Objective To investigate the expressions of matrix metalloproteinases(MMPs) in Kashin-Beck disease(KBD) cartilage as well as in a KBD rat model of T-2 toxin poisoning under selenium deficient conditions, and to investigate the effect of T-2 toxin on MMP-13 expression in human chondrocytes in vitro in order to determine a possible mechanism underlying KBD. Methods Samples of articular cartilage were divided into 2 groups:controls(samples from 5 normal children, traffic accident or operation), and KBD(samples from 5 children with KBD, auctopsy). Thirty-two Sprague-Dawley rats were divided into two groups by body weight using random number table: normal diet group(n = 16) and selenium-deficient diet group(n=16). The selenium level in normal diet was 101.500μg/kg, and in selenium-deficient diet was 1.118μg/kg. Rats were fed for 4 weeks with selenium-deficient or normal diet, respectively. After successful build up of the low selenium rat model, normal diet group was then subdivided into 2 sub-groups: normal group(n = 8) and normal diet plus low T-2 toxin group(n = 8);and selenium-deficient diet group was also subdivided into 2 sub-groups: selenium-deficient group ( n = 8 ) and selenium-deficient diet plus T-2 toxin group ( n = 8 ) . T-2 toxin of 100 μg·kg-1·d-1 was administered by intragastric administration for 30 days. Then the rats were sacrificed, and their knee joints were processed for histopathological evaluation. MMP-1 and MMP-13 locations in cartilages were performed by inmmunohistochemistry. Human chondrocytes C28/I2 were cultured in vitro. The experiment was divided into 4 groups: empty vector plasmid group, MMP-13 promoter plasmid group, MMP-13 promoter plasmid plus 20 μg/L T-2 toxin group and MMP-13 promoter plasmid plus 40 μg/L T-2 toxin group. MMP-13-luciferase reporter plasmid and vector plasmid were transiently transfected into C28/I2 cells for 24 hours, and then treated with 20 - 40 μg/L T-2 toxin for 24 hours. Transactivation of human MMP-13 promoter was analyzed using luciferase reporter constructs containing sequences spanning-1602 to+20 bp in C28/I2 chondrocytes. Results The percentages of chondrocytes staining for MMP-1 in the superficial and middle zones of KBD samples [(29.73 ± 10.12)%, (28.27 ± 0.91)%] were significantly higher than those of controls[(2.47 ± 0.11)%, (0.00 ± 0.00)%, all P < 0.05]. The percentages of chondrocytes staining for MMP-13 in the superficial and middle zones of KBD samples [(13.21 ± 4.32)%, (41.85 ± 6.32)%] were significantly higher than those of controls[(5.72 ± 0.31)%, (0.00 ± 0.00)%, all P<0.05]. The percentages of chondrocytes staining for MMP-13 in the superficial and middle zones of rats fed with selenium-deficient diet plus T-2 toxin group[(13.21 ± 4.32)%, (61.85 ± 8.68)%] were significantly higher than those of the normal and selenium-deficient groups[(2.43 ± 0.22)%, (5.89 ± 0.69)%, (3.03 ± 0.29)%, (25.99 ± 0.57)%, all P < 0.05]. Moreover, T-2 toxin activated the MMP-13 promoter detected with luciferase reporter assays in C28/I2 cells. The luciferase activities in MMP-13 promoter plasmid plus 20 μg/L T-2 toxin group and MMP-13 promoter plasmid plus 40μg/L T-2 toxin group(0.082 78 ± 0.008 40, 0.103 35 ± 0.013 19) were significantly higher than those in empty vector plasmid group and MMP-13 promoter plasmid group(0.024 19 ± 0.000 96, 0.040 32 ± 0.003 56, all P < 0.05). Conclusions These data suggest that T-2 toxin induces cartilage matrix degradation through up-regulation of MMP-13 promoter expression. Increased MMPs staining intensity in KBD cartilage and the rat KBD model of T-2 toxin poisoning under selenium deficient conditions suggest that matrix degradation appear to be driven by MMPs activity.

Objective To study the change of rats serum malondialdehyde (MDA) and the expression levels of 4-hydroxy acid nonene (4-HNE) and 8-hydroxy uridine (8-OHdG) of articular cartilage under low selenium (Se) and T-2 toxin poisoning,to explore oxidative damage of articular cartilage in rats.Methods Thirtytwo healthy male SD rats were divided into two groups by weight which were normal diet group and Se-deficiency group,16 rats in each group.Rats in normal diet group was fed with selenium 101.5 μg/kg diet,and rats in Sedeficiency group was fed with selenium 1.1 μg/kg diet for 30 d.Normal diet group was divided into control group and T-2 toxin group,and low selenium diet group was randomly divided into Se-deficiency group and Se-deficiency plus T-2 toxin group,8 rats in each group.After that,rats in T-2 toxin and Se-deficiency plus T-2 toxin groups were administrated intragastrically with T-2 toxin (100 mg/kg) everyday for 30 d.Rats were put to death,the left knee was taken and stained with hematoxylin-eosin and Safranin-Fast green,pathological changes of rat's knee joint cartilage were observed under light microscopy,expression levels of 8-OHdG and 4-HNE in rat's articular cartilage cells were determined by immunohistochemical method and rat's MDA content was determined by glucosinolates barbituric acid method.Results Chondronecrosis in deep zone of articular cartilage of knee joint stained with hematoxylin-eosin was seen in Se-deficient plus T-2 toxin diet group under light microscope.Significantly less Safranin-Fast green staining was observed in the cartilage of knee joints in the Se-deficient plus T-2 toxin diet group compared to the control group.Compared with control group [(3.41 ± 2.48)％,(2.28 ± 1.74)％],8-OHdG and 4-HNE in Se-deficient plus T-2 toxin group [(62.61 + 10.97)％,(75.03 ± 7.92) ％] positive expression rate increased significantly (F =16.24,18.61,all P ＜ 0.05).Comparison of serum MDA content in each group,the difference was statistically significant (F =4.32,P ＜ 0.05).The Se-deficiency group [(2.803 ± 0.163) μmol/L] was compared with control group [(1.873 ± 0.475) μmol/L] that the contents of serum MDA were increased.The T-2 toxin group [(2.890 ± 0.453) μmol/L] was compared with control group [(1.873 ± 0.475) μmol/L] that the content of serum MDA was increased (P ＜ 0.05).The Se-deficiency plus T-2 toxin group [(3.521 ± 0.292) μmol/L] was compared with Sedeficiency group and control group that the contents of serum MDA were increased (all P ＜ 0.05).Conclusions The marker of peroxidation products are increased in articular cartilage of SD rats under the condition of Sedeficiency and T-2 toxin poisoning.The cartilage damage and chondronecrosis due to Se-deficiency and T-2 toxin poisoning are related to oxidative damage.

