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Biomedical subjects

Yong Jiang

Publications and source records attributed to Yong Jiang.

141 records · Page 8Linked to original sources
PubMed2002

Role of p38 MAPK in ICAM-1 expression of vascular endothelial cells induced by lipopolysaccharide.

Lipopolysaccharide (LPS) stimulation of endothelial cells induces the expression of intercellular adhesion molecule-1 (ICAM-1), a critical adhesion molecule involved in the adhesive interaction between leukocytes and endothelial cells in shock and inflammation. Although there is little literature about role of p38 mitogen-activated protein kinase (MAPK) in ICAM-1 protein expression of LPS-induced endothelial cells, it is still not defined whether gene transcription is regulated by p38 MAPK in ICAM-1 expression of LPS-induced endothelial cells. In this study, the potential role of p38 MAPK in ICAM-1 expression of LPS-induced endothelial cells was studied in vitro and in vivo. In vitro studies, the results showed that compared with basic expression of ICAM-1 protein on cultured human umbilical vein endothelial cells (HUVECs), the ICAM-1 expression was increased initially at 2 h after LPS stimulation, reached peak value at 24 h, and descended at 36 h obviously. A dose-dependent relationship existed between LPS concentration and ICAM-1 expression. The abundance of ICAM-1 mRNA in cytoplasma of endothelial cells was upregulated significantly by LPS stimulation at 2 h and was maintained at a high level from 4 to 36 h. The upregulation of ICAM-1 protein and mRNA expression of LPS-induced HUVECs was markedly inhibited by SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)imidazole], a highly specific inhibitor of p38 MAPK. Activity of p38 MAPK in HUVECs was increased at 15 min after LPS stimulation and reached the maximum at 60 min, then descended significantly. Activity of p38 MAPK was inhibited significantly by SB203580 in vitro. In vivo studies, administration of SB203580 (12.5 or 25 mg/kg, per ora) markedly reduced LPS-induced expression of ICAM-1 protein and mRNA of lung tissues of male BALB/c mice. These data highlight that the upregulation of ICAM-1 expression of LPS-induced endothelial cells in vitro and in vivo is mediated by p38 MAPK pathway at the level of gene transcription. The ICAM-1 expression of LPS-induced endothelial cells is characteristic of time dependence and dose dependence, and tolerates to chronic LPS stimulation. Inhibition of the p38 MAPK signal pathway may be used as an approach to attenuate ICAM-1 production in the treatment of septic shock.

Animals↗
PubMed2002

New approach to treatment of shock--restitution of vasoreactivity.

Our objective was to observe the therapeutic effect of restituting vasoreactivity agent in severe shock. A hemorrhagic shock (HS) model was reproduced in rat and the response of arterioles of spinotrapezius muscle to norepinephrine (NE) in HS was tested. The diameter, blood velocity, and volumetric flow in arteriole, and the mean arterial pressure (MAP) were measured. The therapeutic effect was observed after the treatment of restituting vasoreactivity agent (glybenclamide--an inhibitor of ATP sensitive potassium channel, and tiron--an oxygen free radical scavenger). The arteriolar vasoreactivity was significantly reduced with 15 fold increase of NE threshold 2 h post HS. After treated with restituting agent (RA), the vascular hyporeactivity of rat was apparently recovered, and the increased level of MAP following injection of dopamine was 1.8 times and 1.9 times more than that in NS-treated and DMSO-treated group respectively. After reinfusion of shed blood, the value of systemic blood pressure maintained more than 100 mmHg and volumetric flow in arterioles in RA group were 2 times more than those in NS treated group within the 2 h observation periods. The average survival time in RA treated group was also 1.8 times and 1.6 times longer than that in NS-treated and DMSO-treated group respectively. The restituting vasoreactivity agent is able to recover the lower vasoreactivity with excellent anti-shock effect in severe hemorrhagic shock.

Animals↗
PubMed2002

[Extension of cardiac monitoring function by used of ordinary ECG machine].

