On Confinement and Quarantine Concerns on an SEIAR Epidemic Model with Simulated Parameterizations for the COVID-19 Pandemic

This paper firstly studies an SIR (susceptible-infectious-recovered) epidemic model without demography and with no disease mortality under both total and under partial quarantine of the susceptible subpopulation or of both the susceptible and the infectious ones in order to satisfy the hospital availability requirements on bed disposal and other necessary treatment means for the seriously infectious subpopulations. The seriously infectious individuals are assumed to be a part of the total infectious being described by a time-varying proportional function. A time-varying upper-bound of those seriously infected individuals has to be satisfied as objective by either a total confinement or partial quarantine intervention of the susceptible subpopulation. Afterwards, a new extended SEIR (susceptible-exposed-infectious-recovered) epidemic model, which is referred to as an SEIAR (susceptible-exposed-symptomatic infectious-asymptomatic infectious-recovered) epidemic model with demography and disease mortality is given and focused on so as to extend the above developed ideas on the SIR model. A proportionally gain in the model parameterization is assumed to distribute the transition from the exposed to the infectious into the two infectious individuals (namely, symptomatic and asymptomatic individuals). Such a model is evaluated under total or partial quarantines of all or of some of the subpopulations which have the effect of decreasing the number of contagions. Simulated numerical examples are also discussed related to model parameterizations of usefulness related to the current COVID-19 pandemic outbreaks.The Spanish Institute of Health Carlos III under Grant COV 20/01213, the Spanish Government and the European Commission under Grant RTI2018-094336-B-I00 (MCIU/AEI/FEDER, UE), and the Basque Government under Grant IT1207-19 funded this research. The Spanish Institute of Health Carlos III funded the APC

On contractive cyclic fuzzy maps in metric spaces and some related results on fuzzy best proximity points and fuzzy fixed points

This paper investigates some properties of cyclic fuzzy maps in metric spaces. The convergence of distances as well as that of sequences being generated as iterates defined by a class of contractive cyclic fuzzy mapping to fuzzy best proximity points of (non-necessarily intersecting adjacent subsets) of the cyclic disposal is studied. An extension is given for the case when the images of the points of a class of contractive cyclic fuzzy mappings restricted to a particular subset of the cyclic disposal are allowed to lie either in the same subset or in its next adjacent one.The first author thanks the Spanish Ministry of Economy and Competitiveness for partial support of this work through Grant DPI2012-30651. He also thanks the Basque Government for its support through Grant IT378-10, and to the University of Basque Country by its support through Grant UFI 11/07

List of Prokaryotic names with Standing in Nomenclature (LPSN) moves to the DSMZ

The List of Prokaryotic names with Standing in Nomenclature (LPSN) was acquired in November 2019 by the DSMZ and was relaunched using an entirely new production system in February 2020. This article describes in detail the structure of the new site, navigation, page layout, search facilities and new features

Applying Fixed Point Techniques to Stability Problems in Intuitionistic Fuzzy Banach Spaces

In this paper we investigate Hyers-Ulam-Rassias stability of certain nonlinear functional equations. Considerations of such stabilities in different branches of mathematics have been very extensive. Again the fuzzy concepts along with their several extensions have appeared in almost all branches of mathematics. Here we work on intuitionistic fuzzy real Banach spaces, which is obtained by combining together the concepts of fuzzy Banach spaces with intuitionistic fuzzy sets. We establish that pexiderized quadratic functional equations defined on such spaces are stable in the sense of Hyers-Ulam-Rassias stability. We adopt a fixed point approach to the problem. Precisely, we use a generxalized contraction mapping principle. The result is illustrated with an example.This work was supported by the Basque Government under the Grant IT 1207-1

Tumor Microenvironment Enriches the Stemness Features: The Architectural Event of Therapy Resistance and Metastasis

Cancer divergence has many facets other than being considered a genetic term. It is a tremendous challenge to understand the metastasis and therapy response in cancer biology; however, it postulates the opportunity to explore the possible mechanism in the surrounding tumor environment. Most deadly solid malignancies are distinctly characterized by their tumor microenvironment (TME). TME consists of stromal components such as immune, inflammatory, endothelial, adipocytes, and fibroblast cells. Cancer stem cells (CSCs) or cancer stem-like cells are a small sub-set of the population within cancer cells believed to be a responsible player in the self-renewal, metastasis, and therapy response of cancer cells. The correlation between TME and CSCs remains an enigma in understanding the events of metastasis and therapy resistance in cancer biology. Recent evidence suggests that TME dictates the CSCs maintenance to arbitrate cancer progression and metastasis. The immune, inflammatory, endothelial, adipocyte, and fibroblast cells in the TME release growth factors, cytokines, chemokines, microRNAs, and exosomes that provide cues for the gain and maintenance of CSC features. These intricate cross-talks are fueled to evolve into aggressive, invasive, migratory phenotypes for cancer development. In this review, we have abridged the recent developments in the role of the TME factors in CSC maintenance and how these events influence the transition of tumor progression to further translate into metastasis and therapy resistance in cancer

