Wear Testing of UHMWPE Tibial Components: Influence of Oxidation

1999 ◽  
Vol 122 (1) ◽  
pp. 323-331 ◽  
Author(s):  
Sarah K. Young ◽  
Tony S. Keller ◽  
Keith W. Greer ◽  
Michael C. Gorhan

An AMTI knee simulator was used to evaluate the wear of UHMWPE tibial inserts which were gamma sterilized in air and displayed a high or low level of oxidation. After 5 million cycles, four out of five samples from the high oxidation group displayed subsurface cracking and/or delamination. The five specimens in the low oxidation group experienced burnishing only. These results indicate that gamma irradiation in air together with high oxidation due to shelf aging can increase susceptibility to wear. The appearance of the wear scars indicates that knee simulator testing is a valid method of producing burnishing, cracking, and delamination similar to that seen in-vivo. [S0742-4787(00)04301-0]

1981 ◽  
Vol 10 (3) ◽  
pp. 137-142 ◽  
Author(s):  
R W Treharne ◽  
R W Young ◽  
S R Young

This paper describes a new method for testing total knee prostheses under simulated in vivo conditions. Previous knee simulator work has been summarized and described. The major variables of testing are also described in detail. The results of wear testing five types of knee prostheses were that the wear rate was nearly an inverse relationship with contact area— knees with a higher contact area had lower wear rates.


2015 ◽  
Vol 35 (9) ◽  
pp. 1435-1444 ◽  
Author(s):  
Tingting Dong ◽  
Qi Zhang ◽  
Michael R Hamblin ◽  
Mei X Wu

Vascular damage occurs frequently at the injured brain causing hypoxia and is associated with poor outcomes in the clinics. We found high levels of glycolysis, reduced adenosine triphosphate generation, and increased formation of reactive oxygen species and apoptosis in neurons under hypoxia. Strikingly, these adverse events were reversed significantly by noninvasive exposure of injured brain to low-level light (LLL). Low-level light illumination sustained the mitochondrial membrane potential, constrained cytochrome c leakage in hypoxic cells, and protected them from apoptosis, underscoring a unique property of LLL. The effect of LLL was further bolstered by combination with metabolic substrates such as pyruvate or lactate both in vivo and in vitro. The combinational treatment retained memory and learning activities of injured mice to a normal level, whereas other treatment displayed partial or severe deficiency in these cognitive functions. In accordance with well-protected learning and memory function, the hippocampal region primarily responsible for learning and memory was completely protected by combination treatment, in marked contrast to the severe loss of hippocampal tissue because of secondary damage in control mice. These data clearly suggest that energy metabolic modulators can additively or synergistically enhance the therapeutic effect of LLL in energy-producing insufficient tissue–like injured brain.


2019 ◽  
Vol 159 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Prabakaran Paulraj ◽  
Michelle Bosworth ◽  
Maria Longhurst ◽  
Callie Hornbuckle ◽  
Garrett Gotway ◽  
...  

The role of autosomal recessive (AR) variants in clinically heterogeneous conditions such as intellectual disability and developmental delay (ID/DD) has been difficult to uncover. Implication of causative pathogenic AR variants often requires investigation within large and consanguineous families, and/or identifying rare biallelic variants in affected individuals. Furthermore, detection of homozygous gene-level copy number variants during first-line genomic microarray testing in the pediatric population is a rare finding. We describe a 6.7-year-old male patient with ID/DD and a novel homozygous deletion involving the FRY gene identified by genomic SNP microarray. This deletion was observed within a large region of homozygosity on the long arm of chromosome 13 and in a background of increased low-level (2.6%) autosomal homozygosity, consistent with a reported common ancestry in the family. FRY encodes a protein that regulates cell cytoskeletal dynamics, functions in chromosomal alignment in mitosis in vitro, and has been shown to function in the nervous system in vivo. Homozygous mutation of FRY has been previously reported in 2 consanguineous families from studies of autosomal recessive ID in Middle Eastern and Northern African populations. This report provides additional supportive evidence that deleterious biallelic mutation of FRY is associated with ID/DD and illustrates the utility of genomic SNP microarray detection of low-level homozygosity.


2002 ◽  
Vol 63 (3-6) ◽  
pp. 451-454 ◽  
Author(s):  
Makoto Miyahara ◽  
Akiko Saito ◽  
Hitoshi Ito ◽  
Masatake Toyoda

2018 ◽  
Vol 49 (3) ◽  
pp. 1151-1167 ◽  
Author(s):  
Yuhang Sun ◽  
Zixuan Liu ◽  
Dandan Liu ◽  
Jin Chen ◽  
Fang Gan ◽  
...  

Background/Aims: Swine influenza virus (SIV) is a major pathogen of both animals and humans. Afatoxin B1 (AFB1) is one of the most common mycotoxins in feed and food. However, the central contribution of AFB1 to SIV infection remains unclear. Methods: Here, TCID50 assays, fluorescence-based quantitative real-time PCR, western blotting, immunofluorescence staining, histopathological examination, flow cytometry and scanning electron microscopy were performed to investigate the involvement and underlying mechanism of AFB1 in SIV infection in vivo and in vitro using mouse models and porcine alveolar macrophage (PAM) models, respectively. Results: The in vivo study showed that low levels of AFB1 promoted SIV infection and increased its severity, as demonstrated by the increased mRNA expression of viral matrix protein (M); by the increased protein expression of nucleoprotein (NP), matrix protein 1 and ion channel protein; and by animal weight loss, lung index and lung histologic damage. In addition, the increased occurrence of SIV infection accompanied by increases in the level of IL-10 in sera and lungs, in the spleen index and in the number of CD206-positive mouse alveolar macrophages but decreases in the level of TNF-α in sera and lungs, in the thymus index and in the number of CD80-positive mouse alveolar macrophages was observed in SIV-infected mice after low-level AFB1 exposure. The in vitro study showed that low concentrations of AFB1 promoted SIV infection, as demonstrated by the increases in viral titers and viral M mRNA and NP expression levels in SIV-infected PAMs as well as by the number of cells positive for NP protein expression. Furthermore, AFB1 promoted the polarization of SIV-infected PAMs to the M1 phenotype at 8 hpi and to the M2 phenotype at 24 hpi, as measured by the increases in IL-10 expression and in the number of CD206-positive PAMs as well as by the morphological changes observed by scanning electron microscopy. The administration of the immune stimulant lipopolysaccharide (LPS) reversed the switch in PAM polarization from M2 to M1 and thereby counteracted the promotion of influenza virus infection induced by AFB1. Conclusion: Our results are the first to confirm that low-level exposure to AFB1 promotes SIV infection and modulates a switch in macrophage polarization from M1 to M2. The work reported here provides important data that point to a role for AFB1 in SIV infection, and it opens a new field of study.


Retrovirology ◽  
2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Christine M. Fennessey ◽  
Celine Camus ◽  
Taina T. Immonen ◽  
Carolyn Reid ◽  
Frank Maldarelli ◽  
...  

1988 ◽  
Vol 86 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Gillian R. Cookman ◽  
Susan E. Hemmens ◽  
Gary J. Keane ◽  
William B. King ◽  
Ciaran M. Regan

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