Biomedical subjects
Publications and source records attributed to Hai Wang.
This literature review presents hydrolysis of active pharmaceutical ingredients as well as the effects on dosage form stability due to hydrolysis of excipients. Mechanisms and measurement methods are discussed and recommendations for formulation stabilization are listed.
AIM: To investigate the antagonistic effects of the novel compounds on vasoconstriction induced by ET-1 and the effect on the blood pressure of stroke-prone spontaneously hypertensive rats. METHODS: Organ bath experiment and whole cardiac function experiment were used. RESULTS: The analogues of o-CPhe-D-Trp-D-Phe(-X)-OH showed good ability against endothelin biological effects. When X was displaced by 3-F, 3-Cl or 4-Cl, the novel compounds inhibit the vascular constriction induced by ET-1 in a concentration-dependent manner, the IC50 +/- L95 were (0.09 +/- 0.05), (0.15 +/- 0.06) or (0.11 +/- 0.03) mumol.L-1 respectively. The blood pressure of stroke-prone spontaneously hypertensive rats was decreased. No significant effect on cardiac function of rats was discovered. CONCLUSION: The results demonstrate that among the six kinds of compounds, those with o-CPhe-D-Trp-D-Phe (-X)-OH configuration showed good biological effects.
Glomerular development proceeds through the spatially ordered and sequential recruitment, proliferation, assembly, and differentiation of endothelial, mesangial, and epithelial progenitors. The molecular determinants of cell-cell recognition and targeting in this process have yet to be defined. The Eph/ephrin family of membrane receptors and counter-receptors are critical participants of developmental vascular assembly in extrarenal sites. Renal expression patterns of ephrin-B2 and EphB4 were investigated using mice expressing beta-galactosidase under control of ephrin-B2 or EphB4 promoters. The earliest glomerular expression of ephrin-B2 was identified in a subset of differentiating comma-stage glomerular epithelial cells (podocyte progenitors) adjacent to the vascular cleft where endothelial progenitors are subsequently recruited. Epithelial ephrin-B2 expression was accompanied by expression in endothelial and mesangial cells as capillary assembly progressed. At or near completion of glomerular maturation, epithelial ephrin-B2 expression was extinguished, with persistence in glomerular endothelial cells. Throughout development, one of several ephrin-B2 receptors, EphB4, was persistently and exclusively expressed in endothelial cells of venous structures. The findings show sequential ephrin-B2 expression across glomerular lineages, first in a distinct subset of podocyte progenitors and subsequently in endothelial cells of the developing glomerulus. Given targeting functions for Eph/ephrin family proteins, the findings suggest that ephrin-B2 expression marks podocyte progenitors at the site of vascular cleft formation, where expression may establish an "address" to which endothelial and mesangial progenitors are recruited. Thus, the present results suggest that ephrin-B2 and EphB interactions play an important role in glomerular microvascular assembly.
BACKGROUND: BZLF1, an EBV (Epstein-Barr virus) immediate early gene, is required for EBV lytic replication that causes the death of host cells. EBNA1, the product of EBV latent gene, binds to the family repeats (FR) of the origin of replication (Orip) regulating EBV replication. MATERIALS AND METHODS: A vector pFR-Z (BZLF1 controlled by FR domain of EBV) was constructed and transfected into EBV-positive 5-8F and-negative HNE3 nasopharyngeal carcinoma cells and BZLF1-induced cytotoxicity was tested. RESULTS: EBNA1 expression was detected in 5-8F but not HNE3 cells and, in agreement, pFR controlled luciferase expression was activated in 5-8F cells but inhibited in HNE3 cells. Gardella gel assay demonstrated that pFR-Z effectively induced EBV lytic replication in 5-8F but not HNE3 cells. The lytic cytotoxicity was confirmed by a diminished cell survival and the induction of lytic proteins EA-D and gp125. The cytotoxicity was also strikingly enhanced by addition of GCV (gancyclovir) that kill cells with lytic form EBV. CONCLUSION: pFR-Z is a specific gene therapy vehicle for EBV-positive carcinomas.
BACKGROUND: Vessel dilator and kaliuretic peptide have anticancer effects in human prostate adenocarcinomas. MATERIALS AND METHODS: Vessel dilator, kaliuretic peptide and cyclic GMP's effects on ERK 1/2 kinase were examined in human prostate adenocarcinoma cells. RESULTS: Vessel dilator and kaliuretic peptide decreased the activation of ERK 1/2 over a concentration range of 0.01 microM to 1 microM. Vessel dilator and kaliuretic peptide (each 1 microM) inhibited the phosphorylation of ERK 1/2 kinase 96% (p < 0.0001) and 70% (p < 0.001), respectively. Both had significant effects within five minutes at their 0.01 microM concentrations. The inhibition of ERK 1/2 lasted for at least two hours secondary to both. Their ability to inhibit ERK 1/2 was decreased by cyclic GMP antibody and cyclic GMP itself decreased ERK 1/2 phosphorylation. CONCLUSION: Vessel dilator and kaliuretic peptide both inhibit ERK 1/2 kinase mediated via cyclic GMP as part of their anticancer mechanism(s) of action.
BACKGROUND: Atrial natriuretic peptide (ANP) and long acting natriuretic peptide (LANP) have anticancer effects in human prostate adenocarcinomas. MATERIALS AND METHODS: ANP, LANP and cyclic GMP's effects on extracellular signal-regulated kinase (ERK) 1/2 kinase were examined in human prostate adenocarcinoma cells. RESULTS: ANP and LANP decreased the activation of ERK 1/2 over a concentration range of 0.01 microM to 10 microM. ANP and LANP's maximal inhibition of the phosphorylation of ERK 1/2 kinase were 94% and 88% (p < 0.0001), respectively. ANP had significant effects within five min at its 10 microM concentration. The inhibition of ERK 1/2 lasted for at least two h, where it was maximal, secondary to both peptides. Their ability to inhibit ERK 1/2 was inhibited by cyclic GMP antibody and cyclic GMP itself inhibited ERK 1/2 phosphorylation. CONCLUSION: ANP and LANP both inhibit ERK 1/2 kinase mediated via cyclic GMP as part of their anticancer mechanism(s) of action.