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1.
Polymers (Basel) ; 15(9)2023 Apr 26.
Artículo en Inglés | MEDLINE | ID: mdl-37177211

RESUMEN

A wet electrostatic precipitator (WESP) has much higher capture rate for fine particulate matter, PM2.5, than a traditional dry type electrostatic precipitator does. In order to make full use of existing dust removal equipment and reduce the emissions of smoke and dust to zero, a combination of chemical coagulation and humidification coagulation is proposed using a WESP. The results show that the addition of chemical coagulant can promote the coagulation of coal-fired dust particles. After the addition of pectin (PG), the median diameter of dust particles increases from 28.19 µm to 45.28 µm. Water vapor humidification can promote the coagulation of dust particles. When the water vapor injection rate increases from 0 kg/h to 3.2 kg/h, the median diameter of dust particles increases from 28.19 µm to 36.45 µm. The synergistic effect of the coagulant and water vapor can enhance the chemical coagulation effect; when 1.0 × 10-2 g/L PG and 3.2 kg/h water vapor synergize, the collection efficiency reaches 98.17%, and when 1.0 × 10-2 g/L polyacrylamide (PAM) and 3.2 kg/h water vapor synergize, the collection efficiency reaches 96.68%. Both chemical coagulation and water vapor humidification can promote the condensation of coal dust, which is beneficial to improve the efficient capture of fine particles using WESP.

2.
Chinese Journal of Biologicals ; (12): 742-750, 2023.
Artículo en Chino | WPRIM (Pacífico Occidental) | ID: wpr-996459

RESUMEN

@#The Coronavirus Disease 2019(COVID-19) pandemic is having a dramatic impact on human health,lives,and the global economy. The development of a safe and efficacious vaccine is the most effective intervention to protect the population from the disease and limit the spread of the virus. Based on the current guidelines and research progress of severe acute respiratory symptom coronavirus 2(SARS-CoV-2) vaccines in various countries,this review summarized the research progress on non-clinical safety evaluation of SARS-CoV-2 vaccines by referring to the guidelines and relevant literatures over the world,in order to provide a reference for non-clinical research of SARS-CoV-2 vaccines.

3.
Chem Pharm Bull (Tokyo) ; 69(1): 52-58, 2021 Jan 01.
Artículo en Inglés | MEDLINE | ID: mdl-33087639

RESUMEN

17ß Hydroxysteroid dehydrogenase type 3 (17ß-HSD3) is the key enzyme in the biosynthesis of testosterone, which is an attractive therapeutic target for prostate cancer (PCa). H10, a novel curcumin analogue, was identified as a potential 17ß-HSD3 inhibitor. The pharmacokinetic study of H10 in rats were performed by intraperitoneal (i.p.), intravenous (i.v.) and oral (p.o.) administration. In addition, the inhibitory effects of H10 against liver CYP3A4 were investigated in vitro using human liver microsomes (HLMs). The acute and chronic toxicological characteristics were characterized using single-dose and 30 d administration. All the mice were alive after i.p. H10 with dose of no more than 100 mg/kg which are nearly the maximum solubility in acute toxicity test. The pharmacokinetic characteristics of H10 fitted with linear dynamics model after single dose. Furthermore, H10 could bioaccumulate in testis, which was the target organ of 17ß-HSD3 inhibitor. H10 distributed highest in spleen, and then in liver both after single and multiple i.p. administration. Moreover, H10 showed weak inhibition towards liver CYP3A4, and did not cause significant changes in aspartate transaminase (AST) and alanine transaminase (ALT) levels after treated with H10 for continuously 30 d. Taken together, these preclinical characteristics laid the foundation for further clinical studies of H10.


Asunto(s)
17-Hidroxiesteroide Deshidrogenasas/antagonistas & inhibidores , Curcumina/farmacología , Citocromo P-450 CYP3A/metabolismo , Inhibidores Enzimáticos/farmacología , 17-Hidroxiesteroide Deshidrogenasas/metabolismo , Animales , Curcumina/administración & dosificación , Curcumina/química , Relación Dosis-Respuesta a Droga , Inhibidores Enzimáticos/administración & dosificación , Inhibidores Enzimáticos/química , Humanos , Masculino , Ratones , Ratones Endogámicos , Microsomas Hepáticos/química , Microsomas Hepáticos/metabolismo , Ratas , Ratas Sprague-Dawley , Distribución Tisular
4.
Int J Nanomedicine ; 15: 3087-3098, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32431503

