We treated two cases of flaccidity syndrome,one who was suffering obstinate myasthenia gravis was treated by modified Mahuang Fuzi Xixin decoction which is based on warming Yang and replenishing qi,dredging the meridian passage.The other who was suffering lipid storage myopathy was treated by modified Buzhong Yiqi decoction which is based on strengthening spleen and improving digest,ascending the clear and descending the turbid,supplementing qi and nourishing blood, promoting blood circulation to remove meridian obstruction.Both got the obvious improvement.

Objective To explore the role of oxygen free radicals in the proliferation of ECV304 induced by AngⅡ.Methods The lines of human umbilical vein endothelial cell(ECV304)cultured in vivo were divided into three groups which were treated by AngⅡ,AngⅡ+N-acetyl-L-cysteine(NAC),and normal culture medium.First we observed the proliferous effect of ECV304 induced by AngⅡat different concentration with improved MTT and microscope.Then the contents of oxygen free radicals(?OH)in three groups were detected by spectrophotometer.Results ECV304 incubated with AngⅡ(0.03125～1?mol/L)for 12 hours increased the proliferation rate(P 0.05 vs.control group).Conclusions ECV304 induced by AngⅡcan produce oxygen free radicals(?OH),and the contents of oxygen free radicals(?OH) increase with the prolongation of time and the enlargement of dose;Antioxidant NAC can inhibit the proliferation of ECV304 induced by AngⅡ,this effect may be related with reducing the content of oxygen free radicals(?OH);oxygen free radicals(?OH)may be one of the major mocleculars which play an important role in the signal transduction of ECV304 proliferation.

Hepatolenticular degeneration,namely Wilson's disease,an autosomal recessive disorder of copper metabolism.The author of this article gave a definition to toxin-pathogen,discussed the basic concept of collaterals disease briefly.And pointed out that hepatolenticular degeneration is a disease due to toxin-pathogen invading collaterals,which was caused by disorder of copper metabolism.This can result in toxin stagnating in collaterals and stagnation of blood stasis in collaterals in the initial stage,and collaterals injured at last.To improve QI-blood circulation and regulate the function of zang fu is important in order to accelerate elimination of toxin and prevent copper from stagnating. Specific therapy vary according to different clinical symptoms,such as promoting blood circulation for removing obstruction in collaterals and clearing toxin, clearing heat-fire and clearing toxin and dispersing stagnated liver-qi for promoting bile flow et al.

Objective To investigate the anti-fibrotic effect of Kudancao tablets on bleomycin-induced pulmonary fibrosis in rats . Methods Forty healthy adult SD rats(200±20g)were randomly divided into 4 groups: normal control group(without any treatment),normal saline group(intratracheal instillation of normal saline), model group(intratracheal instillation of 5mg/kg of Bleomycin)and kudancao tablets group(intragastric administration of kudancao tablets suspended in normal saline,0.705g/(100 g.d),2 times/day and for 5 times, then intratracheal instillation of 5 mg/kg of Bleomycin 1h later). Rats in all groups were scraficed 14d and 28d after intratracheal instillation. Alkali hydrolysis method was used to detect the HYP content in lung tissues. The pathological changes were observed with HE staining and silver staining. ResultsCompared with the normal control group and normal saline group,the HYP content in the lung tissues of rats in model group increased significantly (P<0.01). Compared with the model group,the HYP content in the lung tissues of rats in kudancao tablets group decreased significantly(P<0.01). Pathological examination showed that significant fibrotic changes were found in lungs of rats in model group,while the fibrotic changes were ameliorated in lungs of rats in kudancao tablets group. ConclusionKudancao tablets may decrease the hydroxyproline content in lung tissues,and ameliorate the fibrotic degree of lungs of rats with bleomycin-induced pulmonary fibrosis.

