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J Z Shen

Publications and source records attributed to J Z Shen.

10 recordsLinked to original sources
PubMed2006

Technical note: a monoclonal antibody-based immunoassay for determination of ractopamine in swine feeds.

An ELISA was developed for routine screening of ractopamine in swine feeds. Swine feed samples were extracted and purified, and the aqueous portion of the extract was analyzed for ractopamine using ELISA and confirmed by HPLC. For swine complex feeds containing ractopamine at 2.5 to 40 mg/kg, the average recoveries ranged from 73.1 to 86.5% by ELISA and 81.9 to 98.2% by HPLC. For the swine supplement containing ractopamine at 50 to 400 mg/kg, the average recoveries were 105.5 to 111.4% by ELISA and 89.1 to 92.9% by HPLC. The limit of detection was 0.24 microg/g by ELISA and 0.48 microg/g by HPLC, respectively. Results from the swine complex feeds (P = 0.009) and the supplement (P = 0.005) using ELISA and HPLC were not highly correlated. The ELISA was more sensitive and rapid and less expensive than the HPLC method and could be used for ractopamine screening in swine feeds before confirmation and quantification by other methods, such as HPLC.

Adrenergic beta-Agonists↗
PubMed2001

Evidence against inhibition of sarcoplasmic reticulum Ca2+-pump as mechanism of H2O2-induced contraction of rat aorta.

AIM: To test whether inhibition of sarcoplasmic reticulum (SR) Ca2+-pump is involved in H2O2-induced contraction of endothelium-denuded rat aorta. METHODS: Isometric tension recording of H2O2 and cyclopiazonic acid (CPA)-induced contractions of rat aortic rings were compared in the absence or presence of various pharmacological tools to discriminate their signaling pathways involved. RESULTS: Both H2O2 and CPA contracted rat aortic rings, but with different contractile patterns. H2O2 triggered a fast and phasic contraction, whereas CPA elicited a slow and sustained contraction. In Ca2+-free medium, pretreatment of aortic rings with CPA 30 micromol/L but not with H2O2 30 micromol/L nearly abolished phenylephrine (10 micromol/L)-induced contraction. In addition, upon the maximal contraction induced by thapsigargin 30 micromol/L, H2O2 but not CPA further contracted aortic rings. On the other hand, H2O2 (30 micromol/L)- but not CPA (10 micromol/L)-induced contraction could be inhibited by suramin and RB-2 (each 100 micromol/L), two P2-purinoceptor antagonists. Furthermore, although pretreatment with 2-APB, a membrane permeable IP3 receptor blocker, inhibited both H2O2- and CPA-induced contractions, only H2O2 (30 micromol/L)-induced contraction could be depressed, to different degree, by various inhibitors of receptor-coupled or downstream signaling enzymes, including PLC, PKC, PLA2, COX, and protein tyrosine kinases. CONCLUSION: Inhibition of smooth muscle SR Ca2+-pump is unlikely the mechanism responsible for H2O2-induced contraction of endothelium-denuded rat aorta.

Animals↗
PubMed2000

Evidence for P(2)-purinoceptors contribution in H(2)O(2)-induced contraction of rat aorta in the absence of endothelium.

OBJECTIVE: H(2)O(2) can contract many arteries, however the underlying mechanisms are not fully understood. This study aims to test whether H(2)O(2)-induced vasoconstriction could be functionally attributed to the activation of P(2)-purinoceptors in rat aorta and to explore its possible signaling mechanisms. METHODS: Isometric tension recording of H(2)O(2) and ATP-induced contractions of rat aortic rings were compared in the absence or presence of various pharmacological tools to identify their possible common signaling pathways. RESULTS: Both H(2)O(2) and ATP induced transient phasic contractions in a concentration-dependent manner (1-1000 microM). Removal of endothelium potentiated the contractile responses to H(2)O(2) and to ATP. H(2)O(2) (30 microM)-induced phasic contraction could be abolished by catalase (800 U/ml), but not affected by SOD (150 U/ml), DMSO (5 mM) and apyrase (5 U/ml), suggesting no involvement of O(2)(-), hydroxyl free radicals and ATP release. Also, several receptor antagonists including phentolamine, atropine, methysergide and chlorpheniramine (each 3 microM) were without effect on H(2)O(2) (30 microM)-induced phasic contraction, suggesting no involvement of typical neurotransmitter release. However, both H(2)O(2) (30 microM) and ATP (1 mM)-induced phasic contractions not only presented homologous desensitization, but also showed heterogeneous desensitization. Furthermore, the phasic contractions in response to H(2)O(2) (30 microM) or ATP (100 microM) could be inhibited or abolished in a concentration dependent manner by RB-2 and suramin (10-100 microM), two widely used P(2)-purinoceptor antagonists, with only partial inhibition by Evans blue (300 microM), a moderately selective P(2x) receptor blocker, or by alpha-beta-methylene-ATP (100 microM), a selective P(2x) receptor desensitizer. On the other hand, both H(2)O(2) (30 microM) and ATP (100 microM)-induced phasic contractions were also attenuated, to different degree, by inhibitors of several enzymes including PLC, PKC, PLA(2) and cyclooxygenase. Lastly, removal of extracellular Ca(2+) or pretreatment with procaine (10 mM) and dantrolene (30 microM), two putative intracellular Ca(2+) release blockers, or with Ni(2+) (100 microM) and tetrandrine (5 microM), two Ca(2+) channel blockers, all significantly inhibited H(2)O(2) and ATP-induced contractions. However, nifedipine (1 microM), a voltage-dependent L-type Ca(2+) channel blocker, was without effect. CONCLUSIONS: Our results demonstrate that H(2)O(2)-induced phasic contraction of rat aorta involves, at least in part, the activation of P(2)-purinoceptors in the aortic smooth muscle cells

Adenosine Triphosphate↗
PubMed2000

Differential contractile actions of reactive oxygen species on rat aorta: selective activation of ATP receptor by H2O2.

