On Weak Exponential Expansiveness of Evolution Families in Banach Spaces

The aim of this paper is to give several characterizations for the property of weak exponential expansiveness for evolution families in Banach spaces. Variants for weak exponential expansiveness of some well-known results in stability theory (Datko (1973), Rolewicz (1986), Ichikawa (1984), and Megan et al. (2003)) are obtained

Erratum

'Beibinghong': A new grape cultivar for brewing ice red wineVitis 53 (2), 85-89 (2014

'Beibinghong': A new grape cultivar for brewing ice red wine

Research Not

Evaluation of Cardioprotective Effects of Genistein against Diabetes-induced Cardiac Dysfunction in Rats

Purpose: To investigate the possible cardioprotective effects and potential pharmacological mechanism of genistein.Methods: Six-week old ZDF and lean rats were randomized into 4 groups (8 rats/group), including group 1 (control lean rats); group 2 (lean rats treated with genistein, 2.5 mg/kg); group 3 (control ZDF rats); and group 4 (ZDF treated with genistein). Two groups (2 and 4) were treated with genistein for 12 weeks, and cardiac functions and metabolic alterations were determined. Macrophage/monocyte chemo-attractant protein-1 (MCP-1), vascular cellular adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) secretion and their messenger RNA transcription level also were observed.Results: Genistein attenuated diabetes-induced cardiac dysfunction and pathological alterations, by improving glucose tolerance and insulin resistance; facilitating Akt activation and glucose utilization, and attenuating oxidative stress and interrelated MAP kinase and NF-κB signalling pathways. In addition, genistein treatment markedly reduced diabetic-induced MCP-1 (83.33 %), VCAM-1 (74.66 %) and ICAM-1 (71.42 %) secretion and mRNA transcription in ZDF rats.Conclusion: The results demonstrate the putative effects of genistein against cardiovascular dysfunction by improving glucose homeostasis, attenuating oxidative stress and reduced diabeticinduced endothelial dysfunction in ZDF rats. Thus, genistein is a potential candidate for the prevention of cardiovascular diseases.Keywords: Cardiac dysfunction, Genistein, Oxidative stress, Inflammatory response, Insulin resistance, Glucose toleranc

Resolving the Speciation Patterns and Evolutionary History of the Intercontinental Disjunct Genus Corylus (Betulaceae) Using Genome-Wide SNPs

Understanding the underlying mechanisms of species origin, divergence, and distribution patterns of the intercontinental disjunct taxa has long fascinated botanists. Based on 4,894 genome-wide single-nucleotide polymorphism dataset, we present a molecular phylogenetic reconstruction of genus Corylus (Betulaceae), which have a disjunct distribution between Eurasia and North America (NA). The aim is to explore the speciation patterns and evolutionary relationships of Corylus species by establishing a general phylogenetic framework with extensive sampling. Both the molecular phylogeny inferred from recombination-free dataset and structure analysis support the division of Corylus into four major clades (A–D). Recombination tests and hybridization detection reveal extensive recombination and hybridization events among different clades, which have potentially influenced the speciation process of Corylus. Divergence time estimation indicates that recent common ancestor (MRCA) of Corylus occurred in late Eocene (∼36.38 Ma) and subsequent rapid diversification began during Miocene. Ancestral area reconstruction shows that Corylus originated from southwest China. The arrival of two clades (Clades B and C) to NA was well supported by the long distance dispersal crossing the Bering land bridge. The Himalayas, European-Mediterranean area, and other distribution regions are primarily the recipients of dispersal taxa. Vicariance after dispersal plays an important role in speciation

Effects of advanced glycation end-products (AGEs) on skin keratinocytes by nuclear factor-kappa B (NF-κB) activation

