Six N - acylsphingosines with molecular weight 509,537,565,607 and 621 respectively were isolated from the Chinese gorgonia Junceella squamata . The chain length of the carboxylic acid in them were C14,C16,C18,C20,C21 and C22,and the chain length of the bases were all C18. On the basis of their spectra and GCMS of the Chemical reaction products,their structure were elucidated.

Objective To stuty the metabolites of marine fungus Julella avicenniae from the South China Sea.Methods The fungus J.avicenniae was extracted with AcOEt,separated,and purified by column chromatographies on silica gel.All the compounds were identified on the basis of spectral analysis(IR,MS,NMR) and chemical evidence.Results One novel compound was identified from its extract of marine fungus J.avicenniae from the South China Sea.Conclusion One novel compound,avicenniaene,is isolated from the marine fungus J.avicenniae from the South China Sea.

Objective To determine the mechanism underlying the mandibular angle enlargement and to provide a morphological basis for correcting the enlarged mandibular angle. Methods By axial computed tomography, it is possible to measure the width and length of the masseter and the medial pterygoid, the gonial angle, and the vertical height of the posterior mandible. The date were initially analysed by using a simple correctionials and indpendent sample T test. Results The distance between two Go points and gonial angle were significantly related with the thickness of masseter muscle, but the thickness of the medial pterygoid was on the contrary. There was significant differences between the group of prominence and the normal control in the gonial angle, the distance between two Go points and thickness of masseter . But there was no difference between the the two groups in the thickness of medial pterygoid. Conclusion The thickness of the masseter muscle is an important factor that affects the lower facial morphology. The hypertrophy of masserter muscle may cause the mandibular angle enlargement.

Subergorgic acid is one of marine neurotoxins. It has a unique chemical structure. This article reviews its isolation and structural determination, total synthesis,derivatives preparation,biologic activities and potential applications.

Objective To establish a rabbit auricular hematoma model,to observe the process of production and absorption,and to study the location of hematoma and method of its removal Methods Ten health New Zealand rabbits were divided randomly into control group and experimental group.A weight was dropped onto particular locality of auricles 3-6 times until a big hematoma appeared.The pathological processes of hematoma were observed,and the hematoma was formed 1 hour and the hematoma was almost absorbed after 4 days.The drainage experiment was conducted to observe the effect of needle aspiration or incision and drainage on the hematoma.Results All experimen tal auricles formed hematoma.The histopathological study showed that hematoma located between skin and cartilage,did not involve the cartilage.After 4 days,new-formed capillaries and fibroblasts were found,and then hematoma mostly absorbed; fibrous hyperplasia was been found.By cutting the hematoma,the blood clot could be thoroughly removed.Conclusions The auricular hematoma model can be established easily by striking with a heavy weight.Hematoma locates in subcutaneous connective tissue.A large hematoma should be early removed for prevention of auricular deformity.

Objective: To study the effect of rapeseed peptides (RSP) from enzymolysis of rapeseed protein on growth of Sarcoma 180 (S180) cell incubated in vitro and its cell membrane. Methods: S180 cell incubated in vitro was used as model. The change of proliferation of S180 cell, fatty acid and sialic acid in membrane and membrane fluidity of S180 cell were investigated. Results: RSP had inhibitiory ability to S180 cell proliferation and could influence its membrane. Conclusion: RSP had potential in inhibiting tumor growth, so was needed to study further.

AIM To examine the effect of cilostazol, a no vel selective phosphodiesterase type 3 inhibitor, on adherence between neutrophils and human umbilical e ndothelial cells ( HUVECs ) and investigate its possible mechanisms. MET HODS Confluent HUVECs between 4～6 passages were used and stimulated by l ipopolysaccharide (LPS, 5 mg?L -1 ) with or without coincubation of cilosta zol (1～10 ?mol?L -1 ) for 24 h. Soluble cell adhesion molecules (sCAMs), including vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1) and endothelial leukocyte adhesion molecule-1 (sELAM-1, sE-selectin) in cell culture medium were measured by ELISA. RESULTS Cilostazol (1～10 ?mol?L -1 ) inhibited adherence between neutrophils and HUVECs in a dose- dependent manor. At the same time, cilostazol didn't affect sICAM-1 and sE-sel ectin release from LPS-stimulated HUVECs, but in contrast, it significantly inh ibited sVCAM-1 production under the same experiment condition, and this effect was canceled by H-89, an inhibitor of protein kinase A ( PKA ). CONCLUS ION Cilostazol significantly inhibits adherence between neutrophils and H UVECs, and downregulates sVCAM-1 release from LPS-activated HUVECs, and these effects on cytokine-challenged endothelial cells might be via a PKA-dependent pathway. The present result suggests that cilostazol partially eliminates some o f the adherent reactions of HUVECs to LPS, a deleterious cytokine, and it is rea sonable to consider that cilostazol might be a strategy for preventing atheroscl erosis and other cardiovascular diseases.