This study aims to examine the effects of different reactive oxygen species (ROS) on the resting tension of endothelium-denuded rat aortic rings. In these preparations, H2O2 (30 microM) induced a fast and transient contraction, which could be abolished by pretreatment of catalase (800 U/ml), but not affected by superoxide anion scavenger, superoxide dismutase (SOD; 150 U/ml) or the hydroxyl free radical scavenger, DMSO/mannitol (each 3 mM). In contrast, pyrogallol, a putative superoxide anion donor, induced a biphasic contraction, which could be abolished by SOD, but not by catalase or DMSO/mannitol. Unlike H2O2 and pyrogallol, Vitamin C(VitC)/Fe2+ (each 100 microM), a commonly used hydroxyl radical-generating system, triggered a tonic contraction which could be prevented by DMSO/mannitol, but not by SOD or catalase. Interestingly, H2O2-induced contraction could be concentration-dependently (10-100 microM) inhibited by suramin and reactive blue-2 (RB-2), two widely used ATP receptor antagonists. On the other hand, suramin or RB-2, at concentration up to 100 microM, affected neither pyrogallol nor VitC/Fe2+-induced contraction. In conclusion, we showed for the first time that different ROS could contract rat aorta with different mechanisms of action, and H2O2 elicits a transient contraction probably as a result of the ATP receptor activation.

Animals↗
PubMed2000

[The study on the standardization of adults voice acoustic parameters by objective analysis].

OBJECTIVE: To explore the characteristic of normal voice in different age-bracket of Chinese adults and to formulate the normal reference value suited to our country at voice assessment. METHOD: We divided the adults into the youth, the middle-aged and the old groups, and analyzed normal voice samples with Dr. Speech software and computer multimedia technique and compared the following 5 parameters (Jitter, Shimmer, NNE, Fo and SDFo) of different groups divided according to one's age, sex and vowel. RESULT: There is difference among the group of age, sex and vowel in most acoustic parameters in the adults. CONCLUSION: To initiate taking multi-vowels samples and using different normal reference value and multi-parameters analysis according to the difference of age-bracket, sex and vowel in the adults.

Adolescent↗
PubMed1999

Characteristics of impaired endothelium-dependent relaxation of rat aorta after streptozotocin-induced diabetes.

AIM: To study whether impaired endothelium-dependent relaxation (EDR) in early diabetic mellitus in response to different receptor-mediated and nonreceptor-mediated vasodilators ran parallel and its possible mechanism. METHODS: Isometric tension recording in aortic rings from streptozotocin (Str)-induced diabetic and age-matched nondiabetic rats. RESULTS: EDR induced by receptor agonist acetylcholine (ACh), histamine (His) or bradykinin (BK) were all significantly reduced in diabetic rings compared with control rings, whereas nonreceptor agonist calcimycin-induced EDR was well reserved in diabetic rings [IC50 control: (0.13 +/- 0.07) mumol.L-1 diabetic: (0.14 +/- 0.06) mumol.L-1, P > 0.05, n = 7]. Cyclopiazonic acid (CPA) which also is a nonreceptor mediated endothelium-dependent vasorelaxant and cells' capacitative Ca2+ entry stimulant, failed to trigger EDR in diabetic rings. Pretreatment with N omega-nitro-L-arginine methylester (L-NAME, 0.3 mmol.L-1) not only abolished all of the EDR elicited by above mentioned vasodilators in either of diabetic or control rings, but also leveled responses triggered by each of the agonists between diabetic and control rings. Upon the maximal EDR induced by ACh (1 mol.L-1) or CPA (3 mumol.L-1) in phenylephrine (1 mumol.L-1) precontracted rings, calcimycin (1 mumol.L-1) further relaxed diabetic rings, but contracted control preparations. When endothelium was denuded, relaxation evoked by sodium nitroprusside and contractions triggered by CPA or His were all identical between diabetic and control rings. CONCLUSION: Receptor agonists but not nonreceptor agonists-induced EDR are commonly impaired in 4-wk Str-induced diabetic rat aorta, and this defective effect is attributable to the low formation of EDRF/NO which is related to impaired capacitative Ca2+ entry pathway in endothelium.

Acetylcholine↗
PubMed1994

[Active factors released by endothelial cells in acute leukemia].

In recent years, it is known that endothelial cells play an important role in the genesis of some diseases, but there are only few papers dealing with the role of endothelial cells in leukemia. In this study some of the active factors released by the endothelial cells in patients with acute leukemia such as von Willebrand factor, prostaglandin, fibronectin, tissue-type plasminogen activator and its inhibitor were determined. It was found that the levels of these factors changed significantly in patients with acute leukemia, as compared with those in normal controls, especially in cases with bleeding tendency and infection. The possible mechanism and the clinical significance were discussed.

6-Ketoprostaglandin F1 alpha↗