Biomedical subjects

Y Zou

Publications and source records attributed to Y Zou.

At least 127 records · Page 7Linked to original sources

PubMed1999

Surfactant protein B corrects oxygen-induced pulmonary dysfunction in heterozygous surfactant protein B-deficient mice.

Surfactant protein B (SP-B) is a 79-amino acid hydrophobic surfactant protein that plays a critical role in postnatal lung function. Homozygous SP-B (-/-)-deficient mice die of respiratory failure at birth, associated with severe pulmonary dysfunction and atelectasis. Heterozygous SP-B (+/-)-deficient mice have 50% less SP-B protein, proprotein, and SP-B mRNA compared with control mice and are highly susceptible to oxygen-induced lung injury. In the current study, we tested whether the susceptibility of SP-B (+/-) mice to hyperoxia was restored by intratracheal administration of exogenous SP-B. After exposure to 95% oxygen for 3 d, opening pressures were increased and maximal lung volumes were significantly decreased in SP-B (+/-) mice compared with SP-B (+/+) mice. SP-B (+/-) mice were administered purified bovine SP-B (2%) with DL-alpha dipalmitoyl phosphatidylcholine (DPPC) and 1-palmitoyl-2-oleoyl-sn-glycero-3-[phospho-rac-( -glycerol)] (POPG) phospholipids or DPPC and POPG phospholipids intratracheally and exposed to 95% oxygen. SP-B-treated SP-B (+/-) mice survived longer in 95% oxygen. Although decreased lung function in SP-B (+/-) mice exposed to oxygen was not altered by administration of DPPC and POPG, administration of lipids containing 2% purified bovine SP-B restored lung function when assessed after 3 d in oxygen. Abnormalities in pulmonary function in SP-B (+/-) mice after oxygen exposure were associated with increased alveolar capillary leak, which was corrected by administration of SP-B with DPPC and POPG. Likewise, histologic abnormalities caused by oxygen-induced lung injury were improved by administration of SP-B with DPPC and POPG. Administration of phospholipids with the active SP-B peptide was sufficient to restore pulmonary function and prevent alveolar capillary leak after oxygen exposure, demonstrating the protective role of SP-B during oxygen-induced lung injury.

Animals↗

PubMed1999

Control of segmental expression of the cardiac-restricted ankyrin repeat protein gene by distinct regulatory pathways in murine cardiogenesis.

Although accumulating evidence suggests that the heart develops in a segmental fashion, the molecular mechanisms that control regional specification of cardiomyocytes in the developing heart remain largely unknown. In this study, we have used the mouse cardiac-restricted ankyrin repeat protein (CARP) gene as a model system to study these mechanisms. The CARP gene encodes a nuclear co-regulator for cardiac gene expression, which lies downstream of the cardiac homeobox gene, Nkx 2.5, and is an early marker of the cardiac muscle cell lineage. We have demonstrated that the expression of the gene is developmentally down regulated and dramatically induced as part of the embryonic gene program during cardiac hypertrophy. Using a lacZ/knock-in mouse and three lines of transgenic mouse harboring various CARP promoter/lacZ reporters, we have identified distinct 5' cis regulatory elements of the gene that can direct heart segment-specific transgene expression, such as atrial versus ventricular and left versus right. Most interestingly, a 213 base pair sequence element of the gene was found to confer conotruncal segment-specific transgene expression. Using the transgene as a conotruncal segment-specific marker, we were able to document the developmental fate of a subset of cardiomyocytes in the conotruncus during cardiogenesis. In addition, we have identified an essential GATA-4 binding site in the proximal upstream regulatory region of the gene and cooperative transcriptional regulation mediated by Nkx2.5 and GATA-4. We have shown that this cooperative regulation is dependent on binding of GATA-4 to its cognate DNA sequence in the promoter, which suggests that Nkx2.5 controls CARP expression, at least in part, through GATA-4.

