T-2 toxin-induced damage to articular cartilage in rats coincided with impaired autophagy linked to the HIF-1α/AMPK signaling axis.

T-2 toxin is one of the most toxic mycotoxins. People are primarily exposed to T-2 toxin through the consumption of spoiled food, typically over extended periods and at low doses. T-2 toxin can cause damage to articular cartilage. However, the exact mechanism is not fully understood. In this experiment, 36 male rats were divided into a control group, a solvent control group, and a T-2 toxin group. The rats in the T-2 toxin group were orally administered the toxin at a dosage of 100 ng/g BW/Day. The damage to articular cartilage and key proteins associated with the autophagy process and the HIF-1α/AMPK signaling axis was assessed at 4, 8, 12, and 16 weeks. Our findings indicate that T-2 toxin-induced damage to articular cartilage in rats coincided with impaired autophagy linked to the HIF-1α/AMPK signaling pathway. This study offers novel insights into the precise mechanism underlying T-2 toxin-induced damage to articular cartilage.

A study on atypical Kashin-Beck disease: an endemic ankle arthritis.

BACKGROUND: To study the epidemiological characteristics of atypical Kashin-Beck disease cases without characteristic hand lesions such as interphalangeal joint enlargement and brachydactyly and the characteristics of ankle joint lesions. METHODS: We investigated Kashin-Beck in the endemic villages in Heilongjiang Province. The patients were judged according to the "Diagnosis of Kashin-Beck Disease" (WS/T 207-2010). The severity of foot lesions was judged based on the changes of X-ray images. Residents of non-Kashin-Beck disease area were selected as normal controls in Jilin Province. RESULTS: A total of 119 residents over 40 years old were surveyed in a natural village in the non-endemic area. A total of 1190 residents over 40 years old were surveyed in 38 endemic areas of Kashin-Beck disease. A total of 710 patients with Kashin-Beck disease were detected, including 245 patients with grade I, 175 patients with grade II, 25 patients with grade III, and 265 atypical patients. Among all investigated patients, 92.0% (653/710) had ankle joint changes, and it was 80.0% (196/245) in grade I patients and 95.4% (167/175) in grade II. Varying degrees of ankle joint changes were found in both grade III and atypical patients. The grade of Kashin-Beck disease was correlated with the degree of ankle joint change (P < 0.001), and the correlation coefficient rs = 0.376. Atypical Kashin-Beck disease patients in mild and severe endemic area of Kashin-Beck disease were younger than those with typical Kashin-Beck disease. CONCLUSIONS: We found a correlation between the degree of ankle joint change and the grade of Kashin-Beck disease. The higher the grade of Kashin-Beck disease, the more serious the change of the ankle joint.

The urinary levels of CTX-II, C2C, PYD, and Helix-II increased among adults with KBD: a cross-sectional study.

BACKGROUND: Kashin-Beck disease (KBD) is an endemic osteoarthropathy, and its pathogenesis is still not entirely clear. Pathologically, many KBD changes are similar to those of osteoarthritis (OA). Therefore, this study aimed to identify changes in the levels of potential urinary biomarkers for OA, including C-telopeptide of type II collagen (uCTX-II), type II collagen cleavage neoepitope (uC2C), pyridinoline (uPYD), and uHelix-II, among adults with KBD. METHODS: Urinary samples of 83 external control (EC) subjects, 91 KBD patients, and 86 internal control (IC) subjects were tested by ELISA after the subjects completed a questionnaire and X-ray examination. RESULTS: The medians of the four markers in the KBD group were higher than those in the EC group and those in the IC group. The medians in the grade II KBD group were higher than those in the grade I group but were not statistically significant (P = 0.301, P = 0.408, P = 0.204, and P = 0.898 for uCTX-II, uC2C, uPYD, and uHelix-II, respectively). The area under the curve (AUC) of uCTX-II (0.775) was higher than that of the others (0.672, 0.639, and 0.628 for uC2C, uPYD, and uHelix-II, respectively). CONCLUSION: The levels of uCTX-II, uC2C, uPYD, and uHelix-II were elevated in adults with KBD and showed an increasing trend as the severity of KBD increased. The prediction accuracy of uCTX-II was more useful than that of the others for assisting in the diagnosis of KBD.

Serum levels of PIICP, PIIANP, and PIIBNP are decreased in patients with an endemic osteochondropathy, Kashin-Beck disease.

