Analysis of human physical vulnerability using static equilibrium techniques of a Hazard flood for the determination of unsafe areas in the city of Catacaos - Piura, Peru

Heavy rains and El Nio phenomenon are recurring natural phenomena at a national level. These can cause floods due to the overflowing of rivers, which, when close to cities, can cause both human and material losses. The district of Catacaos, located in the city of Piura, was the one with the highest number of injuries due to the flood caused by El Nio phenomenon in 2017. This phenomenon causes a large amounts of rainfalls due to the presence of abnormally warm waters along the northern coast of Peru [1]. It is for this reason that the need arose to carry out an analysis of the physical vulnerability due to instability of people through static equilibrium, in said district, in order to present maps of unsafe areas in the face of this phenomenon. In this investigation, flood hazard maps are generated simulating the one presented in 2017, using 2D hydraulic modeling. For the generation of vulnerability curves, the instability analysis is performed by moment and drag force. Finally, maps with unsafe areas are made using ArcGis software. Where the results obtained indicate that 29.37% of the city was flooded. Likewise, the vulnerability maps generated show us that women and men over 18 years of age in the city of Catacaos would be vulnerable to dragging and overturning in the face of floods in 16.54% and 13.21%, respectively, of the total studied area. This information will be useful for the development of future evacuation plans during floods, carried out by national entities. © Published under licence by IOP Publishing Ltd

Bioassay-guided identification of the antiproliferative compounds of cissus trifoliata and the transcriptomic effect of resveratrol in prostate cancer pc3 cells

The bioassay-guided fractionation of a CHCl3-MeOH extract from the stems of Cissus trifo-liata identified an active fraction against PC3 prostate cancer cells. The treatment for 24 h showed an 80% reduction in cell viability (p ≤ 0.05) by a WST-1 assay at a concentration of 100 µg/mL. The HPLC-QTOF-MS analysis of the fraction showed the presence of coumaric and isoferulic acids, apigenin, kaempferol, chrysoeriol, naringenin, ursolic and betulinic acids, hexadecadienoic and octadecadienoic fatty acids, and the stilbene resveratrol. The exposure of PC3 cells to resveratrol (IC25 = 23 µg/mL) for 24 h induced significant changes in 847 genes (Z-score ≥ ±2). The functional classification tool of the DAVID v6.8 platform indicates that the underlying molecular mechanisms against the proliferation of PC3 cells were associated (p ≤ 0.05) with the process of differentiation and metabolism. These findings provide experimental evidence suggesting the potential of C. trifoliata as a promising natural source of anticancer compounds

Cytotoxic Fractions from <i>Hechtia glomerata</i> Extracts and <i>p</i>-Coumaric Acid as MAPK Inhibitors

Preliminary bioassay-guided fractionation was performed to identify cytotoxic compounds from Hechtia glomerata, a plant that is used in Mexican ethnomedicine. Organic and aqueous extracts were prepared from H. glomerata’s leaves and evaluated against two cancer cell lines. The CHCl3/MeOH (1:1) active extract was fractionated, and the resulting fractions were assayed against prostate adenocarcinoma PC3 and breast adenocarcinoma MCF7 cell lines. Active fraction 4 was further analyzed by high-performance liquid chromatography–quadrupole time-of-flight–mass spectrometry analysis to identify its active constituents. Among the compounds that were responsible for the cytotoxic effects of this fraction were flavonoids, phenolic acids, and aromatic compounds, of which p-coumaric acid (p-CA) and its derivatives were abundant. To understand the mechanisms that underlie p-CA cytotoxicity, a microarray assay was performed on PC3 cells that were treated or not with this compound. The results showed that mitogen-activated protein kinases (MAPKs) that regulate many cancer-related pathways were targeted by p-CA, which could be related to the reported effects of reactive oxygen species (ROS). A molecular docking study of p-CA showed that this phenolic acid targeted these protein active sites (MAPK8 and Serine/Threonine protein kinase 3) at the same binding site as their inhibitors. Thus, we hypothesize that p-CA produces ROS, directly affects the MAPK signaling pathway, and consequently causes apoptosis, among other effects. Additionally, p-CA could be used as a platform for the design of new MAPK inhibitors and re-sensitizing agents for resistant cancers

Cytotoxic Fractions from Hechtia glomerata Extracts and p-Coumaric Acid as MAPK Inhibitors

Preliminary bioassay-guided fractionation was performed to identify cytotoxic compounds from Hechtia glomerata, a plant that is used in Mexican ethnomedicine. Organic and aqueous extracts were prepared from H. glomerata’s leaves and evaluated against two cancer cell lines. The CHCl3/MeOH (1:1) active extract was fractionated, and the resulting fractions were assayed against prostate adenocarcinoma PC3 and breast adenocarcinoma MCF7 cell lines. Active fraction 4 was further analyzed by high-performance liquid chromatography–quadrupole time-of-flight–mass spectrometry analysis to identify its active constituents. Among the compounds that were responsible for the cytotoxic effects of this fraction were flavonoids, phenolic acids, and aromatic compounds, of which p-coumaric acid (p-CA) and its derivatives were abundant. To understand the mechanisms that underlie p-CA cytotoxicity, a microarray assay was performed on PC3 cells that were treated or not with this compound. The results showed that mitogen-activated protein kinases (MAPKs) that regulate many cancer-related pathways were targeted by p-CA, which could be related to the reported effects of reactive oxygen species (ROS). A molecular docking study of p-CA showed that this phenolic acid targeted these protein active sites (MAPK8 and Serine/Threonine protein kinase 3) at the same binding site as their inhibitors. Thus, we hypothesize that p-CA produces ROS, directly affects the MAPK signaling pathway, and consequently causes apoptosis, among other effects. Additionally, p-CA could be used as a platform for the design of new MAPK inhibitors and re-sensitizing agents for resistant cancers