An analytical study of the factors that influence COVID-19 spread

The outbreak of the coronavirus disease 2019 (COVID-19) continues to constitute an international public health emergency. Seasonality is a long-recognized attribute of many viral infections of humans. Nevertheless, the relationship between environmental factors and the spread of infection, particularly for person-to-person communicable diseases, remains poorly understood. This study explores the relationship between environmental factors and the incidence of COVID-19 in 188 countries with reported COVID-19 cases as of April 13, 2020. Here we show that COVID-19 growth rates peaked in temperate zones in the Northern Hemisphere during the outbreak period, while they were lower in tropical zones. The relationships between COVID-19 and environmental factors were resistant to the potentially confounding effects of air pollution, sea level, and population. To prove the effect of those factors, study, and analysis of the prevalence of COVID-19 in Italy, Spain, and China was undertaken. A fuzzy logic system was designed to predict the effects of that variables on the rate of viral spread of COVID-19.     

Antimicrobial resistance patterns among different Escherichia coli isolates in the Kingdom of Saudi Arabia

Antimicrobial resistance patterns among different Escherichia coli isolates in the Kingdom of Saudi Arabia. This study aimed to investigate the patterns of antimicrobial resistance in E. coli isolated from different samples, and to identify potential pathogenic isolates in Riyadh, Kingdom of Saudi Arabia (KSA). In total, 51 bacterial isolates were recovered from 113 samples of human urine, food (raw meat, raw chicken, raw egg surface, and fresh vegetables), water, and air. Twenty-four E. coli isolates were tested for susceptibility to 26 antibiotics. The air sample isolates were most resistant to amoxicillin, ampicillin, amoxicillin/clavulanic acid, amoxicillin/sulbactam, piperacillin/tazobactam, cefalotin, cefuroxime, cefoxitin, cefixime, nitrofurantoin, and trimethoprim/sulfamethoxazol. The isolates from vegetable samples were resistant to amoxicillin, ampicillin, amoxicillin/clavulanic acid, amoxicillin/sulbactam, cefalotin, cefuroxime, cefoxitin, and cefixime. By contrast, the isolates from the water samples were resistant only to amoxicillin and ampicillin. The isolates from the human urine samples were most frequently resistant to norfloxacin (80%) followed by amoxicillin and ampicillin (70%), trimethoprim/sulfamethoxazole (55%), ciprofloxacin and ofloxacin (50%), cefalotin (30%), cefuroxime, cefixime and cefotaxime (25%), ceftazidime, ceftriaxone, cefepime and aztreonam (20%), amoxicillin/clavulanic acid, piperacillin/tazobactam and gentamicin (10%), and amoxicillin/sulbactam and cefoxitin (5%). Almost all (23/25, 95.8%) (n = 23) of the isolates were multi-drug resistant (MDR) (i.e., resistant to 3 or more classes of antibiotics), and 16.7% (n = 4) of those were positive for extended spectrum β-lactamase (ESBL). Of the 4 ESBL-producers, 3 were positive for blaCTX_-M-15 and blaCTX_-M1_group, 2 were positive for blaCMY_-2, and 1 each was positive for blaCTX_{-M-2 group,} blaSHV, and blaOXA_-47. The quinolone resistance gene qnrS was detected in 25% (n = 6) of the E. coli strains isolated from urine (N = 5) and air (N = 1) samples. The considerable number of antimicrobial resistance genes detected among E. coli isolates tested here is alarming and should raise public health concern.     

