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Biomedical subjects

Feng Gao

Publications and source records attributed to Feng Gao.

At least 271 records · Page 15Linked to original sources
PubMed2002

A synthetic analog of prostaglandin E(1) prevents the production of reactive oxygen species in the intestinal mucosa of methotrexate-treated rats.

Administration of methotrexate to rats results in severe enterocolitis and death. Previous our studies showed that a synthetic analog of prostaglandin E(1), OP-1206 [17S, 20-dimethyl-trans-Delta(2)-prostaglandin E(1)] ameliorated the anticancer agent-induced enterocolitis of rats. In the current study, we have focused on the biochemical effect of OP-1206 on the methotrexate-induced intestinal inflammation implicating reactive oxygen species (ROS). Methotrexate (15 mg/kg body weight) was orally administered to rats once daily for 5 days. OP-1206 (0.5 microg/kg body weight) was orally administered to rats twice a day for 5 days. On the 6th day, the chemiluminescence from the jejunum was measured to evaluate the generation of ROS. Spontaneous chemiluminescence from the jejunum of the methotrexate-treated rats increased significantly, compared with the control. Luminol-enhanced chemiluminescence from inflamed mucosal scrapings from the jejunum of the methotrexate-treated rats indicated more remarkable enhancement than the control rats. The treatment of OP-1206 with methotrexate showed significantly lower chemiluminescence of both the jejunum and mucosal scrapings than those of the methotrexate-treated rats. The alkaline phosphatase (ALP) activity, as a marker of small intestinal differentiation, in the intestinal mucosa of the methotrexate-treated rats decreased remarkably, but that of the methotrexate and OP-1206-treated rats was significantly higher than that of the methotrexate-treated rats. Thus, OP-1206 may possibly help the anticancer chemotherapy by protecting the small intestine from the methotrexate-induced damage.

Alprostadil↗
PubMed2002

Comparative analysis of commercial assays for the detection and quantification of Human Immunodeficiency Virus Type 1 (HIV-1) RNA in plasma from patients infected with HIV-1 subtype C.

The commercial assays commonly used to quantify plasma human immunodeficiency virus type 1 (HIV-1) RNA in clinical settings were designed to assess HIV-1 subtype B. We compared the performance of 4 commercial assays (Amplicor versions 1.0 and 1.5 [Roche]; Quantiplex [Chiron]; and NASBA HIV-1 RNA QT [Organon Teknika]) in detecting and quantifying HIV-1 RNA in plasma from HIV-infected persons from Zambia, an area where HIV-1 subtype C is predominant. Each assay detected plasma HIV-1 RNA, but they do not all measure statistically similar quantities of plasma HIV-1 RNA.

Female↗
PubMed2002

Heme oxygenase 1 gene transfer prevents CD95/Fas ligand-mediated apoptosis and improves liver allograft survival via carbon monoxide signaling pathway.

Apoptosis via the CD95/FasL (CD95L) pathway plays an important role in allograft rejection. Heme oxygenase 1 (HO-1), a stress-responsive cytoprotective molecule, may be essential in preventing graft rejection. We used Ad-HO-1 gene transfer to analyze HO-1-mediated effects in a rat allogeneic orthotopic liver transplantation (OLT) model. The cytotoxicity to Fas-bearing YAC-1 target cells and frequency of terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling-positive (TUNEL(+)) cells in vitro were diminished in Ad-CD95L + Ad-HO-1-transfected cells, as compared with Ad-CD95L + Ad-beta-gal controls (p < 0.001). AdHO-1 gene transfer prevented <10-day rejection of dark agouti (DA) livers in Lewis (LEW) rats (survival >32 days), and diminished apoptosis. Unlike Ad-beta-gal OLTs, which showed signs of severe acute rejection, OLTs in the Ad-HO-1 group exhibited mild to moderate rejection and improved function. These beneficial effects were abrogated after adjunctive treatment with tin protoporphyrin (SnPP), an HO-1 antagonist. Intragraft expression of HO-1 and antiapoptotic gene products (Bcl-xl/Bag-1) was enhanced in Ad-HO-1-transduced OLTs, in association with selectively depressed expression of helper T cell type 1 cytokines (interleukin 2 and interferon gamma), as compared with Ad-beta-gal controls. To deliver CO, one of the downstream HO-1 mediators, allogeneic OLT recipients were exposed to methylene chloride. Such treatment prolonged survival to >47 days, diminished apoptosis, and preserved hepatic architecture/function. Thus, Ad-HO-1 gene transfer prevents CD95/FasL-mediated apoptosis, and significantly prolongs allogeneic OLT survival via a downstream HO-1-CO signaling pathway.

