The left and right cardiac function of 11 patients with chronic mountain sickness was studied before and after oxygen administration. It was found that after pure oxygen was inhaled, the internal diameter of the right ventricle, the ratio between right and left ventrcular diameters, and the heart rate were decreased significantly, while the ?-wave excursion of the pulmonary valve and the EF slope of the mitral valve were increased obviously. However there was no change of the systolic time interval of both the ventricles and of the left ventricular systolic function. The results suggest that oxygen inhalation could relieve hypoxic pulmonary hypertension and improve left ventricular diastolic function.

Objective Taking sham electroacupuncture as control, to observe the clinical efficacy of electroacupuncture in treating female stress urinary incontinence (SUI). Method By using central random design, the eligible subjects were randomized into an electroacupuncture group of 42 cases [electroacupuncture at Zhongliao (BL33) and Huiyang (BL35)] and a sham group of 42 cases [sham electroacupuncture at points beside Zhongliao and Huiyang]. The therapeutic efficacy was evaluated by observing the urine leakage volume in the 1-h pad test and International Consultation on Incontinence Questionnaire-Short Form (ICIQ-SF). Result In the electroacupuncture group, the urine leakage volumes in the 4th, 6th, 20th, and 32nd treatment week were significantly lower than that before treatment (P<0.05);the decreases of urine leakage volume in the electroacupuncture group were more significant than that in the sham group in the 4th, 6th, 20th, and 32nd treatment week (P<0.05). In the electroacupuncture group, the ICIQ-SF scores in the 4th, 6th, 20th, and 32nd treatment week were significantly lower than that before treatment (P<0.05); the ICIQ-SF scores were significantly lower in the electroacupuncture group than in the sham group in the 4th, 6th, 20th, and 32nd treatment week (P<0.05). Conclusion Electroacupuncture can effectively improve urine leakage and other urinary symptoms in SUI.

OBJECTIVETo enhance the dissolution rate of daidzein with solid dispersion technique.

METHODSolid dispersions were prepared by the solvent method using water-solubility chitosan as a hydrophilic carrier. DSC, IR and X-ray methods were used to verify the formation of solid dispersion.

RESULTDissolution percentages of solid dispersions were more than 90 percent in the drug-carrier ratio of 1:5 and 1:9. But dissolution percentages of physical mixtures and pure drug were 40 and 38.4 percent respectively. Part of daidzein dispersed in solid dispersion in the form of microcrystalline.

CONCLUSIONWater-soluble chitosan solid dispersion can significantly increase dissolution rate of daidzein.

Calorimetry, Differential Scanning ; Chitosan ; chemistry ; Isoflavones ; chemistry ; Solubility ; Spectrophotometry, Infrared ; Water ; chemistry ; X-Ray Diffraction

Objective To investigate the effect of calcium on the stability of VWF-A2 domain. Methods The crystal structures of A2 (not containing calcium) and A2/Ca2+ (with calcium bound) were downloaded from protein data bank. For A2 domain, the conformational changes, unfolding pathway differences and the exposure degree variance of cleavage sites caused by calcium binding were observed and analyzed by steered Molecular Dynamics simulations under constant force. Results The unfolding pathway of A2 domain and exposure process of cleavage sites were force-dependent. Calcium binding did not affect the unfolding process of A2 in the early stage. As the conformational rearrangement of α3β4-loop reduced its localized dynamic properties, the movement among β1-β4-β5 strands was restrained, which suppressed its further unfolding to stay in the intermediate steady state and delayed the cleavage-site exposure. Conclusions Stretch force could induce β5 strand of A2 unfolding and the cleavage-site exposure, while calcium binding inhibited ADAMTS13 proteolysis efficiency through stabilizing A2 hydrophobic core and covering its cleavage sites. These results way help to understand how ADAMTS13 cleavages the VWF-A2 domain and regulates the hemostatic potential of VWF, and further provide useful guidance on the design of related anti-thrombus drugs.

In resting platelets, the 17 ^th domain of filamin a (FLNa17) constitutively binds to the platelet membrane glycoprotein Ibα (GPIbα) at its cytoplasmic tail (GPIbα-CT) and inhibits the downstream signal activation, while the binding of ligand and blood shear force can activate platelets. To imitate the pull force transmitted from the extracellular ligand of GPIbα and the lateral tension from platelet cytoskeleton deformation, two pulling modes were applied on the GPIbα-CT/FLNa17 complex, and the molecular dynamics simulation method was used to explore the mechanical regulation on the affinity and mechanical stability of the complex. In this study, at first, nine pairs of key hydrogen bonds on the interface between GPIbα-CT and FLNa17 were identified, which was the basis for maintaining the complex structural stability. Secondly, it was found that these hydrogen bonding networks would be broken down and lead to the dissociation of FLNa17 from GPIbα-CT only under the axial pull force; but, under the lateral tension, the secondary structures at both terminals of FLNa17 would unfold to protect the interface of the GPIbα-CT/FLNa17 complex from mechanical damage. In the range of 0~40 pN, the increase of pull force promoted outward-rotation of the nitrogen atom of the 563 ^rd phenylalanine (PHE ⁵⁶³-N) at GPIbα-CT and the dissociation of the complex. This study for the first time revealed that the extracellular ligand-transmitted axial force could more effectively relieve the inhibition of FLNa17 on the downstream signal of GPIbα than pure mechanical tension at the atomic level, and would be useful for further understanding the platelet intracellular force-regulated signal pathway.
Filamins/metabolism* ; Platelet Glycoprotein GPIb-IX Complex/metabolism* ; Molecular Dynamics Simulation ; Ligands ; Protein Binding ; Blood Platelets/metabolism* ; von Willebrand Factor/metabolism*