A Computational Approach for the Ramsey Numbers R(C_4, K_n)

For graphs G and H, the Ramsey number R(G,H) is the least integer n such that every 2-coloring of the edges of K_n contains a subgraph isomorphic to G in the first color or a subgraph isomorphic to H in the second color. Graph G is a (C_4, K_n)-graph if G doesn\u27t contain a cycle C_4 and G has no independent set of order n. Jayawardene and Rousseau showed that 21 \u3c = R(C_4,K_7) \u3c = 22. In this work we determine R(C_4, K_7) = 22 and R(C_4,K_8) = 26, and enumerate various families of (C_4, K_n)-graphs. In particular, we construct all (C_4, K_n)-graphs for n \u3c 7, and all (C_4,K_7)-graphs on at least 19 vertices. Most of the results are based on computer algorithms

Note: Computation of the Ramsey Number R(W5,K5)

We determine the value of the Ramsey number R(W5;K5) to be 27, where W5 = K1 + C4 is the 4-spoked wheel of order 5. This solves one of the four remaining open cases in the tables given in 1989 by George R. T. Hendry, which included the Ramsey numbers R(G;H) for all pairs of graphs G and H having ve vertices, except seven entries. In addition, we show that there exists a unique up to isomorphism critical Ramsey graph for W5 versus K5. Our results are based on computer algorithms

Isolated heart models for studying cardiac electrophysiology: a historical perspective and recent advances

Experimental models used in cardiovascular research range from cellular to whole heart preparations. Isolated whole hearts show higher levels of structural and functional integration than lower level models such as tissues or cellular fragments. Cardiovascular diseases are multi-factorial problems that are dependent on highly organized structures rather than on molecular or cellular components alone. This article first provides a general introduction on the animal models of cardiovascular diseases. It is followed by a detailed overview and a historical perspective of the different isolated heart systems with a particular focus on the Langendorff perfusion method for the study of cardiac arrhythmias. The choice of species, perfusion method, and perfusate composition are discussed in further detail with particular considerations of the theoretical and practical aspects of experimental settings

Computation of the Ramsey Number R(B_3, K_5)

In 1989, George R. T. Hendry presented a table of two-color graph Ramsey numbers R(G,H) for all pairs of graphs G and H having five vertices, with the exception of seven cases. Until now, only two of the these open cases were solved. This work eliminates another one by computing R(B_3,K_5) = 20, where B_3 = K_2 + K_3 is the book graph of order 5. In addition, we show that for these parameters there exists a unique up to isomorphism critical graph. The results are based on computer algorithms. Among the four remaining open cases in Hendry\u27s table, the most notable is that of K_5 versus K_5, for which it is known that 4

PMCA4 (ATP2B4) mutation in familial spastic paraplegia causes delay in intracellular calcium extrusion

Background: Familial spastic paraplegia (FSP) is a heterogeneous group of disorders characterized primarily by progressive lower limb spasticity and weakness. More than 50 disease loci have been described with different modes of inheritance. Recently, we described a novel missense mutation (c.803G>A, p.R268Q) in the plasma membrane calcium ATPase (PMCA4, or ATP2B4) gene in a Chinese family with autosomal dominant FSP. Further to this finding, here we describe the functional effect of this mutation. Methods: As PMCA4 removes cytosolic calcium, we measured transient changes and the time-dependent decay of cytosolic calcium level as visualized by using fura-2 fluorescent dye with confocal microscopy in human SH-SY5Y neuroblastoma cells overexpressing either wild-type or R268Q mutant PMCA4. Results: Overexpressing both wild-type and R268Q PMCA4 significantly reduced maximum calcium surge after KCl-induced depolarization as compared with vector control cells. However, cells overexpressing mutant PMCA4 protein demonstrated significantly higher level of calcium surge when compared with wild-type. Furthermore, the steady-state cytosolic calcium concentration in these mutant cells remained markedly higher than the wild-type after SERCA inhibition by thapsigargin. Conclusion: Our result showed that p.R268Q mutation in PMCA4 resulted in functional changes in calcium homeostasis in human neuronal cells. This suggests that calcium dysregulation may be associated with the pathogenesis of FSP. © 2015 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.published_or_final_versio

PMCA4 (ATP2B4) Mutation in Familial Spastic Paraplegia

Familial spastic paraplegia (FSP) is a heterogeneous group of disorders characterized primarily by progressive lower limb spasticity and weakness. More than 50 disease loci have been described with different modes of inheritance. In this study, we identified a novel missense mutation (c.803G.A, p.R268Q) in the plasma membrane calcium ATPase (PMCA4, or ATP2B4) gene in a Chinese family with autosomal dominant FSP using whole-exome sequencing and confirmed with Sanger sequencing. This mutation co-segregated with the phenotype in the six family members studied and is predicted to be pathogenic when multiple deleteriousness predictions were combined. This novel R268Q mutation was not present in over 7,000 subjects in public databases, and over 1,000 Han Chinese in our database. Prediction of potential functional consequence of R268Q mutation on PMCA4 by computational modeling revealed that this mutation is located in protein aggregation-prone segment susceptible to protein misfolding. Analysis for thermodynamic protein stability indicated that this mutation destabilizes the PMCA4 protein structure with higher folding free energy. As PMCA4 functions to maintain neuronal calcium homeostasis, our result showed that calcium dysregulation may be associated with the pathogenesis of FSP.published_or_final_versio

Assessment of Cellular Estrogenic Activity Based on Estrogen Receptor-Mediated Reduction of Soluble-Form Catechol-O-Methyltransferase (COMT) Expression in an ELISA-Based System

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Rzadki przypadek przerzutu pierwotnego chłoniaka piersi do ciała szklistego

Pierwotny chłoniak piersi (PBL) to rzadko występujący nowotwór, ograniczony w chwili rozpoznania wyłącznie do piersi. Izolowany przerzut chłoniaka do ciała szklistego obserwowany jest wyjątkowo i w związku z tym może stanowić duży problem diagnostyczny. W przedstawionej publikacji opisano przypadek 75-letniej chorej pochodzenia tajwańskiego z pierwotnym rozpoznaniem PBL z limfocytów B, który ustąpił po 6 cyklach chemioterapii CHOP. Dwa lata po uzyskaniu całkowitej odpowiedzi chora zgłosiła się z powodu narastających zaburzeń widzenia, wywołanych obecnością zmętnień w ciele szklistym lewego oka. Wynik badania histologicznego próbek ciała szklistego pobranych w czasie witrektomii oraz całość obrazu klinicznego przemawiały za rozsiewem chłoniaka z limfocytów B. Celem przedstawienia tego przypadku jest poszerzenie wiedzy na temat chłoniaków pozawęzłowych oraz uniknięcie w przyszłości zbędnych opóźnień w leczeniu chorych z podobnym przebiegiem klinicznym choroby

The effect of ex-vivo rotenone intoxication on dopamine re-uptake of LRRK2-R1441G mutant mouse

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