Interactive effects of excessive potassium and Mg deficiency on safflower

In the present work, separate and combined effects of excessive potassium and magnesium deficiency on safflower (Carthamus tinctorius) were studied. Four treatments were considered: C (control treatment: complete medium containing 1.5 mM Mg), +KCl (excessive potassium treatment: complete medium added with 60 mM KCl), ?Mg (Mg-deficient treatment: containing 0.1 mM Mg), and DS (double stress treatment: Mg-deficient medium (0.1 mM Mg) added with 60 mM KCl. Excessive potassium effect on plant growth was more pronounced than that of Mg deficiency. The two stresses impaired differently plant organs; KCl application affected more roots than shoots, whereas Mg deficiency reduced only leaf biomass. Gas exchange and pigment concentrations and patterns were severely impaired by KCl and mainly by interactive effects of the two stresses. This led to obvious lipid peroxidation and electrolyte leakage. Mg deficiency did not induce lipid peroxidation and electrolyte leakage, but as applied with excessive potassium, it doubled the effect of the latter. Mineral analyses showed that major cation nutrition was disturbed by KCl and combined stresses and at a lower level by magnesium deficiency. Plants did not show an enhanced selectivity of Mg and Ca over K but they improved their use efficiencies.     

Sequence-Level Analysis of the Major European Huntington Disease Haplotype

Huntington disease (HD) reflects the dominant consequences of a CAG-repeat expansion in HTT. Analysis of common SNP-based haplotypes has revealed that most European HD subjects have distinguishable HTT haplotypes on their normal and disease chromosomes and that ∼50% of the latter share the same major HD haplotype. We reasoned that sequence-level investigation of this founder haplotype could provide significant insights into the history of HD and valuable information for gene-targeting approaches. Consequently, we performed whole-genome sequencing of HD and control subjects from four independent families in whom the major European HD haplotype segregates with the disease. Analysis of the full-sequence-based HTT haplotype indicated that these four families share a common ancestor sufficiently distant to have permitted the accumulation of family-specific variants. Confirmation of new CAG-expansion mutations on this haplotype suggests that unlike most founders of human disease, the common ancestor of HD-affected families with the major haplotype most likely did not have HD. Further, availability of the full sequence data validated the use of SNP imputation to predict the optimal variants for capturing heterozygosity in personalized allele-specific gene-silencing approaches. As few as ten SNPs are capable of revealing heterozygosity in more than 97% of European HD subjects. Extension of allele-specific silencing strategies to the few remaining homozygous individuals is likely to be achievable through additional known SNPs and discovery of private variants by complete sequencing of HTT. These data suggest that the current development of gene-based targeting for HD could be extended to personalized allele-specific approaches in essentially all HD individuals of European ancestry.     

Retinoid X Receptor-selective Signaling in the Regulation of Akt/Protein Kinase B Isoform-specific Expression

The differentiation and fusion of myoblasts into mature myotubes are complex processes responding to multiple signaling pathways. The function of Akt/PKB is critical for myogenesis, but less is clear as to the regulation of its isoform-specific expression. Bexarotene is a drug already used clinically to treat cancer, and it has the ability to enhance the commitment of embryonic stem cells into skeletal muscle lineage. Whereas bexarotene regulates fundamental biological processes through retinoid X receptor (RXR)-mediated gene expression, molecular pathways underlying its positive effects on myogenesis remain unclear. In this study, we have examined the signaling pathways that transmit bexarotene action in the context of myoblast differentiation. We show that bexarotene promotes myoblast differentiation and fusion through the activation of RXR and the regulation of Akt/PKB isoform-specific expression. Interestingly, bexarotene signaling appears to correlate with residue-specific histone acetylation and is able to counteract the detrimental effects of cachectic factors on myogenic differentiation. We also signify an isoform-specific role for Akt/PKB in RXR-selective signaling to promote and to retain myoblast differentiation. Taken together, our findings establish the viability of applying bexarotene in the prevention and treatment of muscle-wasting disorders, particularly given the lack of drugs that promote myogenic differentiation available for potential clinical applications. Furthermore, the model of bexarotene-enhanced myogenic differentiation will provide an important avenue to identify additional genetic targets and specific molecular interactions that we can study and apply for the development of potential therapeutics in muscle regeneration and repair.     

