Biomedical subjects

Y T Zhao

Publications and source records attributed to Y T Zhao.

At least 19 recordsLinked to original sources

PubMed2000

2-Deoxyglucose-induced long-term potentiation in CA1 is not prevented by intraneuronal chelator.

In hippocampal slices, temporary (10-20 min) replacement of glucose with 10 mM 2-deoxyglucose is followed by marked and very sustained potentiation of EPSPs (2-DG LTP). To investigate its mechanism, we examined 2-DG's effect in CA1 neurons recorded with sharp 3 M KCl electrodes containing a strong chelator, 50 or 100 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). In most cases, field EPSPs were simultaneously recorded and conventional LTP was also elicited in some cells by tetanic stimulation of stratum radiatum. 2-DG potentiated intracellular EPSP slopes by 48 +/- 5.1% (SE) in nine cells recorded with plain KCl electrodes and by 52 +/- 6.2% in seven cells recorded with EGTA-containing electrodes. In four of the latter cells, tetanic stimulation (twice 100 Hz for 1 s) failed to evoke LTP (2 +/- 1.1%), although field EPSPs were clearly potentiated (by 28 +/- 6.9%). Thus unlike tetanic LTP, 2-DG LTP is not readily prevented by postsynaptic intraneuronal injection of EGTA. These findings agree with other evidence that the rise in postsynaptic (somatic) [Ca(2+)](i) caused by 2-DG is not the principal trigger for the subsequent 2-DG LTP and that it may be a purely presynaptic phenomenon.

Animals↗

PubMed2000

2-Deoxyglucose-induced long-term potentiation of monosynaptic IPSPs in CA1 hippocampal neurons.

In previous experiments on excitatory synaptic transmission in CA1, temporary (10-20 min) replacement of glucose with 10 mM 2-deoxyglucose (2-DG) consistently caused a marked and very sustained potentiation (2-DG LTP). To find out whether 2-DG has a similar effect on inhibitory synapses, we recorded pharmacologically isolated mononosynaptic inhibitory postsynaptic potentials (IPSPs; under current clamp) and inhibitory postsynaptic currents (IPSCs; under voltage clamp); 2-DG was applied both in the presence and the absence of antagonists of N-methyl-D-aspartate (NMDA). In spite of sharply varied results (some neurons showing large potentiation, lasting for >1 h, and many little or none), overall there was a significant and similar potentiation of IPSP conductance, both for the early (at approximately 30 ms) and later (at approximately 140 ms) components of IPSPs or IPSCs: by 35.1 +/- 10.25% (mean +/- SE; for n = 24, P = 0.0023) and 36.5 +/- 16.3% (for n = 19, P = 0.038), respectively. The similar potentiation of the early and late IPSP points to a presynaptic mechanism of LTP. Overall, the LTP was statistically significant only when 2-DG was applied in the absence of glutamate antagonists. Tetanic stimulations (in presence or absence of glutamate antagonists) only depressed IPSPs (by half). In conclusion, although smaller and more variable, 2-DG-induced LTP of inhibitory synapses appears to be broadly similar to the 2-DG-induced LTP of excitatory postsynaptic potentials previously observed in CA1.

2-Amino-5-phosphonovalerate↗

PubMed1997

2-Deoxy-D-glucose-induced changes in membrane potential, input resistance, and excitatory postsynaptic potentials of CA1 hippocampal neurons.

