objective To evaluate the relationship between the pulse pressure and the cardiac geometric structure in patients with essential hypertension. Methods Three hundred and ninety-five patients,age ranging from 20 to 77 years,were enrolled into the study. Their clinical systolic and diastolic blood pressure (SBP/DBP) were all above 140/90mmHg. All the patients either were initially diagnosed as having essential hypertension,or confirmed after taking a the placebo for 2 weeks after stopping anti-hypertensive drugs. The cardiac geometric structure was determined by the echocardiography at the same time when the patients untook the 24 hours ambulatory blood pressure monitoring. Results The clinical pulse pressure was significantly different among the groups as divided by the age ( P

Objective To observe the changes in cytokines, oxygen free radicals, acidulous production in serum and to investigate the effectiveness of monitoring metabolism of cells and the method for evaluating cell injury in patients with severe trauma. Method The detailed data of 117 patients rescued and managed carefully from May 2005 to February 2007 were assessed and stratified with ISS and APACHE Ⅱ , and the serum levels of arterial blood lactate(ABL) ,base deficit(BD) ,superoxide(SOD) ,lipid peroxide(LPO) ,TNF-α and IL-6 were measured in real-time according to the condition of the patient. Results The monitoring biomarkers obviously changed with injury severity which endangered the situation of patients after trauma (P < 0.05) , especially in the patients with ischemia , hypoxia, shock, iniection, SIRS, and MODS (P < 0.01). The persistence of extremely elevated levels of biomarkers meant the organ failure and fatality of patients after trauma, and there was a obvious differece between those cases and cases without elevation of biomarkers ( P < 0.01). Conclusions The outcome of patients after trauma is closely correlated with injury severity,infection and MODS,and the levels of biomarkers including ABL, SOD, IPO, TNF-a and IL-6 are useful indicators of outcome measure.

Objective To investigate the effects of deletion of adenosine A2A receptors on peripheral leukocytes on cerebral white matter lesions induced by chronic cerebral hypoperfusion.Methods Twenty-four wild type(WT) male mice were given a ? irradiation of 12.5Gy,followed by receiving bone marrow cells tail vein from female A2A receptor knocked out(KO) mice via tail vein,were assigned as KO→WT group,while those received bone marrow cells from WT female mice were assigned as WT→WT group(n=20).The efficiency of reconstitution of bone marrow cells in recipient mice was assessed 7 weeks after transplantation by PCR and immunofluorescent technique.Then,the recipient mice were subjected to bilateral common carotid artery stenosis with internal diameter of 0.18mm by external banding using microcoils at 8 weeks after transplantation.On 7d,14d and 30d after the surgery,corpus callosum,fiber bundles of Caudoputamen and optic tract were harvested from the cerebral white matter,and stained with Kluver-Barrera staining for observing the changes in nerve fibers,and with GFAP and CD11b immunohistochemistry staining for observing the proliferation of microglia and astrocytes.Results At 7 weeks after successful transplantation,the genotype of sex chromosome in peripheral leukocytes of the male recipient mice was changed into female pattern.The expression rate of A2A receptor was 9.73%?2.05% in KO→WT group and 93.82%?11.24% in WT→WT group,with significant difference between the two groups(P

Objective To observe behavioral characteristics and pathologic changes of chronic cerebral hypoperfusion in mice. MethodsTotally 62 adult C57BL/6 mice were subjected to either sham-operation (n=31) or bilateral common carotid artery stenosis using external microcoils with an inner diameter of 0.18 mm(n=31). At 30 d after the stenosis, the animals of the 2 groups (8 mice for each group) underwent behavioral test of 8-arm radial maze. In 7, 14 and 30 d, the rest mice were sacrificed for their brain tissue samples which were examined with Kluver-Barrera staining and immunohistochemical assay for markers of microglia and astroglia, glial fibrillary acidic protein (GFAP) and CD11b. In 14 d after the model establishment, Evans blue dye extravasation test was performed for the blood-brain barrier function. ResultsThe model group made significantly more errors than sham-operated group in 8-arm radial maze test at 30 d after the surgery. White matter lesions occurred and the proliferation of activated microglia and astroglia were observed in white matter in model mice after 14 and 30 d bilateral common carotid artery stenosis. The disruption of blood-brain barrier function of model mice was indicated in the evans blue extravasation test at 14 d after bilateral common carotid artery stenosis. ConclusionCognitive impairment, white matter lesions and glial activation are successfully induced after bilateral common carotid artery stenosis in mice model of chronic cerebral hypoperfusion.

