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Biomedical subjects

S Q Zhang

Publications and source records attributed to S Q Zhang.

At least 19 recordsLinked to original sources
PubMed2006

Does multiple hosts mean multiple parasites? Population genetic structure of Schistosoma japonicum between definitive host species.

Multi-host parasites, those capable of infecting more than one species of host, are responsible for the majority of all zoonotic, emerging or persistent human and animal diseases and are considered one of the major challenges for the biomedical sciences in the 21st century. We characterized the population structure of the multi-host parasite Schistosoma japonicum in relation to its definitive host species by genotyping miracidia collected from humans and domestic animals across five villages around the Yangtze River in Anhui Province, mainland China, using microsatellite markers. High levels of polymorphisms were observed and two main genetic clusters were identified which separated water buffalo, cattle and humans from goats, pigs, dogs and cats. We thereby believe that we present the first evidence of definitive host-based genetic variation in Schistosoma japonicum which has important epidemiological, evolutionary, medical and veterinary implications.

Animals↗
PubMed2006

Influence of mizolastine on antigen-induced activation of signalling pathways in murine mast cells.

BACKGROUND: There is accumulating evidence that some antihistamines can interrupt intermediate signalling events that regulate cell function. The effect of mizolastine on both the generation and release process of many cytokines in mast cells further implies that the inhibition by mizolastine may target signalling pathways. AIM: To observe the influence of mizolastine on antigen-induced activation of signalling pathways in murine mast cells. METHODS: Western blot analysis and enzyme assay were performed. Immunoblots were prepared from whole cell lysates and probed with antibodies against Fyn, Akt, ERK, p38, phospho-Fyn, phospho-Akt, phospho-ERK and phospho-p38, respectively. RESULTS: Our study showed that signalling molecules such as IP3, Fyn, p38 and ERK were enhanced when mast cells were stimulated by antigen, and that this was not inhibited by treatment with mizolastine. Mizolastine at concentrations from 10(-9) to 10(-5) mol/L could inhibit activation of the PI3K kinase downstream signalling molecule Akt to antigen stimulation. The study also demonstrated that mizolastine exerted inhibitory ability on protein kinase C (PKC) activation in a dose-dependent manner. CONCLUSION: PKC-mediated phosphorylation of Akt can be blocked by mizolastine. There may be a PKC-independent pathway effectively activating MAPK pathways in mast cells in response to antigen induction, which cannot be affected by mizolastine.

Animals↗
PubMed2005

Attenuation of acute lung injury in mice by oxymatrine is associated with inhibition of phosphorylated p38 mitogen-activated protein kinase.

Oxymatrine is one of the alkaloids extracted from Chinese herb Sophora japonica (Sophora flavescens Ait.) with activities of anti-inflammation, inhibiting immune reaction, antivirus, protecting hepatocytes and antihepatic fibrosis. However, the effect of oxymatrine on acute lung injury (ALI) has not been known yet. In this study, the effect of oxymatrine on ALI was investigated using an oleic acid-induced ALI mouse model. Morphological findings showed that the oleic acid group demonstrated a marked lung injury represented by prominent atelectasis, intraalveolar and interstitial patchy hemorrhage, edema, thickened alveolar septum, formation of hyaline membranes and the existence of inflammatory cells in alveolar spaces. While in the oxymatrine/dexamethasone group, these changes were less severe and in the vicinity of the control group. Furthermore, pretreatment with oxymatrine significantly alleviated oleic acid-induced lung injury accompanied by reduction of lung index and wet-to-dry weight ratio, decreases in serum TNF-alpha level and inhibition of phosphorylated p38 MAPK. These findings suggest that oxymatrine has a beneficial effect on acute lung injury induced by oleic acid in mice and may inhibit the production of proinflammatory cytokine, TNF-alpha, by means of the inhibition of p38 MAPK.

Alkaloids↗
PubMed2005

The effect of mizolastine on expression of vascular endothelial cell growth factor, tumour necrosis factor-alpha and keratinocyte-derived chemokine in murine mast cells, compared with dexamethasone and loratadine.

It has been shown that many antihistamines may have anti-inflammatory activity in addition to being H1 antagonists. Mizolastine (MIZ), a novel antihistamine, might also have anti-angiogenesis properties. In this study, we investigated the influence of MIZ on proangiogenesis factors, vascular endothelial cell growth factor (VEGF), tumour necrosis factor (TNF)-alpha and keratinocyte-derived chemokine (KC) in murine mast cells by using ELISA and RT-PCR, as compared with dexamethasone (DEX) and loratadine (LOR). Our results show that MIZ is effective in the inhibition of KC, VEGF and TNF-alpha release induced by an IgE-dependent mechanism, in a time- and dose-dependent manner. The differences between the inhibitory effects of the three drugs on these proangiogenic factors were rather subtle. Semiquantitative analysis using RT-PCR showed that the three drugs significantly reduced VEGF165, VEGF120, TNF-alpha and KC mRNA expression. Statistical results revealed that the effect of DEX on VEGF165 mRNA was different from that of MIZ or LOR (P < 0.01) and the differences between the three drugs on VEGF120, TNF-alpha and KC mRNA were not statistically significant (P > 0.05). These findings raise the possibility that MIZ can mediate anti-angiogenesis activity and that the effect may depend not only on the inhibition on the levels of cytokine proteins but also at the mRNA level.