This paper deals with a portable monitor system on liquid crystal display (LCD) based on this available ordinary ECG machine, which is low power and suitable for China's specific condition. Apart from developing the overall scheme of the system, this paper also has completed the design of the hardware and the software. The 80c196 single chip microcomputer is taken as the central microprocessor and real time electrocardiac single is data treated and analyzed in the system. With the performance of ordinary monitor, this machine also possesses the following functions: five types of arrhythmia analysis, alarm, freeze, and record of automatic pappering, convenient in carrying, with alternate-current (AC) or direct-current (DC) powered. The hardware circuit is simplified and the software structure is optimized in this paper. Multiple low power designs and LCD unit design are adopted and completed in it. Popular in usage, low in cost price, the portable monitor system will have a valuable influence on China's monitor system field.

Arrhythmias, Cardiac↗
PubMed2002

Role of p38 mitogen-activated protein kinase in lipopolysaccharide-induced expression of inducible nitric oxide synthase in human endothelial cells.

OBJECTIVE: To understand the role of p38 mitogen-activated protein kinase (p38MAPK) in the expression of inducible nitric oxide synthase (iNOS) and NO production in human endothelial cells under the stimulation by lipopolysaccharide (LPS). METHODS: NO level in the supernatant of the cell culture media was measured with Griess method, and iNOS protein and mRNA expressions by the cells were detected with immunofluorescence analysis and reverse transcriptase-polymerase chain reaction (RT-PCR) respectively. Immunoprecipitation assay was employed to examine p38 MAPK activity. RESULTS: It was shown that in comparison with the basal level of iNOS expression in cultured endothelial cells line ECV304, iNOS mRNA and protein expressions were significantly increased in the cells after LPS stimulation. In response to LPS treatment, obvious enhancement of p38 MAPK activity in ECV304 took place after the stimulation, with the peak level occurring at 15 min that maintained for approximately 45 min before gradual decline. When treated with SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl) imidazole], a highly specific inhibitor of p38 MAPK, significant inhibition of LPS-induced iNOS protein and mRNA expressions was observed. CONCLUSIONS: p38 MAPK plays an important role in iNOS expression and NO production in ECV304 cells, and, inhibition of the signal transduction pathway may consequently be an effective approach to reduce the production of iNOS and other cytokines for the treatment of septic shock.

Cell Line↗
PubMed2002

[Construction and expression of red fluorescent protein fusion vector incorporating p38 mitogen-activated protein kinase].

OBJECTIVE: To construct the vector that expresses the fusion protein of p38 mitogen-activated protein kinase (MAPK) and red fluorescent protein (RFP) in mammalian cells. METHODS: FLAG-tagged p38 MAPK in pcDNA3 vector was subcloned into RFP vector pDsRed1-N1, the construct of which was then transfected into HeLa cells and observed with fluorescence microscope. RESULTS: The recombinant plasmid was verified by enzyme digestion, PCR and sequence analysis, and p38 MAPK-RFP fusion protein was highly expressed in HeLa cells. Fluorescence microscope found the red fluorescence distributed all over the cytoplasm and in the nuclei as well. CONCLUSION: The expression vector for p38 MAPK-RFP fusion protein is successfully constructed and effective expression of this fusion protein is achieved, which might be instrumental in the study of intracellular localization of p38 MAPK.

Gene Expression↗
PubMed2002

[Effect of infrasound on ultrastructure and permeability of rat's blood-retinal barrier].