Objective To investigate the effect of adenosine A2A receptor deficiency on the ischemic neuronal injury and its potential mechanism.Methods Transient(2 h)cerebral ischemia was induced by the middle cerebral artery occlusion(MCAO)in mice.Adenosine A2A receptor knockout(A2ARKO)mice and their wild-type littermates(A2ARWT)were divided into 2-hour cerebral ischemia group,cerebral ischemia with 22-hour reperfusion group and cerebral ischemia with 46-hour reperfusion group.Cerebral infarction volume was measured by image analysis of brain sections stained with cresyl violet(CV).Brain water content was evaluated with the dry-wet weighing method.The expression of calbindin D-28k(CB)and aquaporin-4(AQP4)in ischemic brain was determined with immunohistochemical methods.Results The cerebral infarction volumes in 2-hour cerebral ischemia group,cerebral ischemia with 22-hour reperfusion group and cerebral ischemia with 46-hour reperfusion group of A2ARKO mice were lesser than those in the corresponding groups of A2ARWT mice.Compared with A2ARWT mice,A2ARKO mice had more CB,lesser AQP4 expressions and lesser brain water contents.Conclusion Adenosine A2A receptor deficiency exerts the protection against ischemic brain injury both in the acute phase and reperfusion phase,and attenuates brain edema caused by cerebral ischemia,which may be due to the inhibition of intracellular calcium overload and AQP4 expression.

Cleidocranial Dysplasia ; pathology ; Diagnosis, Differential ; Dwarfism ; Humans ; Maxillofacial Abnormalities ; Osteosclerosis ; pathology ; Pycnodysostosis ; diagnostic imaging ; etiology ; pathology ; therapy ; Radiography ; Tooth Abnormalities

The effects of the feed attractants on Whitmania pigra were studied. The average weight of Wh. pigra were 5.0 g. Arginine was selected as feed attractants, xanthan gum was selected as feed substrate. The times of Wh. pigra going into the inducing room were recorded. The water temperature was 22-25 degrees C during the whole experiment. Arginine that had better inducing effect was chosen to carry on in the gradient experiment. The results showed that the best inducing effect was found when the added amount of arginine was 0.3%, which was close to the arginine content of the natural body fluid of Wh. Pigra and Bellamya purificata, 2.97 mg x g(-1).
Animal Feed ; analysis ; Animals ; Arginine ; analysis ; metabolism ; Body Weight ; Feeding Behavior ; Leeches ; growth & development ; physiology

OBJECTIVETo observe the protective effects of histone deacetylase inhibitor on stress-induced myocardial injury.

METHODSHealthy male Wistar rats were randomly divided into 3 groups( n = 6), and the stress-induced myocardial injury model was established with chronic restraint stress method. The protective effects of histone deacetylase inhibitor on stress-induced myocardial injury were observed with Trichostatin A (TSA) intervention. Histone acetylation levels in myocardium of rats were detected by Western blot method, spectrophotometry method was used to dynamically determine the activity of rat serum lactate dehydrogenase (LDH), serum creatine kinase isoenzyme-MB (CK-MB) and Caspase 3, and nagar Olsen staining were used to observe the early myocardial damage.

RESULTSRestraint stress could significantly reduce the level of histone acetylation of myocardium in rats, and TSA intervention could inhibit the stress-induced reduction of myocardial levels of histone acetylation. Restraint stress could cause the significant increase of serum LDH activity ( P < 0.05), serum CK-MB activity ( P < 0.05), and the Caspase 3 activity of myocardial tissue (P < 0.05), and early myocardial damage also occurred during restraint stress. ISA intervention could significantly reduce the serum LDH activity (P < 0.05), the serum CK-MB activity (P < 0.05), the activity of myocardial tissue caspase 3 induced by restraint stress (P < 0.05), and the stress-induced myocardial injury was also attenuated by TSA intervention.