Age Factors↗

PubMed1999

Hypertrophic responses of cardiomyocytes induced by endothelin-1 through the protein kinase C-dependent but Src and Ras-independent pathways.

We have previously shown that endothelin-1 (ET-1) modulates mechanical stretch-induced hypertrophic responses such as extracellular signal-regulated protein kinase (ERK) activation in cardiac myocytes. This study was undertaken to elucidate the ET-1-evoked signal transduction pathways leading to ERK activation. ET-1 was added to cultured cardiac myocytes of neonatal rats with or without a variety of inhibitors. ET-1 activated ERKs, which were followed by an increase in protein synthesis, and inhibition of protein kinase C activities by calphostin C completely suppressed the ET-1-induced ERK activation. We next examined whether tyrosine kinases or Ras are involved in ET-1-induced signaling pathways in cardiomyocytes. Pretreatment with a receptor tyrosine kinase inhibitor did not attenuate ET-1-induced activation of ERKs. Also, co-transfection of the dominant-negative mutant of Ras or active mutant of C-terminal Src kinase, a tyrosine kinase which inhibits Src family tyrosine kinases, with hemagglutinin-tagged ERK2 had no effects on ET-1-induced ERK2 activation. On the other hand, blockade of Raf-1 kinase function by overexpression of the dominant-negative mutant of Raf-1 kinase completely inhibited ET-1-induced ERK2 activation. These results suggest that protein kinase C and Raf-1 kinase, but not Src or Ras, are critical to ET-1-induced ERK activation in cardiac myocytes.

Amino Acids↗

PubMed1999

[Determination of 6-methoxy-2-naphthylacetic acid, a major metabolite of nabumetone, in human plasma by HPLC].

This paper reports a sensitive and rapid method for determining 6-methoxy-2-naphthylacetic acid (MNA), a major metabolite of nabumetone in human plasma using naproxen as the internal standard. High performance liquid chromatograph model 680 (Waters, USA) with a variable wavelength UV detector and reversed-phase YWG-C18 column (10 microns, 250 x 4.6 mm) was used. After the addition of acetate buffer(pH3.0), the plasma sample was extracted with methylene chloride. The mobile phase of methanol-pH3.0, 0.02 mol/L acetate buffer(74:26) was pumped at 1.0 ml/min through the column. The detector at 0.01AUFS was set at 270 nm. The retention times for MNA and naproxen were 3.98 min and 4.73 min respectively. Standard curve was linear in the concentration range of 0.5 to 64 mg/L. The detection limit in serum was 0.02 mg/L. Extraction recovery was 88%-94%; method recovery 96%-102%; withinday RSD less than 3.5%; inter-day RSD less than 5%.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1999

[Simultaneous determination of norepinephrine and epinephrime in plasma by using high performance liquid chromatograph].

A sensitive and rapid method was reported for the determination of nerepinephrine (NE) and epinephrine (E) in plasma by using high-performance liquid chromatography with an electrochemical detector (HPLC-EC) and YWG-C18 column(5u). 3,4-Dihydroxybenzylamine(DHBA) was used as an internal standard. The mobile phase of 0.05 mol/L actate buffer(pH3.0)-methanol-0.05 mol/L EDTA-Na2(78:20:2) with of 200 mg/L SDS solution was pumped through the column with a flow rate of 1.0 ml/min. The lengths of retention time for NE, E and DHBA(IS) was 7.3 min, 8.3 min and 10.4 min, respectively. The standard curve was linear within the concentration range of 31.25 to 4000 ng/L for NE and E (NE: r = 0.9999 E: r = 0.9996). The within day RSD (%) were less than 1.87% for NE and less than 2.07% for E, inter-day RSD(%) were less than 8.92% for NE and less than 9.65% for E respectively. The average extraction recovery(%) for NE and E were 93.5% +/- 5.50% and 91.3% +/- 1.77% respectively. This method has been applied to the diagnosis of pheochromocytoma and clinical research.

