Objective To explore the changes of finger artery hemodynamics of patients with pulmonary heart disease, at the same time to search for the relationship with PaO_2.Methods We used American ACUSON128/xp10 and ATL5000 color Doppler ultrasound diagnostic instrument to detect double middle - finger artery hymodynamics items; VSMANX, VDMIN,TAMX , PI and RI. We used Danish ABL5 artery blood gas analysis to monitor PaO_2 and SaO_2.Results PaO_2 ,SaO_2, VSMAX,VDMIN ,TAMX,and PI in control group,pulmonary heart disease remission stage, active attack stage had significant difference (P

Equipping tumor-targeting carrier with cell-penetrating peptide with high transduction efficacy has become a trend. According to the fusion modes and tumor-targeting mechanisms, cell-penetrating peptides can be divided into five categories: first, self-targeting cell-penetrating peptides; second, fusion carriers made of targeting ligands and cell-penetrating peptides; third, cell-penetrating peptide-modified nano-carrier; fourth, tumor-microenvironment-targeting cell-penetrating peptides; fifth, other special cell-penetrating peptides. Fusion carriers, which can not be effectively released into the cytoplasm after transducted into target cells, can be further modified to increase their efficacy. In all, cell-penetrating peptide introduced into tumor-targeting carrier should provide a new era for anti-tumor pharmacy research and cancer therapy.

Objective　To investigate the pattern of human neutrophil degranulation mediated by Fc alpha receptors. Methods　IgA immune complexes (IgA IC) and specific monoclonal antibody were used to stimulate neutrophil degranulation. Lactoferrin released by stimulated neutrophils was quantitatively determined. Results　Monoclonal antibody and IgA IC could both induce neutrophil lactoferrin release. However, monoclonal antibody induced rapid and strong degranulation whilst the effect of IgA IC was much weaker. Conclusion　The pattern of neutrophil degranulation induced by IgA IC and monoclonal antibody is different.

Aim To investigate the toxicity of isopsor-alen in HepG2 cells and its effects on bile acid, bile acid synthesis and transport. Methods Cell viability was evaluated by MTT assay and bile acid was deter-mined inside HepG2 cells, with exposure to various isopsoralen for 24h. The mRNA transcription of BSEP, MRP2, MRP3, NTCP, OATP2, OSTα, CYP7A1, CYP27 A1 , FXR and PXR were assessed by real-time PCR. Results The cell viability was decreased dose-dependently with isopsoralen in HepG2 cells, and IC50 was 118. 1μmol·L-1 exposure to isopsoralen for 24h. Bile acid inside cells significantly increased with 100 and 400 μmol · L-1 isopsoralen. Isopsoralen caused the down-regulation of MRP2 , MRP3 , CYP7 A1 mRNA at 25 μmol · L-1 . Beside these, the up-regulation of OATP2,OSTα,CYP27A1,FXR,PXR with 100 μmol· L-1 isopsoralen, but there was no significant change of BSEP and NTCP. Conclusion The results show that isopsoralen induces bile acid accumulation and cytotox-icity which may be associated with the down-regulation of MRP2, MRP3 in HepG2 cells.

The post-stroke depression (PSD) is one of the common complications of stroke.It can not only delay the recovery of the neurological function in patients, seriously affect the quality of life of patients, but also increase the mortality and morbidity.More and more attention has been paid to the pathogenesis of PSD.Recent studies have confirmed that brain small vessel disease is closely related to the occurrence of PSD.This article reviews relationship between brain small vessel diseases and PSD.

Objective To screen rhEndoglin-binding peptides from phage displayed 12-peptide library. Methods The rhEndoglin was used as target protein for biopanning of phage-displayed 12-peptide library. After three rounds of screening, 16 phage clones were randomly selected and identified by sandwich ELISA. The positive phage clones were sequenced, and the fuse peptides were deduced by the DNA sequence. Further we identified the affinity and speciality by competitive inhibition test. Results Six of 16 phage clones were identified as positive clones by competent ELISA which could bind to rhEndoglin. Five sequences were obtained, and the amino acid sequence in two of these five was AHKHVHHVPVRL. Conclusion The rhEndoglin-binding peptides can be obtained by screening phage random peptide library. It could play an important role in early diagnosis of ovarian cancer.