BACKGROUND: Kashin-Beck disease (KBD) is an endemic, chronic, degenerative osteoarthropathy. KBD is usually diagnosed by using X-ray image and clinical symptoms, lacking of serological biomarkers. The serum level of PIICP, PIIANP, and PIIBNP can specifically reflect the damage of the cartilage. So, in this study, the serum levels of PIICP, PIIANP, and PIIBNP were detected in order to determine whether they can be used as potential biomarkers for the diagnosis of KBD. METHOD: Using a status survey, the survey sites were selected in the KBD historical endemic areas and non-endemic areas in Jilin and Heilongjiang provinces. All local residents have undergone clinical examination, X-ray examination of the hands and knees, and questionnaire survey. A total of 554 people were surveyed, and 184 residents who are eligible for inclusion criteria were selected as our subjects. Fifty-six cases were diagnosed as KBD and 63 individuals were included as internal control and 65 subjects were included as external control. And blood samples of surveyed subjects were collected, and the serum was separated to detect the levels of PIICP, PIIANP, and PIIBNP by ELISA. Statistical analysis was performed using the SPSS software. RESULTS: There were no statistically significant differences in age and sex among the three groups. The Kruskal-Wallis H test showed that the serum levels of PIICP, PIIANP, and PIIBNP were significantly different among the three groups. Multiple comparisons using Dunnett's T3 test revealed that serum levels of PIICP, PIIANP, and PIIBNP were significantly lower in KBD patients than in internal and external control. However, there was no significant difference between the internal and external control. CONCLUSIONS: The results preliminarily indicated that the levels of PIICP, PIIANP, and PIIBNP in serum could reflect the abnormal synthesis of type II collagen in KBD patients and suggested that these indicators might be used as potential biomarkers for the diagnosis of KBD.

Surveys in Areas of High Risk of Iodine Deficiency and Iodine Excess in China, 2012-2014: Current Status and Examination of the Relationship between Urinary Iodine Concentration and Goiter Prevalence in Children Aged 8-10 Years.

OBJECTIVE: We aimed to evaluate goiter prevalence and iodine nutritional status in areas with high levels of water iodine; to monitor the prevalence of iodine deficiency disorders (IDD) in areas at high risk of IDD; and to compare the prevalence of goiter and urine iodine (UI) concentrations between children living in the two areas. METHODS: Based on surveillance from 2012-2014, we analyzed the concentration of UI and prevalence of goiter in 8-10-year-old children from 12 high-risk IDD provinces, and from 8 provinces and municipalities with excessive water iodine. We calculated goiter prevalence for each UI level according to World Health Organization (WHO) standards and constructed predictive prevalence curves. RESULTS: The goiter prevalence and median UI of children from areas with high water iodine were not optimal, being above the WHO standards (5% and 100-199 µg/L, respectively), whereas those in high-risk areas fell within the standard. UI and goiter prevalence exhibited a U-shaped relationship in high-risk endemic areas and a parabolic relationship in areas of iodine excess. CONCLUSION: Iodine surplus in high-iodine areas leads to high goiter prevalence and UI. However, in high-risk areas, UI was optimal and goiter prevalence met the national criteria for IDD elimination.

Iodine Intake Increases IP-10 Expression in the Serum and Thyroids of Rats with Experimental Autoimmune Thyroiditis.

Here, we sought to establish an experimental autoimmune thyroiditis rat model induced by bovine thyroglobulin (bTg) injection and to investigate pathological changes and variations in serum interferon- γ -inducible protein of 10 kDa (IP-10) in thyroid tissue following iodine treatment. Four-week-old female Lewis rats (n = 135) were randomly divided into normal (NC), thyroglobulin (TG), HI, HI+TG, HII, and HII+TG groups; rats in the NC and TG groups drank only distilled water (iodine concentration: 10 µ g/L), rats in the HI and HI+TG groups were given water containing 25.7 mg/L iodine, and rats in the HII and HII+TG groups were given water containing 423.3 mg/L iodine. Rats in the TG, HI+TG, and HII+TG groups were immunized with 0.1 mL bTg (8 mg/mL) in incomplete Freund's adjuvant once every 2 weeks for 6 weeks. Compared with the NC group, the TG, HI+TG, and HII+TG groups exhibited higher iodine intake and increased thyroid weights with increasing iodine doses (P < 0.05). The high iodine intake in the TG group was associated with increased CD4(+) T cells and serum IP-10. Thus, high iodine consumption aggravated the inflammatory reaction in the thyroid and mild high iodine consumption increased serum IP-10 levels after induction with bTg.