Pattern of COVID-19 in Sichuan province, China: A descriptive epidemiological analysis.

This study described the epidemiology of 487 confirmed coronavirus disease 2019 (COVID-19) cases in Sichuan province of China, and aimed to provide epidemiological evidence to support public health decision making. Epidemiological information of 487 COVID-19 cases were collected from the official websites of 21 districts (including 18 cities, 3 autonomous prefecture) health commissions within Sichuan between 21st of January 2020 to 17th of April 2020. We focus on the single-day diagnosis, demographics (gender and age), regional distribution, incubation period and symptoms. The number of single-day confirmed COVID-19 cases reach a peak on January 29 (33 cases), and then decreased. Chengdu (121 cases), Dazhou (39 cases) Nanchong (37 cases) and Ganzi Tibetan Autonomous Prefecture (78 cases) contributed 275 cases (56.5% of the total cases) of Sichuan province. The median age of patients was 44.0 years old and 52.6% were male. The history of living in or visiting Hubei, close contact, imported and unknown were 170 cases (34.9%), 136 cases (27.9%), 21 cases (4.3%) and 160 cases (32.9%) respectively. The interval from the onset of initial symptoms to laboratory diagnosis was 4.0 days in local cases, while that of imported cases was 4.5 days. The most common symptoms of illness onset were fever (71.9%) and cough (35.9%). The growth rate of COVID-19 in Sichuan has significantly decreased. New infected cases have shifted from the living in or visiting Wuhan and close contact to imported. It is necessary to closely monitor the physical condition of imported cases.

Bufadienolides induce apoptosis and autophagy by inhibiting the AKT signaling pathway in melanoma A­375 cells.

The purpose of the present study was to investigate the effect of bufadienolides on the A­375 melanoma cell line, and to delineate the underlying mechanism. A Cell Counting Kit­8 assay was used to determine the viability of the cells, and flow cytometry was used to evaluate apoptosis. Western blot analysis was used to evaluate the expression levels of proteins involved in the AKT pathway that are associated with apoptosis and autophagy. The results demonstrated that bufadienolides reduced the viability of A­375 cells in a dose­ and a time­dependent manner. Following treatment with bufadienolides, A­375 cells exhibited clear properties that were characteristic of apoptosis and autophagy. The expression levels of the pro­apoptotic proteins Bax and p53 were upregulated, whereas those of the anti­apoptotic proteins, Bcl­2 and caspase­3 were downregulated. In addition, the level of a protein known to be associated with autophagy, microtubule­associated proteins 1A/1B light chain 3­II, was increased, whereas that of p62 protein was reduced. Finally, the AKT signaling pathway was blocked in the bufadienolide­treated A­375 cells. In conclusion, these results revealed that bufadienolides effectively induced apoptosis and autophagy in A­375 cells via the AKT pathway, and therefore may be one of the candidate targets for the future development of targeted drugs to treat melanoma.

Baicalin potentiates TRAIL­induced apoptosis through p38 MAPK activation and intracellular reactive oxygen species production.

The combination of tumor necrosis factor­related apoptosis­inducing ligand (TRAIL) with other agents has been recognized as a promising strategy to overcome TRAIL resistance in cancer cells. Baicalin (5, 6­dihydroxy­7­o­glucuronide flavone) is a flavonoid from the root of the medicinal herb Scutellaria baicalensis Georgi, which has been reported to exert antioxidant, anti­inflammatory, antiviral and anticancer activities in vitro. However, the effect of baicalin on TRAIL­induced cytotoxicity has not been previously reported. In the present study, the effect of combining TRAIL and baicalin was investigated in non­small cell lung cancer cell lines. The results revealed that baicalin was able to sensitize A549 and H2009 cells to TRAIL­induced apoptosis. This was detected by the potentiation of poly­adenosine­5'­diphosphate­ribose polymerase cleavage and Annexin V­fluorescein isothiocyanate staining of cells co­treated with baicalin and TRAIL. In addition, p38 mitogen­activated protein kinase was activated in baicalin and TRAIL co­treated cancer cells, whereas the p38 inhibitor SB203580 effectively suppressed cell death within the co­treated cells. Butylated hydroxyanisole and N­acetyl­cysteine, known reactive oxygen species (ROS) scavengers, significantly suppressed the potentiated cytotoxicity induced by baicalin and TRAIL co­treatment. The present study is the first, to the best of our knowledge, to demonstrate that baicalin enhances the anticancer activity of TRAIL via p38 activation and ROS accumulation, and may be exploited for anticancer therapy.