Objective To assess functional affinity of rhEndoglin conjugated eptide in order to identify the affinity.Methods We measured the functional affinity of rhEndoglin conjugated eptide with non-competitive ELISA method.After coating the peptide by BSA binding with glutaral couple,affirming the best concentration,best time of peptide to coat the plate and the coating coefficient,and the proper binding time of peptide to Endoglin to reach an equilibrium,we plotted the standard curve of the binding reaction of peptide and Endoglin.Results The affinity constant of peptide and anti-hEndoglin IgG is respectively(2.956?0.749)?106mol/L and(7.403?10.76) ?108mol/L.Conclusion The peptide we got from the peptide liberary can strongly bind to Endoglin,providing a theoretical basis for its clinical use.

Neovascular glaucoma is a rare and severe complication of hypoperfusion retinopathy.The appearance of hypoperfu- sion retinopathy complicating neovascular glaucoma in ophthalmolscopy and fundus fluorescein angiography shows a special feature. Neovascular glaucoma occurs when new fibrovascular tissues proliferate onto the chamber angle and obstruct the trabecular meshwork. The stenosis or occlusion of internal carotid artery is the most common reason of hypoperfusion retinopathy in elder people.Early recog- nition and treatment of patients with carotid occlusive diseases may prevent more serious complications.

It is a challenging and important project to prolong the in vivo half life of protein and peptide drugs by physicochemical methods without new molecular entities generation. Protein crystallization provides a new strategy for improving the stability and in vivo delivery of these drugs. We show here that recombinant human interferon-alpha (rhIFN) can form spherical crystals. The physical and chemical features of the crystals were characterized, and drug dissolution was determined in vitro. The pharmacokinetics of crystallized interferon after sc injection in rabbit at 1.5 x 10(7) U x kg(-1) was compared to that of soluble form. The crystals were characterized as mono-dispersed spheres, with yield of > 80%, mean diameter size of about 16 microm and crystallinity of 23.2%. The in vitro dissolution behavior of crystallized rhIFN was featured as low initial burst release (21% within the first 2 h) and prolonged cumulative dissolution time up to 72 h without biological potency lost. After sc administration of soluble and crystallized interferon in rabbits, the peak time (T(max)) and half life (t1/2) were prolonged from (1.80 +/- 0.45) h and (1.35 +/- 0.35) h to (13.20 +/- 2.68) h and (10.68 +/- 1.97) h, respectively. The corresponding peak concentration decreased from (1 411.10 +/- 575.28) U x mL(-1) to (721.37 +/- 206.55) U x mL(-1). PK/PD analysis indicated that (96.87 +/- 20.30) % of relative bioavailability was obtained. The research results of this work will provide important academic value and application prospect for improving clinical therapeutic effect and development of biomacromolecules delivery system for protein and peptide drugs.

Objective To investigate the effects of peroxisome proliferators-activated receptorγ(PPARγ)agonist pioglitazone on the expressions of glial fibrillary acidic protein (GFAP) and cyclin D1 in the hippocampal CA1 region after cerebral ischemia in rats.Methods Fifty-four Sprague-Dawley rats were randomly divided into 3 groups:sham operation group,ischemia/reperfusion group,and pioglitazone intervention group (18 in each group).A rat middle cerebral artery occlusion and reperfusion model was induced by the modified suture method.Continuous pioglitazone rosiglitazone gavage (0.65 mg/kg once a day) was conducted for 5 days before modeling in the pioglitazone intervention group.At day 1,3,and 7 after modeling the rats (6 at each time point) were sacrificed and their brains were removed.HE staining was used to detecte the pathological changes of neurons in the hippocampal CA1 region.Immunohistochemical staining was use to detect the expressions of GFAP and cyclin D1 in the hippocampal CA1 region.Results Compared to the sham operation group,at day 3 and 7 after ischemia/reperfusion,the number of neuronal survival in the hippocarmpal CA1 region in the ischemia/reperfusion group was significantly reduced (all P ＜ 0.01).The expressions of GFAP and Cyclin D1 at all time points were significantly upregulated (all P ＜ 0.01).At day 3 and 7 after ischemia/reperfusion,the numbers of neuronal survival in the hippocampal CA1 region in the pioglitazone intervention group were significantly increased (all P ＜0.01).Compared to the ischemia/reperfusion group,the expressions of GFAP and Cyclin D1 at all time points were significantly down-regulated (all P ＜ 0.01).Conclusions PPARγagonist pioglitazone has a significant protective effect on neuron in the hippocampal CA1 region after cerebral ischemia/reperfusion in rats.Its mechanism may be associated with inhibiting GFAP and cyclin D1 expressions.