Biomedical subjects

N Yang

Publications and source records attributed to N Yang.

At least 91 records · Page 5Linked to original sources

PubMed1997

Two-dimensional film dosimetry application in heterogeneous materials exposed to megavoltage photon beams.

Measurement of dose within tissues and tissue interfaces having sharp density discontinuities and heterogeneities (such as in the lung, esophagus, and rectum) is essential for treatment plan verification and accurate prediction of the prescribed dose. This study examines the feasibility and utility of simplifying standard film dosimetry to measure dose distributions deposited by megavoltage beams in tissue substitutes (such as cork for lung) and anthropomorphic phantoms which closely resemble human tissues having large density heterogeneities and having sharp tissue interfaces. In addition, film dosimetry determined the dose distribution involving superposition of multiple radiation fields and helped evaluate the accuracy of a commercial treatment planning program which incorporates tissue heterogeneity effects through the "effective path length" algorithm. This study shows that these treatment planning programs and simple calculations overestimate the dose delivered within the lower density material in heterogeneous regions.

Biophysical Phenomena↗

PubMed1997

Alpha1D-adrenergic receptors and mitogen-activated protein kinase mediate increased protein synthesis by arterial smooth muscle.

Catecholamines may influence vascular smooth muscle cell (SMC) growth and vascular hypertrophic diseases. We previously demonstrated that stimulation of alpha1-adrenoceptors (AR) causes hypertrophy of vascular SMCs in vitro and in situ. Here, we used adult rat aorta SMCs that express alpha1D- and alpha1B-ARs (but not alpha1A-ARs) in vitro to examine the mechanisms and alpha1-AR subtypes involved. Norepinephrine (NE) increased protein synthesis and content in a time- and dose-dependent manner. To identify the responsible alpha1-AR subtype, we first documented the selectivity of two alpha1-AR subtype antagonists, BMY 7378 (alpha1D-AR antagonist) and chloroethylclonidine (CEC; alpha1B-AR antagonist), using Rat-1 fibroblasts stably transfected with the three different rodent alpha1-AR cDNAs. NE dose-dependently increased protein synthesis in each cell line. In alpha1D fibroblasts, BMY 7378 inhibited growth and protected alpha1D-ARs from CEC alkylation while having little blocking or protecting effect on the growth induced by stimulation of fibroblasts that express alpha1A- or alpha1B-ARs. In rat aorta SMCs, pretreatment with CEC in the presence of BMY 7378 to protect alpha1D-ARs had no effect on NE-induced protein synthesis. BMY 7378 inhibited the SMC growth response with a pKb of 8.4. NE caused rapid and transient p42-p44 mitogen-activated protein kinase (MAPK) activation that was alpha1D-AR dependent. Furthermore, NE caused tyrosine phosphorylation of multiple cellular proteins, phosphorylation of Raf-1, and stimulation of c-fos mRNA expression in aorta SMCs. The selective MAPK kinase inhibitor PD 98059 inhibited NE-induced protein synthesis and MAPK activation with IC50 values of 2.3 and 1.6 microM, respectively. These data demonstrate that SMC growth induced by NE is mediated by alpha1D-ARs that couple to activation of the MAPK cascade.

Animals↗

PubMed1997

CRE-like response element regulates expression of rat alpha 2D-adrenergic receptor gene in vascular smooth muscle.

