The Influence of Biomechanical Factors at the Tissue-Biomaterial Interface

1987 ◽  
Vol 110 ◽  
Author(s):  
John B. Brunski ◽  
J. A. Hipp ◽  
G. V. B. Cochran

AbstractWhen an implant is placed into bone, an interface is created. This interface has a critical biomechanical function: it must support the implant in bone. However, failure of implant fixation (i.e., implant “loosening”), continues to be a leading cause of implant failure [1,2]. While there are a number of factors involved in this problem, it is recognized that biomechanical factors play a role, and this paper reviews the more important factors, including relative motion and interfacial stresses and strains. Also, it presents results from a recent in vivo experiment on controlled loading of an interface.

2006 ◽  
Vol 5 (8) ◽  
pp. 1378-1387 ◽  
Author(s):  
Adam K. Kallmeyer ◽  
Kim M. Keeling ◽  
David M. Bedwell

ABSTRACT Protein synthesis requires a large commitment of cellular resources and is highly regulated. Previous studies have shown that a number of factors that mediate the initiation and elongation steps of translation are regulated by phosphorylation. In this report, we show that a factor involved in the termination step of protein synthesis is also subject to phosphorylation. Our results indicate that eukaryotic release factor 1 (eRF1) is phosphorylated in vivo at serine 421 and serine 432 by the CK2 protein kinase (previously casein kinase II) in the budding yeast Saccharomyces cerevisiae. Phosphorylation of eRF1 has little effect on the efficiency of stop codon recognition or nonsense-mediated mRNA decay. Also, phosphorylation is not required for eRF1 binding to the other translation termination factor, eRF3. In addition, we provide evidence that the putative phosphatase Sal6p does not dephosphorylate eRF1 and that the state of eRF1 phosphorylation does not influence the allosuppressor phenotype associated with a sal6Δ mutation. Finally, we show that phosphorylation of eRF1 is a dynamic process that is dependent upon carbon source availability. Since many other proteins involved in protein synthesis have a CK2 protein kinase motif near their extreme C termini, we propose that this represents a common regulatory mechanism that is shared by factors involved in all three stages of protein synthesis.


2018 ◽  
Vol 166 (1) ◽  
pp. 43-45 ◽  
Author(s):  
L. P. Sycheva ◽  
R. A. Shchegoleva ◽  
N. I. Lisina ◽  
A. V. Gordeev ◽  
L. M. Rozhdestvenskii

2020 ◽  
Vol 28 (3) ◽  
pp. 230949902096612
Author(s):  
Jian Yu ◽  
Chao Zhang ◽  
Wen-Ming Chen ◽  
Dahang Zhao ◽  
Pengfei chu ◽  
...  

Purpose: Implant loosening in tibia after primary total ankle replacement (TAR) is one of the common postoperative problems in TAR. Innovations in implant structure design may ideally reduce micromotion at the bone–implant interface and enhance the bone-implant fixation and initial stability, thus eventually prevents long-term implant loosening. This study aimed to investigate (1) biomechanical characteristics at the bone–implant interface and (2) the influence of design features, such as radius, height, and length. Methods: A total of 101 finite-element models were created based on four commercially available implants. The models predicted micromotion at the bone–implant interface, and we investigated the impact of structural parameters, such as radius, length, and height. Results: Our results suggested that stem-type implants generally required the highest volume of bone resection before implantation, while peg-type implants required the lowest. Compared with central fixation features (stem and keel), peripherally distributed geometries (bar and peg) were associated with lower initial micromotions. The initial stability of all types of implant design can be optimized by decreasing fixation size, such as reducing the radius of the bars and pegs and lowering the height. Conclusion: Peg-type tibial implant design may be a promising fixation method, which is required with a minimum bone resection volume and yielded minimum micromotion under an extreme axial loading scenario. Present models can serve as a useful platform to build upon to help physicians or engineers when making incremental improvements related to implant design.


2018 ◽  
Vol 50 (4) ◽  
pp. 1398-1413 ◽  
Author(s):  
Min Li ◽  
Chun-Xia Ren ◽  
Jian-Mei Zhang ◽  
Xiao-Yan Xin ◽  
Teng Hua ◽  
...  

Background/Aims: This study is aimed at identification of miR-195-5p/MMP14 expression in cervical cancer (CC) and their roles on cell proliferation and invasion profile of CC cells through TNF signaling pathway in CC. Methods: Microarray analysis, gene set enrichment analysis (GSEA) and DAVID were used to analyze differentially expressed miRNAs, mRNAs and signaling pathways. MiR-195-5p and MMP14 expression levels in CC cell were determined by qRT-PCR. Western blot was employed to measure MMP14 and TNF signaling pathway-relating protein level. Luciferase reporter system was used to confirm the targeting relationship between MMP14 and miR-195-5p. Cell proliferation and invasion was respectively deeded by CCK8, transwell. In vivo experiment was carried out to study the impact of MMP14 and miR-195-5p on CC development in mice. Results: The microarray analysis and the results of qRT-PCR determined that miR-195-5p was under-expressed and MMP14 was over-expressed in CC cells. GSEA and DAVID analysis showed that TNF signaling pathway was regulated by miR-195-5p/MMP14 and activated in cervical carcinoma cells. The miR-195-5p and MMP14 have a negative regulation relation. In vivo experiment found that down-regulated MMP14 and up-regulated miR-195-5p suppressed the tumor development. Conclusion: Our results suggest that MMP14 is a direct target of miR-195-5p, and down-regulated MMP14 and up-regulated miR-195-5p suppressed proliferation and invasion of CC cells by inhibiting TNF signaling pathway.


