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Jing Zhao

Publications and source records attributed to Jing Zhao.

At least 55 records · Page 3Linked to original sources
PubMed2006

Morphine promotes Jurkat cell apoptosis through pro-apoptotic FADD/P53 and anti-apoptotic PI3K/Akt/NF-kappaB pathways.

Opiates have been shown to inhibit cell growth and trigger apoptosis, but the underlying molecular mechanisms remain unclear. We have previously shown that morphine induces Fas expression and promotes Fas-mediated apoptosis. Here, we investigated the mechanisms by which morphine modulates apoptosis in human Jurkat cells. Morphine-induced apoptosis was inhibited by transfection with a dominant negative Fas-associated death domain (FADD) plasmid, revealing that morphine-induced apoptosis is dependent on FADD. Furthermore, suppression of endogenous p53 expression by RNA interference technology considerably attenuated the morphine-induced apoptosis. In addition, morphine-induced apoptosis seems to be dependent on the activation of phosphatidylinositol 3-kinase (PI3K), as PI3K inhibition by the PI3K inhibitor LY294002 significantly enhanced morphine-induced apoptosis. Moreover, inhibition of Akt or nuclear factor-kappaB (NF-kappaB) expression by RNA interference technology also dramatically increased morphine-induced apoptosis. Our study thus demonstrates that morphine induces Jurkat cell apoptosis through FADD/p53, anti-apoptotic PI3K/Akt and NF-kappaB pathways.

Analysis of Variance↗
PubMed2006

Effect of modified C-reactive protein on complement activation: a possible complement regulatory role of modified or monomeric C-reactive protein in atherosclerotic lesions.

OBJECTIVE: The capacity of human C-reactive protein (CRP) to activate/regulate complement may be an important characteristic that links CRP and inflammation with atherosclerosis. Recent advances suggest that in addition to classical pentameric CRP, a conformationally distinct isoform of CRP, termed modified or monomeric CRP (mCRP), may also play an active role in atherosclerosis. Although the complement activation behavior of CRP has been well established, the capacity of mCRP to interact with and activate the complement cascade is unknown. METHODS AND RESULTS: mCRP bound avidly to purified C1q, and this binding occurred primarily through collagen-like region of C1q. Fluid phase mCRP inhibited the activation of complement cascade via engaging C1q from binding with other complement activators. In contrast, when immobilized or bound to oxidized or enzymatically modified low-density lipoprotein, mCRP could activate classical complement pathway. Low-level generation of sC5b-9 indicated that the activation largely bypassed the terminal sequence of complement, which appears to involve recruitment of Factor H. CONCLUSIONS: These results indicate that mCRP can both inhibit and activate the classical complement pathway by binding C1q, depending on whether it is in fluid phase or surface-bound state.

Atherosclerosis↗
PubMed2006

Safrole oxide induced human umbilical vein vascular endothelial cell differentiation into neuron-like cells by depressing the reactive oxygen species level at the low concentration.

Previously, we found that 5-25 microg/ml safrole oxide could inhibit apoptosis and dramatically make a morphological change in human umbilical vein vascular endothelial cells (HUVECs). But the possible mechanism by which safrole oxide function is unknown. To answer this question, in this study, we first investigated the effects of it on the activity of nitric oxide synthetase (NOS), the expressions of Fas and integrin beta4, which play important roles in HUVEC growth and apoptosis, respectively. The results showed that, at the low concentration (10 microg/ml), safrole oxide had no effects on NOS activity and the expressions of Fas and integrin beta4. Then, we investigated whether HUVECs underwent differentiation. We examined the expressions of neuron-specific enolase (NSE) and neurofilament-L (NF-L). Furthermore, we analyzed the changes of intracellular reactive oxygen species (ROS). After 10 h of treatment with 10 microg/ml safrole oxide, some HUVECs became neuron-like cells in morphology, and intensively displayed positive NSE and NF-L. Simultaneously, ROS levels dramatically decreased during HUVECs differentiation towards neuron-like cells. At the low concentration, safrole oxide induced HUVECs differentiation into neuron-like cells. Furthermore, our data suggested that safrole oxide might perform this function by depressing intracellular ROS levels instead of by affecting cell growth or apoptosis signal pathways.

Blotting, Western↗
PubMed2006

Coupling of cell migration with neurogenesis by proneural bHLH factors.