Contractile and binding studies indicate that alpha 2-adrenergic receptors (ARs) are differentially expressed by vascular smooth muscle cells (SMCs) according to vascular segment (artery, arteriole, vein). In the present study, alpha 2D-AR mRNA was two- to threefold higher in vena cava than in aorta. To understand vascular regulation of alpha 2D-AR expression in these cells, we sequenced 2.8 kb of the 5' flanking region of the alpha 2D-AR gene. Notable features include two potential TATA boxes, an adenosine 3',5'-cyclic monophosphate response element (CRE)-like binding element, and an Sp1 element. Comparison of the rat and human genes revealed an overall homology of 74% over the 1.87-kb sequence 5' to the translation initiator methionine, including complete homology at the distal TATA, CRE-like, and Sp1 sites, alpha 2D-AR transcription starts from the guanine nucleotide 18 base pair downstream from the distal TATA box. Reporter gene constructs demonstrated strong alpha 2D-AR promoter activity, but with several differences in construct activity, in both rat aorta and vena cava SMCs. Analysis of an essential promoter fragment revealed two regions protected by aorta and vena cava SMC nuclear proteins. The core sequences of these protected regions are TGACGCTA and TATAA. The former CRE-like element conferred specific binding of both aorta and vena cava nuclear proteins. In addition, promoter activity was increased 300% by forskolin or 8-bromoadenosine 3',5'-cyclic monophosphate, indicating that the CRE-like element may regulate alpha 2D-AR expression in vascular tissue.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1997

The mouse estrogen receptor-related orphan receptor alpha 1: molecular cloning and estrogen responsiveness.

Estrogen receptor-related orphan receptor alpha 1 is a member of the steroid/thyroid nuclear receptor superfamily. We have previously cloned the human estrogen receptor-related orphan receptor alpha 1 (hERR alpha 1) cDNA and demonstrated that it enhances estrogen responsiveness of the lactoferrin gene promoter in transfected human endometrial carcinoma cells. In the present study, we used the hERR alpha 1 cDNA as a probe and isolated the mouse homologue of ERR alpha 1 from the cDNA libraries of the brain and kidney. Sequence comparison between human and mouse ERR alpha 1 (mERR alpha 1) revealed that the homologies are 89% in nucleotides and 97% in amino acids. By electrophoresis mobility shift assay, we showed that the glutathione S-transferase-mERR alpha 1 fusion protein produced in a bacterial system bound to the human ERR alpha 1 DNA-binding element. Mouse uterine nuclear extract also interacted with this DNA element and produced three complexes in the mobility shift assay, one of which was supershifted by the hERR alpha 1 antiserum. A 2.2 kbp transcript was detected by Northern analysis in all adult mouse tissues tested; however, large variations in the amount of ERR alpha 1 mRNA were found among them. Multiple immunoreactive forms of mouse ERR alpha 1 were detected by Western analysis in non-reproductive tissues, whereas a major 53 kDa protein was found in reproductive tissues such as uterus, cervix and vagina. Diethylstilbestrol (DES) stimulated the expression of ERR alpha 1 mRNA in the uterus of 19-day-old mouse. We showed that DES and estradiol, but not progesterone or dexamethasone, enhanced the level of immunoreactive ERR alpha 1 in the mouse uterus. These results demonstrated that the ERR alpha 1 is an estrogen-responsive gene in the mouse uterus and provides a model system with which to study the biological roles of this nuclear orphan receptor.

Amino Acid Sequence↗

PubMed1997

[Experimental study on effect of zhuyu tongfu mixture on anti-enterogenous infection caused by endotoxin].

OBJECTIVE: To evaluate the effect of Zhuyu Tongfu mixture (ZYTFM) in curing enterogenus infection. METHODS: Experimental model of enterogenous infection in mice caused by endotoxin was used. The positive translocation trate (PTR) and mumber of viable bacteria in viscera and serum level of superoxide dismutase (SOD) were measured before and after ZYTFM treatment. RESULTS: The PTR and number of viable bacteria in liver, spleen and mesocolon in the ZYTFM group were much lower than those in the model group and the placebo group (P < 0.01). Whereas the SOD level of the ZYTFM group was significantly higher than that in the latter two groups (P < 0.05-0.01). Pathological examination displayed that ZYTFM could markedly alleviate the mucosal damage of small intestine. CONCLUSION: ZYTFM has an obvious curative effect on enterogenous infections induced by endotoxin.

