ABM: To introduce the basic methods of gray relational analysis (GRA) and to illustrate its applications in gastroenterology. METHODS: With the essential formulae of GRA and several typically practical examples, the p...ABM: To introduce the basic methods of gray relational analysis (GRA) and to illustrate its applications in gastroenterology. METHODS: With the essential formulae of GRA and several typically practical examples, the procedure of GRA was introduced. Examples were drawn from the gastroenterological studies. Thus the trait of GRA could be demonstrated. RESULTS: The superiority of GRA in gastroenterological study was proved by the examples. CONCLUSION: GRA can be applied mechanically or flexibly in gastroenterology.展开更多
AIM: To explore the effect of sulfated cholecystokinin octapeptide (sCCK-8) on cardiac functions and its receptor mechanism in endotoxic shock (ES) rats. METHODS: The changes of the mean arterial pressure (MAP), heart...AIM: To explore the effect of sulfated cholecystokinin octapeptide (sCCK-8) on cardiac functions and its receptor mechanism in endotoxic shock (ES) rats. METHODS: The changes of the mean arterial pressure (MAP), heart rate (HR), the left ventricular pressure (LVP) and the maximal/minimum rate of LVP (±LVdp/dt max) were measured by using physiological record instrument in eight groups of rats. The expression of cholecystokinin-A receptor (CCK-AR) and cholecystokinin-B receptor (CCK-BR) mRNA of myocardium in ES rats was examined by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: (1) Low doses of sCCK-8 (0.4 μg/kg) caused tachycardia (441±27, normal control 391±22 s/min) and slight increase in MAP, LVP and ±LVdp/dtmax (16.96±1.79, 18.21±1.69 and +768.85±31.28/-565.04±27.71 kPa, respectively, all P<0.01), while medium doses (4.0 μg/kg) and high doses of sCCK-8 (40 μg/kg) elicited bradycardia and marked increase in MAP, LVP and ±LVdp/dtmax (17.29±1.63, 19.46±2.57 and +831.46±22.57/-606.08 ±31.32; 17.46±1.08, 19.83±2.91 and +914.52±35.95/ -639.15±30.23 kPa, respectively, all P<0.01). Proglumide (1.0 mg/kg), a nonselective antagonist of CCK-receptor (CCK-R), significantly inhibited the pressor effects of sCCK-8 (15.96±1.38, 17.36±0.66 and +748.18±19.29/-512.12±14.39 kPa, respectively, all P<0.01), whilst reversing the bradycardiac responses. (2) High doses of LPS (8 mg/kg) elicited marked decrease in MAP, LVP and ±LVdp/dtmax. (7.16±0.59, 7.6±0.68 and +298.01±25.52/ -166.96±19.25 kPa, respectively, all P<0.01). Pretreatment with sCCK-8 (40 μg/kg) could reverse the decline of cardiac functions (10.71±0.45, 11.7±1.26 and +446.04±67.18/ -347.90±36.98 kPa, respectively, all P<0.01), while proglumide could cause further decline of cardiac function in ES rats (4.71±0.67, 5.58±1.25 and +226.48±15.84/ -142.83±20.23 kPa, respectively, all P<0.01). (3) CCK-A/BR mRNAs were expressed in myocardium of control rats. Gene expression of CCK-AR and CCK-BR significantly increased in展开更多