OBJECTIVE: To investigate the possible effect of infrasound on the ultra-structure and permeability of rat's blood-retinal barrier (BRB). METHODS: Ultra-structural changes of BRB were observed through the injection of lanthanum nitrate (La), which was used as a tracer to demonstrate the breakdown of the BRB, into blood vessels. Fifteen mature male rats divided into 5 groups were exposed to infrasound at a 8 Hz frequency, 130 dB sound pressure level in a pressure chamber especially designed for the experiment for 0, 1, 7, 14, 21 days, respectively. RESULTS: Under the action of infrasound, along with the prolongation of exposure, the damage of BRB was severer and severer. On the 1st day, there was no significant change in La leakage. On the 7th day, La diffused in the interphotoreceptor space at nuclear level. On the 14th day, La granules could be seen in the space of nervous cells. Finally, on the 21st day, La was found between synapses, synapses and nerve cells, as well as between the nerve cells and supporting cells, then sometimes reached vitreous body. Under the electron microscope, there were no significant morphological changes, but changes related to metabolism, such as edematous mitochondria, dilated rough endoplasmic reticula, precipitation of glycogen grandules, widening of perinuclear space, etc. CONCLUSIONS: The results thus suggest that the exposure to infrasound cause the breakdown of rat's blood-retinal barrier and visual impairment.

Animals↗
PubMed2002

[The application and development of artificial intelligence in medical diagnosis systems].

This paper has reviewed the development of artificial intelligence in medical practice and medical diagnostic expert systems, and has summarized the application of artificial neural network. It explains that a source of difficulty in medical diagnostic system is the co-existence of multiple diseases--the potentially inter-related diseases. However, the difficulty of image expert systems is inherent in high-level vision. And it increases the complexity of expert system in medical image. At last, the prospect for the development of artificial intelligence in medical image expert systems is made.

Artificial Intelligence↗
PubMed2002

[Response of N transformation related soil enzyme activities to inhibitor applications].

With an aerobic incubation test, this paper studied the response of soil urease, nitrate reductase, nitrite reductase, and hydroxylamine reductase to urease inhibitor hydroquinone (HQ) applied in combination with nitrification inhibitor encapsulated calcium carbide (HQ + ECC) or dicyandiamide (HQ + DCD). The results showed that HQ + DCD could inhibit urease activity and increase activities of nitrate reductase, nitrite reductase, and hydroxylamine reductase significantly in comparison with CK, HQ and HQ + ECC. Under the condition of our test, there existed a significant relationship between soil urease, nitrate reductase, nitrite reductase, and hydroxylamine reductase activities and soil NH4+ and NO3- contents, NH3 volatilization and N2O emission rate, and regression analysis indicated that there were significantly positive relationships between soil urease, nitrite reductase and hydroxylamine reductase activities.

Ammonia↗
PubMed2001

Glutathione S-transferase pi Protects Serum Depletion-induced Cell Death by Inhibiting ASK1-MKK7-JNK Pathway in the 293 Cells.

Glutathione S-transferase pi (GSTpi) protects cells from death by altering intracellular oxidative stress. In order to understand the mechanism of GSTpi protection, a cell death model induced by serum depletion as the stress was established. Cotransfection of apoptosis signal-regulating kinase 1 (ASK1) and GSTpi cDNA was performed to elucidate the impact of GSTpi on ASK1 activity, as well as on its downstream signals, MKK7 and JNK, and to elucidate the potential protection of GSTpi on 293 cell death induced by serum depletion. The dominant negative mutant of JNK was used to explore if the blocking of the JNK pathway led to cell death inhibition. It was found that GSTpi had a dose-dependent inhibitory effect on activation induced by serum depletion, and also on inhibition both on MKK7 and JNK. Intracellular expression of GSTpi significantly inhibited serum depletion-induced cell death. Blocking the JNK pathway by transfection of a dominant negative form of JNK (JNK (APF)) brought about significant inhibition of cell death induced by serum depletion with an inhibiting rate as high as 15%. All the results suggest that the mechanism of GSTpi protection on serum depletion-induced cell death works through an ASK1-MKK7-JNK pathway.

Journal Article↗
PubMed2000

Signal Transduction in TNF-alpha-induced c-jun Gene Expression.