RESUMEN

PURPOSE: Aldo-ketoreductase (AKR) 1C3 is crucial for testosterone synthesis. Abnormally high expression/activity of AKR1C3 can promote castration-resistant prostate cancer (CRPC). A mansonone derivative and AKR1C3 inhibitor, 6e, was combined with 4D5 (extracellular fragment of the monoclonal antibody of human epidermal growth factor receptor-2)-modified chitosan to achieve a nanodrug-delivery system (CS-4D5/6e) to treat CRPC. MATERIALS AND METHODS: Morphologies/properties of CS-4D5/6e were characterized by atomic force microscopy, zeta-potential analysis, and Fourier transform-infrared spectroscopy. CS-4D5/6e uptake was measured by immunofluorescence under confocal laser scanning microscopy. Testosterone in LNCaP cells overexpressing human AKR1C3 (LNCaP-AKR1C3) and cell lysates was measured to reflect AKR1C3 activity. Androgen receptor (AR) and prostate-specific antigen (PSA) expression was measured by Western blotting. CS-4D5/6e-based inhibition of AKR1C3 was evaluated in tumor-xenografted mice. RESULTS: CS-4D5/6e was oblate, with a particle size of 200-300 nm and thickness of 1-5 nm. Zeta potential was 1.39±0.248 mV. 6e content in CS-4D5/6e was 7.3±1.4% and was 18±3.6% for 4D5. 6e and CS-4D5/6e inhibited testosterone production significantly in a concentration-dependent manner in LNCaP-AKR1C3 cells, and a decrease in expression of AKR1C3, PSA, and AR was noted. Half-maximal inhibitory concentration of CS-4D5/6e on LNCaP-AKR1C3 cells was significantly lower than that in LNCaP cells (P<0.05). CS-4D5/6e significantly reduced growth of 22Rv1 tumor xenografts by 57.00% compared with that in the vehicle group (P<0.01). CONCLUSION: We demonstrated the antineoplastic activity of a potent AKR1C3 inhibitor (6e) and its nanodrug-delivery system (CS-4D5/6e). First, CS-4D5/6e targeted HER2-positive CRPC cells. Second, it transferred 6e (an AKR1C3 inhibitor) to achieve a reduction in intratumoral testosterone production. Compared with 6e, CS-4D5/6e showed lower systemic toxicity. CS-4D5/6e inhibited tumor growth effectively in mice implanted with tumor xenografts by downregulating testosterone production mediated by intratumoral AKR1C3. These results showed a promising strategy for treatment of the CRPC that develops invariably in prostate-cancer patients.


Asunto(s)
Miembro C3 de la Familia 1 de las Aldo-Ceto Reductasas/antagonistas & inhibidores , Antineoplásicos/química , Antineoplásicos/farmacología , Terapia Molecular Dirigida/métodos , Neoplasias de la Próstata Resistentes a la Castración/tratamiento farmacológico , Animales , Anticuerpos Monoclonales/química , Antineoplásicos/administración & dosificación , Línea Celular Tumoral , Quitosano/química , Sistemas de Liberación de Medicamentos/métodos , Humanos , Masculino , Ratones Endogámicos BALB C , Nanoestructuras/administración & dosificación , Nanoestructuras/química , Naftoquinonas/química , Antígeno Prostático Específico/metabolismo , Neoplasias de la Próstata Resistentes a la Castración/metabolismo , Neoplasias de la Próstata Resistentes a la Castración/patología , Receptor ErbB-2/inmunología , Receptores Androgénicos/metabolismo , Sesquiterpenos/química , Testosterona/metabolismo , Ensayos Antitumor por Modelo de Xenoinjerto
5.
Front Pharmacol ; 11: 637, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32457626

RESUMEN

The 17ß-hydroxysteroid dehydrogenase type 3 (17ß-HSD3) enzyme is a potential therapeutic target for hormone-dependent prostate cancer, as it is the key enzyme in the last step of testosterone (T) biosynthesis. A curcumin analog, H10, was optimized for inhibiting T production in LC540 cells that stably overexpressed 17ß-HSD3 enzyme (LC540 [17ß-HSD3]) (P < 0.01), without affecting progesterone (P) synthesis. H10 downregulated the production of T in the microsomal fraction of rat testes containing the 17ß-HSD3 enzyme from 100 to 78.41 ± 7.41%, 51.86 ± 10.03%, and 45.14 ± 8.49% at doses of 10, 20, and 40 µM, respectively. There were no significant differences among the groups with respect to the protein expression levels of 17ß-HSD3, 3ßHSD1, CYP17a1, CYP11a1, and STAR, which participate in 17ß-HSD3-mediated conversion of androgens to T (P > 0.05). This indicated that H10 only inhibited the enzymatic activity of 17ß-HSD3 in vitro. Furthermore, H10 inhibited the adione-stimulated growth of xenografts established from LNCaP cells in nude mice in vivo. We conclude that H10 could serve as an effective inhibitor of 17ß-HSD3, which in turn would inhibit the biosynthesis of androgens and progression of prostate cancer.

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