刺松藻(Codium fragile)经水提-醇沉获得粗多糖,进一步将刺松藻粗多糖(CFP)通过Q-Sepharose Fast Flow(QFF)阴离子交换柱纯化得到6个多糖组分CFP1~CFP6,其中,在CFP6中发现纯度较高的阿拉伯聚糖.采用高效凝胶渗透色谱与十八角激光散射...刺松藻(Codium fragile)经水提-醇沉获得粗多糖,进一步将刺松藻粗多糖(CFP)通过Q-Sepharose Fast Flow(QFF)阴离子交换柱纯化得到6个多糖组分CFP1~CFP6,其中,在CFP6中发现纯度较高的阿拉伯聚糖.采用高效凝胶渗透色谱与十八角激光散射仪联用法和1-苯基-3-甲基-5-吡唑啉酮(PMP)柱前衍生高效液相色谱法对CFP6的分子量及单糖组成进行了分析.结果表明,CFP6是一种分子量为79290的多糖,由阿拉伯糖(Ara)和半乳糖(Gal)组成,二者摩尔比为14. 8∶1. 0.通过多维核磁共振波谱、液相色谱-质谱联用及二级质谱等方法对CFP6的糖苷键连接方式及其寡糖序列结构进行表征,进一步阐明了该复杂多糖的特征结构.经判断,CFP6主链由Ara组成,通过β-(1→3)糖苷键连接,在Ara的C2位存在分支结构,硫酸基位于Ara的C4或C2位.展开更多
基金Supported by the National Natural Science Foundation of China, No. 30271158
文摘ABM: To introduce the basic methods of gray relational analysis (GRA) and to illustrate its applications in gastroenterology. METHODS: With the essential formulae of GRA and several typically practical examples, the procedure of GRA was introduced. Examples were drawn from the gastroenterological studies. Thus the trait of GRA could be demonstrated. RESULTS: The superiority of GRA in gastroenterological study was proved by the examples. CONCLUSION: GRA can be applied mechanically or flexibly in gastroenterology.
基金Supported by the projects of Health Committee and Education Committee of Hebei Province, No. 2K002, and No. 200122
文摘AIM: To explore the effect of sulfated cholecystokinin octapeptide (sCCK-8) on cardiac functions and its receptor mechanism in endotoxic shock (ES) rats. METHODS: The changes of the mean arterial pressure (MAP), heart rate (HR), the left ventricular pressure (LVP) and the maximal/minimum rate of LVP (±LVdp/dt max) were measured by using physiological record instrument in eight groups of rats. The expression of cholecystokinin-A receptor (CCK-AR) and cholecystokinin-B receptor (CCK-BR) mRNA of myocardium in ES rats was examined by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: (1) Low doses of sCCK-8 (0.4 μg/kg) caused tachycardia (441±27, normal control 391±22 s/min) and slight increase in MAP, LVP and ±LVdp/dtmax (16.96±1.79, 18.21±1.69 and +768.85±31.28/-565.04±27.71 kPa, respectively, all P<0.01), while medium doses (4.0 μg/kg) and high doses of sCCK-8 (40 μg/kg) elicited bradycardia and marked increase in MAP, LVP and ±LVdp/dtmax (17.29±1.63, 19.46±2.57 and +831.46±22.57/-606.08 ±31.32; 17.46±1.08, 19.83±2.91 and +914.52±35.95/ -639.15±30.23 kPa, respectively, all P<0.01). Proglumide (1.0 mg/kg), a nonselective antagonist of CCK-receptor (CCK-R), significantly inhibited the pressor effects of sCCK-8 (15.96±1.38, 17.36±0.66 and +748.18±19.29/-512.12±14.39 kPa, respectively, all P<0.01), whilst reversing the bradycardiac responses. (2) High doses of LPS (8 mg/kg) elicited marked decrease in MAP, LVP and ±LVdp/dtmax. (7.16±0.59, 7.6±0.68 and +298.01±25.52/ -166.96±19.25 kPa, respectively, all P<0.01). Pretreatment with sCCK-8 (40 μg/kg) could reverse the decline of cardiac functions (10.71±0.45, 11.7±1.26 and +446.04±67.18/ -347.90±36.98 kPa, respectively, all P<0.01), while proglumide could cause further decline of cardiac function in ES rats (4.71±0.67, 5.58±1.25 and +226.48±15.84/ -142.83±20.23 kPa, respectively, all P<0.01). (3) CCK-A/BR mRNAs were expressed in myocardium of control rats. Gene expression of CCK-AR and CCK-BR significantly increased in