The Harbola-Sahni exchange potential is the work needed to move an electron against the electric field of its hole charge distribution. We prove that it is not the exact exchange potential of density-functional theory, by showing that it yields the wrong second-order gradient expansion in the slowly varying limit. But we also discover that it yields the correct local-density approximation. Thus the Harbola-Sahni potential is a more physically correct version of the Slater potential, one that is better suited for molecular and solid-state applications. As a step in our derivation, we present the third-order gradient expansion of the exchange hole density, and discuss its structure. We also describe a new version of the Harbola-Sahni potential which corrects its path dependence. The exact exchange potential for an atom is given by the optimized potential model (OPM) of Talman and Shadwick. By using enhanced numerics, we confirm that the OPM potential satisfies the Levy-Perdew virial relation and exhibits correct -1/r behavior at large r. Numerical calculations also show that the intershell maxima in the exact exchange potential are needed to lower the total energy. These ``bumps'' are missing from the Harbola-Sahni and Slater potentials.
Objective:To detect the VEGF expression in gliomas and the relationships between VEGF and the occurrence,progression,histological classification,grade,and diagnosis,prognosis of human gliomas.Methods:132 gliomas were detected by means of immunohistochemical S-P method.Results:VEGF expression was seen in 87 out of 132 gliomas(65.91%),in 1 of 9 NB(11.11%).The positive expression and quantitative analysis scores were 44.44% and 2.09±2.63,74.00% and 3.48±2.47,96.43% and 5.04±1.97 in BG,MG,HMG respectively.VEGF level in HMG were considerably higher than those in MG and BG(P0 05).VEGF expression was observed in 10 out of 11 medulloblastomas(Meds).VEGF expression was found in cytoplasma of oligodendrogliomas.Conclusion:The VEGF expression level rises with the grade and plays an important role in the occurrence,transformation and progression of gliomas.
The human VEGF 121 cDNA was amplified by RT PCR, and was inserted into the Pichia pastoris expression vector pPIC9K to form the expression plasmid p9KVEGF 121 . This recombinant plasmid was transformed into GS115. Transformants were screened by G418 YPD plates and were induced by methanol. The expression product of r hVEGF 121 amounted to 900 mg/L by a 5 liter fermentor, over 70% of the total secreted protein. The purified r hVEGF 121 can stimulate the proliferation of bovine capillary endothelial cells and shows high vascular permeability.
Objective To explore the effect of antisense VEGF121 on cell proliferation in pancreatic cancer cell line in vitro,so as to elucidate the depression of tumor growth by antisense VEGF121.Methods Pancreatic Cancer cell BxPC-3 was transfected with pcDNA3-ASVEGF121 and pcDNA3 as control.VEGF expression was tested by RT-PCR and ELISA.Colony forming test and growth curve MTT assay were carried out to assess the proliferation potency.Culture cells were labeled by Annexin Ⅴ-FITC and PI,then apoptosis was tested by flow cytometry.Results VEGF protein was decreased in the culture media from transfected cell.Cells transfected with antisense VEGF121 vector had a lower colony forming rate,while cell growth is significantly inhibited in the growth curve test.It was also put into evidence that antisense VEGF121 vector could promote apoptosis in the pancreatic cancer in vitro.Conclusions Antisense VEGF121 vector can inhibit the VEGF expression of pancreatic cancer cell line in vitro,and can inhibit cell growth as well as promote cell apoptosis.
The aging process is obvious in the cardiovascular system in older people. Stiffening of the arterial tree alters afterload and left ventricular geometry. Although resting left ventricular systolic function is maintained, left ventricular diastolic function changes substantially. Cardiovascular function in older people during exercise is also significantly altered but can be modified by exercise training in older adults. Age related changes in cardiovascular structure and function also lower the threshold at which cardiac diseases become apparent. The changes in cardiovascular structure and function at rest and during exercise in older people and highlights their consequences are reviewed.
Abstract Airway re‐modelling in asthma usually results in an irreversible weakness of pulmonary ventilation, however, its initiating or controlling mechanism remains unclear. In this study, we hypothesize that signal communication between airway epithelial cells and sub‐mucosal fibroblast cells may play an important role in the maintenance of structure homeostasis in a physiologic condition and in initiation of airway remodelling in a stressed condition. To test the hypothesis, a co‐cultured system of human bronchial epithelial cells (BEC) and human lung fibroblasts (HLF) were designed to observe the effects of BEC, in the normal state or in a BRS‐3 activated state, on the proliferation and collagen synthesis of HLF. The results showed that the proliferation activities of both BEC and HLF inhibited each other under the normal state. BRS‐3‐activated BEC can transform the reciprocal inhibition into promoting effects. The secretion of TGF‐β1 increased and the synthesis of PGE2 decreased from BRS‐3‐activated BEC, which were correlated with the proliferation and collagen synthesis of HLF. The proliferation activities of HLF were weakened by co‐culture with TGF‐β1 antisense oligonucleotides (ASO) treated BEC. It was concluded that, in the normal state, BEC inhibits the activities of fibroblasts through release of PGE2 to maintain the airway homeostasis; however when stressed, for example by BRS‐3 activation, BEC promote the activities of fibroblasts mediated by TGF‐β1, thereby facilitating the airway re‐modelling.