Animals↗

PubMed1997

[Effect of recombinant growth hormone on amino acids metabolism in blood and urine after major operation].

To determine the effects of recombinant human growth hormone (GH) on postoperative amino acids metabolism, we performed a placebo-controlled randomized double-blind trial in 18 patients after elective gastrectomy or colectomy. The same amount of calories and amino acids were administered. Research group was daily injected growth hormone 0.15 IU/(kg.day) and control group was given placebo during the first postoperative week. All urine were analyzed for nitrogen balance and excretion of 3-methylhistidine. On the seventh postoperative day while the parenteral nutrients were being infused, amino acid exchange across the forearm was measured. On the seventh postoperative day all patients' amino acids in plasma were slightly increased by comparing with preoperative day but was not statistical significance. Forearm arterial-venous difference (A-V) measured on POD + 7 was markedly different between groups. There was continued release of amino acids from the forearm in the control subjects, while there was marked amino acid uptake in the GH patients (total amino acid nitrogen exchange was -398 +/- 158 mumol/L vs +165 +/- 61 mumol/L, P < 0.01). Excretion of urinary 3-methylhistidine in control group loss more than in GH group (7.3 +/- 1.0 mumol/(kg.24 h) vs 4.4 +/- 0.3 mumol/(kg.24 h), P < 0.05). The results demonstrated that GH can increase the uptake of amino acid from forearm and decrease the excreation of 3-methylhistidine in urine after operation, but did not disturb the balance of amino acids in plasma.

Amino Acids, Branched-Chain↗

PubMed1997

[Simultaneous determination of matrine and oxymatrine in jieeryin and fuyanshuan by RP-HPLC].

Matrine and oxymatrine in Jieeryin and Fuyanshuan were separated and determined by Reversed Phase High Performance Liquid Chromatography, A chromatographic method for the separation and determination of matrine and oxymatrine in these preparations was established. Chromatographic coditions: ODS column with methanol-water-triethylamine(55:45:0.02) as the mobil phase, and UV detection at 215 nm. The method is simple, sensitive and accurate. This study provides the scientific basis for quality evaluation and quality control in making these preparations.

Alkaloids↗

PubMed1997

[Studies on hydrolysis of anti-HRV IgY and its oral passive immunity effect to human rotavirus].

In this paper, hens of fine breed were immunized with human rotavirus (HRV), and the anti-HRV IgY was isolated and purified from their eggs collected daily. In addition, the resistance of anti-HRV IgY to hydrolysis of gastric juice and proteases in human digestive tract, the safety of IgY and the effectiveness of IgY in clinical use were observed as well. The results showed that anti-HRV IgY has a fairly good resistance to gastroinstestinal proteases. The safety of using anti-HRV IgY was affirmed by oral administration to mice of a solution of IgY. In clinical test the IgY has been proved to be anti-HRV and, therefore, effective against infections of infant diarrhea induced by HRV.

Administration, Oral↗

PubMed1997

TNF-alpha up-regulates renal MIF expression in rat crescentic glomerulonephritis.

