An animal model of Kashin–Beck disease induced by a low-nutrition diet and exposure to T-2 toxin

Kang, Pengde; Yao, Y F; Yang, Jing; Shen, Bo; Zhou, Zongke; Pei, Fuxing

doi:10.1016/j.joca.2013.05.005

Cited by 27 publications

(25 citation statements)

References 27 publications

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“…A recent study also showed that the NOD2 deficiency mice protect from Ag-induced arthritis characterized by cartilage degradation 30 , and activated NOD2 could also promote and exacerbate the inflammation in proteoglycan-induced arthritis mice 31,32 . In fact, we also found the expression of NOD2 increased in articular chondrocyte from T-2 treated rats which show similar pathological changes to KBD patients 17 . These findings imply the importance of NOD2 in the cartilage damage of arthritis.…”

Section: Discussionsupporting

confidence: 78%

NOD2 pathway via RIPK2 and TBK1 is involved in the aberrant catabolism induced by T-2 toxin in chondrocytes

Jiang

Zhu

et al. 2015

Osteoarthritis and Cartilage

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Section: Discussionsupporting

confidence: 78%

NOD2 pathway via RIPK2 and TBK1 is involved in the aberrant catabolism induced by T-2 toxin in chondrocytes

Jiang

Zhu

et al. 2015

Osteoarthritis and Cartilage

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“…This disease was initially reported in Russia by Kashin then Beck in 1848 and 1906, respectively (Allander 1994), where it was later proposed to be caused by a mycotoxin. Current focus on KBD is in northeastern and southwestern China, where it is endemic, affecting approximately 2.5 million people in 15 provinces (Kang et al 2013). Disease onset begins in children between the ages of 4 and 13 years, with boys being more susceptible than girls (Zhai et al 1990).…”

Section: Kashin-beck Diseasementioning

confidence: 99%

Public Health Impacts of Foodborne Mycotoxins

Groopman

Pestka

2014

Annu. Rev. Food Sci. Technol.

497

314

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Mycotoxins are toxic and carcinogenic metabolites produced by fungi that colonize food crops. The most agriculturally important mycotoxins known today are aflatoxins, which cause liver cancer and have also been implicated in child growth impairment and acute toxicoses; fumonisins, which have been associated with esophageal cancer (EC) and neural tube defects (NTDs); deoxynivalenol (DON) and other trichothecenes, which are immunotoxic and cause gastroenteritis; and ochratoxin A (OTA), which has been associated with renal diseases. This review describes the adverse human health impacts associated with these major groups of mycotoxins. First, we provide background on the fungi that produce these different mycotoxins and on the food crops commonly infected. Then, we describe each group of mycotoxins in greater detail, as well as the adverse effects associated with each mycotoxin and the populations worldwide at risk. We conclude with a brief discussion on estimations of global burden of disease caused by dietary mycotoxin exposure.

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“…MRI is generally accepted as the best method to show epiphyseal plate and cartilage, but there is no report about observations of early lesions of the epiphyseal plate or epiphyseal end in a rat model of KBD with 7.0 T MRI. This model of KBD induced by a low-nutrition diet and T-2 toxin exposure could demonstrate radiographic and histopathological abnormalities of the proximal epiphyseal plate and the tibial metaphysis that are very similar to the bony changes found in patients with KBD [23]. Four weeks old Wistar rats are usually selected in this model given the fact that KBD mainly invades the developing bone during endochondral ossification in children.…”

Section: Introductionmentioning

confidence: 99%

“…Four weeks old Wistar rats are usually selected in this model given the fact that KBD mainly invades the developing bone during endochondral ossification in children. Therefore, in this study, ultra-high field MRI technology was used to study the knee joint MRI of a rat KBD model [23] and compare with X-ray imaging to summarize and analyze the possible MRI manifestations of KBD rat model. Tthe study also aimed to explore ways to determine the pathological damage of KBD rat model in the early stage to further provide a method for etiological research on and the prevention and treatment of KBD.…”

Section: Introductionmentioning

confidence: 99%

Magnetic resonance imaging at 7.0 T for evaluation of early lesions of epiphyseal plate and epiphyseal end in a rat model of Kashin-Beck disease

Kang

Zhou

et al. 2020

BMC Musculoskelet Disord

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Background: Kashin-Beck disease (KBD) is a disabling osteoarticular disease involving growth and joint cartilage. Early diagnosis can effectively prevent the progress of the disease. However, the early diagnosis of it is still very difficult. Our aim was to study the knee joint lesions of a rat KBD model using ultra-high field magnetic resonance imaging (MRI) and compare it with X-ray imaging to analyze the possible MRI manifestations of KBD, and to further explore ways to determine the pathological damage of KBD in the early stage. Methods: A total of 96 Wistar rats were selected and randomly divided into 4 groups: normal diet (Group A), KBDaffected diet (Group B), normal diet+T-2 toxin (Group C), and KBD-affected diet+T-2 toxin (Group D). T-2 toxin was administered at a dose of 0.1 mg/kg/day. In the 4th week, 8th week, and 12th week, eight rats randomly selected in each group were sacrificed by cervical dislocation after undergoing X-ray and 7.0 T MRI imaging, and then knee joints were harvested, sliced, and subjected to hematoxylin-eosin (H&E) staining. Results: Characteristic image changes including of continuity interruption and early closure and fusion of epiphyseal plates were observed on T1WI in rat model of KBD. The total necrosis rates in the H&E stain of group A to group D were 4.35, 52.38, 33.3, and 73.68%, respectively. The positive rate of image change under 7.0 T MRI was 0.833 VS. that under X-ray was 0.33 (P = 0.001). Conclusions: MRI at 7.0 T is highly sensitive to the early pathological changes of the epiphysis, epiphyseal plate, and metaphyseal end, which can improve imaging positive rate of KBD and decrease the rate of missed diagnosis. This imaging modality can be used for research on early joint lesions and for early diagnosis of KBD.

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An animal model of Kashin–Beck disease induced by a low-nutrition diet and exposure to T-2 toxin

Cited by 27 publications

References 27 publications

NOD2 pathway via RIPK2 and TBK1 is involved in the aberrant catabolism induced by T-2 toxin in chondrocytes

NOD2 pathway via RIPK2 and TBK1 is involved in the aberrant catabolism induced by T-2 toxin in chondrocytes

Public Health Impacts of Foodborne Mycotoxins

Magnetic resonance imaging at 7.0 T for evaluation of early lesions of epiphyseal plate and epiphyseal end in a rat model of Kashin-Beck disease

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