Analysis of product shrinkage and waste in a potato bagging plant

Nowadays, an average of 2 kg of waste per person are generated in Spain. Furthermore, the household consumption is rising and, as a consequence, the waste production is also increasing. This trend presents a direct impact in the environment. Moreover, after two years of COVID-19 pandemic, it has been detected a stronger rise in consumption per person, while consumption through professional commercial channels for hospitality industry has been lower. This paper analizes the waste generation and product shrinkage in a potato bagging plant, which addresses its production to both final consumers and retailers. The raw materials washing line, as well as the production line, are taken into consideration in the analysis, while new uses to the produced waste are proposed, aiming at providing new useful life, such as the production of bioplastics or the production of biodiesel. As a consequence, the environment impact is minimized and new products are obtained

Elevated PAF1-RAD52 Axis Confers Chemoresistance to Human Cancers

Cisplatin- and gemcitabine-based chemotherapeutics represent a mainstay of cancer therapy for most solid tumors; however, resistance limits their curative potential. Here, we identify RNA polymerase II-associated factor 1 (PAF1) as a common driver of cisplatin and gemcitabine resistance in human cancers (ovarian, lung, and pancreas). Mechanistically, cisplatin- and gemcitabine-resistant cells show enhanced DNA repair, which is inhibited by PAF1 silencing. We demonstrate an increased interaction of PAF1 with RAD52 in resistant cells. Targeting the PAF1 and RAD52 axis combined with cisplatin or gemcitabine strongly diminishes the survival potential of resistant cells. Overall, this study shows clinical evidence that the expression of PAF1 contributes to chemotherapy resistance and worse clinical outcome for lethal cancers

Associations between tamoxifen, estrogens, and FSH serum levels during steady state tamoxifen treatment of postmenopausal women with breast cancer

<p>Abstract</p> <p>Background</p> <p>The cytochrome P450 (CYP) enzymes 2C19, 2D6, and 3A5 are responsible for converting the selective estrogen receptor modulator (SERM), tamoxifen to its active metabolites 4-hydroxy-tamoxifen (4OHtam) and 4-hydroxy-<it>N</it>-demethyltamoxifen (4OHNDtam, endoxifen). Inter-individual variations of the activity of these enzymes due to polymorphisms may be predictors of outcome of breast cancer patients during tamoxifen treatment. Since tamoxifen and estrogens are both partly metabolized by these enzymes we hypothesize that a correlation between serum tamoxifen and estrogen levels exists, which in turn may interact with tamoxifen on treatment outcome. Here we examined relationships between the serum levels of tamoxifen, estrogens, follicle-stimulating hormone (FSH), and also determined the genotypes of CYP2C19, 2D6, 3A5, and SULT1A1 in 90 postmenopausal breast cancer patients.</p> <p>Methods</p> <p>Tamoxifen and its metabolites were measured by liquid chromatography-tandem mass spectrometry. Estrogen and FSH levels were determined using a sensitive radio- and chemiluminescent immunoassay, respectively.</p> <p>Results</p> <p>We observed significant correlations between the serum concentrations of tamoxifen, <it>N</it>-dedimethyltamoxifen, and tamoxifen-<it>N</it>-oxide and estrogens (p < 0.05). The genotype predicted CYP2C19 activity influenced the levels of both tamoxifen metabolites and E1.</p> <p>Conclusions</p> <p>We have shown an association between tamoxifen and its metabolites and estrogen serum levels. An impact of CYP2C19 predicted activity on tamoxifen, as well as estrogen kinetics may partly explain the observed association between tamoxifen and its metabolites and estrogen serum levels. Since the role of estrogen levels during tamoxifen therapy is still a matter of debate further prospective studies to examine the effect of tamoxifen and estrogen kinetics on treatment outcome are warranted.</p

Partial Inhibition of Estrogen-Induced Mammary Carcinogenesis in Rats by Tamoxifen: Balance between Oxidant Stress and Estrogen Responsiveness

Epidemiological and experimental evidences strongly support the role of estrogens in breast tumor development. Both estrogen receptor (ER)-dependent and ER-independent mechanisms are implicated in estrogen-induced breast carcinogenesis. Tamoxifen, a selective estrogen receptor modulator is widely used as chemoprotectant in human breast cancer. It binds to ERs and interferes with normal binding of estrogen to ERs. In the present study, we examined the effect of long-term tamoxifen treatment in the prevention of estrogen-induced breast cancer. Female ACI rats were treated with 17β-estradiol (E2), tamoxifen or with a combination of E2 and tamoxifen for eight months. Tissue levels of oxidative stress markers 8-iso-Prostane F2α (8-isoPGF2α), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, and oxidative DNA damage marker 8-hydroxydeoxyguanosine (8-OHdG) were quantified in the mammary tissues of all the treatment groups and compared with age-matched controls. Levels of tamoxifen metabolizing enzymes cytochrome P450s as well as estrogen responsive genes were also quantified. At necropsy, breast tumors were detected in 44% of rats co-treated with tamoxifen+E2. No tumors were detected in the sham or tamoxifen only treatment groups whereas in the E2 only treatment group, the tumor incidence was 82%. Co-treatment with tamoxifen decreased GPx and catalase levels; did not completely inhibit E2-mediated oxidative DNA damage and estrogen-responsive genes monoamine oxygenase B1 (MaoB1) and cell death inducing DFF45 like effector C (Cidec) but differentially affected the levels of tamoxifen metabolizing enzymes. In summary, our studies suggest that although tamoxifen treatment inhibits estrogen-induced breast tumor development and increases the latency of tumor development, it does not completely abrogate breast tumor development in a rat model of estrogen-induced breast cancer. The inability of tamoxifen to completely inhibit E2-induced breast carcinogenesis may be because of increased estrogen-mediated oxidant burden