胰脏弹性酶制造法

1.发明的名称胰脏弹性酶制造法 2.专利范围 以在动物胰脏中加入曲霉属(状菌属)或酒曲菌属(根霉菌属)的微生物发酵产生的酸性蛋白酶,使胰脏中弹性酶原激活为特征的胰弹性酶制造法。 3.发明的详细说明 本发明是关于胰弹性酶(下称:前脂酶)的制造方法,本法收率较高。 弹性酶存在于一般哺乳动物中,是以惰性的弹性酶原存在的,因而在制造弹性酶时,必须对前脂酶进行激活。 过去,前脂酶的激活方法有:①自溶法;②加含有胰蛋白酶或肠激肽酶的十二指肠或它的抽提液的方法等。①法收率低;

He－Ne激光和CO_2激光针灸的研究

本文对Ｈｅ－Ｎｅ激光和ＣＯ２激光在针灸治疗中的应用进行了研究，根据“八纲论治”的基本思想和激光与生物组织的作用规律，归纳总结出它们在针灸治疗中的一般方法。并从传统的针灸理论和现代光生物学出发，对Ｈｅ－Ｎｅ激光和ＣＯ２激光针灸治疗的机理提出了两种新的解释。

幽门螺杆菌是肝性脑病的危险因素吗?

肝性脑病的确切发病机理仍未明了,但氨可能是主要的原因之一。氨主要在结肠腔内由能分解尿素的细菌产生,但也可以在胃粘膜中通过尿素酶的激活而产生。作者观察了Hp作为尿素分解细菌,对肝性脑病的作用。 1994年检查了248例慢性酒精性肝病患者。

偏食挑食对儿童身体有危害

科研人员最近研究证实,儿童 出现的异常情绪或行为,除一些疾 病引起外,还与挑食、偏食等不良 生活习惯有关。他们认为,偏食或 挑食,使孩子体内某些营养成分过 多或不足,影响了体内酶的激活, 损害大脑,最后导致他们生理或心 理出现异常。挑食偏食对儿童的危 害有:

cytoplasmic domain of tissue factor promotes liver fibrosis in mice

To evaluate the role of tissue factor (TF) and protease activated receptor (PAR)-2 in liver fibrosis. METHODSUsing CCl4 administration for eight weeks, we induced hepatic fibrosis in wild-type C57BL/6 mice and in mice with deletion of the cytoplasmic signalling domain of TF (TF§CT/§CT), deletion of PAR-2 (PAR-2-/-) and combined deletion of TF signalling domain and PAR-2 (TF§CT/§CT/PAR-2-/-). Hepatic fibrosis area was assessed by quantitative imaging of picrosirius red staining. Hepatic collagen content was assessed by hydroxyproline levels. Hepatic stellate cells (αSMA positive) and hepatic macrophages (CD68 positive) were identified by immunohistochemistry. Hepatic gene expression was determined by PCR and liver TGFβ1 content by ELISA. RESULTSCCl4 treated mice with deletion of the PAR-2 gene (PAR-2-/-) and the cytoplasmic domain of TF (TF§CT/§CT) developed significantly less hepatic fibrosis, characterised by reduced liver fibrosis area and hydroxyproline content, compared to control wildtype mice treated with CCl4. The observed reduction in histological fibrosis was accompanied by a significant decrease in the hepatic content of TGFβ, the prototypic fibrogenic cytokine, as well as fewer activated hepatic stellate cells and hepatic macrophages. Deletion of the TF cytoplasmic signalling domain reduced hepatic fibrosis to levels similar to those observed in mice lacking PAR-2 signalling but combined deletion provided no added protection against fibrosis indicating a lack of mutual modulating effects that have been observed in other contexts such as angiogenic responses. CONCLUSIONTissue factor cytoplasmic domain is involved in TF-PAR-2 signalling initiating hepatic fibrosis and is a potential therapeutic target, as its deletion would not impact coagulation.

Visceral hypersensitivity in inflammatory bowel diseases and irritable bowel syndrome: The role of proteases

Proteases, enzymes catalyzing the hydrolysis of peptide bonds, are present at high concentrations in the gastrointestinal tract. Besides their well-known role in the digestive process, they also function as signaling molecules through the activation of protease-activated receptors(PARs). Based on their chemical mechanism for catalysis, proteases can be classified into several classes: serine, cysteine, aspartic, metallo- and threonine proteases represent the mammalian protease families. In particular, the class of serine proteases will play a significant role in this review. In the last decades, proteases have been suggested to play a key role in the pathogenesis of visceral hypersensitivity, which is a major factor contributing to abdominal pain in patients with inflammatory bowel diseases and/or irritable bowel syndrome. So far, only a few preclinical animal studies have investigated the effect of protease inhibitors specifically on visceral sensitivity while their effect on inflammation is described in more detail. In our accompanying review we describe their effect on gastrointestinal permeability. On account of their promising results in the field of visceral hypersensitivity, further research is warranted. The aim of this review is to give an overview on the concept of visceral hypersensitivity as well as on the physiological and pathophysiological functions of proteases herein.