2018 ◽  
Vol 7 (10) ◽  
pp. 548-560 ◽  
Author(s):  
I. Qayoom ◽  
D. B. Raina ◽  
A. Širka ◽  
Š. Tarasevičius ◽  
M. Tägil ◽  
...  

During the last decades, several research groups have used bisphosphonates for local application to counteract secondary bone resorption after bone grafting, to improve implant fixation or to control bone resorption caused by bone morphogenetic proteins (BMPs). We focused on zoledronate (a bisphosphonate) due to its greater antiresorptive potential over other bisphosphonates. Recently, it has become obvious that the carrier is of importance to modulate the concentration and elution profile of the zoledronic acid locally. Incorporating one fifth of the recommended systemic dose of zoledronate with different apatite matrices and types of bone defects has been shown to enhance bone regeneration significantly in vivo. We expect the local delivery of zoledronate to overcome the limitations and side effects associated with systemic usage; however, we need to know more about the bioavailability and the biological effects. The local use of BMP-2 and zoledronate as a combination has a proven additional effect on bone regeneration. This review focuses primarily on the local use of zoledronate alone, or in combination with bone anabolic factors, in various preclinical models mimicking different orthopaedic conditions. Cite this article: I. Qayoom, D. B. Raina, A. Širka, Š. Tarasevičius, M. Tägil, A. Kumar, L. Lidgren. Anabolic and antiresorptive actions of locally delivered bisphosphonates for bone repair: A review. Bone Joint Res 2018;7:548–560. DOI: 10.1302/2046-3758.710.BJR-2018-0015.R2.


2021 ◽  
pp. 29-31
Author(s):  
Анна Георгиевна Калинина ◽  
Ирина Михайловна Абрамова ◽  
Наталья Евгеньевна Головачёва ◽  
Светлана Семеновна Морозова ◽  
Любовь Павловна Галлямова

Результаты исследования в опыте in vivo подтвердили снижение негативных последствий при хронической интоксикации животных для образцов настойки сладкой крепостью 20 %, содержащей черносмородиновый спиртованный морс, по сравнению с раствором этилового спирта аналогичной крепости. The results of the study in the in vivo experiment confirmed a reduction in the negative consequences of chronic intoxication of animals for samples of tincture with a sweet strength of 20 %, containing blackcurrant alcoholic mors, compared with a solution of ethyl alcohol of a similar strength.


2020 ◽  
Vol 39 (5) ◽  
pp. 477-490
Author(s):  
Attalla Farag El-kott ◽  
Ali S. Alshehri ◽  
Heba S. Khalifa ◽  
Abd-El-karim M. Abd-Lateif ◽  
Mohammad Ali Alshehri ◽  
...  

This study investigated whether the mechanism underlying the neurotoxic effects of cadmium chloride (CdCl2) in rats involves p66Shc. This study comprised an initial in vivo experiment followed by an in vitro experiment. For the in vivo experiment, male rats were orally administered saline (vehicle) or CdCl2 (0.05 mg/kg) for 30 days. Thereafter, spatial and retention memory of rats were tested and their hippocampi were used for biochemical and molecular analyses. For the in vitro experiment, control or p66Shc-deficient hippocampal cells were treated with CdCl2 (25 µM) in the presence or absence of SP600125, a c-Jun N-terminal kinase (JNK) inhibitor. Cadmium chloride impaired the spatial learning and retention memory of rats; depleted levels of glutathione and manganese superoxide dismutase; increased reactive oxygen species (ROS), tumor necrosis factor α, and interleukin 6; and induced nuclear factor kappa B activation. Cadmium chloride also decreased the number of pyramidal cells in the CA1 region and induced severe damage to the mitochondria and endoplasmic reticulum of cells in the hippocampi of rats. Moreover, CdCl2 increased the total unphosphorylated p66Shc, phosphorylated (Ser36) p66Shc, phosphorylated JNK, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, cytochrome c, and cleaved caspase-3. A dose–response increase in cell death, ROS, DNA damage, p66Shc, and NADPH oxidase was also observed in cultured hippocampal cells treated with CdCl2. Of note, all of these biochemical changes were attenuated by silencing p66Shc or inhibiting JNK with SP600125. In conclusion, CdCl2 induces hippocampal ROS generation and apoptosis by promoting the JNK-mediated activation of p66Shc.


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