The trial was registered at clinicaltrials.gov (NCT01700855).

This study indicates that TSN pretreatment reduces infarct size and improves cardiac dysfunction after I/R injury in diabetic rats. This was accompanied with decreased cardiac apoptosis and inflammation. The possible mechanism responsible for the effects of TSN is associated with the PI3K/Akt-dependent pathway.

SummaryElectroacupuncture has been demonstrated to be effective at alleviating pain and postoperative side-effects. Our aim was to investigate whether transcutaneous electric acupoint stimulation, a low-skill alternative to needle-based electroacupuncture, could improve the quality of recovery after ambulatory surgery. Seventy-two women scheduled for cosmetic breast surgery were randomly allocated to transcutaneous electric acupoint stimulation or sham groups. Patients in the transcutaneous electric acupoint stimulation group received 30 min of electrical stimulation at three acupoints located on the hand and forearm before the induction of general anaesthesia. We found significant mean (SD) differences between the transcutaneous electric acupoint stimulation and sham groups in the mean (SD) length of recovery room stay (35.6 (12.9) min vs 48.3 (16.3) min, p = 0.01), time to removal of the laryngeal mask airway (10.2 (2.5) min vs 17.8 (4.4) min, p = 0.01), and time to reorientation of the patient (14.6 (3.2) min vs 26.5 (5.0) min, p = 0.01). Further, postoperative pain scores and the incidence of side-effects were all lower in the transcutaneous electric acupoint stimulation group. In conclusion, transcutaneous electric acupoint stimulation can significantly improve the quality of recovery and decrease the incidence of anaesthesia-related side-effects for patients undergoing ambulatory surgery.

Objective To investigate whether mechanical stress induces mineral deposits that contribute to matrix degradation at the onset of osteoarthritis (OA) in temporomandibular joint (TMJ) cartilage. Design Female Spragueee–Dawley rats were subjected to an unilateral anterior crossbite (UAC) procedure. Histology, electron microscopy, and energy dispersive spectrometer (EDS) were used to examine cartilage matrix structures and composition of mineral deposit in the affected TMJ cartilage. Protein and/or RNA expression of phenotypic markers and mineralization modulators and matrix degradation was analyzed by immunohistochemistry and/or real-time PCR. Synthetic basic calcium phosphate (BCP) and calcium pyrophosphate dehydrate (CPPD) crystals were used to stimulate ATDC5 cells for their impact on cell differentiation and gene expression. Results Fragmented and disorganized collagen fibers, expanded fibrous spaces, and enhancement of matrix vesicle production and mineral deposition were observed in matrices surrounding hypertrophic chondrocytes in cartilage as early as 2-weeks post-UAC and exacerbated with time. The mineral deposits in TMJ cartilage at 12- and 20-weeks post-UAC had Ca/P ratios of 1.42 and 1.44, which are similar to the ratios for BCP. The expression of mineralization inhibitors, NPP1, ANK, CD73, and Matrix gla protein (MGP) was decreased from 2 to 8 weeks post-UAC, so were the chondrogenic markers, Col-2, Col-X and aggrecan. In contrast, the expression of tissue-nonspecific alkaline phosphatase (TNAP) and MMP13 was increased 4-weeks post-UAC. Treating ADTC5 cells with BCP crystals increased MMPs and ADAMTS5 expression, but reduced matrix production in a time-dependent manner. Conclusion UAC induces deposition of BCP-like minerals in osteoarthritic cartilage, which can stimulate matrix degradation by promoting the expression of cartilage-degrading enzymes to facilitate OA progression.