Adrenal Gland Neoplasms↗

PubMed1999

[Changes on positive rate and distribution of Helicobacter pylori during progression of gastric cancer].

We observed changes on the positive rate and the distribution of helicobacter pylori (HP) in 7 case during early stage of gastric cancer and in 42 cases during middle-late stage of gastric cancer. The results showed that 1. the positive rate during early stage of gastric cancer was 57.1%, the positive rate during middle-rate stage of gastric cancer was 23.8%, 2. HP was not found within the gastric cancer lesions, 3. for HP positive cases, HP distribution during early stage of gastric cancer was more sparse than during middle-late stage of gastric cancer. These results suggested that HP can hardly live within the gastric cancer tissue, so the progression of gastric cancer is probably independent of HP. It may be a question that HP eradication can prevent later development of gastric cancer.

Adenocarcinoma↗

PubMed1999

[Determination of serum calicotonin gene-related peptide in patients with duodenal ulcer infected with Helicobacter pylori].

OBJECTIVE: To investigate the effect of calicotonin gene-related peptide(CGRP) on duodenal ulcer caused by Helicobacter pylori infection. METHOD: The serum levels of CGRP were determined by radioimmunoassay in 30 patients with duodenal ulcer associated with Helicobacter pylori infection and 20 healthy volunteers. RESULTS: The mean CGRP serum level was higher in duodenal ulcer associated with Helicobacter pylori group than that in the healthy group. CONCLUSION: The CGRP level might be one of the important factors in which Helicobacter pylori infections induce duodenal ulcer.

Adult↗

PubMed1999

[Computer-aided legal medical examination of body surface].

This paper provides a package of automatic and semi-automatic methods for computing the area of different kinds of body surface injuries. Compared with traditional methods, these processes of examination are faster and the conclusions are more precise and objective. Also presented are the authors classify the items into many types by standards which are necessary to let computer draw conclusions automatically. This software is conducive to improvement in work efficiency and convenience for judicial supervision.

Algorithms↗

PubMed1999

Preliminary observation of one-site combined trabeculectomy and phacoemulsification in the management of cataract patients with drug-controllable glaucoma.

PURPOSE: To evaluate the effect of one-site combined phacoemulsification and trabeculectomy in the management of cataract patients with drug-controllable glaucoma. METHODS: Twenty-four cases (25 eyes) of cataract patients with glaucoma whose intraocular pressure could be controlled by drugs were observed. All had undergone one-site combined phacoemulsification and trabeculectomy. Intraocular pressure and visual acuity were observed. RESULTS: The follow-up was 1-21 months. Postoperative visual acuity was 0.4-0.6 in 9 eyes, 0.7-0.9 in 7 eyes and 1.0 or better in 9 eyes. Postoperative intraocular pressure was 2.17 +/- 0.764 kPa (16.28 +/- 5.73 mmHg), 1.83 +/- 0.90 kPa (13.74 +/- 6.77 mmHg) lower than that before surgery (t = 11.89, P < 0.01). Only one eye needed one drug to control intraocular pressure after surgery. CONCLUSIONS: One-site combined phacoemulsification and trabeculectomy is a safe, effective and convenient technique for the management of cataract patients with drug-controllable glaucoma.

Aged↗

PubMed1999

[Determination of lead in tinplate by ICP-AES].

The determination of lead in tinplate by ICP-AES was presented in this paper. The tinplate samples were pretreated with NaOH-H2O2 for dissolving tin and lead,and the spectral interferences from iron could thus be avoided. The lead content in the sample was determined in the range of 0.14-0.38 microg/cm2. The recovery and the relative standard deviation (RSD) were in the ranges of 96.1%-103.2% and 2.6%-3.8%, respectively. The method was simple,rapid and efficient.

Food Packaging↗

PubMed1998

[Use of the primed in situ labeling technique for a rapid detection of chromosomes X, 18].

