Objective To observe the effect of muscone on the blood-brain barrier and neuropathological changes after complete cerebral ischemia/reperfusion of rats.Methods The global cerebral ischemia/reperfusion injury model was established by the four-vessel occlusion(4VO) method,and then the model animals were given high-,middle-and low-dose muscone.Meanwhile,sham-operation group,model group,and positive control group were also set up.The rats neuroethology behavior,and the contents of superoxide dismutase(SOD),malondialdehyde(MDA) and excitatory amino acid(EAA) in ischemic brain tissue were examined.Results Muscone increased SOD content,lowered MDA content,reduced the increase of EAA content caused by ischemia and hypoxia,and inhibited the excitatory neurotoxicity caused by EAA.Conclusion Muscone has obvious protective effect on rats with complete cerebral ischemia/reperfusion injury.

OBJECTIVETo compare the influence of different Bupleurun chinense composition to the degree of hepatotoxicity damage to rats and oxidative damage mechanism.

METHODTo successively lavage alcohol extracted and water extracted B. chinense composition to rats for 30 days, the general conditions were observed and the related index of liver function, the content of total-SH in serum, the content of MDA, the activity of SOD and the content and activity of GSH and GSH-Px in serum and liver tissue were detected.

RESULTAlcohol and water extracted B. chinense composition all could induce the increases of the activity of ALT and AST in serum, liver weight and the ratio of liver to body, and the content of MDA and induce the decreses of the content of total -SH in serum, the content of GSH, and the activity of SOD and GSH-Px in serum and liver tissue. The above-mentioned changes gradually aggravated with dose increasing, and there was significant difference compared with control group with distilled water.

CONCLUSIONThe different B. chinense composition all can induce hepatotoxicity damage, and the channel of hepatic damage is related with the peroxidative damage mechanism. The degree of hepatotoxicity damage caused by the alcohol extracted composition is more serious than that by the water extracted composition.

Animals ; Bupleurum ; chemistry ; Dehydroascorbic Acid ; analogs & derivatives ; metabolism ; Female ; Liver ; drug effects ; enzymology ; metabolism ; Male ; Oxidative Stress ; drug effects ; Plant Extracts ; administration & dosage ; toxicity ; Random Allocation ; Rats ; Rats, Wistar ; Superoxide Dismutase ; metabolism

Objective To compare the value of conventional ultrasound,hydrosonography and double-contrast enhanced ultrasound in the display capacity of periampullary carcinoma and its relationship with the surrounding tissue.Methods A total of 18 patients with the periampullary carcinoma were diagnosed pathologically or by endoscopic biopsy.Each patient had three imaging modalities by conventional ultrasound,hydrosonography and double-contrast enhanced ultrasound.The display capacity and the relationship between the mass and surrounding tissue were compared with three modalities.Results The display rates of limpid visibilities of carcinoma on conventional ultrasound,hydrosonography and double-contrast enhanced ultrasound were 16.7%(3/18),22.2%(4/18) and 94.4%(17/18),respectively;The display rates of duodenum protrusion on three modalities were 0(0/18),38.9% (7/18) and 72.2% (13/18),respectively,with significant differences among conventional ultrasound,hydrosonography and double-contrast enhanced ultrasound.The double-contrast enhanced ultrasound showed two cases of peripheral vascular invasion and one case of intrahepatic metastasis.Conclusion The double-contrast enhanced ultrasound can increase the display capacity of periampullary carcinoma as a new diagnostic modality for periampullary carcinoma.

OBJECTIVETo investigate the expression and distribution of mast cell tryptase (MCT) in scar, and to discuss the different MCT gene expression in keloid, hypertrophic scar and normal skin.

METHODS20 samples of keloid, 20 samples of hypertrophic scar and 20 samples of normal skin were collected. The distribution of MCT was investigated by immunofluorescence histochemistry, and the MCT mRNA expression was detected by Relative Quantification real-time fluorescent PCR.

RESULTSMCT gene was mainly located in the collagen fiber bundles of the scar, especially in the superficial layer of scar. MCT mRNA expression was significantly higher in keloid than that in hypertrophic scar and normal skin (P < 0.01). Averagely, the MCT gene expression in keloid was 2.5 times and 5.4 times of that in hypertrophic scar and normal skin.

CONCLUSIONSMCT gene may play a role in the pathogenesis of scar.

Adolescent ; Adult ; Cicatrix, Hypertrophic ; metabolism ; pathology ; Humans ; Keloid ; metabolism ; pathology ; RNA, Messenger ; genetics ; Skin ; metabolism ; pathology ; Tryptases ; genetics ; metabolism ; Young Adult

OBJECTIVETo identify the genetic susceptibility to Kashin-Beck disease (KBD) and explore the interaction between low selenium (Se) and the susceptibility gene loci in KBD.

METHODSThe DNA samples collected from 23 KBD nuclear families were analyzed using PCR and GeneScan Analysis 3.7 and Genotyper3.7 software. The haplotype relative risk (HRR) and transmission disequilibrium test (TDT) were used to test the data of the genotypes. The serum selenium (Se) concentration was measured by atomic fluorescence spectrometry, and the interaction between low Se and the susceptibility loci was calculated using a binary logistic regression.