Animals↗
PubMed2002

Diversity considerations in HIV-1 vaccine selection.

Globally, human immunodeficiency virus-type 1 (HIV-1) is extraordinarily variable, and this diversity poses a major obstacle to AIDS vaccine development. Currently, candidate vaccines are derived from isolates, with the hope that they will be sufficiently cross-reactive to protect against circulating viruses. This may be overly optimistic, however, given that HIV-1 envelope proteins can differ in more than 30% of their amino acids. To contend with the diversity, country-specific vaccines are being considered, but evolutionary relationships may be more useful than regional considerations. Consensus or ancestor sequences could be used in vaccine design to minimize the genetic differences between vaccine strains and contemporary isolates, effectively reducing the extent of diversity by half.

AIDS Vaccines↗
PubMed2002

Maps of optical differential pathlength factor of human adult forehead, somatosensory motor and occipital regions at multi-wavelengths in NIR.

The optical differential pathlength factor (DPF) is an important parameter for physiological measurement using near infrared spectroscopy, but for the human adult head it has been available only for the forehead. Here we report measured DPF results for the forehead, somatosensory motor and occipital regions from measurements on 11 adult volunteers using a time-resolved optical imaging system. The optode separation was about 30 mm and the wavelengths used were 759 nm, 799 nm and 834 nm. Measured DPFs were 7.25 for the central forehead and 6.25 for the temple region at 799 nm. For the central somatosensory and occipital areas (10 mm above the inion), DPFs at 799 nm are 7.5 and 8.75, respectively. Less than 10% decreases of DPF for all these regions were observed when the wavelength increased from 759 nm to 834 nm. To compare these DPF maps with the anatomical structure of the head, a Monte Carlo simulation was carried out to calculate DPF for these regions by using a two-layered semi-infinite model and assuming the thickness of the upper layer to be the sum of the thicknesses of scalp and skull, which was measured from MRI images of a subject's head. The DPF data will be useful for quantitative monitoring of the haemodynamic changes occurring in adult heads.

Brain↗
PubMed2002

Idoxifene causes endothelium-dependent, nitric oxide-mediated vasorelaxation in male rats.

Selective estrogen receptor modulators are estrogen-like compounds that lack the deleterious effects of estrogen. The present study was designed to determine whether idoxifene, a new selective estrogen receptor modulator, may have a vasodilatory effect on aortic vessels from male animals, and if so, to investigate the mechanism (i.e., endothelium-independent, direct vasorelaxation vs. endothelium-dependent, nitric oxide mediated vasorelaxation) by which idoxifene may exert its vasodilatory effect. Superior mesenteric arterial rings from adult male Sprague-Dawley rats were suspended in Krebs-Henseleit ring baths. Rings were contracted with 50 nM U-46619 (9,11-epoxymethano-PGH(2)), a thromboxane A(2) mimetic. Cumulative dose-response vasorelaxation to idoxifene (0.01 to 3 microM) was studied in the presence and absence of 200 microM N(omega)-nitro-L-arginine methyl ester (L-NAME, a nitric oxide synthase (NOS) inhibitor). The results obtained from idoxifene were compared with those from 17beta-estradiol. Our experimental results demonstrated that addition of idoxifene to superior mesenteric arterial rings isolated from male rats resulted in a dose-dependent vasorelaxation in the range of 0.1 microM (minimal vasodilatory concentration) to 3 microM (maximal vasodilatory concentration). Pre-treatment with L-NAME to block nitric oxide (NO) production virtually abolished idoxifene-induced vasodilatation, indicating that idoxifene caused an NO-mediated vasorelaxation in vessels from male animals. Addition of 17beta-estradiol also resulted in an endothelium-dependent vasorelaxation in aortic rings from male rats. However, these vessels were 30-fold less sensitive to 17beta-estradiol than to idoxifene in their vasorelaxation responses. Taken together, these results demonstrate that selective estrogen receptor modulators are superior to traditional estrogen in their vascular protection and may thus have potential therapeutic use in protection against cardiovascular disease, especially in male patients.

Animals↗
PubMed2002

Prediction of volume of distribution values in humans for neutral and basic drugs using physicochemical measurements and plasma protein binding data.