Angiogenesis Inducing Agents↗
PubMed2001

Sleep-promoting activity of prolactin-releasing peptide (PrRP) in the rat.

The present study examines whether or not prolactin-releasing peptide (PrRP) infused intracerebroventricularly (i.c.v.) affects sleep and the release of prolactin (PRL) and growth hormone (GH) in rats. At a dose of 0.1 nmol, PrRP promoted rapid-eye-movement (REM) sleep, whereas 1.0 nmol increased both non-REM and REM sleep and 10.0 nmol enhanced only non-REM sleep. During the i.c.v. infusion of PrRP with 0.1 nmol, levels of plasma PRL were elevated, but GH levels were significantly decreased. Since it is reported that PrRP fails to induce PRL release from the male pituitary, the stimulatory effects of PrRP on PRL release observed here seem to be indirect. However, PRL stimulated by i.c.v.-infused PrRP could take part in the REM sleep-promoting activity of PrRP.

Animals↗
PubMed2001

Multiple dose study of interactions between artesunate and artemisinin in healthy volunteers.

AIMS: To investigate whether coadministration of the antimalarials artesunate and artemisinin alters the clearance of either drug. METHODS: Ten healthy Vietnamese males (Group AS) were randomized to receive a single dose of 100 mg oral artesunate (pro-drug of dihydroartemisinin) on day -5 and then once daily for 5 consecutive days (days 1-5). Oral artemisinin (500 mg) was coadministered on days 1 and 5. Another 10 subjects (Group AM) were given 500 mg oral artemisinin on day -5 and then further doses on days 1-5. Artesunate 100 mg was given on days 1 and 5. Artemisinin and dihydroartemisinin plasma concentrations on days -5, 1 and 5 were quantified by h.p.l.c. with on-line postcolumn derivatization and u.v. detection. RESULTS: In Group AS, dihydroartemisinin oral clearance values (mean (95% CI)) were similar on day 1 (32 (22, 47)) l h(-1) and day 5 (38 (28, 51)) l h(-1) of daily artesunate administration but these mean values were approximately three fold higher compared with day -5 after a single dose (95 (56, 159)). In this group, artemisinin oral clearance increased from 196 (165, 232) l h(-1) on day 1-315 (241, 410) l h(-1) on day 5. In Group AM, dihydroartemisinin oral clearance on day 1 was 39 (34, 46) l h(-1) and increased 1.6 fold to 64 (48, 85) l h(-1) on day 5. In this group, artemisinin oral clearance increased sequentially (1.5 and 4.7 fold, respectively) from 207 (151, 285) l h(-1) on day -5-308 (257, 368) l h(-1) on day 1 and to 981 (678, 1420) l h(-1) on day 5. The increase in artemisinin oral clearance between days -5 and 1 (in the absence of artesunate) was similar to that between days 1 and 5 in Group AS subjects who took daily artesunate. Dihydroartemisinin was not a significant metabolite of artemisinin. CONCLUSIONS: Artesunate (dihydroartemisinin) did not alter the elimination of artemisinin. However, dihydroartemisinin elimination was inhibited by artemisinin. Artemisinin induced its own elimination even 5 days after a single oral dose. There was no evidence for the formation of dihydroartemisinin from artemisinin.

Administration, Oral↗
PubMed2001

Basal forebrain microinjections of L-3,3',5-triiodothyronine modify sleep in hypothyroid rats.

Male rats were injected bilaterally with various doses of L-3,3',5-triiodothyronine (T3) into basal forebrain areas. The electroencephalogram (EEG), electromyogram (EMG) and brain temperature (Tbr) were then measured in 8-h studies. In the medial preoptic area (MPA), a 4 microg dose of T3 caused significant elevations in REM sleep as compared to control injections. In the median preoptic nucleus (MnPO), both 2 and 4 microg doses of T3 significantly inhibited non-REM sleep. Injections to the diagonal band of Broca did not alter EEG-defined sleep. Influences on Tbr were not significant for any of the treatments. Since these effects of T3 were demonstrated after acute injections, the data are consistent with possible non-genomic actions of thyroid hormones in adult brain.

Animals↗
PubMed2001

Relationship between changes in the guard cell abscisic-acid content and other stress-related physiological parameters in intact plants.

