scholarly journals Numerical Simulation of Bone Remodeling Coupling the Damage Repair Process in Human Proximal Femur

2020 ◽  
Vol 125 (2) ◽  
pp. 829-847
Author(s):  
Chuanyong Qu ◽  
Hui Yuan
Keyword(s):  
Numerical Simulation ◽  
Bone Remodeling ◽  
Proximal Femur ◽  
Repair Process ◽  
Damage Repair

Bone Distribution Simulation during Damage-Repair Bone Remodeling in Human Proximal Femur

2013 ◽  
Vol 634-638 ◽  
pp. 883-891
Author(s):  
Bing Hui Zhao ◽  
Chuan Yong Qu ◽  
Qing Hua Qin
Keyword(s):  
Mathematical Model ◽  
Bone Remodeling ◽  
Proximal Femur ◽  
Ansys Software ◽  
Governing Equations ◽  
Damage Repair ◽  
The Mathematical Model ◽  
Novel Model ◽  
Element Algorithm ◽  
Repair Cycle

A new damage-adaptive bone remodeling model, in which an algorithm incorporating both strain and damage stimuli, is developed in this paper. Typically, a human proximal femur model is established to predict the bone mass distribution during bone remodeling process. And human physiology damage-repair cycle is considered in the model. The governing equations of the mathematical model, digesting the predecessors’ ideas, are numerically solved and implemented into ANSYS software via the user interface of finite element algorithm. With the aid of this novel model, the whole healing behavior of human proximal femur is elucidated properly.

scholarly journals The emerging role of RNAs in DNA damage repair

2017 ◽  
Vol 24 (4) ◽  
pp. 580-587 ◽  
Author(s):  
Ben R Hawley ◽  
Wei-Ting Lu ◽  
Ania Wilczynska ◽  
Martin Bushell
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Critical Role ◽  
Repair Process ◽  
Rna Molecules ◽  
Processing Enzymes ◽  
Damage Repair ◽  
New Findings ◽  
Integral Role ◽  
Repair Mechanisms

Abstract Many surveillance and repair mechanisms exist to maintain the integrity of our genome. All of the pathways described to date are controlled exclusively by proteins, which through their enzymatic activities identify breaks, propagate the damage signal, recruit further protein factors and ultimately resolve the break with little to no loss of genetic information. RNA is known to have an integral role in many cellular pathways, but, until very recently, was not considered to take part in the DNA repair process. Several reports demonstrated a conserved critical role for RNA-processing enzymes and RNA molecules in DNA repair, but the biogenesis of these damage-related RNAs and their mechanisms of action remain unknown. We will explore how these new findings challenge the idea of proteins being the sole participants in the response to DNA damage and reveal a new and exciting aspect of both DNA repair and RNA biology.

scholarly journals A Review on DNA Repair Inhibition by PARP Inhibitors in Cancer Therapy

Folia Medica ◽  
2018 ◽  
Vol 60 (1) ◽  
pp. 39-47 ◽  
Author(s):  
Ashish P. Shah ◽  
Chhagan N. Patel ◽  
Dipen K. Sureja ◽  
Kirtan P. Sanghavi
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Cancer Therapy ◽  
Repair Process ◽  
Parp Inhibitors ◽  
Brca Mutations ◽  
Development Of Resistance ◽  
Damage Repair ◽  
Future Therapy

AbstractThe DNA repair process protects the cells from DNA damaging agent by multiple pathways. Majority of the cancer therapy cause DNA damage which leads to apoptosis. The cell has natural ability to repair this damage which ultimately leads to development of resistance of drugs. The key enzymes involved in DNA repair process are poly(ADP-ribose) (PAR) and poly(ADP-ribose) polymerases (PARP). Tumor cells repair their defective gene via defective homologues recombination (HR) in the presence of enzyme PARP. PARP inhibitors inhibit the enzyme poly(ADP-ribose) polymerases (PARPs) which lead to apoptosis of cancer cells. Current clinical data shows the role of PARP inhibitors is not restricted to BRCA mutations but also effective in HR dysfunctions related tumors. Therefore, investigation in this area could be very helpful for future therapy of cancer. This review gives detail information on the role of PARP in DNA damage repair, the role of PARP inhibitors and chemistry of currently available PARP inhibitors.