Differentiation of NIH3T3 fibroblasts into adipocytes induced by peroxisome proliferator activated receptor γ2 expression

Objective To express mouse peroxisome proliferator activated receptor γ2 (mPPARγ2) in NIH3T3 fibroblasts mediated by the recombinant retrovirus and study its function.Methods The mPPARγ2 gene was subcloned into retrovirus vector pGCEN to generate the recombinant pGCEN/mPPARγ2. Then it was packaged into PA317 cells and selected with G418. Viral supernatants were harvested and then used to infect NIH3T3 fibroblasts. PPARγ activator 5,8,11,14-eicosatetraynoic acid (ETYA) was used to induce the mPPARγ2-expressing NIH3T3 cells into adipocyte differentiation.Results The recombinant retrovirus pGCEN/mPPARγ2 was constructed, and the higher titers of the viral supernatants were obtained. mPPARγ2 was expressed in NIH3T3 cells mediated by the recombinant retrovirus. Lipid accumulation obviously existed in these induced adipocytes which morphologically resembled mature adipocytes in vivo and expressed tissue specific adipocyte P2 (AP2) and Leptin genes.Conclusions An adipocyte differentiation model in vitro was successfully established. The work is the basis for further research on the molecular mechanism of adipocyte differentiation induced by PPARγ2.

Effect of acupuncture plus mild hypothermia on MAPK/ERK pathway of brain tissues in rats with cerebral ischemia-reperfusion injury

Objective： To observe the protective effect of acupuncture plus mild hypothermia on brain tissues in rats with cerebral ischemia-reperfusion injury （CIRI）, and the influence on protein expression levels of phosphorylated Raf-1, MEK-2 and ERK3/2 in the mitogen-activated protein kinase （MAPK）/extracellular regulated protein kinases （ERK） pathway, and to explore the mechanism of acupuncture plus mild hypothermia therapy for the ischemic stroke. Methods： Ninety Sprague-Dawley （SD） rats were randomly divided into a blank control group, a sham operation group, a model group, an acupuncture group, a mild hypothermia group and an acupuncture plus mild hypothermia group, 15 rats in each group. Except the rats in the blank control group, the remaining rats were used to prepare the middle cerebral artery occlusion （MCAO） models according to the modified occlusion method using lines, while only the occlusion lines were inserted without blocking the brain arteries of rats in the sham operation group. When the vital signs of rats were stable, rats in the blank control group did not receive any intervention; rats in the sham operation group and the model group received fastening without treatment; rats in the acupuncture group, the mild hypothermia group, and the acupuncture plus mild hypothermia group were treated with the corresponding therapeutic methods. 72 h later, observed neurologic injury score, evaluated infarction area ratio by 2,3,5-tripheyl tetrazolium chloride （TTC） staining, determined apoptosis by TUNEL assay, and measured the phosphorylated Raf-1, MEK-2 and ERK3/2 protein expression levels in rat ischemic hippocampal tissues by Western blot assay. Results： Compared with the blank control group and the sham operation group, after modeling, the neurologic injury score, infarction area ratio and apoptotic cells were increased, and phosphorylated Raf-1, MEK-2 and ERK：1/2 protein expression levels were significantly increased in the model group; the differences were statistically significant （P〈0.05 or P〈0.01）. Compared with the model group, after acupuncture or mild hypothermia therapy, neurologic injury score and infarction area ratio were decreased; apoptotic cells and phosphowlated Raf-1, MEK-2 and ERK1/2 protein expression levels were significantly decreased; the differences were statistically significant （P〈0.05 or P〈0.01）. Compared with the acupuncture group, neurologic injury score and phosphorylated Raf-1, MEK-2 and ERK3/2 protein expression levels were decreased in the acupuncture plus mild hypothermia group; differences between the groups were statistically significant （P〈0.05 or P〈0.01）. Compared with the mild hypothermia group, phosphorylated Raf-1, MEK-2 and ERK1/2 protein expression levels decreased in the acupuncture plus mild hypothermia group, and differences were statistically significant （P〈0.01）. Conclusion： Acupuncture or mild hypothermia therapy can improve neurologic injury, reduce infarction area and apoptosis, which brought about protective effect on the brain tissues, in the MCAO model. The protective effect of acupuncture plus mild hypothermia group is the strongest. The mechanism may involve the MAPK/ERK pathway, by reducing the phosphorylated Raf-l, MEK-2 and ERK：1/2 protein expression levels.