The relationships of guard cell ABA content to eight stress-related physiological parameters were determined on intact Vicia faba L. plants that were grown hydroponically with split-root systems. Continuous stress was imposed by the addition of PEG to part of the root system. The water potentials of roots sampled after the addition of PEG were 0.25 MPa lower than the water potentials of other roots of the same plant, which were similar to the roots of untreated plants. The leaflet water potentials of plants sampled within 2 h of stress imposition were similar to those of control plants. However, leaf conductance was lower in plants sampled after only 20 min of stress imposition, and the root- and leaflet apoplastic ABA concentrations of these plants were higher than those of untreated plants. As the essence of this report, there was a linear relationship between guard cell ABA content and leaf conductance. Leaflet apoplastic ABA concentrations <150 nM were also linearly related to leaf conductance, but higher leaflet apoplastic ABA concentration did not cause equally large further declines in leaf conductance. It is suggested that evaporation from guard cell walls caused ABA to accumulate in the guard cell apoplast and this pool was saturated at high leaflet apoplastic ABA concentrations.

Abscisic Acid↗
PubMed2001

[Features of breast ultrasound image and its correlation with estradiol and progesterone level in different phases of menstrual cycle in normal women].

OBJECTIVE: To determine the features of the breast ultrasound image and its correlation with estrogen and progestogen level during different phases of menstrual cycle in normal women. METHODS: Breast ultrasound was performed during luteal phase and late follicular phase in 50 women aged 25-45, with normal menstrual cycle and no distinct breast disease. Breast section thickness, ductal width, breast structure and blood flow were measured. Initial time and persistent days of the cyclic breast pain were recorded. Serum estradiol (E2) and progesterone (P) levels were measured by enzyme immunoassay on the day of ultrasound performed. RESULTS: Breast glandular section was thicker (increasing by 7.3%) in luteal phase than that in late follicular phase and breast ductal was wider (increasing by 13%) in late follicular phase than that in luteal phase. However, both of them had no significant difference. Thirty women (60%) experienced cyclic premenstrual mastalgia, lasting 4 days. Twenty four women (48%) had breast structure changes, nineteen (63.3%) of 30 women with cyclic mastalgia, but only 5 (25%) of 20 women without breast pain had breast structure change (chi 2, P < 0.01). Average serum E2 level of women with or without cyclic breast pain in luteal phase were 365.0 pmol/L and 335.3 pmol/L respectively (P > 0.05), serum progesterone level were 73.3 nmol/L and 66.1 nmol/L respectively (P > 0.05). Serum E2 levels of women with or without cyclic breast pain in late follicular phase were 299.9 pmol/L and 385.8 pmol/L respectively (P = 0.05). Average serum E2 levels of women with or without breast structure change in luteal phase were 368.1 pmol/L and 322.7 pmol/L respectively (P < 0.05). Serum P levels were 78.8 nmol/L and 62.2 nmol/L respectively (P = 0.05); Estradiol levels in late follicular phase were 301.9 pmol/L and 364.2 pmol/L respectively (P > 0.05). CONCLUSIONS: Image of breast ultrasound changed following menstrual cycle in normal menstrual women. Breast structure changes is related to breast pain. Breast pain and breast structure changes may be caused by higher E2 and P level in luteal phase and lower E2/P ratio in late follicular phase.

Adult↗
PubMed2000

Granulocyte-macrophage colony-stimulating factor modulates rapid eye movement (REM) sleep and non-REM sleep in rats.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a hematopoietic cytokine that may affect various functions of the CNS because the molecule and its receptors are expressed in the brain. The present study examines the effects of GM-CSF on sleep using rats and the secretion of three neurotransmitters/hormones that are involved in sleep regulation. When infused intracerebroventricularly at doses as low as 10 pmol for 10 hr during the dark period, GM-CSF promoted predominantly rapid eye movement (REM) sleep and moderate amounts of non-REM sleep without eliciting fever. An injection of GM-CSF (3.0 pmol) into the arcuate nucleus increased the release of nitric oxide (NO) from the hypothalamus but did not alter plasma levels of growth hormone. The release of somatostatin (SRIF) from the medial basal hypothalamus was stimulated by 1 x 10(-)(11) M GM-CSF. These findings indicated that centrally administered GM-CSF stimulates SRIF release through activation of the NO system in the hypothalamus. Because SRIF promotes REM sleep, it may also mediate the effects of GM-CSF on REM sleep. The present study indicates a novel central effect of GM-CSF that modulates sleep, supporting the notion that hematopoietic cytokines also play roles in the CNS.

Animals↗
PubMed2000

Recruitment of the IKK signalosome to the p55 TNF receptor: RIP and A20 bind to NEMO (IKKgamma) upon receptor stimulation.