Temporary block of glycolysis by 2-deoxy-D-glucose (2-DG) reversibly suppresses synaptic transmission in the CA1 region of hippocampal slices. Recovery of responses is followed by a sustained potentiation of field excitatory postsynaptic potentials (EPSPs) (2-DG-LTP). To investigate the mechanisms involved in this type of LTP, we studied the effects of 2-DG on membrane properties of CA1 neurons (in slices from Sprague-Dawley rats), recorded with sharp intracellular electrodes containing 3 M KCl, as well as patch electrodes, filled mainly with 150 mM KMeSO4 and Hepes. The predominant change produced by 15- to 20-min applications of 2-DG (10 mM, replacing glucose) was hyperpolarization (-5.6 +/- 1.1 mV for 18 intracellular recordings and -7.2 +/- 0.80 mV for 17 whole-cell recordings) accompanied by a fall in resistance (-33 +/- 2.5% for 14 intracellular recordings and -11.6 +/- 7.1% for 15 whole-cell recordings). Virtually identical hyperpolarizations were recorded in the presence of 20 microM glyburide (-5.5 +/- 1.5 mV, n = 6), but they were abolished by adenosine antagonists 8-(p-sulfophenyl)theophylline (8-SPT) and 8-cyclopentyl-3,7-dihydro-1,3-dipropyl-1H-purine-2,6-dione (DPCPX) (2.8 +/- 1.6 and 4.0 +/- 1.7 mV, respectively; n = 5 for both). It was concluded that the hyperpolarization is most likely caused by an increase in K+ conductance, activated by a 2-DG-induced rise in adenosine release. After such applications of 2-DG, a sustained potentiation of EPSPs (similar to the 2-DG-LTP of field EPSPs) was evident in five neurons recorded with intracellular electrodes but not in any of nine whole-cell recordings, where it was replaced by sustained, LTD-like depression. We conclude that a factor essential for 2-DG-LTP induction is lost during whole-cell recording.

Animals↗

PubMed1997

[Distribution of obese protein in the mouse tissue].

In the present study, the contents of obese protein of tissue from liver, brain, abdominal wall fat, skeletal muscle and the contents of plasma OP of mice were measured with radio immunoassay. The results showed that the contents of OP were much higher in the brain than that in the abdominal wall fat tissue (P < 0.01). The liver and the skeletal muscle tissue did not show the presence of OP. The contents of OP of abdominal wall fat tissue were lower in the female than that in the male mice (P < 0.05).

Abdominal Muscles↗

PubMed1995

Vasodilator effect of human adrenomedullin(13-52) on hypertensive rats.

Human adrenomedullin (hADM) is a newly isolated peptide with hypotensive activity in normotensive rats. The objective of this study was to investigate the effect of hADM(13-52) on hypertensive animals. hADM(13-52) induced a dose-dependent decrease in the blood pressure of spontaneously hypertensive rats and renal hypertensive rats. This result suggests that hADM is a novel antihypertensive peptide. In isolated rat aortic arteries, hADM(13-52) produced nitric oxide dependent relaxation and inhibited endothelin 1 and angiotensin II release. These in vitro effects may represent the molecular mechanisms underlying the hypotensive action of hADM in vivo.

Adrenomedullin↗

PubMed1995

[A study on hypotensive mechanism of adrenomedullin (13-52)].

In the present study the hypotensive mechanism of AdM (13-52) was investigated in rats, both in vitro and in vivo. It was found that the hypotensive effect of AdM (13-52) could be partially inhibited by L-NG-nitro-arginine (LNNA), an inhibitor of nitric oxide synthase. The vasodilator effect of AdM (13-52) was dependent on vascular endothelium and inhibited by LNNA in a dose-dependent manner. This LNNA induced inhibitory effect could be reversed with L-Arginine. In addition, the vasodilator effect of AdM (13-52) disappeared with methylene blue (MB), which blocked cGMP formation. Using radioimmunoassay it was shown that LNNA lowered, but AdM (13-52) elevated the vascular cGMP content, while vascular cGMP content was not altered by co-application of AdM (13-52) and LNNA. The above results suggest that the vasodilator effect of AdM (13-52) might be mediated by nitric oxide.

Adrenomedullin↗

PubMed1994

Involvement of nitric oxide in the vasodilator and depressor effect of calcitonin gene-related peptide.