CONCLUSIONThe histone deacetylase inhibitor TSA can protect stress-induced myocardial injury.

Acetylation ; Animals ; Cardiotonic Agents ; pharmacology ; Caspase 3 ; blood ; Creatine Kinase, MB Form ; blood ; Histone Deacetylase Inhibitors ; pharmacology ; Hydroxamic Acids ; pharmacology ; L-Lactate Dehydrogenase ; blood ; Male ; Myocardium ; pathology ; Rats ; Rats, Wistar ; Restraint, Physical ; Stress, Physiological

OBJECTIVETo study the chemical constituents from Anemone flaccida.

METHODChemical constituents were isolated by repeated column chromatography (silica gel, Toyopearl HW-40C and preparative HPLC). The structures were elucidated on the basis of spectral data analysis.

RESULTTwelve triterpenes were isolated and their structures were identified as follow: oleanolic acid (1), oleanolic acid 3-O-beta-D-glccopyranosyl-(1-->2)-beta-D-xylopyranoside (2), eleutheroside K (3), oleanolic acid 3-O-alpha-L-rhamnopyranosyl-(1-->2)-beta-D-xylopyranoside (4), oleanolic acid 3-O-beta-D-glccopyranosyl-(1-->2)-alpha-L-arabinofurnoside (5), oleanolic acid 3-O-beta-D-glccuronopyranose (6), oleanolic acid 3-O-beta-D-glccuronopyranose methyl ester (7), oleanolic acid 28-O-alpha-L-rhamnopyranosyl(1-->4)-beta-D-glccopyranosyl (1-->6)-beta-D-glccopyranosyl (8), oleanolic acid 3-O-beta-D-glccuronopyranose 28-O-alpha-L-rhamnopyranosyl (1-->4)-beta-D-glccopyranosyl (1-->6)-beta-D-glccopyranoside (9), oleanolic acid 3-O-beta-D-glccopyranosyl methyl ester 28-O-alpha-L-rhamnopyranosyl (1-->4)-beta-D-glccopyranosyl (1-->6)-beta-D-glccopyranoside (10), oleanolic acid 3-O-beta-D-glccopyranosyl-(1-->2)-beta-D-xylopyranosyl-28-O-alpha-L-rhamnopyranosyl (1-->4)-beta-D-glccopyranosyl (1-->6)-beta-D-glccopyranoside (11), oleanolic acid 3-O-alpha-L-rh-amnopyranosyl-(1-->2)-alpha-L-arabinopyrnosyl-28-O-alpha-L-rhamnopyranosyl (1-->4)-beta-D-glccopyranosyl (1-->6)-beta-D-glccopyranoside (12).

CONCLUSIONcompounds 5-8, 10, 12 were isolated from this plant for the first time. Compounds 2, 5 and 11 showed positive anti-tumor activities.

Anemone ; chemistry ; Antineoplastic Agents ; chemistry ; pharmacology ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; Eleutherococcus ; chemistry ; Glycosides ; chemistry ; pharmacology ; HeLa Cells ; Humans ; Magnetic Resonance Spectroscopy ; Oleanolic Acid ; chemistry ; pharmacology ; Plant Extracts ; chemistry ; pharmacology ; Rhizome ; chemistry ; Spectrometry, Mass, Electrospray Ionization

Primary biliary cholangitis is a chronic intrahepatic cholestatic liver disease and has increasing incidence and prevalence rates, as is reported in the literature. Examination of specific antibodies including serum anti-mitochondrial antibody subtype M2 and liver histopathological examination help to make a definite diagnosis of this disease. Ursodeoxycholic acid (UDCA) is often used for the treatment of this disease, but patients with an unsatisfactory biochemical response to UDCA tend to have rapid disease progression. At present, there are no effective treatment methods for such patients. The addition of budesonide, fenofibrate, bezafibrate, or obeticholic acid may be effective in these patients, but this needs to be verified by further clinical studies.