Radial symmetry for a generalized nonlinear fractional p-Laplacian problem

This paper first introduces a generalized fractional p-Laplacian operator (–Δ)sF;p. By using the direct method of moving planes, with the help of two lemmas, namely decay at infinity and narrow region principle involving the generalized fractional p-Laplacian, we study the monotonicity and radial symmetry of positive solutions of a generalized fractional p-Laplacian equation with negative power. In addition, a similar conclusion is also given for a generalized Hénon-type nonlinear fractional p-Laplacian equation

Radial symmetry of a relativistic Schrödinger tempered fractional p-Laplacian model with logarithmic nonlinearity

In this paper, by introducing a relativistic Schrödinger tempered fractional p-Laplacian operator (–Δ)p,λs,m, based on the relativistic Schrödinger operator (–Δ + m2)s and the tempered fractional Laplacian (Δ + λ)β/2, we consider a relativistic Schrödinger tempered fractional p-Laplacian model involving logarithmic nonlinearity. We first establish maximum principle and boundary estimate, which play a very crucial role in the later process. Then we obtain radial symmetry and monotonicity results by using the direct method of moving planes

Aberrant DNA methylation of drug metabolism and transport genes in nodular goiter

The genes encoding drug-metabolizing enzymes and transporters play an important role in maintaining the normal life processes of human body. Their disorder or defect will lead to the occurrence and development of various diseases. Currently, most of studies have focused on genetic variations in these genes, however, in the present study, we analyzed promoter methylation of 11 drug metabolism and transport genes in a cohort of nodular goiter and normal thyroid tissues using methylation-specific PCR (MSP). Our data first revealed a distinct methylation profiling in drug metabolism and transport genes between nodular goiter and normal thyroid tissues, particularly ABCB4, CYP1B1 and CYP24A1 and SLC1A2. Given these genes contribute to the development and progression of various diseases, such as multidrug resistance and tumorigenesis, these epigenetic events may thus play a critical role in the pathogenesis of nodular goiter

A New Approach for the Preparation of Variable Valence Rare Earth Alloys from Nano Rare Earth Oxides at a Low Temperature in Molten Salt

The solubility of RE2O3 (RE = Eu, Sm, and Yb) with variable valence in molten salts is extremely low. It is impossible to directly obtain variable valence metals or alloys from RE2O3 using electrolysis in molten salts. We describe a new approach for the preparation of variable valence rare earth alloys from nano rare earth oxide. The excellent dispersion of nano–Eu2O3 in LiCl–KCl melts was clearly observed using a luminescent feature of Eu3+ as a probe. The ratio of solubility of nano-Sm2O3/common Sm2O3 is 16.98. Electrochemical behavior of RE2O3 on a molybdenum and Al electrode in LiCl–KCl melts containing AlCl3 at 480 °C was investigated by different electrochemical techniques, such as cyclic voltammetry (CV), square wave voltammetry, and chronopotentiometry. Prior to the reduction peak of Al, the reduction peaks of Sm(III)/Sm(II), Yb(III)/Yb(II), and Eu(III)/Eu(II) were observed at about −0.85, −0.45, and 0.39 V insquare wave voltammetry, respectively. The underpotential deposition of RE on pre-deposited aluminum leads to the formation of Al–RE alloy. The structure, morphology, and energy dispersion analysis of the deposit obtained by potentiostatic electrolysis are analyzed. Al2Sm and Al3Sm alloys were successfully obtained from nano–Sm2O3

Genome dynamics and diversity of Shigella species, the etiologic agents of bacillary dysentery