Autophagy and apoptosis are closely associated. In previous studies, pseudolaric acid B (PAB), a diterpene acid isolated from the root and trunk bark of Pseudolarix kaempferi Gordon (Pinaceae), was demonstrated to induce apoptosis in various cell lines. However, in L929 murine fibrosarcoma and SW579 human thyroid squamous cell carcinoma cells, only autophagy was induced. In the present study, another cell line, MRC5 human lung fibroblast cells, was identified in which PAB only induced autophagy. The relationship between apoptosis and autophagy subsequent to PAB treatment in MRC5 cells was explored. When autophagy was inhibited by 3‑methyladenine (3MA), apoptosis was induced in the PAB‑treated MRC5 cells. To study the mechanism for the promotion of apoptosis by 3MA in the PAB‑treated cells, the expression of members from the apoptotic signal pathways was assessed. As Bcl‑2, Bcl‑2 associated X and pro‑caspase‑9 expression following PAB treatment was not affected by 3MA treatment, it was determined that apoptosis was induced independent of the mitochondrial pathway of apoptosis. As Fas and pro‑caspase‑8 expression following PAB treatment were not altered by 3MA, it was further determined that the death receptor pathway was not induced. However, the phosphorylation of c‑Jun‑N‑terminal kinase and the expression of pro‑caspase‑3 were upregulated, and the phosphorylation of extracellular signal‑regulated kinase downregulated, by the combination of PAB and 3MA treatment compared with PAB alone. It was also observed that 3MA did not affect the microtubule aggregation ability of PAB. Therefore, inhibiting autophagy in MRC5 cells did not affect the role of PAB in microtubule aggregation, while apoptosis was induced. This may present a strategy to enhance the anti‑tumor effects of PAB.
IgA nephropathy (IgAN) is characterized by predominant IgA deposition in the glomerular mesangium. It has been considered that the deposited IgA is synthesized by B cells, although recent reports have suggested the implication of other cell types. Therefore, the present study investigated whether glomerular mesangial cells could produce IgA by themselves. Semi‑quantitative reverse transcription-polymerase chain reaction, and immunostaining analysis revealed that the IgA protein and gene transcripts were expressed in primary human renal mesangial cells (HRMCs). Furthermore, the IgA heavy chain (α1 and α2) and the light chain (κ and λ) were localized in the cytoplasm or were located on the cell membranes of human mesangial cells (HMCs). Mass spectrometry results indicated that Ig α1 and Ig α2 were secreted in the culture media of HMCs. The transcripts of Ig α, Ig κ and Ig λ constant regions were detected. The predominant rearrangement pattern of the variable region of Ig κ, was Vκ3‑20*01/Jκ1*01 in HMCs and Vκ1‑12*01/Jκ4*01 in HRMCs. In addition, knockdown of Ig α1 expression by small interfering RNA (siRNA) inhibited cell adhesion and promoted apoptosis. Our findings demonstrate that HMCs can express IgA, and that this expression is associated with cell functions, which may contribute to the deposition of IgA in patients with IgAN.
Objective To investigate the effects of FHIT gene on the malignant growth of lung cancer cells with different gene background and its mechanism of cancer inhibition. Methods A mammalian expression vector PEGFP-FHIT was transfected into the lung cancer lines by lipofectamine.We tested the transfected cancer cell lines by RT-PCR,immunochemical stain and Western blot.The inhibition growth efficacy of extraneous FHIT was evaluated by clonogenic survival assay and flow cytometry.The expression of p21~(Waf/cip) protein was examined by Western blot.Results All of the transfected cancer cell lines had the expression of FHIT gene and protein.The clonal formation rate of 801D-FHIT(46.3%),A2-FHIT(43.7%),A549-FHIT(32.7%) was lower than that of 801D(58.2%),A2(60.3%),A549(52.8%)(P0.01).Cell cycle analysis by FACS showed that 801D-FHIT,A2FHIT and A549-FHIT cells were blocked at G_1,S and G_2 phase,respectively.A significant increase in p21~(Waf/cip) protein expression was noticed in FHIT expression clones 801D-FHIT,A2-FHIT and A549-FHIT compared with that of the control parental cell lines.Conclusion Extrogenous FHIT gene can suppress the proliferation in different FHIT gene status and regulate the cell cycle.There is a different cell cycle arrest in three sorts of lung cancer cell lines with different expression of FHIT gene.Our data suggests that observed growth-inhibitory effect in FHIT-reexpressioning cells could be related to cell cycle arrest and linked to the increased p21~(Waf/cip) protein expression.
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