RESULTSIn the 23 nuclear families, the alleles of D2S151 (248 bp), D2S305 (320 bp), and D11S4094 (194 bp) showed significant correlation to KBD (P<0.05). Serum Se concentrations in the studied individuals was 0.037 µg/ml. No significant statistical interaction was observed between low Se exposure and the susceptibility loci (P>0.05).

CONCLUSIONThe polymorphisms in the STR loci D2S305, D2S151, and D11S4094 or the polymorphism loci near them might been related to KBD susceptibility. Low Se exposure shows no significant interaction with the susceptibility loci.

Adolescent ; Adult ; Alleles ; Child ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Kashin-Beck Disease ; blood ; etiology ; genetics ; Male ; Microsatellite Repeats ; Middle Aged ; Pedigree ; Selenium ; blood ; Young Adult

【Objective】To study retrospectively the serum hepatitis B surface antigen（HBsAg）and HBsAg normal⁃ ized to the same hepatic parenchyma cell volume（HPCV），namely，the same hepatic cell quantities，between HBeAg- positive and HBeAg-negative chronic hepatitis B（CHB）.【Methods】A total of 168 CHB patients who had undergone liv⁃ er biopsy and test of serum HBsAg levels due to their disease in the Third Affiliated Hospital of SunYat-sen University were selected as the study subjects. The serum HBsAg levels，as well as HBsAg levels normalized to HPCV（hepatic cell quantities）were compared between HBeAg-positive and HBeAg-negative CHB，respectively.【Results】There was statis⁃ tically significant difference in serum HBsAg levels between HBeAg-positive and HBeAg-negative CHB（P = 0.028）， while there was no statistical difference in HBsAg normalized to HPCV（P = 0.073）. There were no correlations between serum HBsAg and liver inflammation grades（HBeAg-positive：r s = 0.020，P = 0.876 & HBeAg-negative：r s = 0.037，P =0.711）. Similarly，there were no correlations between HBsAg and hepatic fibrosis stages（HBeAg-positive：r s = 0.087， P = 0.488 & HBeAg-negative：r s = 0.144，P = 0.148）. Nevertheless，statistically significant positive correlations were shown between HBsAg normalized to HPCV and liver inflammation grades（HBeAg-positive：r s = 0.309，P = 0.012 & HBeAg-negative：r s = 0.389，P < 0.001）. Similarly，the HBsAg normalized to HPCV and hepatic fibrosis stages were shown to be statistically significantly correlated（HBeAg-positive：r s = 0.490，P < 0.001 & HBeAg-negative：r s = 0.599， P < 0.001）.【Conclusions】Serum HBsAg normalized to HPCV but not HBsAg levels，is correlated with liver inflamma⁃ tion grades as well as hepatic fibrosis stages positively in both HBeAg-positive and HBeAg-negative CHB. But there is no difference in serum HBsAg levels normalized to HPCV between HBeAg-positive and HBeAg-negative CHB.

OBJECTIVE: To quantify the purine concentrations of the acupoints along the pericardium and nonpericardium meridians under healthy and myocardial ischemia conditions to investigate the relationship between acupoint purine change and body functional status in rats. METHODS: A total of 70 rats underwent an operation for myocardial ischemia, while 40 of them survived. They were randomly assigned to the following 5 subgroups: Neiguan (PC 6), Quze (PC 3), Tianquan (PC 2), Quchi (LI 11), and Jianyu (LI 15). Simultaneously, another 40 healthy rats were also randomized into the same 5 subgroups as the control group. The tissue fluids at the acupoints were collected by microdialysis for 30 min. Subsequently, the concentration of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and adenosine (ADO) were quantified using the high-performance liquid chromatography method. RESULTS: Compared with the healthy group, the ADO at PC 6 (P=0.012), PC 3 (P=0.038), PC 2 (P=0.024), and LI 15 (P=0.042) obviously increased in the model group, while no significant difference was observed at LI 11 (P=0.201). However, ATP, ADP, and AMP manifested no significant changes in these areas, except for ATP at LI 15 (P=0.036). CONCLUSIONS Myocardial ischemia could induce an increase in ADO at acupoints of the upper arm and shoulder area, suggesting that the body functional status could affect the responsiveness of acupoints. The status of these acupoints could be pathogenically activated by disease, and distribution following some specific courses.

Unlike healthy, non-transformed cells, the proteostasis network of cancer cells is taxed to produce proteins involved in tumor development. Cancer cells have a higher dependency on molecular chaperones to maintain proteostasis. The chaperonin T-complex protein ring complex (TRiC) contains eight paralogous subunits (CCT1-8), and assists the folding of as many as 10% of cytosolic proteome. TRiC is essential for the progression of some cancers, but the roles of TRiC subunits in osteosarcoma remain to be explored. Here, we show that CCT4/TRiC is significantly correlated in human osteosarcoma, and plays a critical role in osteosarcoma cell survival. We identify a compound anticarin-β that can specifically bind to and inhibit CCT4. Anticarin-β shows higher selectivity in cancer cells than in normal cells. Mechanistically, anticarin-β potently impedes CCT4-mediated STAT3 maturation. Anticarin-β displays remarkable antitumor efficacy in orthotopic and patient-derived xenograft models of osteosarcoma. Collectively, our data uncover a key role of CCT4 in osteosarcoma, and propose a promising treatment strategy for osteosarcoma by disrupting CCT4 and proteostasis.