Objective To observe the impact of hypoxia/reoxygenation on myocardial cytoskeletal proteins (α-actinin protein,tubulin protein,desmin protein) and to investigate EPO lessening the damage of myocardial cytoskeleton proteins in rats proved by culturing hypoxia/reoxygenation injured myocardial cells in presence of EPO.Methods The rat model of asphyxia-induced cardiac arrest was performed by turning-off the ventilator and clamping the endotracheal tube.After asphyxia for 8 minutes,CPR was carried out.A total of 24 rats were divided into normal group,ischemia/resuscitation (I/R) group and the EPO group (n =8).The model of myocardial dysfunction was determined 2 hours after restoration of spontaneous circulation (ROSC).The rats of EPO group were given EPO 5000 U/kg after ROSC.The rat heart specimens were collected.Actinin,Tubulin and Desmin protein were observed by SABC immunohistochemistry.The cultured cardiomyocytes were taken from neonatal rats and were divided into three groups:the normal group,the hypoxia/reoxygenation (H/R) group (hypoxia 10 h/reoxygenate 4h),the EPO group (hypoxia 10 h/reoxygenate 4 h,plus 10 U/mL EPO).The changes of tubulin and actinin in cultured cardiomyocytes were observe by Immunofluorescence.Results From immunohistochemistry,there were no significant difference in the optical density of actinin,tubulin and desmin among the normal,I/Rand EPO groups.After H/R injury,the structures of the actinin,tubulin protein were destroyed,the network structure of both protein were unclear in cultured myocardial cells.The grades of fluorescence intensity of actinin and tubulin in H/R group were significant lower than those in normal group,but there was no significant difference between H/R group and EPO group.Conclusions The damage of cytoskeleton during ischemia/reperfusion may be time-dependent.EPO has no beneficial effect on the cytoskeleton after I/R injury.

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Objective:To investigate the effect of lipopolysaccharide (LPS) on primary neonatal rat cardiomyocytes (CMs) and human induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs).Methods:The hiPS-CMs and primary neonatal rat CMs were treated with different concentrations of LPS for 24 to 48 h. Then the cellular viability was analyzed by the xCELLigence RTCA Cardio system. The measurement of NPPB gene was studied by qRT-PCR and the gene expression analysis was performed by the qPCR array, in order to evaluate the cardiac inflammation effect induced by LPS.Results:The LPS exposure led to dysfunction in the primary neonatal rat CMs, which shown as an increase in beating rate and a decrease in contraction amplitude ( P<0.01), accompanied by an increased NPPB mRNA level ( P<0.01). There was no significant alteration in beating rate and the contraction amplitude in the corresponding concentration of the primary neonatal rat CMs ( P>0.05), as well as the NPPB mRNA level ( P>0.05). However, the expression of NPPB mRNA in hiPS-CMs was significantly different at a higher concentration of LPS (5 μg/mL~40 μg/mL) ( P<0.01), but the beating rate and the contraction amplitude showed no significant change, even the concentration of LPS up to 40 μg/mL ( P>0.05). Finally, the genes of C3, Gpnmb, Atf3, Il6r and Ly96 upregulated to 1.5 folds in the primary neonatal rat CMs. In comparison with primary neonatal rat CMs, the AK4, TOLLIP, SPP1, FABP1, IL6R, LY96 and C3 were over expression to 1.5 folds in the hiPS-CMs. Conclusions:In comparison with primary neonatal rat CMs, hiPS-CMs are markedly less injured by LPS and show a different pattern of inflammation gene expression.