We present a method for the prediction of volume of distribution in humans, for neutral and basic compounds. It is based on two experimentally determined physicochemical parameters, ElogD(7.4) and f(i(7.4)), the latter being the fraction of compound ionized at pH 7.4 and on the fraction of free drug in plasma (f(u)). The fraction unbound in tissues (f(ut)), determined via a regression analysis from 64 compounds using the parameters described, is then used to predict VD(ss) via the Oie-Tozer equation. Accuracy of this method was determined using a test set of 14 compounds, and it was demonstrated that human VD(ss) values could be predicted, on average, within or very close to 2-fold of the actual value. The present method is as accurate as reported methods based on animal pharmacokinetic data, using a similar set of compounds, and ranges between 1.62 and 2.20 as mean-fold error. This method has the advantage of being amenable to automation, and therefore fast throughput, it is compound and resources sparing, and it offers a rationale for the reduction of the use of animals in pharmacokinetic studies. A discussion of the potential errors that may be encountered, including errors in the determination of f(u), is offered, and the caveats about the use of computed vs experimentally determined logD and pK(a) values are addressed.

Blood Proteins↗
PubMed2002

Microwave assisted template removal of siliceous porous materials.

Organic templates of meso- and macro-porous siliceous materials can be completely removed within minutes by microwave digestion, resulting in highly ordered inorganic frameworks with higher surface areas, larger pore volumes, lower structural shrinkage and richer silanol groups compared with those from conventional template removal methods.

Journal Article↗
PubMed2002

Imaging of in vitro chicken leg using time-resolved near-infrared optical tomography.

Near-infrared optical imaging gains much attention because of its noninvasiveness and deep penetration depths into tissue. Here, we report near-infrared optical tomographic imaging of an in vitro chicken leg from time-resolved measurements. The in vitro chicken leg, dipped in a cylindrical container filled with diluted Intralipid-10% solution, was imaged with a multichannel time-resolved imaging system. A two-dimensional reconstruction algorithm based on a modified generalized pulse spectrum technique has been developed to reconstruct the images of both the absorption and reduced scattering coefficients simultaneously and quickly. The results demonstrate that a simultaneous reconstruction of absorption and reduced scattering coefficients from time-resolved measurement has a potential to reveal the changes in the optical properties associated with not only the physiological information but also the anatomical structure of the organ.

Algorithms↗
PubMed2002

Immunopathogenesis of accelerated allograft rejection in sensitized recipients: humoral and nonhumoral mechanisms.

INTRODUCTION: Accelerated rejection (AccR) in sensitized recipients (second-set rejection) is considered a classic humorally mediated form of allograft rejection, although additional effector mechanisms may be involved. METHODS: We developed a model of AccR in which C57BL6 mice are sensitized by BALB/c skin grafts, followed 10 days later by transplantation of BALB/c hearts. We undertook analysis of various humoral and cellular components in this model using knockout or monoclonal antibody-treated allograft recipients. RESULTS: Sensitized mice rejected cardiac allografts in 34+/-7 hr. AccR was accompanied by endothelial deposition of immunoglobulins, complement, and fibrin, but also by dense expression of multiple chemokines and a mixed polymorphonuclear and mononuclear cellular infiltrate. Whereas neutrophil or complement depletion had no significant effect on the tempo of AccR, surprisingly B cell-deficient recipients still underwent AccR (41+/-7 hr) in conjunction with T cell and macrophage recruitment. In contrast, T cell-deficient (nude) mice maintained functioning cardiac allografts for >720 hr despite prior skin engraftment. CONCLUSIONS: AccR in sensitized experimental recipients involves multiple effector pathways. Although most previous studies have emphasized the key role of humoral pathways in mediating AccR, our data indicate that T cell-dependent mechanisms can also promote AccR, alone or in conjunction with humoral responses.

Animals↗
PubMed2002

Load-dependent and -independent regulation of proinflammatory cytokine and cytokine receptor gene expression in the adult mammalian heart.