After cell birth, almost all neurons in the mammalian central nervous system migrate. It is unclear whether and how cell migration is coupled with neurogenesis. Here we report that proneural basic helix-loop-helix (bHLH) transcription factors not only initiate neuronal differentiation but also potentiate cell migration. Mechanistically, proneural bHLH factors regulate the expression of genes critically involved in migration, including down-regulation of RhoA small GTPase and up-regulation of doublecortin and p35, which, in turn, modulate the actin and microtubule cytoskeleton assembly and enable newly generated neurons to migrate. In addition, we report that several DNA-binding-deficient proneural genes that fail to initiate neuronal differentiation still activate migration, whereas a different mutation of a proneural gene that causes a failure in initiating cell migration still leads to robust neuronal differentiation. Collectively, these data suggest that transcription programs for neurogenesis and migration are regulated by bHLH factors through partially distinct mechanisms.

Actins↗
PubMed2006

Nociceptor-derived brain-derived neurotrophic factor regulates acute and inflammatory but not neuropathic pain.

Conditional mouse knock-outs provide an informative approach to drug target validation where no pharmacological blockers exist or global knock-outs are lethal. Here, we used the Cre-loxP system to delete BDNF in most nociceptive sensory neurons. Conditional null animals were healthy with no sensory neuron loss. However, pain-related behavior was substantially altered. Baseline thermal thresholds were reduced. Carrageenan-induced thermal hyperalgesia was inhibited. Formalin-induced pain behavior was attenuated in the second phase, and this correlated with abolition of NMDA receptor NR1 Ser896/897 phosphorylation and ERK1 and ERK2 activation in the dorsal horn; AMPA receptor phosphorylation (GluR1/Ser831) was unaffected. NGF-induced thermal hyperalgesia was halved, and mechanical secondary hyperalgesia caused by intramuscular NGF was abolished. By contrast, neuropathic pain behavior developed normally. Nociceptor-derived BDNF thus plays an important role in regulating inflammatory pain thresholds and secondary hyperalgesia, but BDNF released only from nociceptors plays no role in the development of neuropathic pain.

Acute Disease↗
PubMed2006

Intermedin1-53 activates L-arginine/nitric oxide synthase/nitric oxide pathway in rat aortas.

Intermedin (IMD), a novel member of the calcitonin/calcitonin gene-related peptide (CGRP) family, has similar or more potent vasodilatory and hypotensive actions than adrenomedullin (ADM) and CGRP. The present study was designed to observe the effects of synthetic rat IMD1-53 on L-arginine (L-Arg) cellular transport, nitric oxide synthase (NOS) activity, and nitric oxide (NO) production in the isolated rat aortic ring to illustrate its direct effect on the L-Arg/NOS/NO pathway in vasculature. IMD1-53 significantly increased NO production and cNOS activity in rat aortas and was more potent than equivalent ADM. But the peptides of both IMD and ADM had no effect on inducible NOS expression and activity. Otherwise, IMD1-53 induced a concentration-dependent increase in [3H]L-Arg transport and its effect was more potent than that of an equivalent concentration of ADM. Semiquantitative RT-PCR revealed that IMD1-53 significantly increased cationic amino acid transport (CAT)-1 and CAT-2B mRNA expression, and its effect was similar to that of ADM. All these results suggest that IMD1-53 might regulate vessel function homeostasis via upregulating the L-Arg/NOS/NO pathway.

Adrenomedullin↗
PubMed2006

Tamoxifen-inducible NaV1.8-CreERT2 recombinase activity in nociceptive neurons of dorsal root ganglia.

To explore the function of genes expressed in adult mouse nociceptive neurons, we generated heterozygous knock-in mice expressing the tamoxifen-inducible Cre recombinase construct CreERT2 downstream of the Na(V)1.8 promoter. CreERT2 encodes a Cre recombinase (Cre) fused to a mutant estrogen ligand-binding domain (ERT2) that requires the presence of tamoxifen for activity. We have previously shown that heterozygous Na(V)1.8-Cre mice will delete loxP flanked genes specifically in nociceptive sensory neurons from embryonic day 14. We therefore used the same strategy of homologous recombination and mouse generation, substituting the Cre cassette with CreERT2. No functional Cre recombinase activity was found in CreERT2 mice crossed with reporter mice in the absence of tamoxifen. We found that, as with Na(V)1.8-Cre mice, functional Cre recombinase was present in nociceptive sensory neurons after tamoxifen induction in vivo. However, the percentage of dorsal root ganglion (DRG) neurons expressing functional Cre activity was much reduced (<10% of the number found in the Na(V)1.8-Cre mouse). We also examined Cre recombinase activity in sensory neurons in culture. After treatment with 1 muM tamoxifen for 48 h, 15% of DRG neurons showed Cre activity. Na(V)1.8-CreERT2 animals may thus be useful for single cell studies of the functional consequences of gene ablation in culture, but are unlikely to be useful for behavioral studies.