Investigation of Osteoclast Resorption Mechanisms in a Hybrid Cellular Automaton Model of Bone Remodeling

2007 ◽  
Author(s):  
Charles L. Penninger ◽  
Ryan K. Roeder ◽  
Glen L. Niebur ◽  
John E. Renaud
Keyword(s):  
Cellular Automaton ◽  
Bone Remodeling ◽  
Mechanical Loading ◽  
Living Tissue ◽  
Basic Multicellular Unit ◽  
Mechanical Loads ◽  
Continuous Formation ◽  
Damage Repair ◽  
Biological Environment ◽  
Osteoclast Resorption

Bone is a living tissue which is continually adapting to its biological environment via continuous formation and resorption. It is generally accepted that bone remodeling occurs in response to daily mechanical loading. The remodeling process enables various functions, such as damage repair, adaptation to mechanical loads, and mineral homeostasis [1]. The cells that are responsible for the bone remodeling process are the bone resorbing osteoclasts and the bone forming osteoblasts. These cells closely coordinate their actions in a basic multicellular unit to renew “packets” of bone.

scholarly journals Tailoring Ovarian Cancer Treatment: Implications of BRCA1/2 Mutations

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 416 ◽  
Author(s):  
Ainhoa Madariaga ◽  
Stephanie Lheureux ◽  
Amit Oza
Keyword(s):  
Ovarian Cancer ◽  
Brca Mutation ◽  
Repair Process ◽  
Resistance Mechanisms ◽  
Tumour Suppressor Genes ◽  
Brca1 And Brca2 ◽  
Brca Mutations ◽  
Damage Repair ◽  
Brca Mutation Carriers ◽  
Drug Efflux Pumps

High grade serous ovarian cancer (HGSOC) is the most common epithelial ovarian cancer, harbouring more than 20% germline or somatic mutations in the tumour suppressor genes BRCA1 and BRCA2. These genes are involved in both DNA damage repair process via homologous recombination (HR) and transcriptional regulation. BRCA mutation confers distinct characteristics, including an increased response to DNA-damaging agents, such us platinum chemotherapy and poly-ADP ribose polymerase inhibitors (PARPi). However, several mechanisms of resistance to these agents have been described, including increased HR capacity through reverse BRCA mutations, non-homologous end-joint (NHEJ) repair alterations and drug efflux pumps. Current treatments of ovarian cancer including surgery, chemotherapy, targeted treatment and maintenance strategies, as well as resistance mechanisms will be reviewed, focusing on future trends with respect to BRCA mutation carriers.

scholarly journals Crystal structure of RecR, a member of the RecFOR DNA-repair pathway, fromPseudomonas aeruginosaPAO1

2018 ◽  
Vol 74 (4) ◽  
pp. 222-230
Author(s):  
Shiyou Che ◽  
Yujing Chen ◽  
Yakun Liang ◽  
Qionglin Zhang ◽  
Mark Bartlam
Keyword(s):  
Crystal Structure ◽  
Dna Damage ◽  
Homologous Recombination ◽  
Analytical Ultracentrifugation ◽  
Repair Process ◽  
Asymmetric Unit ◽  
Homologous Recombination Pathway ◽  
Damage Repair ◽  
Important Regulator ◽  
Recombination Pathway

DNA damage is usually lethal to all organisms. Homologous recombination plays an important role in the DNA damage-repair process in prokaryotic organisms. Two pathways are responsible for homologous recombination inPseudomonas aeruginosa: the RecBCD pathway and the RecFOR pathway. RecR is an important regulator in the RecFOR homologous recombination pathway inP. aeruginosa. It forms complexes with RecF and RecO that can facilitate the loading of RecA onto ssDNA in the RecFOR pathway. Here, the crystal structure of RecR fromP. aeruginosaPAO1 (PaRecR) is reported.PaRecR crystallizes in space groupP6122, with two monomers per asymmetric unit. Analytical ultracentrifugation data show thatPaRecR forms a stable dimer, but can exist as a tetramer in solution. The crystal structure shows that dimericPaRecR forms a ring-like tetramer architectureviacrystal symmetry. The presence of a ligand in the Walker B motif of one RecR subunit suggests a putative nucleotide-binding site.

Etiology of Exercise-Induced Muscle Damage

1999 ◽  
Vol 24 (3) ◽  
pp. 234-248 ◽  
Author(s):  
Priscilla M. Clarkson ◽  
Stephen P. Sayers
Keyword(s):  
Muscle Damage ◽  
Eccentric Exercise ◽  
Muscle Function ◽  
Stress Proteins ◽  
Repair Process ◽  
Cellular Level ◽  
Muscle Stiffness ◽  
Damage Repair ◽  
Exercise Induced ◽  
Shock Proteins

Muscle damage is caused by strenuous and unaccustomed exercise, especially exercise involving eccentric muscle contractions, where muscles lengthen as they exert force. Damage can be observed both directly at the cellular level and indirectly from changes in various indices of muscle function. Several mechanisms have been offered to explain the etiology of the damage/repair process, including mechanical factors such as tension and strain, disturbances in calcium homeostasis. the inflammatory response, and the synthesis of stress proteins (heat shock proteins). Changes in muscle function following eccentric exercise have been observed at the cellular level as an impairment in the amount and action of transport proteins for glucose and lactate/H+, and at the systems level as an increase in muscle stiffness and a prolonged loss in the muscle's ability to generate force. This paper will briefly review factors involved in the damage/repair process and alterations in muscle function following eccentric exercise. Key words: eccentric exercise, inflammation, stress proteins, muscle function

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