BACKGROUND: Although previous studies have examined the effects of acute hemodynamic pressure overload on proinflammatory cytokine gene expression, the effects of sustained hemodynamic overloading have not been examined. METHODS AND RESULTS: Sustained hemodynamic pressure overloading was produced in mice by transverse constriction of the aorta. Proinflammatory cytokine and cytokine receptor gene expression were determined by ribonuclease protection assays (RPA) at 6 hours and at 3, 7, 14 and 35 days after banding. M-mode echocardiography was used to assess left ventricular structure and function at identical time points. RPA showed that tumor necrosis factor (TNF), interleukin (IL)-1beta, and IL-6 mRNA levels were maximal at 6 hours and returned to baseline levels within 72 hours. There was a significant increase in IL-1RII and IL-6Ralpha receptor mRNA levels after overloading but no significant increase in TNFR1, TNFR2, IL-1RI, or gp130 mRNA levels. The transient increase in expression of proinflammatory cytokine gene expression was not explained by changes in left ventricular loading conditions, left ventricular wall stress, desensitization of proinflammatory genes, or decreased nuclear factor-kappaB activation. It is interesting that transverse constriction of the aorta provoked an increase in the expression of tristetraprolin, a homeostatic zinc finger protein that is known to destabilize TNF mRNA. CONCLUSION: Sustained hemodynamic overloading provokes a transient increase in proinflammatory cytokine and cytokine receptor gene expression; however, the decrease in proinflammatory cytokine gene expression occurred in the absence of changes in loading conditions, suggesting that the expression of proinflammatory cytokines in the heart is regulated, at least in part, by load-dependent and load-independent mechanisms.

Animals↗
PubMed2002

Nitric oxide mediates the antiapoptotic effect of insulin in myocardial ischemia-reperfusion: the roles of PI3-kinase, Akt, and endothelial nitric oxide synthase phosphorylation.

BACKGROUND: Recent evidence from cultured endothelial cell studies suggests that phosphorylation of endothelial nitric oxide synthase (eNOS) through the PI3-kinase-Akt pathway increases NO production. This study was designed to elucidate the signaling pathway involved in the antiapoptotic effect of insulin in vivo and to test the hypothesis that phosphorylation of eNOS by insulin may participate in the cardioprotective effect of insulin after myocardial ischemia and reperfusion. METHODS AND RESULTS: Male Sprague-Dawley rats were subjected to 30 minutes of myocardial ischemia and 4 hours of reperfusion. Rats were randomized to receive vehicle, insulin, insulin plus wortmannin, or insulin plus L-NAME. Treatment with insulin resulted in 2.6-fold and 4.3-fold increases in Akt and eNOS phosphorylation and a significant increase in NO production in ischemic/reperfused myocardial tissue. Phosphorylation of Akt and eNOS and increase of NO production by insulin were completely blocked by wortmannin, a PI3-kinase inhibitor. Pretreatment with L-NAME, a nonselective NOS inhibitor, had no effect on Akt and eNOS phosphorylation but significantly reduced NO production. Moreover, treatment with insulin markedly reduced myocardial apoptotic death (P<0.01 versus vehicle). Pretreatment with wortmannin abolished the antiapoptotic effect of insulin. Most importantly, pretreatment with L-NAME also significantly reduced the antiapoptotic effect of insulin (P<0.01 versus insulin). CONCLUSIONS: These results demonstrated that in vivo administration of insulin activated Akt through the PI3-kinase-dependent mechanism and reduced postischemic myocardial apoptotic death. Phosphorylation of eNOS and the concurrent increase of NO production contribute significantly to the antiapoptotic effect of insulin.

Androstadienes↗
PubMed2002

Purification, crystallization and preliminary X-ray diffraction studies of a Ca2+-binding protein, human S100P.

S100P, a Ca(2+)-binding protein, is a member of the S100 family. Its presence is associated with the development of prostate cancer, but its cellular function is not known. Recombinant human S100P has been expressed and purified in bacterial cells and crystals of human S100P in the calcium-bound state have been grown using the vapour-diffusion technique with PEG 4000 as precipitant. Diffraction data have been obtained to a resolution of 2.0 A from a single frozen S100P crystal which belongs to the space group P4(1)2(1)2, with unit-cell parameters a = b = 60.8, c = 47.6 A.

Calcium-Binding Proteins↗
PubMed2002

[Promotion of growth of human breast cancer cells MDA231 by human sperm membrane-bound hyaluronidase: an experimental study].