The Shigella bacteria cause bacillary dysentery, which remains a significant threat to public health. The genus status and species classification appear no longer valid, as compelling evidence indicates that Shigella, as well as enteroinvasive Escherichia coli, are derived from multiple origins of E.coli and form a single pathovar. Nevertheless, Shigella dysenteriae serotype 1 causes deadly epidemics but Shigella boydii is restricted to the Indian subcontinent, while Shigella flexneri and Shigella sonnei are prevalent in developing and developed countries respectively. To begin to explain these distinctive epidemiological and pathological features at the genome level, we have carried out comparative genomics on four representative strains. Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants. The Shigella chromosomes share most of their genes with that of E.coli K12 strain MG1655, but each has over 200 pseudogenes, 300∼700 copies of insertion sequence (IS) elements, and numerous deletions, insertions, translocations and inversions. There is extensive diversity of putative virulence genes, mostly acquired via bacteriophage-mediated lateral gene transfer. Hence, via convergent evolution involving gain and loss of functions, through bacteriophage-mediated gene acquisition, IS-mediated DNA rearrangements and formation of pseudogenes, the Shigella spp. became highly specific human pathogens with variable epidemiological and pathological features

Characterization of an Artificial Swine-Origin Influenza Virus with the Same Gene Combination as H1N1/2009 Virus: A Genesis Clue of Pandemic Strain

Pandemic H1N1/2009 influenza virus, derived from a reassortment of avian, human, and swine influenza viruses, possesses a unique gene segment combination that had not been detected previously in animal and human populations. Whether such a gene combination could result in the pathogenicity and transmission as H1N1/2009 virus remains unclear. In the present study, we used reverse genetics to construct a reassortant virus (rH1N1) with the same gene combination as H1N1/2009 virus (NA and M genes from a Eurasian avian-like H1N1 swine virus and another six genes from a North American triple-reassortant H1N2 swine virus). Characterization of rH1N1 in mice showed that this virus had higher replicability and pathogenicity than those of the seasonal human H1N1 and Eurasian avian-like swine H1N1 viruses, but was similar to the H1N1/2009 and triple-reassortant H1N2 viruses. Experiments performed on guinea pigs showed that rH1N1 was not transmissible, whereas pandemic H1N1/2009 displayed efficient transmissibility. To further determine which gene segment played a key role in transmissibility, we constructed a series of reassortants derived from rH1N1 and H1N1/2009 viruses. Direct contact transmission studies demonstrated that the HA and NS genes contributed to the transmission of H1N1/2009 virus. Second, the HA gene of H1N1/2009 virus, when combined with the H1N1/2009 NA gene, conferred efficient contact transmission among guinea pigs. The present results reveal that not only gene segment reassortment but also amino acid mutation were needed for the generation of the pandemic influenza virus

(+)-Rutamarin as a Dual Inducer of Both GLUT4 Translocation and Expression Efficiently Ameliorates Glucose Homeostasis in Insulin-Resistant Mice

Glucose transporter 4 (GLUT4) is a principal glucose transporter in response to insulin, and impaired translocation or decreased expression of GLUT4 is believed to be one of the major pathological features of type 2 diabetes mellitus (T2DM). Therefore, induction of GLUT4 translocation or/and expression is a promising strategy for anti-T2DM drug discovery. Here we report that the natural product (+)-Rutamarin (Rut) functions as an efficient dual inducer on both insulin-induced GLUT4 translocation and expression. Rut-treated 3T3-L1 adipocytes exhibit efficiently enhanced insulin-induced glucose uptake, while diet-induced obese (DIO) mice based assays further confirm the Rut-induced improvement of glucose homeostasis and insulin sensitivity in vivo. Subsequent investigation of Rut acting targets indicates that as a specific protein tyrosine phosphatase 1B (PTP1B) inhibitor Rut induces basal GLUT4 translocation to some extent and largely enhances insulin-induced GLUT4 translocation through PI3 kinase-AKT/PKB pathway, while as an agonist of retinoid X receptor α (RXRα), Rut potently increases GLUT4 expression. Furthermore, by using molecular modeling and crystallographic approaches, the possible binding modes of Rut to these two targets have been also determined at atomic levels. All our results have thus highlighted the potential of Rut as both a valuable lead compound for anti-T2DM drug discovery and a promising chemical probe for GLUT4 associated pathways exploration