Alleles↗
PubMed2006

Quality evaluation of Cordyceps through simultaneous determination of eleven nucleosides and bases by RP-HPLC.

A new RP-HPLC method has been developed for the simultaneous determination of 11 nucleosides and bases, including adenosine, cordycepin, cytidine, guanosine, inosine, thymidine, uridine, cytosine, guanine, thymine, and uracil in Cordyceps. Determination was achieved on a Zorbax 300SB C18 analytical column (4.6 x 250 mm id, 5 mm) using gradient elution with diode-array detection. All calibration curves showed good linearity (r2 > 0.9995) within the test ranges. The developed method was simple, rapid, and accurate, and showed good reproducibility for the quantification of 11 nucleosides and bases in natural and cultured Cordyceps with both intra- and inter-day variations of less than 1.8%. Furthermore, hierarchical clustering analysis based on the typical peaks of adenosine, cordycepin, and inosine in HPLC profiles from the 11 tested samples showed that natural and cultured Cordyceps were in different clusters, which could provide a means of discriminating between Cordyceps of different origins. Thus, adenosine, cordycepin, and inosine could be used as markers for quality control of Cordyceps.

Calibration↗
PubMed2006

Management of involved or close resection margins in 120 patients with colorectal liver metastases: edge cryotherapy can achieve long-term survival.

BACKGROUND: The liver resection margin is prognostically significant for patients with colorectal liver metastases. Management plans for patients with suboptimal resection margins have not been adequately addressed. This article reports the long-term results of edge cryotherapy in 120 patients with suboptimal resection margins. METHODS: A retrospective analysis of prospectively collected clinical data of 120 patients with suboptimal hepatic resection margins was performed. Morbidity, mortality, recurrence, and survival results were analyzed. RESULTS: The median length follow-up was 30 months (range 1 to 139). The median disease-free interval was 19 months (range 2 to 139). Cryosite, remaining liver, and extrahepatic recurrence rates were 10%, 36%, and 47%, respectively. The median survival was 39 months (range 1 to 139), and 1-, 3-, and 5-year survival rates were 89%, 55%, and 36%, respectively. Cryosite and extrahepatic recurrence were independently associated with a reduced survival outcome. COMMENTS: Edge cryotherapy to suboptimal liver resection margins can achieve a lower local recurrence rate and a longer survival advantage.

Adult↗
PubMed2006

Activation of DNA enzyme 10-23 by tethering an intercalator to its backbone.

The activity of RNA cleaving DNA enzyme 10-23 is greatly improved by covalently introducing an intercalator, such as azobenzene, anthraquinone, 2-stilbazole, and pyrene. The intercalator is attached via an amide bond to D-threoninol, which inserts into the backbone of DNA with typical phosphoramidite chemistry. The increase of cleavage activity is observed only when an intercalator is tethered at the junction point between the catalytic loop and the binding arm at 3' side. Structures of the introduced intercalator itself as well as the linker for tethering it greatly influence the cleavage activity. In the case of anthraquinone, the most efficient activator we investigated, about eight folds of activity increase are obtained in comparison with the native DNA enzyme.

Azo Compounds↗
PubMed2006

Altered L-arginine/nitric oxide synthase/nitric oxide pathway in the vascular adventitia of rats with sepsis.

