Objective To discuss the ultrastructural pathological characteristics and dynamic changes of brain vessel after subarachnoid hemorrhage(SAH),and the mechanism of these changes in delayed cerebral vasospasm.Methods SAH model was made by infusing blood twice into the cistern magna of Japanese rabbits.The animals were divided randomly into SAH group,saline group,puncture group and blank group,at 1 h,3 d,5 d,7 d and 10 d after the first infusion the animals were perfused and basilar artery was harvested.Ultrastructural changes were observed under light microscope and electron microscope.Results Under the light microscope,the vessel wall became thick,the vessel cavity became narrow,the endothelia cells became swollen,vacuoles could be found in the chromatin,inner elastic membrane became reductus and broke.Under the electron microscope,the close connection between the endothelial cells disappeared,the membrane of the cells fell off,and the mitochondria became swollen,vacuoles could be seen,the chromatin became concentrated,heterochromatin could be seen,smooth muscle became deformed,chromatin became uneven, myofilament had derangement and fragmentation and dissolved,vacuolus could be seen in the kytoplasm,mitochondrion became swollen.The structural change of basilar artery under the light microscope got similar to that under the electron microscope;slight change was observed right after 1 h of SAH,significant change was observed at 3 d,and most obvious change was observed between 5 d and 7 d.Conclusion Ultrastructural changes were observed in the basilar artery after SAH,and significant dynamic changes were observed in the progress.The damage of endothelia cells may be the important factors which cause delayed cerebral vasospasm.

We study the techniques of synthesis of disulfide bond-bearing cyclopeptides FIK. This experimentation with the material of Fmoc-aa use Solid-Phase synthesis after condensation by HBTU/HOBt/DIEA to synthesize linear peptide, then cyclopeptide was synthesized by creation of intramolecular disulfide bond by means of 12 oxidation of bis cysteine sulfhydryl of the linear peptide. The crude production was cleaved from the resin together with all protecting group and identified and separated by MALDI-MS and RP-HPLC. The peptide yield was 18%, after purification the purity was more than 97%. It was identified on MALDI-MS and Ellman reagent detection. This method is effective, simple, rapid and obtained good yield, and it's fit for the large-scale production.
Amino Acids ; chemistry ; Combinatorial Chemistry Techniques ; methods ; Disulfides ; chemistry ; Fluorenes ; chemistry ; Molecular Structure ; Peptides, Cyclic ; chemical synthesis ; chemistry ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

The aim of this study was to investigate the inhibitory effect and the underlying mechanism of ethacrynic acid (EA) on the contraction in mice. BL-420S force measuring system was used to measure the tension of mouse tracheal rings. The whole cell patch clamp technique was utilized to record the channel currents of airway smooth muscle (ASM) cells. The calcium imaging system was used to determine the intracellular Ca concentration ([Ca]) in ASM cells. The results showed that EA significantly inhibited the high K (80 mmol/L) and acetylcholine (ACh, 100 µmol/L)-induced contraction of mouse tracheal rings in a dose-dependent manner. The maximal relaxation percentages were (97.02 ± 1.56)% and (85.21 ± 0.03)%, and the median effective concentrations were (40.28 ± 2.20) μmol/L and (56.22 ± 7.62) μmol/L, respectively. EA decreased the K and ACh-induced elevation of [Ca] from 0.40 ± 0.04 to 0.16 ± 0.01 and from 0.50 ± 0.01 to 0.39 ± 0.01, respectively. In addition, EA inhibited L-type voltage-dependent calcium channel (LVDCC) and store-operated calcium channel (SOCC) currents in ASM cells, and Ca influx. Moreover, EA decreased the resistance of the respiratory system (Rrs) in vivo in mice. These results indicated that EA inhibits LVDCC and SOCC, which results in termination of Ca influx and decreases of [Ca], leading to relaxation of ASM. Taken together, EA might be a potential bronchodilator.
Animals ; Calcium ; metabolism ; Calcium Channels, L-Type ; Enzyme Inhibitors ; pharmacology ; Ethacrynic Acid ; pharmacology ; Mice ; Muscle Contraction ; drug effects ; Muscle, Smooth ; drug effects ; Respiratory System ; cytology ; drug effects

Objective To investigate the risk factors associated with epididymitis after transurethral resection of prostate.Methods A retrospective analysis of 352 patients with benign prostatic hyperplasia (BPH) who underwent transurethral resection of prostate in X'an Aerospace General Hospital from January 2015 to December 2017 was performed.There were 14 cases of epididymitis and 338 cases of nonepididymitis.Measurement data were expressed as ((x) ± s),t test was used for comparison between groups;count data was expressed by rate (％),and chi-square test was used for comparison between groups.Univariate and multivariate logistic regression analyses were used for factors that may lead to post-urethral epididymitis.Results Univariate logistic regression analysis showed that preoperative leukocytic positive,urine glucose positive and prostate volume had significant effects on postoperative epididymitis (P ＜ 0.05).Multivariate logistic regression analysis showed that prostate volume increased (OR =0.182,P =0.005)was an independent risk factor for postoperative epididymitis.Conclusion The enlargement of prostate volume is an independent risk factor for postoperative epididymitis.For large-volume prostate surgery,the purpose of relieving obstruction can be achieved.