Rare Earth Dy3+ Activated MgSrAl10O17 Phosphors for Luminescence

MgSrAl10O17:xDy3+ nanophosphors were fabricated by combustion method for different concentrations (x = 0, 0.0005, 0.001, 0.005, 0.01 and 0.02 mol) of Dysprosium (Dy). The synthesized nanophosphors were characterized by XRD, SEM, TEM, FTIR, PL and TL. The XRD (X-ray diffraction) showed crystalline hexagonal structure with preferred orientation of (107) plane. SEM (Scanning electron microscope) result shows the formation of nanosheets in irregular shape. TEM (transmission electron microscope) study revealed the nanoparticles within average diameter size of 30 nm. The FTIR ( fourier transform infrared spectrum) shows absorption peaks in numerous regions. TL (thermo-luminescence) properties included TL glow curves and TL response for different concentrations of Dy after exposure of 700 Gy gamma rays. TL intensity was found to increase with increase in concentration of dopant Dy and was found to show best result for x=0.02. Further PL (photoluminescence) characterization ofMgSrAl10O17:0.02 Dy3+ phosphor exhibits two main emission peaks at 484 and 575 nm due to Dy3+ ion, when excited with 350 nm wavelength.

Evaluation of the effect of some medicinal plants on cultured Trichomonas Vaginalis

Introduction: Trichomoniasis is a worldwide sexually transmitted disease caused by Trichomonas vaginalis. It inflicts severe complications to the human genitourinary system. The devastating negative effects and the emergence of resistance to common medication impose the search for safer and effective alternatives. This research aimed to investigate the effect of the Allium sativum, Nigella sativa crude extracts (NsCE) and the combination between their most effective doses with metronidazole. Methodology: Vaginal swabs were obtained from symptomatic patients, and cultured on Diamond's medium. Assessment of various concentrations of these herbs at different follow-up periods was done by counting the number of dead T. vaginalis trophozoites using the hemocytometer and trypan blue staining. Transmission electron microscope study was done. Results: NsCE 9 mg/mL yielded the highest lethal effect on T. vaginalis trophozoites after 72 hours, compared with metronidazole. Combination of NsCE 9 mg/mL and metronidazole 50 µg/mL gave the best result. Additionally, Tomex90 µg/mL, represents a tolerable effect after 72 hours, but metronidazole 100 µg/mL still has higher effect. These results were confirmed by the ultrastructural changes observed in T. vaginalis trophozoites, signifying severe damage of nucleus and cytoplasm with large vacuolization and cell membrane defects. Conclusions: NsCE is a promising anti-Trichomonas especially its combination with metronidazole which showed a high synergistic effect.

TLR4 Activation Promotes the Progression of Experimental Autoimmune Myocarditis to Dilated Cardiomyopathy by Inducing Mitochondrial Dynamic Imbalance

Mitochondrial dynamic imbalance associates with several cardiovascular diseases. However, the role of mitochondrial dynamics in TLR4 activation-mediated dilated cardiomyopathy (DCM) progress remains unknown. A model of experimental autoimmune myocarditis (EAM) was established in BALB/c mice on which TLR4 activation by LPS-EB or TLR4 inhibition by LPS-RS was performed to induce chronic inflammation for 5 weeks. TLR4 activation promoted the transition of EAM to DCM as demonstrated by increased cardiomyocyte apoptosis, myocardial fibrosis, ventricular dilatation, and declined heart function. TLR4 inhibition mitigated the above DCM changes. Transmission electron microscope study showed that mitochondria became fragmented, also with damaged crista in ultrastructure in EAM mice. TLR4 activation aggravated the above mitochondrial aberration, and TLR4 inhibition alleviated it. The mitochondrial dynamic imbalance and damage in DCM development were mainly associated with OPA1 downregulation, which may be caused by elevated TNF-α level and ROS stress after TLR4 activation. Furthermore, OMA1/YME1L abnormal degradation was involved in the OPA1 dysfunction, and intervening OMA1/YME1L in H9C2 significantly alleviated mitochondrial fission, ultrastructure damage, and cell apoptosis induced by TNF-α and ROS. These data indicate that TLR4 activation resulted in OPA1 dysfunction, promoting mitochondrial dynamic imbalance and damage, which may involve in the progress of EAM to DCM.