In present study, we examined the effects of NG-nitro-L-arginine (LNNA), an inhibitor of nitric oxide synthase (NOS), and/or methylene blue (MB), a blocker of guanylate cyclase on the vasodilator response of isolated rat arteries including aorta and mesenteric artery to calcitonin gene-related peptide (CGRP) by in vitro vasoconstriction experiment, and the effect of LNNA on the depressor action of CGRP by in vivo hemodynamic experiment. Furthermore, the effect of CGRP on NOS activity and cyclic guanylate monophosphate (cGMP) content were also examined by NOS activity assay and radioimmunoassay (RIA), respectively. The results showed that LNNA and/or MB significantly decreased, but not abolished, the vasodilator response of isolated rat aorta and mesenteric artery to CGRP. The depressor effect of CGRP on LNNA-induced hypertensive rats (LHR) was obviously weaker than that on spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR) and normotensive rats (NWR). In addition, CGRP (0.5 nmol/kg) increased the NOS activity of rat aorta tissue by 1.3 times (P < 0.05) and resulted in an increase of cGMP content of aorta (1.27 times, P < 0.05) and myocardium (1.38 times, P < 0.05). The results suggested that NO is involved in the action of CGRP.

Animals↗

PubMed1993

[A clinical and basic study on the relationship between acute myocardial infarction and endothelin].

The level of plasma endothelin (ET) was studied in 40 cases with acute myocardial infarction (AMI) with radioimmunoassay. The results showed that plasma ET level reached its peak value (46.01 +/- 1.64 pg/ml) immediately after AMI attack and dropped down (39.37 +/- 0.47 pg/ml) on the first day; The value was still high (15.56 +/- 1.40 pg/ml) on the twenty-eight day: this was significant higher than that in control group (6.35 +/- 0.44 pg/ml, P < 0.001). It was found that height of plasma ET level was closely correlated with severity of myocardial damage and degree of cardiac insufficiency. In order to evaluate the pathogenic role of ET in AMI, the effect of ET-antiserum on myocardial infarction (MI) was investigated on infarct model produced by ligature of left anterior descending coronary artery in rats. The results showed that plasma ET levels elevated significantly in rats with MI (8.4 +/- 1.0, sham 3.1 +/- 0.2 pg/ml, P < 0.01) and ET-antiserum administration dramatically decreased plasma ET level 65% (P < 0.01), lowered plasma content of lipid peroxide 27% (P < 0.01) and reduced infarct size 48% (P < 0.01). It is suggested that ET is an important factor which contributes to the pathogenesis of MI. Limb ischemia and reperfusion study was carried out in rats also. Metallothionein (MT) was found to antagonize markedly ET-induced vasoconstriction and lower the release of ET stimulated by angiotensin II in a dose-dependent manner. It is suggested that under certain pathological conditions MT may exert its injury--resistant and cell protective action.

Adult↗

PubMed1993

[Immunohistochemical study on human papillomavirus infection of the vulva].

Two hundred and sixteen cases of human papillomavirus infection of the vulva from 1984 to 1991 in the Affiliated Hospital of Qingdao Medical College were reviewed, and were immunohistochemically studied by ABC method to detect HPV-Ag. The results showed that the demonstration of diagnostic koilocytes is very important in diagnosis of HPV infection in routine tissue slides examination. But in cases of atypical morphological changes; when diagnostic koilocytes were not formed in early stage, the demonstration of brown color granules in the nuclei of prickle cells is very diagnostic for positive HPV infection. In occasional cases, the diagnostic koilocytes do not demonstrate brown color granules in their nuclei. The explanation is that HPV-Ag was exhausted during metabolism. Besides, the cell membrane of basal cells are stained with brown color granules, while the morphological changes of upper layers of squamous epithelium have not appeared yet, therefore, there were no HPV-Ag positive reactive cells. It is probably showed that the HPV-Ag is primarily formed and appeared in the cell membrane of basal cells.

Antigens, Viral↗

PubMed1990

[Plasma calcitonin gene-related peptide (CGRP) level in patients with essential hypertension].

Calcitonin gene-related peptide (CGRP) is a 37-amine acid bioactive polypeptide and known to be a powerful vascular relaxant. CGRP was measured in 45 cases with essential hypertension (EH). The results suggested that plasma CGRP level in patients with EH was lower than that in normal subjects (P less than 0.001). It was found that decrease of plasma CGRP was closely related with the severity of hypertension. However, the level of plasma atrial natriuretic factor (ANF) in EH patients was significantly increased as compared with normal subjects (P less than 0.01). A negative correlation between plasma CGRP and ANF (r = -0.3615, P less than 0.02) was found. These data suggested that decrease of plasma CGRP may play an important role in the pathogenesis of hypertension.

