126 research outputs found

    One-Parameter Homothetic Motion in the Hyperbolic Plane and Euler-Savary Formula

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    In \cite{Mul} one-parameter planar motion was first introduced and the relations between absolute, relative, sliding velocities (and accelerations) in the Euclidean plane E2\mathbb{E}^2 were obtained. Moreover, the relations between the Complex velocities one-parameter motion in the Complex plane were provided by \cite{Mul}. One-parameter planar homothetic motion was defined in the Complex plane, \cite{Kur}. In this paper, analogous to homothetic motion in the Complex plane given by \cite{Kur}, one-parameter planar homothetic motion is defined in the Hyperbolic plane. Some characteristic properties about the velocity vectors, the acceleration vectors and the pole curves are given. Moreover, in the case of homothetic scale hh identically equal to 1, the results given in \cite{Yuc} are obtained as a special case. In addition, three hyperbolic planes, of which two are moving and the other one is fixed, are taken into consideration and a canonical relative system for one-parameter planar hyperbolic homothetic motion is defined. Euler-Savary formula, which gives the relationship between the curvatures of trajectory curves, is obtained with the help of this relative system

    Common coeliacomesenteric trunk: a computed tomography radiological study

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    Background: There is an increasing trend for administration of invasive radiological interventions, laparoscopic surgery, and transplantation procedures in recent years, and determining the vascular variations prior to these procedures is crucially important. Coeliacomesenteric trunk (CMT) is among these variations. This study aimed to retrospectively evaluate this rare anomaly by computed tomography (CT). Materials and methods: A total of 1000 CT angiography images were analysed retrospectively, and the patients with mesenteric and coeliac arteries arising from the abdominal aorta with a single root were identified. The level that CMT arose, and its branching patterns were determined individually for all patients. Results: Ten patients (6 males and 4 females) with a mean age of 50.2 years (17–87 years) had CMT in CT images. Conclusions: The knowledge of variations in the CMT prior to vascular or laparoscopic interventions will contribute to early intervention in case of a complication, or to avoid from a potential damage

    The conserved C-terminus of the PcrA/UvrD helicase interacts directly with RNA polymerase

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    Copyright: © 2013 Gwynn et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: This work was supported by a Wellcome Trust project grant to MD (Reference: 077368), an ERC starting grant to MD (Acronym: SM-DNA-REPAIR) and a BBSRC project grant to PM, NS and MD (Reference: BB/I003142/1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewedPublisher PD

    Transcription-replication conflicts: How they occur and how they are resolved

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    The frequent occurrence of transcription and DNA replication in cells results in many encounters, and thus conflicts, between the transcription and replication machineries. These conflicts constitute a major intrinsic source of genome instability, which is a hallmark of cancer cells. How the replication machinery progresses along a DNA molecule occupied by an RNA polymerase is an old question. Here we review recent data on the biological relevance of transcription-replication conflicts, and the factors and mechanisms that are involved in either preventing or resolving them, mainly in eukaryotes. On the basis of these data, we provide our current view of how transcription can generate obstacles to replication, including torsional stress and non-B DNA structures, and of the different cellular processes that have evolved to solve them

    Comparative study on cellular entry of incinerated ancient gold particles (Swarna Bhasma) and chemically synthesized gold particles

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    Gold nanoparticles (AuNPs) are used for a number of imaging and therapeutic applications in east and western part of the world. For thousands of years, the traditional Indian Ayurvedic approach to healing involves the use of incinerated gold ash, prepared with a variety of plant extracts and minerals depending on the region. Here, we describe the characterization of incinerated gold particles (IAuPs) in HeLa (human cells derived from cervical cancer) and HFF-1 (human foreskin fibroblast cells) in comparison to synthesized citrate-capped gold nanoparticles (AuNPs). We found that while individual IAuP crystallites are around 60 nm in size, they form large aggregates with a mean diameter of 4711.7 nm, some of which can enter cells. Fewer cells appeared to have IAuPs compared to AuNPs, although neither type of particle was toxic to cells. Imaging studies revealed that IAuPs were in vesicles, cytosol, or in the nucleus. We found that their nuclear accumulation likely occurred after nuclear envelope breakdown during cell division. We also found that larger IAuPs entered cells via macropinocytosis, while smaller particles entered via clathrin-dependent receptor-mediated endocytosis

    XRN2 Links Transcription Termination to DNA Damage and Replication Stress

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    We thank the Proteomics Core Facility. We thank Dr. Robert J. Crouch for providing us with GFP- and GFP-RNase H expression plasmids. We also thank Dr. Stephen H. Leppla for providing us with antibodies directed against RNA:DNA hybrids (R loops) (S9.6). We thank Novus Biologicals for generously providing XRN2 and Rrp45 antibodies. We also thank the members of the Boothman lab for critical reading of this manuscript.Author Summary Genomic instability is one of the primary causes of disease states, in particular cancer. One major cause of genomic instability is the formation of DNA double strand breaks (DSBs), which are one of the most dangerous types of DNA lesions the cell can encounter. If not repaired in a timely manner, one DSB can lead not only to cell death. If misrepaired, one DSB can lead to a hazardous chromosomal aberration, such as a translocation, that can eventually lead to cancer. The cell encounters and repairs DSBs that arise from naturally occurring cellular processes on a daily basis. A number of studies have demonstrated that aberrant structures that form during transcription under certain circumstances, in particular RNA:DNA hybrids (R loops), can lead to DSB formation and genomic instability, especially during DNA synthesis. Thus, it is important to understand how the cell responds and repairs transcription-mediated DNA damage in general and R loop-related DNA damage in particular. This paper both demonstrates that the XRN transcription termination factor links transcription and DNA damage, but also provides a better understanding of how the cell prevents transcription-related DNA damage.Yeshttp://www.plosgenetics.org/static/editorial#pee

    C9orf72 Expansion Disrupts ATM-mediated Chromosomal Break Repair

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    A hexanucleotide repeat expansion represents the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, though the mechanisms by which the expansion cause neurodegeneration are poorly understood. We report elevated levels of DNA/RNA hybrids (R-loops) and double-strand breaks (DSBs) in rodent neurons, human cells, and in C9orf72-ALS patient spinal cord tissues. Accumulation of endogenous DNA damage is concomitant with defective ATM-mediated DNA repair signalling and accumulation of protein-linked DNA breaks. We further reveal that defective ATM-mediated DNA repair is a consequence of p62 accumulation, which impairs H2A ubiquitylation and perturbs ATM signalling. Adeno-associated virus- mediated expression of C9orf72-related RNA and dipeptide repeats in the murine central nervous system causes elevated DSBs, ATM defects, and triggers neurodegeneration. These findings identify R-Loops, DSBs, and defective ATM-mediated repair as pathological consequences of C9orf72 expansions, and suggest that C9orf72-linked neurodegeneration is driven, at least in part, by genomic instability
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