1. In recent studies, the vascular adventitia has been established as an important source of inducible nitric oxide synthase (iNOS) and subsequent nitric oxide (NO) production, even more powerful than the media in response to certain inflammatory factors, such as lipopolysaccharide (LPS). The adventitia has an independent L-arginine (L-Arg)/NOS/NO pathway and is involved in the regulation of vascular function. In the present study, we explored the changes in and the pathophysiological significance of the L-Arg/NOS/NO pathway in the adventitia of rats with sepsis. 2. Sepsis was induced by caecal ligation and puncture in order to observe changes in L-Arg transport, NOS gene expression and activity and NO generation in the vascular adventitia to determine the mechanism of activation of the L-Arg/NOS/NO pathway. 3. Severe sepsis resulted in severe disturbance of haemodynamic features, with decreased mean arterial blood pressure, brachycardia and inhibited cardiac function (decreased left ventricular +/-dP/dt(max)). Left ventricular end-diastolic pressure was elevated threefold (P < 0.01) under anaesthesia. Rats with sepsis showed severe glucopenia and lacticaemia. Plasma levels of the inflammatory factors macrophage chemoattractant protein-1 and interleukin-8 were increased five- and 29-fold, respectively (P < 0.01). 4. In the adventitia of the thoracic and abdominal aortas, the L-Arg/NO pathway was similarly characterized: the uptake of [(3)H]-L-Arg was Na(+) independent, with the peak occurring at approximately 40 min incubation. Total NOS activity was largely calcium independent (> 90%). The V(max) of L-Arg transport in the sepsis group was increased by 83.5% (P < 0.01), but the K(m) value was not significantly different compared with controls. 5. The mRNA levels of cationic amino acid transporter (CAT)-1 and CAT-2B in the sepsis group were increased by 86 and 62%, respectively (both P < 0.01). Inducible NOS activity was increased 2.8-fold compared with controls (P < 0.01) and iNOS mRNA levels were elevated approximately sixfold (P < 0.01). The NO levels in the plasma and incubation media (incubation for 40 min) in the sepsis group were increased by 144 and 273%, respectively (both P < 0.01). 6. The Arg/NOS/NO pathway was activated in the vascular adventitia of rats with sepsis shock. The L-Arg/NOS/NO pathway in the aortic adventitia may play an important role in the pathogenesis of sepsis and septic shock.

Animals↗
PubMed2006

Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats.

AIM: To investigate the role of the endogenous cystathionine gamma-synthase (CSE)/hydrogen sulfide (H2S) pathway in vascular calcification in vivo. METHODS: A rat vascular calcification model was established by administration of vitamin D3 plus nicotine (VDN). The amount of CSE and osteopontin (OPN) mRNA was determined by using semi-quantitative reverse-transcription polymerase chain reaction. The calcium content, 45Ca2+ accumulation and alkaline phosphatase (ALP) activity were measured. H2S production and CSE activity were measured. RESULTS: von Kossa staining produced strong positive black/brown staining in areas among the elastic fibers of the medial layer in the calcified aorta. The calcium content, 45Ca2+ accumulation and ALP activity in calcified arteries increased by 6.77-, 1.42-, and 1.87-fold, respectively, compared with controls. The expression of the OPN gene was upregulated (P<0.01). Expression of the CSE gene was downregulated. However, calcium content, 45Ca2+ uptake and ALP activity in the VDN plus NaHS group was lower than that in the VDN group. The content of calcium and 45Ca2+ accumulation and activity of ALP in the aorta were 34.8%, 40.75% and 63.5% lower in the low-dosage NaHS group than in the VDN group, respectively (P<0.01), and the calcium content and deposition of 45Ca2+ and activity of ALP was 83.9%, 37.8 % and 46.2% lower in the aorta in the high-dosage NaHS group than in the VDN group, respectively (P<0.01). The expression of the OPN gene was downregulated. CONCLUSION: The production of H2S, and CSE activity were decreased and CSE gene expression was downregulated in rats with vascular calcification. H2S can ameliorate vascular calcification, suggesting that the H2S/CSE pathway plays a regulatory role in the pathogenesis of vascular calcification.

Animals↗
PubMed2006

Advances in contemporary nanosphere lithographic techniques.

Nanosphere lithography (NSL) is an inexpensive, high throughput, materials general nanofabrication technique capable of producing a large variety of nanoscale structures including well-ordered 2 dimensional nanoparticle arrays. In this review, we will summarize the most recent advances in the fabrication of size-tunable nanoparticles using NSL. Four examples of new NSL-derived materials will be described: (1) The development of a method to release NSL nanoparticles from the substrate for applications in solution environments, (2) the fabrication of triangular nanoholes with reactive ion etching, (3) the electrochemical fine tuning of the structure of a silver nanoparticle and the wavelength of its localized surface plasmon resonance (LSPR), and (4) the growth of ultra thin protective dielectric layers on NSL-fabricated Ag nanotriangles using atomic layer deposition (ALD).

Crystallization↗
PubMed2006

Expression of cytoskeleton and apoptosis related genes after cerebral infarction.