OBJECTIVE: To develop a rapid method for detection of chromosomes. METHODS: Chromosomes X, 18 were detected by the primed in situ labeling(PRINS) in eight samples of female peripheral blood cultures. RESULTS: Specific chromosomes were obtained on both metaphase and interphase nuclei. The efficiency of labeling was 84%-92%(mean=89%) in chromosome 18, and 73%-87%(mean=84%) in chromosome X. The pretreatment of slides by proteinase K markedly raised the efficiency of labeling and increased the intensity of signals. PRINS reaction could be performed automatically with a programmable thermocycler in less than one hour. CONCLUSION: The results suggest that PRINS is a fast and specific method for identifying chromosomes. It may be a reliable technique for detecting aneuploid in prenatal diagnosis.

Chromosomes, Human, Pair 18↗

PubMed1998

Mechanical stretch induces hypertrophic responses in cardiac myocytes of angiotensin II type 1a receptor knockout mice.

Many lines of evidence have suggested that angiotensin II (AngII) plays an important role in the development of cardiac hypertrophy through AngII type 1 receptor (AT1). To determine whether AngII is indispensable for the development of mechanical stress-induced cardiac hypertrophy, we examined the activity of mitogen-activated protein kinase (MAPK) family and the expression of the c-fos gene as hypertrophic responses after stretching cultured cardiac myocytes of AT1a knockout (KO) mice. When cardiac myocytes were stretched by 20% for 10 min, extracellular signal-regulated protein kinases (ERKs) were strongly activated in KO cardiomyocytes as well as wild type (WT) myocytes. Both basal and stimulated levels of ERKs were higher in cardiomyocytes of KO mice than in those of WT mice. Activation of another member of the MAPK family, p38(MAPK), and expression of the c-fos gene were also induced by stretching cardiac myocytes of both types of mice. An AT1 antagonist attenuated stretch-induced activation of ERKs in WT cardiomyocytes but not in KO cardiomyocytes. Down-regulation of protein kinase C inhibited stretch-induced ERK activation in WT cardiomyocytes, whereas a broad spectrum tyrosine kinase inhibitor (genistein) and selective inhibitors of epidermal growth factor receptor (tyrphostin, AG1478, and B42) suppressed stretch-induced activation of ERKs in KO cardiac myocytes. Epidermal growth factor receptor was phosphorylated at tyrosine residues by stretching cardiac myocytes of KO mice. These results suggest that mechanical stretch could evoke hypertrophic responses in cardiac myocytes that lack the AT1 signaling pathway possibly through tyrosine kinase activation.

Animals↗

PubMed1998

Hydrophobic forces dominate the thermodynamic characteristics of UvrA-DNA damage interactions.

The Escherichia coli DNA repair proteins UvrA, UvrB and UvrC work together to recognize and incise DNA damage during the process of nucleotide excision repair (NER). To gain an understanding of the damage recognition properties of UvrA, we have used fluorescence spectroscopy to study the thermodynamics of its interaction with a defined DNA substrate containing a benzo[a]pyrene diol epoxide (BPDE) adduct. Oligonucleotides containing a single site-specifically modified N2-guanine (+)-trans-, (-)-trans-, (+)-cis-, or (-)-cis-BPDE adducts were ligated into 50-base-pair DNA fragments. All four stereoisomers of DNA-BPDE adducts show an excitation maximum at 350 nm and an emission maximum around 380 to 385 nm. Binding of UvrA to the BPDE-DNA adducts results in a five to sevenfold fluorescence enhancement. Titration of the BPDE-adducted DNA with UvrA was used to generate binding isotherms. The equilibrium dissociation constants for UvrA binding to (+)-trans-, (-)-trans-, (+)-cis-, and (-)-cis- BPDE adduct were: 7.4+/-1.9, 15. 8+/-5.4, 11.3+/-2.7 and 22.4+/-2.0 nM, respectively. There was a large negative change in heat capacity DeltaCpo,obs, (-3.3 kcal mol-1 K-1) accompanied by a relatively unchanged DeltaGoobs with temperature. Furthermore, varying the concentration of KCl showed that the number of ions released upon formation of UvrA-DNA complex is about 3.4, a relatively small value compared to the contact size of UvrA with the substrate. These data suggest that hydrophobic interactions are an important driving force for UvrA binding to BPDE-damaged DNA.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed1998

Effective treatment of early endobronchial cancer with regional administration of liposome-p53 complexes.