AIM: To investigate the urinary protein (UP) excretion in rats suffering from renal ischemia-reperfusion (I-R) and effect of nitric oxide on it. METHODS: SD rats were used to establish the renal I-R model. Sodium nitroprusside (SNP), N ?-nitro-L-arginine (L-NNA) and aminoguanidine (AG) were used to determine the effect of nitric oxide on UP excretion under renal I-R. Quantitative analysis of UP was made by chromatometry. UP species were separated by SDS-PAGE. RESULTS: Renal I-R caused significant increase in UP ( P

AIM: To study the role of polymorphonuclear neutrophile(PMN) in lipopolysaccharide (LPS)- induced acute lung injury (ALI) and the protective effect of interleukin - 10(IL - 10) on ALI. METHODS: LPS alone (100 ?g) or LPS+ IL-10 (l ug) was instilled intratracheally into rats. PMN numbers, protein content and malondialdehyde (MDA) content in bronchoalveolar lavage fluid (BALF) were measured. Histological change of lung was also observed. RESULTS: LPS increased significantly PMN numbers, protein content and MDA content in BALF. Histological finding shows PMN accumulation in lung. IL - 10+LPS reduced remarkably PMN numbers ,pro- tein content and MDA content in BALF than those caused by LPS. PMN decreasing was also identified by light microscopy. CONCLUSION: LPS instilled intratracheally causes PMN accumulation in lung and ALI, while IL - 10 could alleviate ALI through reducing PMN accumulation.

AIM: To study the up-regulation of inducible nitric oxide synthase (iNOS) in lung of pulmonary fibrosis and its relationship with fibrosis. METHODS: The changes of amount of iNOS positive stain cells and type Ⅰ?Ⅲ collagen were examined on the day 7, 14 and 30 after intratracheal administration of bleomycin A_5. The contents of NO-_2/NO-_3 (nitrite/nitrate) in out-flowing pulmonary blood (OPB), hydroxyproline in lung and the histological changes were detected after iNOS was blocked by aminoguanidine (AG). RESULTS: (1) The number of iNOS-positive stain cells increased significantly in BLMA_5 7 d, 14 d and 30 d groups compared with that in control group (P

Objective To evaluate the relationship between the expression of MMP-2,MMP-9 and invasion of gallbladder carcinoma.Method Seventeen specimens of gallbladder carcinoma,9 cases of gallbladder adenoma and 9 cases of chronic cholecystis were assessed by using immunohistochemical method(S-P method).Results There were no significant difference in MMP-2 and MMP-9 expressions between gallbladder carcinoma and adenoma,but they were significantly higher than that of chronic cholecystis.The expressions of MMP-2 and MMP-9 had no correlation with the histological differentiation or Nevin staging.Conclusion MMP-2 and MMP-9 may play an important role in tumor invasion and metastasis in gallbladder carcinoma.

Objective To investigate the effects of ischemic postconditioning (I-post) on intestinal mucosa mitochondrion after ischemia-reperfusion (IR) injury in rat intestine.Methods By using rat model of intestine IR injury,male Sprague-Dawley rats were divided into 4 groups:sham-operation group (S),IR group (IR),ischemic preconditioning group (IPC),and I-post group.Intestinal mucosa mitochondrial ultrastructural changes were observed by using transmission electron microscope (TEM).Mucosal cellular mitochondrial respiration function was studied by measuring the mitochondrial dehydrogenase-dependent reduction of MTT to its formazan derivative,and intestinal mucosal mitochondrial membrane potential was detected by confocal laser scanning microscopy.Results Compared with that in IR group,the injury of mitochondrion in I-post group and IPC group began to recover.The mitochondrial respiratory function and the mitochondrial membrane potential were significantly improved in I-post group and IPC group (P0.05).Conclusion The mechanism of ischemic postconditioning against IR injury of intestine in rats is partly related to maintaining the mitochondrial ultrastructural changes and respiratory function and improving mitochondrial membrane potential.

As a tool for the research of periodical literature data,core journal was initially used in optimizing selection of journals for libraries and information institutes and in providing access for readers to selection of journals.But in recent years,the primitive function of core journal has began to weaken and its negative effects to generalize,mainly in the value orientation deviation of academic periodicals and in the generalization of the evaluation function.Due to these effects,bad results have emerged in periodical circle,academia and even in scientific research management,therefore,rational cognition may be required on the functional effects of core journals.