OBJECTIVE: The aim of the study was to investigate the expression and regulation of cytoskeleton and apoptosis related genes in several brain areas after cerebral infarction. METHODS: Tissues were collected from ten autopsy brains from cerebral infarction patients. Using immunohistochemistry, several cytoskeleton and apoptosis related genes were examined in these tissues. The genes included microtubule-associated protein (MAP), glial fibrillary acidic protein (GFAP), neurofilament protein (NF-200), apoptosis gene bc1-2 and factor VIII related antigen (F-VIII). Based on morphological changes in the damaged areas after infarction, the focus and the surrounding areas of injured brain were divided into four areas. RESULTS: In area 0, there was almost no cell survival after infraction, and all markers mentioned above were negative in this area. In addition, both MAP-2 and NF200 like immunoreactivities were dramatically down-regulated in area 1. However, in area 2 and area 3, MAP-2 and NF-200 expressed at normal level. GFAP- and F-VIII immunoreactive cells could hardly found in areas 0 and 1. In the short phase of ischemia, both GFAP and F-immmunoreactive cells could be seen in areas 2 and 3, and the number of GFAP and F (positive cells) was strongly increased in the long phase of ischemia. Bcl-2 immunoreactive cells were only seen in area 2. CONCLUSION: Cerebral infarction causes cell death and physipathological changes of cytoskeleton and apoptosis related genes.

Aged↗
PubMed2006

[Detecting of mtDNA mutations at position A3243G and G3316A in patients with type 2 diabetes mellitus in Wenzhou].

To investigate the frequencies of mitochondria DNA (mtDNA) tRNA(Leu (UUR)) point mutation A3243G and NADH dehydronase subunit 1(ND1) gene point mutation G3316A in Wenzhou area of Zhejiang Province, and to explore the correlation between these mutations and the clinical manifestations in patients with type 2 mellitus diabetes(T2DM). Two hundreds and forty-four unrelated patients with T2DM and 156 healthy subjects without family history of T2DM were enrolled in Wenzhou area in this study and screened for the point mutations mentioned above with polymerase chain reaction (PCR) and restricted fragment length polymorphism(RFLP) analysis. The heterogeneous mutations were confirmed with DNA sequencing and denaturing high performance liquid chromatography (DHPLC) following T-A cloning of PCR products. The percentage of A3243G mutation in group of patients with T2DM and control were 0.410% and 0.0% (1/244 vs 0/156), respectively; however, there's not any significant difference between these two groups in frequency of A3243G mutation (P>0.05). G3316A mutation was detected in 4 of 244 cases with T2DM (1.639%) and 2 of 156 healthy controls (1.282%), showing that there's also no statistic difference between these two groups in frequency of G3316A mutation (P>0.05). It's shown that the frequency of mtDNA tRNA(Leu (UUR)) A3243G mutation is fairly low in patients with T2DM in Wenzhou area. Thus it's reasonable to assume that this mutation may not be involved in the development and progression of T2DM. Furthermore, it's demonstrated that the rate of G3316A mutation of mtDNA ND1 gene is rare in patients with T2DM in Wenzhou area and this mutation also happened in healthy control. It's suggested that G3316A mutation is just a gene polymorphism of mtDNA and not related to the pathogenesis of T2DM.

Asian People↗
PubMed2006

[Progress on Agrobacterium-mediated transformation of banana].

The development of improved Musa by conventional breeding remains to be a difficult endeavor because of the long generation times, various levels of ploidy, sterility of most edible cultivars and limited genetic variability. Therefore, genetic engineering may offer an alternative method for crop enhancement. The transformation system mediated by Agrobacterium tumefaciens has been used successfully to transform banana during the past 10 years. This article reviews recent progresses on transformation of banana mediated by Agrobacterium tumefaciens and summarizes the factors affecting transformation efficiency. Existing problems and its prospects are briefly discussed.

Agrobacterium tumefaciens↗
PubMed2006

Expression of soluble and functional snake venom fibrinolytic enzyme fibrolase via the co-expression of DsbC in Escherichia coli.

Fibrolase is a non-hemorrhagic zinc metalloproteinase found in southern copperhead snake venom (Agkistrodon contortrix contortrix). It is capable of degrading fibrin clots that result from purified fibrinogen or blood plasma. The DNA of fibrolase was amplified by recursive PCR, and cloned into the pET25b(+) expression vector. The effect of co-expression of signalless versions of catalysts or molecular chaperones FkpA, Skp and DsbC in cytoplasm was examined. When co-expressed with DsbC, compared to the totally insoluble inclusion bodies of fibrolase expressed separately, more than 90 % of recombinant fibrolase was soluble, according to denaturing polyacrylamide gel electrophoresis analysis. We also determined that FkpA and Skp had no effects on the solubility of target protein when co-expressed with fibrolase in Escherichia coli. Fibrolase was successfully purified using metal ion affinity chromatography and hydrophobic chromatography, and a maximum yield of 20 mg/L fibrolase was obtained. Fibrinolytic activity of recombinant fibrolase was demonstrated using fibrin plate assays and fibrinogen hydrolysis.

Agkistrodon↗