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1.
Biomed Chromatogr ; 38(4): e5827, 2024 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-38287211

RESUMEN

In recent years, researchers have shown a growing interest in the interactions between different pharmaceutical agents. An intriguing instance lies in the possible interaction between nimodipine and vitamin C. To investigate the pharmacokinetic and pharmacodynamic effects of vitamin C on nimodipine in rats, rats were randomly divided into a nimodipine only group and a combination group (nimodipine + vitamin C). The two groups were given intragastric administration and nimodipine blood concentrations were determined using high-performance liquid chromatography-tandem mass spectrum at different time points. Blood pressure and heart rate were measured via carotid artery cannulation. Pharmacokinetic differences were observed between the nimodipine only group and the combination group at the same dose. Compared with the nimodipine only group, the combination group's main pharmacokinetic parameters of peak concentration and area under the curve increased significantly, and the difference was statistically significant (p < 0.05); furthermore, the combination group exhibited a significant reduction in average blood pressure, while no significant effects on heart rate were observed. Vitamin C did not affect the activity of CYP450 in rat liver. The pharmacokinetic characteristics and pharmacodynamics of nimodipine were changed by vitamin C administration in rats.


Asunto(s)
Ácido Ascórbico , Nimodipina , Ratas , Animales , Cromatografía Líquida de Alta Presión , Sistema Enzimático del Citocromo P-450
2.
Opt Express ; 31(15): 24926-24938, 2023 Jul 17.
Artículo en Inglés | MEDLINE | ID: mdl-37475308

RESUMEN

We demonstrate a transmitter and receiver in a silicon photonics platform for O-band optical communication that monolithically incorporates a modulator driver, traveling-wave Mach-Zehnder modulator, control circuitry, photodetector, and transimpedance amplifier (TIA) in the GlobalFoundries Fotonix (45SPCLO) platform. The transmitter and receiver show an open 112 Gbps PAM4 eye at a 4.3 pJ/bit energy efficiency, not including the laser. Extensive use of gain-peaking enables our modulator driver and TIA to achieve the high bandwidths needed in the 45 nm CMOS-silicon photonics process. Our results suggest an alternative to the frequent approach of bump-bonding BiCMOS drivers and TIAs to silicon photonics.

3.
Onco Targets Ther ; 12: 11691-11700, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-32021247

RESUMEN

INTRODUCTION: The breast cancer stem cells contribute to the initiation, progression, recurrence, metastasis as well as resistance of breast cancer. However, the mechanisms underlying the maintenance of breast cancer stemness have not been fully understood. MATERIALS AND METHODS: TCGA and GEO data were used for measuring miR-520b expression in breast cancer tissues. Kaplan-meier analysis was used for determining the relationship between miR-520b expression level and the prognosis of patients. Genetic manipulation was performed by lentivirus system and miR-520b inhibitor was used for knockdown of miR-520b. qRT-PCR and Western blot were employed to determine the mRNA and protein levels, respectively. The stemness and EMT (Epithelial to mesenchymal transition) were assessed by sphere-formation and transwell assay as well as the expression of the related markers. The target genes of miR-520b were identified using the online database starBase V3.0. RESULTS: miR-520b is upregulated in cancer tissues of breast cancer patients and predicts poor prognosis. Upregulation of miR-520b was found in breast cancer stem cells. Ectopic expression of miR-520b promotes the stemness of the breast cancer cells, conversely, depletion of miR-520b attenuates the stemness of these cells. miR-520b positively regulates Hippo/YAP signaling pathway and overexpression of LAST2 abolished the effect of miR-520b on the stemness of breast cancer cells. CONCLUSION: miR-520b promotes the stemness of breast cancer patients by activating Hippo/YAP signaling via targeting LATS2.

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