Differentiation of <Emphasis Type="Italic">Aspergillus niger</Emphasis> by random amplification of polymorphic DNA

The randomly amplified polymorphic DNA (RAPD) patterns of whole-cell lysates from five Aspergillus niger isolates, including one reference strain, two isolated from deep freeze, and two environmental strains from soil and plant infections, were investigated. PCR-RAPD analysis of genomic DNA was performed using eight primers (Tube-A1, Tube-A6, Tube-A17, Tube-B8, Tube-B11, Tube-B15, Tube-C5, Tube-C6). The RAPD assay discriminated between all strains. Comparison of deep freeze isolates showed identical RAPD patterns in some of the reference and environmental isolates. The data indicates that the RAPD technique is useful for fingerprinting A. niger.     

Binding of the universal minicircle sequence binding protein at the kinetoplast DNA replication origin

Kinetoplast DNA, the mitochondrial DNA of trypanosomatids, is a remarkable DNA structure that contains, in the species Crithidia fasciculata, 5000 topologically linked duplex DNA minicircles. Their replication initiates at two conserved sequences, a dodecamer, known as the universal minicircle sequence (UMS), and a hexamer, which are located at the replication origins of the minicircle L and H strands, respectively. A UMS-binding protein (UMSBP) binds specifically the 12-mer UMS sequence and a 14-mer sequence that contains the conserved hexamer in their single-stranded DNA conformation. In vivo cross-linking analyses reveal the binding of UMSBP to kinetoplast DNA networks in the cell. Furthermore, UMSBP binds in vitro to native minicircle origin fragments, carrying the UMSBP recognition sequences. UMSBP binding at the replication origin induces conformational changes in the bound DNA through its folding, aggregation and condensation.     

Effects of CaCl2 pretreatment on antioxidant enzyme and leaf lipid content of faba bean (Vicia faba L.) seedlings under cadmium stress

Most polyploids can survive better under multiple stress conditions than their corresponding diploid; however, there is no established theory that can adequately explain this phenomenon at the molecular or physiological level. Here, we attempt to explain this interesting but puzzling problem from the perspectives of resource requirement and antioxidant response. In this experiment, we compared the antioxidative response and stomatal behavior of two ploidy levels of tobacco plants (tetraploid and its colchicine-induced octaploid) under drought, cold and nutrient deficit stress conditions. In comparison to tetraploid, less H₂O₂ accumulation and stronger reactive oxygen scavenging capacity (antioxidant enzyme activities and DPPH radical scavenging capacity) were observed in octaploid under stress free or stressful conditions. In accordant with these, less oxidative damage and higher redox values (ASC/DHA and GSH/GSSG) were also monitored in the octaploid than in the tetraploid under same conditions. In addition, a higher net rate of photosynthesis (Pn) and slower decline in the concentration of intercellular CO₂(Ci) were measured in the octaploid compared to the tetraploid following high concentration ABA treatment (20 mg L⁻¹), with more severe oxidative damage observed in the tetraploid than in the octaploid. On the basis of the resource acquisition theory, we consider that any environmental stress that can lower plant resource availability would favor survival in a slow-growing polyploid compared with that in a fast-growing diploid.     

A delta-catenin signaling pathway leading to dendritic protrusions

Delta-catenin is a synaptic adherens junction protein pivotally positioned to serve as a signaling sensor and integrator. Expression of delta-catenin induces filopodia-like protrusions in neurons. Here we show that the small GTPases of the Rho family act coordinately as downstream effectors of delta-catenin. A dominant negative Rac prevented delta-catenin-induced protrusions, and Cdc42 activity was dramatically increased by delta-catenin expression. A kinase dead LIMK (LIM kinase) and a mutant Cofilin also prevented delta-catenin-induced protrusions. To link the effects of delta-catenin to a physiological pathway, we noted that (S)-3,5-dihydroxyphenylglycine (DHPG) activation of metabotropic glutamate receptors induced dendritic protrusions that are very similar to those induced by delta-catenin. Furthermore, delta-catenin RNA-mediated interference can block the induction of dendritic protrusions by DHPG. Interestingly, DHPG dissociated PSD-95 and N-cadherin from the delta-catenin complex, increased the association of delta-catenin with Cortactin, and induced the phosphorylation of delta-catenin within the sites that bind to these protein partners.