Injuries associated with the cartilages of the foot

There is a growing body of evidence that uniaxial or biaxial ossification of the cartilages of the foot should not be discounted as irrelevant in a lame horse, especially if extensive. Potential causes of pain and lameness include primary injury of an ossified cartilage and/or the ipsilateral aspect of the distal phalanx, injury of the chondrocoronal or chondrosesamoidean ligaments and desmopathy of the collateral ligaments of the distal interphalangeal joint.     

Injury Induces a Change in the Functional Characteristics of Cells Recovered from Equine Tendon

Injury initiates a repair process characterized by influx of fibroblasts and the rapid formation of fibrous scar tissue and subsequent tissue contraction. The response to injury and behavior of the different tendon fibroblast populations, however, has been poorly characterized. We hypothesized that the fibroblasts recovered from tendon with acute injury would exhibit different cell properties relating to adhesion, migration and tensegrity. To test this hypothesis we evaluated the ability of fibroblasts recovered from normal and injured equine superficial digital flexor tendons (SDFTs). The injured tendon-derived cells showed greater contraction of the collagen gel but poorer adhesion to pepsin-digested collagen, and migration over extracellular matrix proteins compared to normal SDFT-derived fibroblasts. Thus, the cells present within the tendon after injury display different behavior related to wound healing.     

Differential response of zucchini varieties to low storage temperature

Several parameters related to cold damage in zucchini have been measured in fruits from different varieties cultivated in the province of Almería (south-eastern Spain). The purpose of this work is to correlate physiological parameters with commercial quality and chilling damage, in order to establish reliable criteria for selecting varieties having better genetic adaptation to low-temperature storage. The results show that, for varieties harvested during February, the variety Natura was the best adapted to storage at 4 °C, as its fruits suffered less from chilling injuries, had a lower weight loss, and the levels of metabolites malonyldialdehyde and H₂O₂ were not as high as in the other varieties. Genetic variation was detected for some of the parameters analysed. The positive correlation among the levels of MDA, H₂O_2, and chilling injury, as well as the negative correlation among catalase and chilling injury, makes these parameters good indicators of chilling damage in our system.     

Effect of ischemic post-conditioning on myocardial mitochondrial function in isolated rat heart

AIM: To investigate the protective effect of ischemic post-conditioning on isolated rat myocardial mitochondrial function during ischemia/reperfusion, and to study the role of mitochondrial ATP-sensitive potassium channel (mitoK_ATP) in myocardial protection. METHODS: Sprague-Dawley male rats were randomized into 4 groups (n=8 in each group): control group (C), model group (M), ischemic post-conditioning group (IPO) and 5-hydroxydecanoate plus IPO group (5-HD+IPO). The hearts isolated from the SD rats were mounted on a Langendorff apparatus and started with a 20-minute perfusion for equilibration. In C group, the hearts went on perfusion for another 70 min after equilibration. In M group, 4 ℃ St. Thomas cardioplegic solution was administered prior to ischemia, followed by ischemia for 40-minute, and reperfusion for another 30 min. In IPO group, the hearts underwent 40-minute global ischemia after equilibration, then perfusion for 10 s and ischemia for another 10 s. The procedure was repeated 6 times before 28-minute reperfusion. In 5-HD+IPO group, the hearts were perfused with 5-HD (100 μmol/L in K-H solution) and treated as that in IPO group, then reperfusion for 23 min. The reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and respiratory function of myocardial mitochondria were measured at the ends of equilibration and reperfusion. RESULTS: (1) Compared with the data collected at the end of equilibrium, the MMP was obviously decreased at the end of reperfusion in all groups, The highest in C group. MMP in 5-HD+IPO group was markedly higher than that in IPO group and M group. MMP in IPO group was higher than that in M group. (2) In contrast to that at the end of equilibrium, ROS was obviously increased at the end of reperfusion in all groups. However, ROS was observably higher in M group than that in the other 3 groups, and ROS in 5-HD+IPO group was markedly higher than that in IPO group and C group. ROS in IPO group was higher than that in C group. (3) The respiratory function of mitochondria was obviously injured at the end of reperfusion in all groups. The arrangement of the mitochondrial respiratory function from the best to the worse was C group > IPO group > 5-HD+IPO group > M group. CONCLUSION: Ischemic post-conditioning attenuates myocardial reperfusion injury by maintaining the stability of MMP, decreasing the generation of ROS and preserving the respiratory chain function of mitochondria. The mitoK_ATP antagonist 5-HD can not completely block the myocardial protective effect of ischemic post-conditioning. Myocardial protective effect of ischemic post-conditioning may achieve by activating mitoK_ATP, meanwhile the other factors may also take part in the myocardial protective processes.     

Protective effect of recombinant SCR15-18 domain of human complement receptor type 1 on intestinal ischemia and reperfusion injury

AIM: To investigate the protective effect of recombinant SCR15-18 domain of human complement receptor type 1 (CR1-SCR-15-18) on intestinal ischemia and reperfusion in a rat model. METHODS: Sprague-Dawley rats were randomly divided into 3 groups: sham operation(SO) group, ischemia and reperfusion (I/R) group and CR1-SCR15-18 treatment group. The superior mesenteric artery of the rats was clamped for 30 min followed by 60 min of reperfusion. PBS alone or CR1-SCR15-18 protein (30 mg/kg) in PBS was intravenously administered 5 min before reperfusion. Intestinal vascular permeability, myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. The histopathological changes of intestinal mucosa were examined by HE staining and complement 3 was detected by immunohistochemical analysis. RESULTS: Compared with SO group, the vascular permeability, the activity of MPO and the content of MDA in I/R group were significantly increased, and the activity of SOD was decreased. HE staining demonstrated that I/R induced severe intestinal histological damages and the increased amount of complement 3 and its derivates were deposited in the necrosis area. Compared with I/R group, the vascular permeability, the activity of MPO and the content of MDA were decreased and the activity of SOD was significantly increased in CR1-SCR15-18 treatment group. CR1-SCR15-18 also significantly attenuated intestinal histological injury, and reduced the deposition of complement 3 and its derivates in the necrosis zone. CONCLUSION: sCR1-SCR15-18 protein exerts a protective effect against intestinal I/R injury in rats, possibly by inhibiting the activation of complement.     

Effect of autophagy in traumatic brain injury

Autophagy is a metabolic process of eukaryotic cells. When lacking of nutrient and energy, the cells obtain biosynthetic materials by degrading the organelles and recycling the proteins to maintain homeostasis. Traumatic brain injury (TBI) is a common kind of mechanic injury, usually with a poor outcome. Accumulated evidence indicates that the activity of autophagy increases after TBI. However, its implication for nervous tissue is still controversy. On one hand, autophagy exerts a protective effect on the neural cells. On the other hand, autophagy can also induce cell death exacerbating neural injury. This review focuses on the processes of autophagy and its roles in TBI, which may provide some novel therapeutic strategies.