BACKGROUND: Macrophage migration inhibitory factor (MIF) is a potent proinflammatory mediator that participates in the pathogenesis of endotoxemia and experimental crescentic glomerulonephritis. However, very little is known about how MIF production is regulated in disease. We therefore examined whether tumor necrosis factor alpha (TNF-alpha), a known inducer of MIF expression by macrophages in vitro, up-regulates local and systemic MIF expression in a macrophage-mediated rat model of crescentic glomerulonephritis. MATERIALS AND METHODS: Anti-glomerular basement membrane (GBM) glomerulonephritis was induced in groups of six primed rats. Animals were treated with 1 mg/kg soluble TNF-alpha receptor (TNFbp) or saline from the time of disease induction until they were killed on Days 1, 7, or 14. Renal MIF expression was assessed by in situ hybridization, immunohistochemistry, and ELISA, and compared with macrophage accumulation and indices of renal damage. RESULTS: Although TNFbp treatment on Day 1 of the disease had only a partial effect upon the up-regulation of glomerular MIF expression, on Days 7 to 14 it almost completely abrogated the increase in glomerular and interstitial MIF mRNA and protein expression. In addition, TNFbp treatment significantly inhibited MIF secretion by cultured glomeruli and reduced serum MIF levels. The inhibition of renal MIF expression was paralleled by a significant inhibition of glomerular and interstitial macrophage infiltration (p < 0.001 versus saline treated), a significant suppression of renal injury (proteinuria and serum creatinine), and a marked reduction in histologic damage (glomerular hypercellularity, crescent formation, and interstitial fibrosis; all p < 0.01 versus saline treated). CONCLUSIONS: This study demonstrates for the first time that TNF-alpha up-regulates local MIF expression by both infiltrating macrophages and resident kidney cells in rat crescentic glomerulonephritis. In addition, TNF-alpha regulates systemic MIF production. Thus, TNF-alpha, together with MIF, may play a pathological role in immunologically induced renal disease.

Animals↗

PubMed1997

Macrophage apoptosis in rat crescentic glomerulonephritis.

The fate of macrophages at the site of inflammation is unknown. We investigated this question in a macrophage-mediated model of crescentic glomerulonephritis in which macrophage accumulation is relatively stable despite the presence of high levels of local macrophage proliferation. Accelerated anti-glomerular basement membrane glomerulonephritis was induced in groups of six rats that were killed on day 1, 7, 14, or 21. Macrophage apoptosis was demonstrated in kidney sections by three methods: in situ terminal deoxyribonucleotide transferase (TdT)-mediated dUTP nick end labeling (TUNEL) combined with ED1 antibody immunostaining of macrophages, ED1 immunostaining combined with classical nuclear morphology, and electron microscopy. Substantial macrophage apoptosis became evident on day 14 of the disease, following the appearance of high levels of macrophage proliferation. The parallel relationship between proliferation and apoptosis is the likely explanation for the stabilization of macrophage numbers within the inflamed kidney. A striking feature was that macrophage proliferation and apoptosis was largely restricted to areas of focal damage, such as in the development of glomerular crescents. Increasing levels of macrophage proliferation and apoptosis were evident as crescents developed from a cellular to a fibrocellular phenotype, with a dramatic reduction in both of these processes in the progression to a fibrotic phenotype, suggesting an important role for macrophage apoptosis in the resolution of fibrocellular crescents to an acellular fibrotic structure. In conclusion, this study has identified apoptosis as an important mechanism counterbalancing local proliferation in the regulation of macrophage accumulation at sites of inflammation. Indeed, apoptosis may be a central regulator of the progression and resolution of macrophage-mediated tissue injury.

Animals↗

PubMed1997

Macrophage and myofibroblast proliferation in remnant kidney: role of angiotensin II.

Local macrophage proliferation has been shown to be a major mechanism of macrophage accumulation in several immunologically-induced animal models of renal diseases. This study has explored whether local proliferation of macrophages and myofibroblasts contribute to their accumulation in rat remnant kidney model and investigated the role of angiotensin II (Ang II) in these cellular pathological events by blocking the angiotensin II activity with ramipril, and angiotensin converting enzyme (ACE) inhibitor, or valsartan, an Ang II type 1 receptor antagonist. There was local proliferation of macrophages and myofibroblasts within renal parenchyma following renal ablation, contributing significantly to macrophage and myofibroblasts accumulation, renal dysfunction and fibrosis. Both treatment resulted in inhibition of local proliferation of macrophages and myofibroblasts and this was associated with attenuation of renal injury. In conclusion, inhibition of local macrophage and myofibroblast proliferation may be an important mechanism by which Ang II blockade attenuated renal injury following renal ablation.