Advance glycation end-products (AGEs) are produced in patients with long-term hyperglycemia metabolic disorder and responsible for multiple symptoms including impaired wound healing. This study was designed to reveal the roles and possible mechanism of AGE in diabetic wound healing. Sixteen Sprague-Dawley (SD) rats were divided into two groups randomly; the streptozotocin (STZ) induced diabetic group and the normal group. Eight weeks later, epidermal growth factor (EGF) and AGE levels, nuclear factor-kappa B (NF-κB) localization and cell viability were measured in vivo. Keratinocytes from normal skin were cultured in AGE-enriched conditional media, and the cell viability, apoptosis, adhesion and migration were detected in order to find the directed evidence between AGE and keratinocytes. AGE content was higher and NF-κB expression was more localized in the nuclear of keratinocytes in diabetic skins. AGE could inhibit normal cell growth by inducing apoptosis and arresting cell division cycle, inhibiting cell adhesion and promoting migration which might be mediated by NF-κB in vitro. Blocking NF-κB activity could reverse effects of AGE on cell proliferation and migration, but not adhesion. Therefore, AGE could damage the skin keratinocytes function in vivo and in vitro, and the activation of NF-κB is involved in this process.Key words: AGE, NF-kappaB, keratinocytes, diabetes, wound healing

Stress-related disorders and subsequent cancer risk and mortality : a population-based and sibling-controlled cohort study in Sweden

Funding Information: This research was supported by the Swedish Research Council through the Swedish Initiative for research on Microdata in the Social and Medical Sciences (SIMSAM) framework. Funding Information: This work was supported by Swedish Cancer Society (20 0846 PjF to F. Fang), 1.3.5 Project for Disciplines of Excellence, West China Hospital, Sichuan University (ZYYC21005 to H. Song), and the National Natural Science Foundation of China (81971262 to H. Song). Publisher Copyright: © 2022, The Author(s).Prior research has suggested a potential role of psychological stress on cancer development while the role of familial factors on this association is underexplored. We conducted a nationwide cohort study including 167,836 individuals with a first-onset stress-related disorder (including post-traumatic stress disorder, acute stress reaction, adjustment disorder and other stress reactions) diagnosed between 1981 and 2016 in Sweden (i.e., exposed patients), 1,631,801 birth year- and sex-matched unexposed individuals, and 179,209 unaffected full siblings of the exposed patients. Cox models were used to estimate the hazard ratios (HRs) of newly diagnosed cancer and cancer-related death, beyond 1 year after diagnosis of stress-related disorders. We further examined the potential mediation roles of behavior-related morbidities in the associations of stress-related disorders with smoking or alcohol-related cancer incidence and mortality. We found modestly elevated risks of cancer incidence and mortality among exposed patients compared with matched unexposed individuals (incidence: HR = 1.03, 95% CI 1.01–1.06; mortality: HR = 1.13, 95% CI 1.07–1.18), while not when comparing with full siblings (incidence: HR = 1.03, 95% CI 0.99–1.08; mortality: HR = 1.09, 95% CI 1.00-1.19). Similarly, the suggested elevations in incidence and mortality of individual cancer sites (or groups) in the population-based comparison attenuated towards null in the between-sibling comparison. The risk elevations for smoking or alcohol-related cancers in the population-based comparison (incidence: HR = 1.18, 95% CI 1.11–1.24; mortality: HR = 1.20, 95% CI 1.12–1.29) were partially mediated by alcohol-related morbidities during follow-up. Collectively, our findings suggest that the association between stress-related disorders and cancer risk and mortality is largely explained by familial factors, including shared behavioral hazards.Peer reviewe

(Imidazole-κN 3){N-[1-(2-oxidophenyl)ethylidene]-l-valinato-κ3 O,N,O′}copper(II)

In each of the two independent mol­ecules in the asymmetric unit of the title compound, [Cu(C13H15NO3)(C3H4N2)], the CuII atom is four-coordinated by two O atoms and the N atom of the tridentate Schiff base ligand and one N atom from the imidazole ligand in a distorted square-planar geometry. In the crystal structure, mol­ecules are linked by inter­molecular N—H⋯O hydrogen bonds