation of orbital tumors between Xinjiang and other areas in general, in addition orbital hydatid which was closely related to regional characteristic of Xinjiang, Surgical excision is the main and effective treatment, the prognosis is related to the local tissue extension of tumor, comprehensive pre-operation preparations, careful operation, appropriate post-operative managements and rich clinic experience of doctor.