OBJECTIVE: To study the mechanism how human sperm membrane-bound hyaluronidase (PH20) promotes the gowth of human breast cancer. METHODS: Full-length cDNA of human PH20 was transfected into human breast cancer cell line MDA231. The transfectant MDA231-PH20 was then implanted into the chorio-allantoic membrane (CAM) of chicken embryo to form a tumor. Four days after implantation, the tumors were resected to be weighed. The angiogenesis in tumor tissue was examined by immunohistochemistry. Trans-well cell culture was used to study the effect of MDA231-PH20 on the growth of adult bovine aortic endothelial cells (ABAE). The expression of fibroblast growth factor-2 (FGF-2) in the tumor cells was investigated by Western blotting. ELISA was used to examine the secretion of FGF-2 and hyaluronic acid. The same amount of empty vector pcDNA3, instead of PH20, was transfected into human breast cancer cell line MDA231 as control group. RESULTS: The average weight of tumor four days after implantation was 44.7 mg +/- 10.2 mg in the MDA231-PH20 group, and was 21.3 mg +/- 2.8 mg in the control group (t = 2.418, P = 0.038). Neogenetic vessels increased remarkably in MDA231-PH20 tumor tissues. The expression of FGF-2 protein was much higher in MDA231-PH20 cells. The FGF content and HA secretion were higher in the MDA231-PH20 group than in the control group (8.10 pg/ml +/- 1.56 pg/ml vs. 3.94 pg/ml +/- 0.82 pg/ml, and 1 220 ng/ml +/- 254 ng/ml vs. 462 ng/ml +/- 96 ng/ml, all P < 0.01). The growth of ABAE cells was significantly accelerated after co-culture with MDA231-PH20 transfectant. CONCLUSION: PH20 may promote the growth of human breast cancer by accelerating the release of FGF-2 from tumor cells, decomposing HA into small fragments, and promoting angiogenesis.

Animals↗
PubMed2002

p38 MAPK inhibition reduces myocardial reperfusion injury via inhibition of endothelial adhesion molecule expression and blockade of PMN accumulation.

BACKGROUND: In vitro evidence suggests that the p38 mitogen-activated protein kinase (p38 MAPK) plays a crucial role in PMN activation and inflammatory cytokine production. However, the effect of p38 MAPK on myocardial reperfusion injury, a pathologic condition involving a typical inflammatory response, has not been fully examined. In the present study, we investigated the effect of SB 239063, a specific p38 MAPK inhibitor, on myocardial injury in a murine ischemia/reperfusion (I/R) model and elucidated the mechanism by which p38 MAPK inhibitor may exert its protective effect against I/R injury. METHODS AND RESULTS: I/R resulted in a significant myocardial injury (myocardial infarct 45 +/- 2.9%) and marked PMN accumulation (myeloperoxidase activity 1.03 +/- 0.16 U/100 g tissue). Administration of SB 239063 significantly inhibited the myocardial inflammatory response as evidenced by reduced PMN accumulation in I/R myocardial tissue (0.62 +/- 0.008 U/100 g tissue, P<0.01 vs. vehicle), and markedly attenuated myocardial reperfusion injury (myocardial infarct size: 28 +/- 2.4%, P<0.01 vs. vehicle). Moreover, treatment with SB 239063 significantly attenuated I/R-induced P-selectin and ICAM-1 upregulation (13.8 +/- 2.7 vs. 23.9 +/- 3.1%, and 29.4 +/- 1.6 vs. 56.3 +/- 4.8%, respectively P<0.01). In addition, pre-treatment with R15.7, a monoclonal antibody against CD 18 adhesion molecule on PMN surface that virtually abolished PMN accumulation in ischemic-reperfused myocardial tissue, significantly, but not completely, blocked the cardioprotection exerted by SB 239063. CONCLUSION: These results demonstrated for the first time that p38 MAPK activation plays a significant role in adhesion molecule upregulation on ischemia-reperfused endothelial cells and is an important signaling step in the pathogenesis of PMN-mediated tissue injury.

Analysis of Variance↗
PubMed2002

Improvement of image quality in diffuse optical tomography by use of full time-resolved data.

In the field of diffuse optical tomography (DOT), it is widely accepted that time-resolved (TR) measurement can provide the richest information on photon migration in a turbid medium, such as biological tissue. However, the currently available image reconstruction algorithms for TR DOT are based mostly on the cw component or some featured data types of original temporal profiles, which are related to the solution of a time-independent diffusion equation. Although this methodology can greatly simplify the reconstruction process, it suffers from low spatial resolution and poor quantitativeness owing to the limitation of effectively applicable data types. To improve image quality, it has been argued that exploiting the full TR data is essential. We propose implementation of a DOT algorithm by using full TR data and furthermore a variant algorithm with time slices of TR data to alleviate the computational complexity and enhance noise robustness. Compared with those algorithms where the featured data types are used, our evaluations on the spatial resolution and quantitativeness show that a significant improvement in imaging quality can be achieved when full TR data are used, which convinces the DOT community of the potential advantage of the TR domain over cw and frequency domains.

Humans↗