BACKGROUND: Lung cancer originates in a diffusely damaged bronchial epithelium as a result of sequential and cumulative genetic alterations. We investigated the feasibility of in vivo gene replacement in endobronchial precancerous and cancerous cells by a regionally administered nonviral delivery system. METHODS: After evaluating the in vitro transfection efficiency and cytotoxicity of a variety of cationic liposome-p53 formulations, a specific formulation, DP3-p53, was selected for further in vitro and in vivo evaluation. The ability of DP3-p53 to introduce the p53 gene in the normal bronchial epithelium was studied in transgenic mice that lack the p53 gene. The therapeutic effect of DP3-p53 administered intratracheally was studied in two nude mouse models of endobronchial human lung cancer by use of H358 (p53-null) and H322 (p53-mutant) cells. RESULTS: DP3-p53 was able to effectively introduce and express the p53 gene and induce G1 arrest and apoptosis in H358 cells in vitro and to introduce and transcribe the p53 gene in the bronchial epithelium of transgenic mice that lack the p53 gene in vivo. In therapeutic experiments using groups of four or five mice each, administration of five intratracheal doses of DP3-p53 (2 microg or 8 microg DNA per dose) on days 4, 8, 12, 16, and 20 after intratracheal tumor inoculation significantly inhibited lung tumor formation and prolonged by approximately twofold the survival of mice bearing H358 or H322 endobronchial tumor cells in contrast to the survival among untreated mice and mice treated with the DP3-empty vector (P = .007 [two-sided logrank test] for mice bearing H358 cells and P = .008 [two-sided logrank test] for those bearing H322 cells). CONCLUSIONS/IMPLICATIONS: Liposome-based p53 delivery through the airways is a potentially effective strategy for the treatment of early endobronchial cancer. These results have important implications for the gene therapy and prevention of human lung cancer.

Animals↗

PubMed1998

Involvement of molecular chaperonins in nucleotide excision repair. Dnak leads to increased thermal stability of UvrA, catalytic UvrB loading, enhanced repair, and increased UV resistance.

UvrA is one of the key Escherichia coli proteins involved in removing DNA damage during the process of nucleotide excision repair. The relatively low concentrations (nanomolar) of the protein in the normal cells raise the potential questions about its stability in vivo under both normal and stress conditions. In vitro, UvrA at low concentrations is shown to be stabilized to heat inactivation by E. coli molecular chaperones DnaK or the combination of DnaK, DnaJ, and GrpE. These chaperone proteins allow sub-nanomolar concentrations of UvrA to load UvrB through >10 cycles of incision. Guanidine hydrochloride-denatured UvrA was reactivated by DnaK, DnaJ, and GrpE to as much as 50% of the native protein activity. Co-immunoprecipitation assays showed that DnaK bound denatured UvrA in the absence of ATP. UV survival studies of a DnaK-deficient strain indicated an 80-fold increased sensitivity to 100 J/m2 of ultraviolet light (254 nm) as compared with an isogenic wild-type strain. Global repair analysis indicated a reduction in the extent of pyrimidine dimer and 6-4 photoproduct removal in the DnaK-deficient cells. These results suggest that molecular chaperonins participate in nucleotide excision repair by maintaining repair proteins in their properly folded state.

