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OBJECTIVE To establish the characteristic chromatogram of Chaenomeles sinensis， determine the contents of rutin， hyperin and quercitrin， and to identify C. sinensis and C. speciosa. METHODS HPLC method was performed on Agilent 5 TC-C18 column， with acetonitrile-0.2% formic acid solution as the mobile phase for gradient elution， at the flow rate of 1.0 mL/min. The column temperature was 30 ℃ . The detection wavelength was 330 nm in characteristic chromatogram and 350 nm in content determination. The characteristic chromatogram of C. sinensis was established and similarity was evaluated by the Similarity Evaluation System for Chromatographic Fingerprint of TCM （2012 edition）. Hierarchical cluster analysis of 15 batches of C. sinensis （S1-S15） was performed by using SPSS 23.0 software. The contents of 3 flavones in 15 batches of C. sinensis and 7 batches of C. speciosa （S16-S22） were determined， while their characteristic chromatograms were compared. RESULTS The similarities of the characteristic chromatogram for 15 batches of C. sinensis ranged from 0.783 to 0.969， and 11 characteristic peaks were confirmed. Four constituents were identified as chlorogenic acid， rutin， hyperin and quercitrin. The medicinal materials in 15 batches of C. sinensis could be divided into 2 categories： S5-S8 were one category， and the others belonged to one category. The characteristic chromatogram of C. sinensis was obviously different from C. speciosa. The contents of rutin， hyperin and quercitrin in 15 batches of C. sinensis were 48.99-294.45， 3.49-102.55， 31.98-149.49 μg/g， respectively. The content of rutin in C. speciosa was lower than that in C. sinensis. None of hyperin （except for S20） and quercitrin were detected in C. speciosa. CONCLUSIONS The characteristic chromatogram and the method for content determination of 3 flavones in C. sinensis are established successfully and can be used for the quality control of C. sinensis and its identification from C. speciosa.
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The presence of tension blister often predicts severe soft tissue damage，which not only increases the risk of wound complications but also prolongs the surgical treatment time. However，the developed tension blister has been proposed as a potential decompressive approach for it may relieve the pressure of osteofascial compartment and improve the likelihood of relieving clinical symptoms，as well as avoid unnecessary surgery in cases of suspected osteofascial compartment syndrome. Recently，the osteofascial system has been increasingly recognized that associations were found between the tension blister and osteofascial self-release processing. Thus，the timing of blister occurrence and regression substantially influences physicians′ clinical decisions，making blister management as part of the treatment of fractures. In this review，the authors give an overview of the characteristics，mechanism，stress reduction effect，prevention，current treatment status and complications of the fracture-related tension blister，hoping to help orthopedic physicians understand and treat the tensile blister.
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Osteofascial compartment syndrome (OFCS) is clinically common and is well known to orthopedic surgeons.Clinicians attach great importance to OFCS because of its severe clinical consequences,and decompression of fascial compartment is often performed in emergency treatment.This article reviews the literature on the threshold of fascial compartment decompression proposed by many scholars in the past and discusses the problems in the clinical diagnosis of acute compartment syndrome,especially the inconsistent pressure thresholds as the indication for emergency decompression surgery.By observing calf fractures patients with tension blister,we found that the pressure of fascia decreased sharply upon the appearance of blisters.Meanwhile,the swelling gradually subsided as well as the clinical manifestations of pain and parasthsia.In view of the uncertainty of various thresholds of fascial decompression and self-decompression,the concepts of myofascial self-release law and muscle-swelling syndrome were first proposed.The author believes that when intracompartmental pressure rises to a point,some unknown mechanisms of fascia can achieve self-decompression.Therefore,no compartment syndrome will take place.We also emphasize that the ' muscle-swelling syndrome'should be strictly distinguished from the soft tissue necrosis caused by crush syndrome and acute limb vascular injury,so as to provide more precise treatment.We believe that without external restrictions such as casts,splints and compression bandages,the muscle-swelling syndrome can achieve self decompression by releasing the pressure in the compartment through tension blisters,and there is no need for fasciotomy.
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Aim To investigate the effect of sphingo-sine kinase 1 (SphK1 )on unilateral ureteral obstruc-tion(UUO)-induced tubulointerstitial fibrosis and ex-plore the possible mechanism.Methods The CD-1 mice were randomly divided into four groups:sham-op-eration group(Sham),PF-543 treatment control group (Sham +PF-543),model group(UUO)and PF-543 treatment group(UUO +PF-543).On 1 ,3,7 and 1 4 d after operation,eight mice were selected randomly from each group and sacrificed.The protein expressions of SphK1 ,mature TGF-β1 ,FN,ColⅠ,LC3,Beclin1 ,Atg5 and Atg1 2 were observed by Western blot.The histo-logical changes were examined by Masson′s trichrome stain.Immunhistochemistry was performed to measure the levels of expression of SphK1 ,FN and Col Ⅰ. Transmission electron microscope was used to observe the autophagic body.Results SphK1 expression and autophagy were both upregulated in a mouse model of kidney fibrosis induced by UUO. Meanwhile, in-creased mature TGF-β1 and deposition of extracellular matrix(ECM)were observed in tubulointerstitial areas compared with sham-operated mice.After intraperito-neal injection with the SphK1 specific inhibitor PF-543 in UUO mice,enhanced expression of SphK1 and acti-vated autophagy were significantly abrogated.Howev-er,aggravation of renal fibrosis was detected when SphK1 inhibitor PF-543 was applied to suppress SphK1 expression in UUO mice.Conclusion SphK1 activa-tion is renoprotective through the induction of autoph-agy in the pathogenesis of kidney fibrosis.