Mid-infrared fiber spectroscopy for detection of cartilage degeneration in osteoarthritis (Conference Presentation)

Author(s):  
Olga A. Bibikova ◽  
Valentin Mironovich ◽  
Iskander Usenov ◽  
Elena Feliksberger ◽  
Alexey Bocharnikov ◽  
...  
Author(s):  
Rubina Shaikh ◽  
Ervin Nippolainen ◽  
Vesa Virtanen ◽  
Lassi Rieppo ◽  
Julian Haas ◽  
...  

2005 ◽  
Vol 14 ◽  
pp. 337-342 ◽  
Author(s):  
M. Dolci ◽  
G. Valentini ◽  
O. Straniero ◽  
G. Di Rico ◽  
M. Ragni ◽  
...  

1999 ◽  
Vol 12 (02) ◽  
pp. 56-63 ◽  
Author(s):  
C. R. Bellenger ◽  
P. Ghosh ◽  
Y. Numata ◽  
C. Little ◽  
D. S. Simpson

SummaryTotal medial meniscectomy and caudal pole hemimeniscectomy were performed on the stifle joints of twelve sheep. The two forms of meniscectomy produced a comparable degree of postoperative lameness that resolved within two weeks of the operations. After six months the sheep were euthanatised and the stifle joints examined. Fibrous tissue that replaced the excised meniscus in the total meniscectomy group did not cover as much of the medial tibial condyle as the residual cranial pole and caudal fibrous tissue observed following hemimeniscectomy. The articular cartilage from different regions within the joints was examined for gross and histological evidence of degeneration. Analyses of the articular cartilage for water content, glycosaminoglycan composition and DNA content were performed. The proteoglycan synthesis and release from explanted articular cartilage samples in tissue culture were also measured. There were significant pathological changes in the medial compartment of all meniscectomised joints. The degree of articular cartilage degeneration that was observed following total meniscectomy and caudal pole meniscectomy was similar. Caudal pole hemimeniscectomy, involving transection of the meniscus, causes the same degree of degeneration of the stifle joint that occurs following total meniscectomy.The effect of total medial meniscectomy versus caudal pole hemimeniscectomy on the stifle joint of sheep was studied experimentally. Six months after the operations gross pathology, histopathology, cartilage biochemical analysis and the rate of proteoglycan synthesis in tissue culture were used to compare the articular cartilage harvested from the meniscectomised joints. Degeneration of the articular cartilage from the medial compartment of the joints was present in both of the groups. Caudal pole hemimeniscectomy induces a comparable degree of articular cartilage degeneration to total medial meniscectomy in the sheep stifle joint.


2018 ◽  
Author(s):  
Y. H. Kan ◽  
Changying Zhao ◽  
Zhuomin M. Zhang

2011 ◽  
Vol 28 (1) ◽  
pp. 33-48 ◽  
Author(s):  
Oto Hanuš ◽  
Václava Genčurová ◽  
Yunhai Zhang ◽  
Pavel Hering ◽  
Jaroslav Kopecký ◽  
...  

Milk acetone determination by the photometrical method after microdiffusion and via FT infra-red spectroscopyMilk acetone (AC) and betahydroxybutyrate (BHB) are important indicators of the energy metabolism of cows (ketosis occurrence) and an effective method for their determination, with reliable results, is of great importance. The goal of this work was to investigate the infrared method MIR-FT in terms of its calibration for milk AC and to develop a usable procedure. The microdiffusion photometric (485 nm; Spekol 11) method was used with salicylaldehyde as a reference (Re) and mid infrared spectroscopy FT (MIR-FT: Lactoscope FT-IR, Delta; MilkoScan FT 6000, M-Sc) as an indirect method. The acetone addition to milk had no recovery using MIR-FT (Delta). The reference AC set must have acceptable statistics for good MIR-FT calibration (M-Sc) and they were: 10.1 ± 9.74 at a geometric mean of 7.26 mg l-1, and a variation range from 1.98 to 33.66 mg l-1. The AC correlation between Re and MIR-FT (Delta) was low at 0.32 (P>0.05 but the Log AC relationship between Re and MIR-FT (M-Sc) was markedly better at 0.80 (P<0.01). The conversion of >10 mg l-1 as an AC subclinical ketosis limit could be > -0.80 (feedback 0.158 mmol l-1 = 9.25 mg l-1) and > -1.66. This could be important for ketosis monitoring (using M-Sc).


2008 ◽  
Vol 31 (4) ◽  
pp. 2
Author(s):  
Tom Appleton ◽  
Shirine Usmani ◽  
John Mort ◽  
Frank Beier

Background: Articular cartilage degeneration is a hallmark of osteoarthritis (OA). We previously identified increased expression of transforming growth factor alpha (TGF?) and chemokine (C-C motif) ligand 2 (CCL2) in articular cartilage from a rat modelof OA (1,2). We subsequently reported that TGF? signalling modified chondrocyte cytoskeletal organization, increased catabolic and decreased anabolic gene expression and suppressed Sox9. Due to other roles in chondrocytes, we hypothesized that the effects ofTGF? on chondrocytes are mediated by Rho/ROCK and MEK/ERK signaling pathways. Methods: Primary cultures of chondrocytes and articularosteochondral explants were treated with pharmacological inhibitors of MEK1/2(U0126), ROCK (Y27632), Rho (C3), p38 MAPK (SB202190) and PI3K (LY294002) to elucidate pathway involvement. Results: Using G-LISA we determined that stimulation of primary chondrocytes with TGF? activates RhoA. Reciprocally, inhibition of RhoA/ROCK but not other signalling pathways prevents modification of the actin cytoskeleton in responseto TGF?. Inhibition of MEK/ERKsignaling rescued suppression of anabolic gene expression by TGF? including SOX9 mRNA and protein levels. Inhibition of MEK/ERK, Rho/ROCK, p38 MAPK and PI3K signalling pathways differentially controlled the induction of MMP13 and TNF? gene expression. TGF? also induced expression of CCL2 specifically through MEK/ERK activation. In turn, CCL2 treatment induced the expression of MMP3 and TNF?. Finally, we assessed cartilage degradation by immunohistochemical detection of type II collagen cleavage fragments generated by MMPs. Blockade of RhoA/ROCK and MEK/ERK signalling pathways reduced the generation of type IIcollagen cleavage fragments in response to TGF? stimulation. Conclusions: Rho/ROCK signalling mediates TGF?-induced changes inchondrocyte morphology, while MEK/ERK signalling mediates the suppression ofSox9 and its target genes, and CCL2 expression. CCL2, in turn, induces the expression of MMP3 and TNF?, two potent catabolic factors known to be involved in OA. These pathways may represent strategic targets for interventional approaches to treating cartilage degeneration in osteoarthritis. References: 1. Appleton CTG et al. Arthritis Rheum 2007;56:1854-68. 2. Appleton CTG et al. Arthritis Rheum 2007; 56:3693-705.


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