Adenosine Triphosphatases↗

PubMed1998

Acute pressure overload could induce hypertrophic responses in the heart of angiotensin II type 1a knockout mice.

Increasing evidence has suggested that locally produced angiotensin II (Ang II) plays an important role in the development of cardiac hypertrophy through the Ang II type 1 receptor (AT1). We and others have recently reported that Ang II is critical for mechanical stress-induced hypertrophic responses in vitro. Using AT1a knockout (KO) mice, we examined whether Ang II is indispensable for pressure overload-induced cardiac hypertrophy in the present study. Reverse-transcriptase polymerase chain reaction analysis revealed that AT1 mRNA levels were <10% in the heart of KO mice compared with wild-type (WT) mice, but the Ang II type 2 receptor gene was expressed at almost the same levels in the hearts of both mice. Intravenous infusion of subpressor dose of Ang II induced c-fos gene expression in the hearts of WT mice but not KO mice. Acute pressure overload, however, induced expressions of immediate-early response genes and activations of mitogen-activated protein kinases in the hearts of KO mice as well as WT mice. Both basal and activated levels of all these responses were significantly higher in KO mice than in WT mice. Pressure overload markedly increased the heart weight-to-body weight ratio in both mice strains at 14 days after aortic banding. These results suggest that acute hypertrophic responses could be induced by pressure overload in the in vivo heart without AT1 signaling.

Angiotensin II↗

PubMed1998

[Polymorphism analysis of 4 loci of X-chromosome in a Chinese population of the Han nationality].

OBJECTIVE: To investigate the polymorphism of 4 loci of X-chromosome in the Hans. METHODS: Using PCR-SSLP, the authors analysed the polymorphism of DXS1068, DXS7132, DXS6804 and DXS6799 in the X-chromosome in 70 randomly selected female Hans. RESULTS: The number of alleles in the 4 loci were 5,5,5 and 6 respectively; there were no significant differences between the observed and estimated and genotype probabilities of the 4 loci; the estimates of heterozygosity of 4 loci were 0.6819, 0.6895, 0.7659 and 0.6483 respectively and there were no significant differences between the observed and estimated heterozygosity of the 4 loci. CONCLUSION: The distribution of alleles and genotype probabilities of 4 loci all observe the Hardy-Weinberg equilibrium.

Asian People↗

PubMed1998

Role of ion channels and exchangers in mechanical stretch-induced cardiomyocyte hypertrophy.

We have previously reported that stretching of cardiomyocytes activates the phosphorylation cascade of protein kinases, including Raf-1 kinase and mitogen-activated protein (MAP) kinases, followed by an increase in protein synthesis partly through enhanced secretion of angiotensin II and endothelin-1. Membrane proteins, such as ion channels and exchangers, have been postulated to first receive extracellular stimuli and evoke intracellular signals. The present study was performed to determine whether mechanosensitive ion channels and exchangers are involved in stretch-induced hypertrophic responses. Neonatal rat cardiomyocytes cultured on expandable silicone dishes were stretched after pretreatment with a specific inhibitor of stretch-sensitive cation channels (gadolinium and streptomycin), of ATP-sensitive K+ channels (glibenclamide), of hyperpolarization-activated inward channels (CsCl), or of the Na+-H+ exchanger (HOE 694). Pretreatment with gadolinium, streptomycin, glibenclamide, and CsCl did not show any inhibitory effects on MAP kinase activation by mechanical stretch. HOE 694, however, markedly attenuated stretch-induced activation of Raf-1 kinase and MAP kinases by approximately 50% and 60%, respectively, and attenuated stretch-induced increase in phenylalanine incorporation into proteins. In contrast, HOE 694 did not inhibit angiotensin II-and endothelin-1-induced Raf-1 kinase and MAP kinase activation. These results suggest that among many mechanosensitive ion channels and exchangers, the Na+-H+ exchanger plays a critical role in mechanical stress-induced cardiomyocyte hypertrophy.

Angiotensin II↗