Angiotensin II↗

PubMed1997

[The decrease of gastric mucosal blood flow in obstructive jaundice under stress].

OBJECTIVE: To investigate the cause of decrease of gastric mucosal blood flow (GMBF) in obstructive jaundice under stress. METHODS: With common bile duct ligation (CBDL) in Wistar rats under cold restraint stress, GMBF and the content of Endothelin-1, Angiotensin-II, H2, alpha 1 receptor in gastric mucosa were measured. Before stress anti-ET-1 serum, Enalapril, Cimentidine and Phetolamins were administrated, and the change of GMBF was studied. RESULTS: GMBF was significantly decreased in CBDL in stress than those in control subjects. The content of ET1 and Ang-II was significantly increaced, the density of H2 and alpha 1 receptor was significantly decreased. Before stress antagonist was administrated, and GMBF was significantly increased. CONCLUSION: GMBF was decreased by increased ET, Ang-II and decreased H2, alpha 1 receptor in CBDL, under stress. Antagonist improved gastric mucosal blood flow. They had protection from gastric mucosa.

Angiotensin II↗

PubMed1996

Self-association of LIM-kinase 1 mediated by the interaction between an N-terminal LIM domain and a C-terminal kinase domain.

LIM-kinase 1 (LIMK1) and 2 (LIMK2) are members of a novel class of protein kinases containing two LIM motifs at the N-terminus. The LIM motif is thought to be involved in protein-protein interactions. We report here evidence that LIMK1 self-associates and also associates with LIMK2. In vivo and in vitro binding analyses using variously deleted mutants of LIMKI revealed that the self-association of LIMK1 was caused by interaction between the N-terminal LIM domain and the C-terminal kinase domain. The association of LIMK1 with itself and with LIMK2 is important for understanding how activities and functions of LIMK family kinases are regulated.

Animals↗

PubMed1996

Estrogen-related receptor, hERR1, modulates estrogen receptor-mediated response of human lactoferrin gene promoter.

We have shown previously that estrogen-stimulated transcription from the human lactoferrin gene in RL95-2 endometrium carcinoma cells is mediated through an imperfect estrogen response element (ERE) at the 5 -flanking region of the gene. Upstream from the ERE, a DNA sequence (-418 to -378, FP1) was selectively protected from DNase I digestion by nuclear extracts from endometrial and mammary gland cell lines. In this report, using the electrophoresis mobility shift assay, site-directed mutagenesis, and DNA methylation interference analyses, we show that three different nuclear proteins bind to the FP1 region (C1, C2, and C3 sites). The nuclear receptor, COUP-TF, binds to the C2 site. Mutations in the C1 binding region abolish C1 complex formation and reduce estrogen-dependent transcription from the lactoferrin ERE. When the imperfect ERE of the lactoferrin gene is converted to a perfect palindromic structure, the enhancing effect of the C1 binding element for estrogen responsiveness was abolished. We isolated a complementary DNA (cDNA) clone from an RL95-2 expression library that encodes the C1 site-binding protein. The encoded polypeptide maintains 99% amino acid identity with the previously described orphan nuclear receptor hERR1. A 2.2-kilobase mRNA was detected in RL95-2 cells by the newly isolated cDNA but not by the first 180 base pair of the published hERR1 sequence. By Western analysis, a major 42-kDa protein is detected in the RL95-2 nuclear extract with antibody generated against GST-hERR1 fusion protein. Finally, we show that the hERR1 interacts with the human estrogen receptor through protein-protein contacts.

Amino Acid Sequence↗

PubMed1996

Spectral editing in 13C CP/MAS experiments at high magnetic field.

