Traversability and connectivity of the middle graph of a graph

AbstractWe define a graph M(G) as an intersection graph Ω(F) on the point set V(G) of any graph G. Let X(G) be the line set of G and F = V′(G) ∪ X(G), where V′(G) indicates the family of all one point subsets of the set V(G). Let M(G) = Ω(F). M(G) is called the middle graph of G. The following theorems result: 1.Theorem 1. Let G be any graph and G+ be a graph constructed from G. Then we have L(G+)≅M(G), where L(G+) is the line graphof G+2.Theorem 2. Let G be a graph. The middle graph M(G) of G is hamiltonian if and only if G contains a closed spanning trail.3.Theorem 3. If a graph G is eulerian, then the middle graph m(G) of G is eulerian and hamiltonian.4.Theorem 4. If M(G) is eulerian, then G is eulerian and M(G) is hamiltonian.5.Theorem 5. Let G be a graph. The middle graph M(G) of G contains a closed spanning trail if and only if G is connected and without points of degree ⩽ 1.6.Theorem 6. If a graph G is n-line connected, then the middle graph M(G) is n-connected

Circadian clock determines the timing of rooster crowing

SummaryCrowing of roosters is described by onomatopoetic terms such as ‘cock-a-doodle-doo’ (English), ‘ki-ke-ri-ki’ (German), and ‘ko-ke-kok-koh’ (Japanese). Rooster crowing is a symbol of the break of dawn in many countries. Indeed, crowing is frequently observed in the morning [1]. However, people also notice that crowing is sometimes observed at other times of day. Therefore, it is yet unclear whether crowing is under the control of an internal biological clock, or is simply caused by external stimuli. Here we show that predawn crowing is under the control of a circadian clock. Although external stimuli such as light and crowing by other individuals also induce roosters’ crowing, the magnitude of this induction is also regulated by a circadian clock

Protein phosphatase 1 is involved in the dissociation of Ca2+/calmodulin-dependent protein kinase II from postsynaptic densities

AbstractAutophosphorylation-dependent translocation of Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) to postsynaptic densities (PSDs) from cytosol may be a physiologically important process during synaptic activation. We investigated a protein phosphatase responsible for dephosphorylation of the kinase. CaM kinase II was shown to be targeted to two sites using the gel overlay method in two-dimensional gel electrophoresis. Protein phosphatase 1 (PP1) was identified to dephosphorylate CaM kinase II from its complex with PSDs using phosphatase inhibitors and activators, and purified phosphatases. The kinase was released from PSDs after its dephosphorylation by PP1

Lignin Modification by Termite and Its Symbiotic Protozoa

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Pharmacological inhibition of sodium-calcium exchange activates NADPH oxidase and induces infection-independent NETotic cell death

In addition to its function of innate immunity against invading pathogens, neutrophil extracellular traps (NETs) promote thrombosis, autoimmune disease, and cancer metastasis; therefore, unnecessary exposure to the triggers of infection-independent NET generation should be avoided. We herein show that inhibition of forward-mode Na⁺/Ca²⁺ exchange by amiloride analogs, 5-(N-ethyl-N-isopropyl)amiloride (EIPA) and 5-(N-Methyl-N-isobutyl)amiloride (MIA), triggers NETotic cell death independently of infectious stimuli. Isolated human neutrophils treated with EIPA and MIA undergo NETotic cell death by an increase of intracellular Ca²⁺ following activation of NADPH oxidase and the resultant upregulation of intracellular ROS. EIPA- and MIA-mediated intracellular Ca²⁺ increase is attributed to the competitive binding of EIPA and MIA against Na⁺ to Na⁺/Ca²⁺ exchanger 1 (NCX1). These results demonstrate a new mechanism of infection-independent NET generation and implicate NCX1 as a physiologic regulator of intracellular calcium balance and NETotic cell death

A new application of the SFDA-staining method to assessment of the freezing tolerance in leaves of alpine plants

For the first time, this study used 5- (6-) sulfofluorescein diacetate (SFDA), a fluorescent product in plant cells converted by esterase activity to fluorescein-5- (and 6-) sulfonic acid (FSA), to assess the freezing tolerance of leaf cells. We were able to readily distinguish living and dead cells, and detect differences in freezing tolerance among five alpine plants using the SFDA-staining method. We also compared this method with two conventional methods, the electrolyte leakage test and fluorescein diacetate (FDA) staining method. The electrolyte leakage test often over- or underestimated freezing injury. With the uninjured control samples, the FDA-staining method failed to stain all leaf cells, while the SFDA-staining method stained almost 100%. From these results, we concluded that SFDA-staining is a more convenient, accurate and reproducible method for analyses of freezing tolerance

Estimating the False Discovery Rate Using Mixed Normal Distribution for Identifying Differentially Expressed Genes in Microarray Data Analysis

The recent development of DNA microarray technology allows us to measure simultaneously the expression levels of thousands of genes and to identify truly correlated genes with anticancer drug response (differentially expressed genes) from many candidate genes. Significance Analysis of Microarray (SAM) is often used to estimate the false discovery rate (FDR), which is an index for optimizing the identifiability of differentially expressed genes, while the accuracy of the estimated FDR by SAM is not necessarily confirmed. We propose a new method for estimating the FDR assuming a mixed normal distribution on the test statistic and examine the performance of the proposed method and SAM using simulated data. The simulation results indicate that the accuracy of the estimated FDR by the proposed method and SAM, varied depending on the experimental conditions. We applied both methods to actual data comprised of expression levels of 12,625 genes of 10 responders and 14 non-responders to docetaxel for breast cancer. The proposed method identified 280 differentially expressed genes correlated with docetaxel response using a cut-off value for achieving FDR <0.01 to prevent false-positive genes, although 92 genes were previously thought to be correlated with docetaxel response ones

The mutual relationship between the host immune system and radiotherapy: stimulating the action of immune cells by irradiation

The effects of irradiation on tumor tissue and the host immune system are interrelated. The antitumor effect of irradiation is attenuated in the immunocompromised hosts. In addition, radiation alone positively and negatively influences the host immune system. The positive effects of radiation are summarized by the ability to help induce and enhance tumor-antigen-specific immune responses. The cancer-immunity cycle is a multistep framework that illustrates how the tumor-antigen-specific immune responses are induced and how the induced antigen-specific immune cells exert their functions in tumor tissues. Irradiation affects each step of this cancer-immunity cycle, primarily in a positive manner. In contrast, radiation also has negative effects on the immune system. The first is that irradiation has the possibility to kill irradiated effector immune cells. The second is that irradiation upregulates immunosuppressive molecules in the tumor microenvironment, whereas the third is that irradiation to the tumor condenses immunosuppressor cells in the tumor microenvironment. When used in conjunction with radiotherapy, immune checkpoint inhibitors can further leverage the positive effects of radiation on the immune system and compensate for the negative effects of irradiation, which supports the rationale for the combination of radiotherapy and immune checkpoint inhibitors. In this review, we summarize the preclinical evidence for the reciprocal effects of radiation exposure and the immune system, and up-front topics of the combination therapy of immune checkpoint inhibitors and radiotherapy