The adapter protein RIP plays a crucial role in NF-kappaB activation by TNF. Here we show that triggering of the p55 TNF receptor induces binding of RIP to NEMO (IKKgamma), a component of the I-kappa-B-kinase (IKK) "signalosome" complex, as well as recruitment of RIP to the receptor together with the three major signalosome components, NEMO, IKK1 and IKK2, and some kind of covalent modification of the recruited RIP molecules. It also induces binding of NEMO to the signaling inhibitor A20, and recruitment of A20 to the receptor. Enforced expression of NEMO in cells revealed that NEMO can both promote and block NF-kappaB activation and dramatically augments the phosphorylation of c-Jun. The findings suggest that the signaling activities of the IKK signalosome are regulated through binding of NEMO to RIP and A20 within the p55 TNF receptor complex.

Antigens, CD↗
PubMed2000

Effects of prolactin-releasing peptide (PrRP) on sleep regulation in rats.

The present study examined in rats how prolactin-releasing peptide (PrRP), a new hypothalamic hormone, infused centrally during the dark period affects sleep and plasma levels of prolactin (PRL). At a dose of 0.1 nmol, PrRP increased only rapid eye movement (REM) sleep, whereas with 1.0 nmol both non-REM sleep and REM sleep were enhanced. However, 10.0 nmol of PrRP increased only non-REM sleep with a febrile response. The levels of plasma PRL were elevated during the infusion of PrRP with 0.1 and 1.0 nmol. Consequently, the increased release of PRL correlated with significant increases in REM sleep, but not in non-REM sleep.

Animals↗
PubMed2000

[Fusion expression of cecropin X including the cleavage of FXa in Escherichia coli].

PCR method was used to introduce the code sequence of Factor Xa cleavage site to the 5' end of cecropin CMIV mutant gene X, then the gene was cloned into the expression vector pGEX-KG, and was highly expressed in E. coli BL21 by IPTG induction. The fusion protein was purified by affinity-chromatography and was cleaved by Factor Xa. Cecropin X with antibacterial activity was obtained after purified by ion-exchange chromatography.

Antimicrobial Cationic Peptides↗
PubMed2000

Effect of PKC-zeta mediating Ang II-stimulated activation of CCDPK on rat cardiac fibroblast proliferation.

AIM: To investigate whether the effect of angiotensin (Ang) II or epidermal growth factor (EGF) on cardiac fibroblast proliferation involved in activation of extracellular signal-regulated kinase (ERK) 1/2 or Ca(2+)-calmodulin dependent protein kinase(CCDPK) mediated by protein kinase C (PKC)-zeta. METHODS: Relative activity of CCDPK was measured by Western blotting. DNA synthesis was assayed by [3H]thymidine incorporation. RESULTS: PDBU caused no decrease in Ang II- and 10% FCS-stimulated CCDPK activity and DNA synthesis. In contrary, 65% or 75% EGF- or tetradecanoylphorbol acetate (TDPA, formally called PMA)--stimulated CCDPK activity and 38% or 42% [3H]thymidine incorporation treated by PDBU were inhibited, respectively. Meanwhile 70% and 72% CCDPK activities induced by Ang II and EGF were inhibited by PD 98059, respectively. CONCLUSION: PKC-zeta mediated Ang II-induced activation of CCDPK and cardiac fibroblast proliferation.

Angiotensin II↗
PubMed2000

[Ultrastructural observation of E. coli K12 treated with antibacterial peptide CM4].

The effect of antibacterial peptide CM4 of Bombyx mori against E. coli K12 was investigated using scanning electron microscopy(SEM) and transmission electron microscopy (TEM). The ultrastructural changes of E. coli K12 were observed by the challenge of the purified antibacterial peptide CM4. The results showed that the antibacterial peptide caused a series of pathological changes on E. coli. SEM and TEM revealed aggregates of bacteria and SEM revealed wrinkled bacterial surfaces in the early stage. Thereafter, plasmolysis was observed with irregular holes appearing in the two ends of bacteria and the cytoplasmic contents of the cells leaking out. Finally, bacteria became empty vesicles and disintegrated into small fragments subsequently. Comparatively, the bacterial membrane was normal and the bacterial structure remained intact in the control group.

Animals↗
PubMed2000

[Antibacterial and antifungal effects of Agkistrodon halys Pallas: purification of its antibacterial protein--LAO].

This paper reports the venom from Agkistrodon halys Pallas have inhibitory activity against fungi and E. coli by tested in a disc diffusion assay. An antibacterial component--LAO from the venom were purified to homogeneous. It had not only antibacterial effect, but L-amino acid oxidase activity. And its enzymatic specific activity was 808 U/mg. The venom had at least 3 antibacterial components (I, II, III) as determined by acid polyacrilamide gel electrophoresis, LAO is the antibaterial components II.

Agkistrodon↗