Antimicrobial modification of PLA scaffolds with ascorbic and fumaric acids via plasma treatment

An optimal medical scaffold should be biocompatible and biodegradable and should have adequate mechanical properties and scaffold architecture porosity, a precise three-dimensional shape, and a reasonable manufacturing method. Polylactic acid (PLA) is a natural biodegradable thermoplastic aliphatic polyester that can be fabricated into nanofiber structures through many techniques, and electrospinning is one of the most widely used methods. Medical fiber mat scaffolds have been associated with inflammation and infection and, in some cases, have resulted in tissue degradation. Therefore, surface modification with antimicrobial agents represents a suitable solution if the mechanical properties of the fiber mats are not affected. In this study, the surfaces of electrospun PLA fiber mats were modified with naturally occurring L-ascorbic acid (ASA) or fumaric acid (FA) via a plasma treatment method. It was found that 30 s of radio-frequency (RF) plasma treatment was effective enough for the wettability enhancement and hydroperoxide formation needed for subsequent grafting reactions with antimicrobial agents upon their decomposition. This modification led to changes in the surface properties of the PLA fiber mats, which were analyzed by various spectroscopic and microscopic techniques. FTIR-ATR confirmed the chemical composition changes after the modification process and the surface morphology/topography changes were proven by SEM and AFM. Moreover, nanomechanical changes of prepared PLA fiber mats were investigated by AFM using amplitude modulation-frequency modulation (AM-FM) technique. A significant enhancement in antimicrobial activity of such modified PLA fiber mats against gram-positive Staphylococcus aureus and gram-negative Escherichia coli are demonstrated herein. © 2020 The AuthorsQatar National Research Fund (a member of The Qatar Foundation) [22-076-1-011]; Qatar University Collaborative Grant [QUCG-CAM-20/21-3]; Czech Science FoundationGrant Agency of the Czech Republic [19-16861S

Activation of Multiple Apoptotic Pathways in Human Nasopharyngeal Carcinoma Cells by the Prenylated Isoflavone, Osajin

Osajin is a prenylated isoflavone showing antitumor activity in different tumor cell lines. The underlying mechanism of osajin-induced cancer cell death is not clearly understood. In the present study, the mechanisms of osajin-induced cell death of human nasopharyngeal carcinoma (NPC) cells were explored. Osajin was found to significantly induce apoptosis of NPC cells in a dose- and time-dependent manner. Multiple molecular effects were observed during osajin treatment including a significant loss of mitochondrial transmembrane potential, release of cytochrome c into the cytosol, enhanced expression of Fas ligand (FasL), suppression of glucose-regulated protein 78 kDa (GRP78), and activation of caspases-9, -8, -4 and -3. In addition, up-regulation of proapoptotic Bax protein and down-regulation of antiapoptotic Bcl-2 protein were also observed. Taken together, osajin induces apoptosis in human NPC cells through multiple apoptotic pathways, including the extrinsic death receptor pathway, and intrinsic pathways relying on mitochondria and endoplasmic reticulum stress. Thus, osajin could be developed as a new effective and chemopreventive compound for human NPC

Wpływ niedokrwienno-reperfuzyjnego uszkodzenia jelita na poziom określonych genów u szczurów

The small intestine is an organ with very well developed immunological activity. There are specific cells in the mucosa of the small intestine responsible for releasing the inflammatory mediators that can lead to Multiple Organ Dysfunction Syndrome (MODS), which is a very complex process that can occur after ischemia-reperfusion injury. The accumulation of specific inflammatory mediators in the wall of the small intestine also increases the expression of apoptotic genes. The aim of this study was to detect and analyse the changes in the expression of apoptotic genes (Bax, Bcl2) and the genes responsible for the production of cytokines (TNFα, IL1β, IL6, IL10) and tumour growth factor beta (TGFβ). Male Wistar rats underwent ischemia performed by complete occlusion of the mesenteric artery. Ischemia was followed by reperfusion periods of 1 hour, 24 hours, and 30 days. Subsequently, the total RNA was isolated from the complete wall of the small intestine and RT-PCR (real-time) was performed. There was a significant increase in the levels of specific genes (Bax, Bcl2, TNFα, IL1β, IL6, IL10, TGFβ) after one hour of reperfusion and a decreased tendency after 24 hours and 30 days.Jelito cienkie jest narządem o bardzo dobrze rozwiniętej aktywności immunologicznej. W błonie śluzowej jelita cienkiego znajdują się specjalne komórki odpowiedzialne za uwalnianie mediatorów zapalenia, mogące wywołać zespół niewydolności wielonaczyniowej (ang. Multiple Organ Dysfunction Syndrome (MODS)), który jest bardzo złożonym procesem, jaki może wystąpić po uszkodzeniu niedokrwienno-reperfuzyjnym. Nagromadzenie swoistych mediatorów zapalenia w ścianie jelita cienkiego zwiększa również ekspresję genów apoptotycznych. Celem tej pracy było wykrycie i analiza zmian w ekspresji genów apoptotycznych (Bax, Bcl2) oraz genów odpowiedzialnych za wytwarzanie cytokin (TNFα, IL1β, IL6, IL10), a także transformującego czynnika wzrostu beta (TGFβ). U samców szczurów rasy Wistar wywoływano niedokrwienie poprzez całkowite zamknięcie tętnicy krezkowej, po czym następowały okresy reperfuzji trwające 1 godzinę, 24 godziny i 30 dni. Następnie z całej ściany jelita cienkiego izolowano RNA całkowite i przeprowadzono badanie RT-PCR (w czasie rzeczywistym). Stwierdzono istotny wzrost poziomów określonych genów (Bax, Bcl2, TNFα, IL1β, IL6, IL10, TGFβ) po jednej godzinie reperfuzji oraz trend spadkowy po 24 godzinach i 30 dniach

Environmental pressures on stomatal size may drive plant genome size evolution: evidence from a natural experiment with Cape geophytes

Background and Aims The idea that genome (size) evolution in eukaryotes could be driven by environmental factors is still vigorously debated. In extant plants, genome size correlates positively with stomatal size, leading to the idea that conditions enabling the existence of large stomata in fossil plants also supported growth of their genome size. We test this inductive assumption in drought-adapted, prostrate-leaved Cape (South Africa) geophytes where, compared with their upright-leaved geophytic ancestors, stomata develop in a favourably humid microclimate formed underneath their leaves. Methods Stomatal parameters (leaf cuticle imprints) and genome size (flow cytometry) were measured in 16 closely related geophytic species pairs from seven plant families. In each pair, representing a different genus, we contrasted a prostrate-leaved species with its upright-leaved phylogenetic relative, the latter whose stomata are exposed to the ambient arid climate. Key Results Except for one, all prostrate-leaves species had larger stomata, and in 13 of 16 pairs they also had larger genomes than their upright-leaved relatives. Stomatal density and theoretical maximum conductance were less in prostrate-leaved species with small guard cells (1 pL). Giant stomata were observed in the prostrate-leaved Satyrium bicorne (89–137 µm long), despite its relatively small genome (2C = 9 Gbp). Conclusions Our results imply that climate, through selection on stomatal size, might be able to drive genome size evolution in plants. The data support the idea that plants from ‘greenhouse’ geological periods with large stomata might have generally had larger genome sizes when compared with extant plants, though this might not have been solely due to higher atmospheric CO2 in these periods but could also have been due to humid conditions prevailing at fossil deposit sites