Adult↗

PubMed1989

[Changes in the level of plasma atrial natriuretic factor in patients with chronic renal failure].

Changes of plasma atrial natriuretic factor (ANF) levels in 89 patients with different kinds of renal diseases (including 39 patients treated with hemodialysis) were studied. The results showed: 1. The mean value of plasma ANF level was significantly increased in patients with renal diseases than that in healthy subjects. The increase was positively correlated with the change of creatinine, serum potassium, mean arterial pressure and ptfV1. The plasma ANF level was markedly decreased after hemodialysis. 2. The right atrial pressure of 8 patients with chronic renal failure measured by right heart catheterization was normal. No significant changes occurred after hemodialysis. 3. Impedance cardiogram and mechanical cardiogram showed that left heart function was significantly improved after hemodialysis. 4. ANF was detected in ultrafiltration liquid. 5. There was no difference of the ANF content between the serum of the first and maintenance hemodialysis. The authors thought that the main causes of increase of plasma ANF level are decrease of catabolic metabolism in renal failure, stimulation of ANF secretion by left heart failure and increased loading of left atrium and increased production of ANF by body compensation as the result of mean arterial pressure increase. The decrease of ANF after hemodialysis was mainly due to improvement of renal and cardiac function, lessening of the left atrial loading, the reduced mean arterial pressure and its direct elimination by hemodialysis.

Adolescent↗

PubMed1989

[Pro-and anti-nucleation activity of biliary proteins in gallbladder bile with and without gallstones].

The proteins of pro-and anti-nucleation activity in gallbladder bile were isolated by chromatography on Bio Gel P-100 and Con A Sepharose. The authors for the first time showed the evidence of presence of pro-and anti-nucleation activity proteins co-existing in gallbladder bile of patients with and without cholesterol gallstones. The result of further study showed that Transferrin, one of the glycoproteins in gallbladder bile, had the effect of promoting nucleation activity on rapid formation of cholesterol crystal in artificial supersaturated bile. The difference in pro-and anti-nucleation proteins of gallbladder bile between patients with and those without cholesterol gallstones were also shown in this paper.

Bile↗

PubMed1989

[Dynamic changes of superoxide dismutase in patients with myocardial infarction. A clinical study].

The activity of serum superoxide dismutase (SOD) was studied in 35 cases of acute myocardial infarction (AMI) and 12 cases of angina pectoris (AP). The results suggested that serum MnSOD activity reached its peak value (18.7 +/- 6.39) immediately after AMI attack and gradually dropped down on the second day. The activity was no more detected on the seventh day. The value of serum MnSOD in patients with AMI within 24 hours was significantly different (P less than 0.05) or very significantly different (P less than 0.01-0.001) from that in patients with AMI after 2 days and AP and in the control group. The positive rate of early diagnosis in the three groups was 100%, 71% and 66% respectively. It was found that the height of serum MnSOD activity was closely correlated with the seriousness of myocardial damage, therefore, serum MnSOD activity may be one of the sensitive indices for the early diagnosis of AMI. In has also certain clinical value in the judgement of the extent of infarction and of prognosis.

Aged↗

PubMed1989

[The changes in serum TXB2 and 6-keto-PGF1 alpha in 62 cases with renal disease].

Measurement of serum thromboxane B2 (TXB2) and 6-keto-prostaglandins F1 alpha (6-keto-PGF1 alpha) was carried out in 62 patients of renal diseases. The results showed that decrease of TXB2 and 6-Keto-PGF1 alpha values and TXB2/6-Keto-PGF1 alpha ratio was correlated with the decrease of the renal function and was negatively correlated with the level of serum creatinine. The values of TXB2 and 6-Keto-PGF1 alpha were markedly elevated after hemodialysis in 19 patients. It was found that the difference between patients with and without renal hypertension was statistically significant (P less than 0.05). The results indicated that the inbalance of PG value was one of the causes of uremic hemorrhage, PG takes part in the development of renal hypertension.

6-Ketoprostaglandin F1 alpha↗

PubMed1987