Our previous studies demonstrated that p38 mitogen-activated protein (MAP) kinase regulated the c-jun protein expression through phosphorylation of transcription factors of myocyte enhancer factors 2 (MEF2) family. There was a MEF2 binding site in the promoter of c-jun gene. Members of the MEF2 family of trans-cription factors bound as homo- and heterodimers to this MEF2 binding site. Here the potential role of the p38 and BMK1 MAP kinases in the regulation of c-jun expression induced by TNF-alpha was examined. It was shown that p38 MAP kinase up-regulated the transcription activity of MEF2A, while BMK1 MAP kinase up-regulated not only the transcription activity of MEF2A, but also MEF2D. The p38 and BMK1 MAP kinases had coordinated effect on the regulation of c-jun transcription. TNF-alpha induced the formation of MEF2A/MEF2D hete-rodimer. Over-expression of homodimer of MEF2 proteins inhibited c-jun transcription induced by TNF-alpha, while over-expression of heterodimer MEF2A/MEF2D enhanced c-jun transcription induced by TNF-alpha. Phosphorylation of MEF2A and MEF2D by p38 and BMK1 respectively appeared very important in TNF-alpha induced MEF2A/MEF2D heterodimer formation to enhance c-jun gene expression.

Journal Article↗
PubMed1999

Studies on the flow and distribution of leukocytes in mesentery microcirculation of rats.

AIM:To study the effect of leukocyte-endothelium interaction (LEI) on the flow and distribution of leukocytes in microcirculation under physiological condition.METHODS:A microcirculation image multiple parameter computer analysis system (MIMPCAS) was used to study the flow and distribution of leukocytes in mesentery microcirculation of rats in vivo.RESULTS:The difference of visible leukocyte flux (VLF) was as high as 131 times in the arterioles and venules with similar diameter and blood velocity. The visible leukocytes rolled along the blood vessel wall as a jerky movement. The frequency distribution of the visible leukocyte velocity (VLV) showed a two peak curve. The low peak value was on 10&mgr;m/s-15&mgr;m/s while the high peak fell between 25&mgr;m/s-30&mgr;m/s. With the increase of diameter of venules, VLF increased while the VLV remained at the same level. With the increase of RBC velocity, VLV trends to elevate and VLF to fall down.CONCLUSION:The results herein might provide a basic theory for the study on the mechanism of LEI under physiological condition and novel methods for the prevention and treatment of high LEI in many pathological processes.

Journal Article↗
PubMed1999

p38 MAPK Signal is Necessary for TNF-alpha Gene Expression in RAW Cells.

The luciferase reporter gene system driven by the TNF-alpha promoter was constructed for the studies of the effect of p38 MAPK signal transduction pathway on the gene expression of TNF-alpha. In the experiments of co-transfection in RAW cells it was found that there was a significant relevance between the activation of p38 by LPS and the induction of TNF-alpha reporter gene transcription. The induction of TNF-alpha expression was not shown after transfection of p38 only co-transfection of p38 with the active mutant of its upstream kinase, MKK6b, however, did induce the high expression of luciferase. Further studies showed that the induction of TNF-alpha promoter activity by MKK6b(E) and LPS was similar. In addition, the dominant negative form of p38 or p38 inhibitor gave an inhibitory effect on the TNF-alpha promoter activity induced by MKK6b(E) or LPS. All these results suggest that a possible mechanism for TNF-alpha production in endotoxic shock is the increase in gene transactivity induced by LPS in monocytes/macrophages, and that p38 MAPK signal pathway participates in the regulation of TNF-alpha gene expression induced by LPS.

Journal Article↗
PubMedDate not supplied

New diterpenoids from Semiaquilegia adoxoides.

Two new ent-kaurane-type diterpenoids, E-semiaquilegin (1) and Z-semiaquilegin (2), together with eight known compounds (3-10) were isolated from the dried roots of Semiaquilegia adoxoides (DC.) Makino. The structures of compounds 1 and 2 were elucidated mainly by 2D NMR techniques including 1H-1H COSY, HSQC, HMBC, NOESY as 16alpha-hydroxy-ent-kaurane-17,20-di-(3,4-dihydroxy-E-cinnamoyl) ester and its (Z)-isomer.

Diterpenes↗