BACKGROUND:Papain-induced rat knee osteoarthritis is a common modeling method, which can obtain a stable osteoarthritis model.
OBJECTIVE:To observe the change of ultrastructure of chondrocytes in the early process of papain-induced rat knee osteoarthritis under transmission electron microscope.
METHODS:A total of 18 Sprague-Dawley rats were randomly divided into three groups. Two rats were considered as a normal control group, without intervention. The mixture of papain and L-cysteine was injected in right knee joint cavity of 16 rats to induce osteoarthritis models (osteoarthritis model group). Physiological saline was injected in the left side (physiological saline control group). At 1, 2, 4 and 6 weeks after injection, samples were col ected. Transmission electron microscope was used to observe the change of cartilage ultrastructure of the medial femoral condyle joint.
RESULTS AND CONCLUSION:For the normal control group and physiological saline control group, their cytoplasm contained abundant rough endoplasmic reticulum and mitochondria. After 1 week of injection,
mitochondria vacuoles and light expanded rough endoplasmic reticulum were visible. Two weeks later, lipid droplets appeared, mitochondria degeneration was distinct, vacuolization was serious and its number was reduced, and rough endoplasmic reticulum expansion was obvious. Four weeks later, lipid droplets became increased, and the number of mitochondria decreased significantly. Most of the rough endoplasmic reticula were highly expanded, and part of the rough endoplasmic reticula were dissolved and fractured. Six weeks later, a number of lipid droplets were visible in cytoplasm, most of the mitochondria disappeared, only a smal number of mitochondria existed, and most of the rough endoplasmic reticula were dissolved and fractured. These results confirmed that cartilage ultrastructure changes gradual y in the early process of papain-induced rat knee osteoarthritis under transmission electron microscope.

Effective cost control and structure optimization of medical consumables in public hospitals can facilitate a shift from extensive cost control to scientific and refine management.On the premise of ensuring medical quality,reducing the burden of patients'diagnosis and treatment and meeting the actual needs of hospital management,this approach aims to realize valuable healthcare outcomes.This study was conducted in a tertiary hospital,which balanced both the medical and economic val-ue of medical consumables.Using an integrated approach to specialty capacity building and disease structure optimization,the hospital restructured the use of medical consumables in Transcatheter Arterial Embolization(TAE)procedures.It developed standardized pathways and usage protocols tailored to specific diseases and surgical requirements.A targeted consumable usage policy framework was introduced,comprising"one department,one policy;one surgery type,one policy;and one consumable,one policy."This included initiatives such as validating the use of drug-loaded embolic microspheres,conducting multi-depart-mental review meetings,strictly regulating indications for these microspheres,limiting personnel involvement,and negotiating re-duced pricing on imported microspheres.Following implementation,the average case-mix index(CMI)for discharged patients undergoing TAE increased from 2.23 to 2.34(P＜0.001),while the average per-case cost of consumables decreased from 19 600 to 15 600(P＜0.001).These measures offer valuable decision-making and operational reference for hospitals nation-wide,supporting efficient,quality-focused consumables management.

Objective In the context of expanding in size and improving the quality of medical consumables,the"one product,one policy"approach has brought challenges to the management of consumables in public hospitals.This study investi-gated the potential management problems in the process of centralized procurement with volume of medical consumables in a pub-lic tertiary hospital in Guangdong Province,and accordingly worked out the corresponding management countermeasures and then assessed their implementation effects.Methods The fishbone diagrams was applied to systematically analyze the potential prob-lems in the implementation process of centralized procurement with volume of medical consumables.Targeted measures were worked out from May to July 2023 in the hospital.The time series data of centralized procurement of coronary stents,pacemak-ers,tubular/end-to-end anastomoses,and spinal products from December 2022 to December 2023 were analyzed.Changes in the monthly implementation rate and contract completion volume pre-and post-intervention were measured to evaluate the effectiveness of the intervention.Results The fishbone diagrams analysis revealed that the primary factors impeding procurement implementa-tion were internal system flaws,personnel management inadequacy,supply issues,and an absence of an information system.Post-intervention,the monthly implementation rate(t=-4.19,P＜0.05)and contract completion(t=-2.38,P＜0.05)significantly improved.Conclusion The implementation of intervention management for centralized procurement with volume of medical consumables can effectively promote the related implementation effect in the department.In the context of centralized pro-curement,clinical and health management personnel need to bolster their professionalism to ensure the procurement management efficiency and quality.It is crucial to deepen policy understanding and implementation,enhance production and distribution process supervision and disciplinary mechanisms,ensure multi-departmental coordination for supply security,and improve hospi-tal information systems and procurement platforms.