COMMON FIXED POINT THEOREM FOR A PAIR OF WEAKLY COMPATIBLE SELF-MAPPINGS IN FUZZY METRIC SPACE USING (CLRG) PROPERTY

In this paper we prove a common fixed point theorem for a pair of weakly compatible self-mappings in fuzzy metric space by using (CLRg) property. The result is extended for two finite families of self-mappings infuzzy metric space by using the concept of pairwise commuting. An example is provided which demonstrates the validity of main theorem

Eyring Powellnanofluid flow over a rotating disk with Activation energy and thermal radiation

This paper's goal is to investigate the Eyring-Powell nano liquid past rotating disk. Thermalradiation and chemical reaction have been used to study heat and mass transmission. Convectivecharacteristics, as well as heat and mass conditions, are studied. Through appropriatetransformations, highly non-linear partial differential equation systems are transformed into nonlinearordinary differential equations. Implementing bvp4c uses the transmuted ordinary differentialequations. Through graphical representation, the effects of promising physical characteristics havebeen investigated

Structural Alignment Using Graphs

ABSTRAC

A Fast Data Structure for Anagrams

In this paper, we are presenting a data structure, which stores the given dictionary data in a hash table called PRIME , by using fundamental theorem on Arithmetic to generate a key for each dictionary word, and stores the word in the hash table based on the key. As compared to tree-based techniques PRIME table generates anagram for the given random word in O(1) time, time to construct a PRIME table depends on the number of words in the dictionary. If dictionary has ‘n’ words then the time to develop the PRIME table is O(n). Categories and Subject descriptors: Problem solving, search and control methods

Performance of magnetic dipole contribution on ferromagnetic non-Newtonian radiative MHD blood flow: An application of biotechnology and medical sciences

Casson flow ferromagnetic liquid blood flow over stretching region is studied numerically. The domain is influence by radiation and blood flow velocity and thermal slip conditions. Blood acts an impenetrable magneto-dynamic liquid yields governing equations. The conservative governing nonlinear partial differential equations, reduced to ODEs by the help of similarity translation technique. The transport equations were transformed into first order ODEs and the resultant system are solved with help of 4th order R-K scheme. Performing a magnetic dipole with a Casson flow across a stretched region with Brownian motion and Thermophoresis is novelty of the problem. Significant applications of the study in some spheres are metallurgy, extrusion of polymers, production in papers and rubber manufactured sheets. Electronics, analytical instruments, medicine, friction reduction, angular momentum shift, heat transmission, etc. are only few of the many uses for ferromagnetic fluids. As ferromagnetic interaction parameter value improves, the skin-friction, Sherwood and Nusselt numbers depreciates. A comparative study of the present numerical scheme for specific situations reveals a splendid correlation with earlier published work. A change in blood flow velocity magnitude has been noted due to Casson parameter. Increasing change in blood flow temperature noted due to Casson parameter. Skin-friction strengthened and Nusselt number is declined with Casson parameter. The limitation of current work is a non-invasive magnetic blood flow collection system using commercially available magnetic sensors instead of SQUID or electrodes.Unai Fernandez-Gamiz was supported by Government of the Basque Country [ELKARTEK21/10KK-2021/00014 & ELKARTEK22/85]. Irfan Nurhidayat was supported by King Mongkut’s Institute of Technology Ladkrabang (KMITL), Bangkok, Thailand [KDS2020/045]

Sirtuin 2 Inhibition Modulates Chromatin Landscapes Genome-Wide To Induce Senescence in ATRX-Deficient Malignant Glioma