We show that the spinning side-bands of protonated and non-protonated carbon atoms can be well separated by means of the standard SCP and LCPD experiments at a relatively slow sample spinning rate or at high magnetic field. These experiments offer a promising way of measuring the principal values of chemical shift anisotropies via spinning side-band analysis in a moderately complex system. General spectral editing in 13C cross-polarization magic-angle spinning (CP/MAS) experiments at high field is achieved by incorporating the total side-band suppression (TOSS) pulse sequence into the standard series of spectral editing pulse sequences. It is confirmed that the relative signal intensity for a certain kind of functional group obtained at different polarization, polarization-inversion and depolarization times is about the same as that obtained at low magnetic field, and that the signal intensity distortion introduced by the TOSS sequence for resonances having different chemical shift anisotropies does not interfere with the spectral editing process. However, quantitative results can only be expected in those cases where full restoration of the intensity of the central band can be achieved by the TOSS sequence. This new strategy at high field is demonstrated by using fumaric acid monoethyl ester as a model compound. A typical application to a Chinese resin is presented, where the relative ratio of each functional group in the aliphatic portion to the total number of aliphatic carbon atoms is determined from only three experimental spectra.

Anisotropy↗

PubMed1996

High resolution 1H spectra of powdered solids observed by Hahn echo pulse sequence with magic-angle spinning.

The 1H magic-angle spinning (MAS) spectrum for a typical powdered solid is composed of a high resolution component and a broadline component. The high resolution component can be well isolated from the broadline component by the Hahn echo sequence with a long echo time. Compared with CRAMPS experiment, which measures the proton system as a whole, the high resolution echo-MAS method measures only a fraction of the solid, which is usually small at room temperature and quite different from the majority of the solid in both molecular motion and chemical environment. It is shown that for a sample of fumaric acid monoethyl ester, the chemical shifts of the high resolution component are apparently distinguishable from the isotropic chemical shifts of the broadline component in the CRAMPS spectrum as the temperature approaches the melting point. In addition, for a sample of malonic acid, the echo-MAS spectrum is sensitive to moisture and temperature, while its corresponding CRAMPS spectrum is not. It is suggested that the molecules which produce the high resolution component are related to the lattice defects in a solid, including the surface disorder of the polycrystallites, while the molecules that generate the broadline component are located on the rigid lattice of the solid.

Chemical Phenomena↗

PubMed1996

Molecular basis of charge movement in voltage-gated sodium channels.

Voltage-dependent movement of a sodium channel S4 segment was examined by cysteine scanning mutagenesis and testing accessibility of the residues to hydrophilic cysteine-modifying reagents. These experiments indicate that 2 charged S4 residues move completely from an internally accessible to an externally accessible location in response to depolarization by passage through a short "channel" in the protein. The energetic problems of S4 movement have thus been solved in the same way that may ion channels achieve highly selective and rapid ion permeation through an open pore, by restricting the contact region between the permion and its channel.

Amino Acid Sequence↗

PubMed1996

[Selective arterial catheterization in the management of drug-resistant choriocarcinoma].

OBJECTIVE: In order to save the life of the patients with drug-resistant choriocarcinoma due to improper treatment, selective arterial catheterization was used. METHODS: All the 71 cases were treated with systemic chemotherapy together with pelvic selective arterial chemotherapy. 5 of them had arterial chemotherapy plus arterial embolization for hemorrhage. In 13 patients who had lung metastasis, intraarterial injection of methotrexate (MTX) through bronchial arterial was added. RESULTS: 55 of 71 (77.8%) achieved complete remission and 10 (14.1%) had partial remission. One patient failed to follow-up. 5 died of various causes during hospitalization. On Follow-up 12 had survived for more than 5 years with no signs of recurrence. 2 of them had childbirth after recovery. CONCLUSION: Systemic intravenous infusion chemotherapy in combination with arterial chemotherapy is useful for drug-resistant choriocarcinoma. In patients with intraperitoneal hemorrhage caused by tumor rupture, selective arterial embolization should be used as emergency treatment to effectively control the bleeding, in order that patients will have a chance for further chemotherapy.

Antineoplastic Combined Chemotherapy Protocols↗