BACKGROUND: Functional inactivation of ATRX characterizes large subgroups of malignant gliomas in adults and children. ATRX deficiency in glioma induces widespread chromatin remodeling, driving transcriptional shifts and oncogenic phenotypes. Effective strategies to therapeutically target these broad epigenomic sequelae remain undeveloped. METHODS: We utilized integrated multiomics and the Broad Institute Connectivity Map (CMAP) to identify drug candidates that could potentially revert ATRX-deficient transcriptional changes. We then employed disease-relevant experimental models to evaluate functional phenotypes, coupling these studies with epigenomic profiling to elucidate molecular mechanism(s). RESULTS: CMAP analysis and transcriptional/epigenomic profiling implicated the Class III HDAC Sirtuin2 (SIRT2) as a central mediator of ATRX-deficient cellular phenotypes and a driver of unfavorable prognosis in ATRX-deficient glioma. SIRT2 inhibitors reverted Atrx-deficient transcriptional signatures in murine neuroepithelial progenitor cells (mNPCs), impaired cell migration in Atrx/ATRX-deficient mNPCs and human glioma stem cells (GSCs), and increased expression of senescence markers in glioma models. Moreover, SIRT2 inhibition impaired growth and increased senescence in ATRX-deficient GSCs in vivo. These effects were accompanied by genome-wide shifts in enhancer-associated H3K27ac and H4K16ac marks, with the latter in particular demonstrating compelling transcriptional links to SIRT2-dependent phenotypic reversals. Motif analysis of these data identified the transcription factor KLF16 as a mediator of phenotype reversal in Atrx-deficient cells upon SIRT2 inhibition. CONCLUSIONS: Our findings indicate that SIRT2 inhibition selectively targets ATRX-deficient gliomas for senescence through global chromatin remodeling, while demonstrating more broadly a viable approach to combat complex epigenetic rewiring in cancer

NSs Encoded by Groundnut Bud Necrosis Virus Is a Bifunctional Enzyme

Groundnut bud necrosis virus (GBNV), a member of genus Tospovirus in the family Bunyaviridae, infects a large number of leguminosae and solanaceae plants in India. With a view to elucidate the function of nonstructural protein, NSs encoded by the small RNA genome (S RNA), the NSs protein of GBNV- tomato (Karnataka) [1] was over-expressed in E. coli and purified by Ni-NTA chromatography. The purified rNSs protein exhibited an RNA stimulated NTPase activity. Further, this activity was metal ion dependent and was inhibited by adenosine 5′ (β, γ imido) triphosphate, an ATP analog. The rNSs could also hydrolyze dATP. Interestingly, in addition to the NTPase and dATPase activities, the rNSs exhibited ATP independent 5′ RNA/DNA phosphatase activity that was completely inhibited by AMP. The 5′ α phosphate could be removed from ssDNA, ssRNA, dsDNA and dsRNA thus confirming that rNSs has a novel 5′ α phosphatase activity. K189A mutation in the Walker motif A (GxxxxGKT) resulted in complete loss of ATPase activity, but the 5′ phosphatase activity was unaffected. On the other hand, D159A mutation in the Walker motif B (DExx) resulted in partial loss of both the activities. These results demonstrate for the first time that NSs is a bifunctional enzyme, which could participate in viral movement, replication or in suppression of the host defense mechanism

Interplay Between Atrx and IDH1 Mutations Governs Innate Immune Responses in Diffuse Gliomas

Stimulating the innate immune system has been explored as a therapeutic option for the treatment of gliomas. Inactivating mutations in ATRX, defining molecular alterations in IDH-mutant astrocytomas, have been implicated in dysfunctional immune signaling. However, little is known about the interplay between ATRX loss and IDH mutation on innate immunity. To explore this, we generated ATRX-deficient glioma models in the presence and absence of the IDH1R132H mutation. ATRX-deficient glioma cells are sensitive to dsRNA-based innate immune agonism and exhibit impaired lethality and increased T-cell infiltration in vivo. However, the presence of IDH1R132H dampens baseline expression of key innate immune genes and cytokines in a manner restored by genetic and pharmacological IDH1R132H inhibition. IDH1R132H co-expression does not interfere with the ATRX deficiency-mediated sensitivity to dsRNA. Thus, ATRX loss primes cells for recognition of dsRNA, while IDH1R132H reversibly masks this priming. This work reveals innate immunity as a therapeutic vulnerability of astrocytomas