PubMed Health⌕ Search

Biomedical subjects

Y Y Jiang

Publications and source records attributed to Y Y Jiang.

At least 19 recordsLinked to original sources
PubMed2006

Effect of B vitamins-fortified foods on primary school children in Beijing.

The objective of this study is to investigate the effect of B vitamins-fortified foods on primary school children. A controlled trial was conducted in 101 normal primary school children aged 9-11 years. They were randomly assigned to supplemental control group (S-control, n=36), riboflavin supplementation group (+riboflavin 0.625 mg/day, n=32), and B vitamin compound supplementation group (+riboflavin 0.625 mg/day, +thiamin 0.512 mg/day, +nicotinic acid 0.365 mg/day, +folic acid 0.13 mg/day, n=33) based on school classes. Urinary riboflavin excretion and erythrocyte glutathione reductase activity coefficient (EGRAC) along with erythrocyte transketolase activity (ETKA) were used to evaluate B vitamin levels in the children. AYP index, an index reflecting the brain performance ability, was chosen to assess the children's study abilities. Health education was carried out to help children and their parents adopt scientific dietary concepts. The urinary riboflavin excretion was higher in two supplementation groups (435.24 +/- 153.3 microg/g creatinine, 374.6 +/- 144.6 microg/g creatinine) than in S-control group (235.1 +/- 86.2 microg/g creatinine). Average values of EGRAC were lower in two supplementation groups (0.90 +/- 0.11, 0.80 +/- 0.10) than in S-control group (1.08 +/- 0.25). At the same time, the percentage of thiamine pyrophosphate (TPP%) decreased from 63.69 +/- 28.04 to 42.16 +/- 16.31 in B vitamin compound supplementation group. Meanwhile, AYP index increased at the end of the supplementation in two supplementation groups. B vitamins supplementation can significantly increase B vitamin level in children. Biochemical activities of riboflavin and thiamin can improve with the intake of fortified foods. The effect of B vitamin compound supplementation is better than that of single riboflavin supplementation when the effect of riboflavin's biofunction is considered. In addition, micronutrient supplementation appears to assist children's study abilities.

Child↗
PubMed2004

Synthesis, in vitro anticancer evaluation, and interference with cell cycle progression of N-phosphoamino acid esters of zidovudine and stavudine.

A series of N-diisopropylphosphoryl (DIPP) L-amino acid ester prodrugs of zidovudine (AZT) (3a-3e) and stavudine (d4T) (4a-4e) has been prepared. The activity of these compounds against MCF-7 cells (human pleural effusion breast adenocarcinoma cell line) and K562 cells (human chronic myeloid leukemia (CML) cell line) was evaluated. In difference from that of AZT amino acid phosphoramidates, the alophatic amino acid esters of AZT were found to be more cytotoxic than the aromatic analogues toward MCF-7 cell. Two DIPP-L-amino acid esters of d4T 4b (CC50 = 83 microM) and 4c (CC50 = 182 microM) were found to be more cytotoxic than the parent drug toward K562 cells. MCF-7 and K562 cell cycle disturbance was investigated showing detectable blockade in the S phase when exposed to biologically active AZT, 3a, 3b, 3c, 4b and 4c, indicating that they inhibit cell growth by blocking cell cycle progression. Together with previous reports, present findings suggest that anti-breast cancer activity of AZT may be due to hamper DNA synthesis.

Antineoplastic Agents↗
PubMed2000

New products from alkali fusion of ginkgolides A and B.

Alkali fusion of ginkgolides A and B has afforded five unexpected products 3-7. Their structures were established from their spectral data and chemical reactions. They were evaluated for their in vitro activity to inhibit the platelet-activating factor-induced aggregation of rabbit platelets and show less potency than ginkgolides A and B.

Animals↗
PubMed1997

Piperbetol, methylpiperbetol, piperol A and piperol B: a new series of highly specific PAF receptor antagonists from Piper betle.

Piperbetol, methylpiperbetol, piperol A, and piperol B, isolated from Piper betle, selectively inhibited the washed rabbit platelet aggregation induced by platelet activating factor (PAF) in a concentration-dependent manner. The IC50 values of piperbetol, methylpiperbetol, piperol A, piperol B, and ginkgolide B were about 18.2, 10.6, 114.2, 11.8, and 4.8 mumol/l, respectively. The inhibitory potency of ginkgolide B was about 2.8, 1.2, 22.8, and 1.4 times higher than those of piperbetol, methylpiperbetol, piperol A, and piperol B. The concentration-response curve of PAF-induced platelet aggregation was shifted to the right by 50 mumol/l of piperbetol, methylpiperbetol, piperol A, piperol B, and ginkgolide B. The EC50 of PAF was increased by these compounds from 1.5 nmol/l to 14.3, 23.1, 2.4, 20.6, and 47.2 nmol/l, respectively. The compounds also inhibited the binding of [3H]-PAF to washed rabbit platelets with IC50 values of 8.7, 5.3, 88, 6.2, and 1.8 mumol/l. Correlating with the inhibitory potency for platelet aggregation, the inhibitory potency of ginkgolide B for binding of PAF was about 3.8, 1.9, 48, and 2.4 times higher than those of piperbetol, methylpiperbetol, piperol A, and piperol B. However, the aggregation of washed rabbit platelets induced by threshold ADP and arachidonic acid were unaffected by piperbetol, methylpiperbetol, piperol A, and piperol B. Furthermore, piperbetol, methylpiperbetol, piperol A, and piperol B had no effects on the cAMP contents in rest washed rabbit platelets. In conclusion, these data indicate that piperbetol, methylpiperbetol, piperol A, and piperol B are effective PAF receptor antagonists in vitro.

Animals↗
PubMed1997

Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study.

OBJECTIVE: Individuals with impaired glucose tolerance (IGT) have a high risk of developing NIDDM. The purpose of this study was to determine whether diet and exercise interventions in those with IGT may delay the development of NIDDM, i.e., reduce the incidence of NIDDM, and thereby reduce the overall incidence of diabetic complications, such as cardiovascular, renal, and retinal disease, and the excess mortality attributable to these complications. RESEARCH DESIGN AND METHODS: In 1986, 110,660 men and women from 33 health care clinics in the city of Da Qing, China, were screened for IGT and NIDDM. Of these individuals, 577 were classified (using World Health Organization criteria) as having IGT. Subjects were randomized by clinic into a clinical trial, either to a control group or to one of three active treatment groups: diet only, exercise only, or diet plus exercise. Follow-up evaluation examinations were conducted at 2-year intervals over a 6-year period to identify subjects who developed NIDDM. Cox's proportional hazard analysis was used to determine if the incidence of NIDDM varied by treatment assignment. RESULTS: The cumulative incidence of diabetes at 6 years was 67.7% (95% CI, 59.8-75.2) in the control group compared with 43.8% (95% CI, 35.5-52.3) in the diet group, 41.1% (95% CI, 33.4-49.4) in the exercise group, and 46.0% (95% CI, 37.3-54.7) in the diet-plus-exercise group (P < 0.05). When analyzed by clinic, each of the active intervention groups differed significantly from the control clinics (P < 0.05). The relative decrease in rate of development of diabetes in the active treatment groups was similar when subjects were stratified as lean or overweight (BMI < or > or = 25 kg/m2). In a proportional hazards analysis adjusted for differences in baseline BMI and fasting glucose, the diet, exercise, and diet-plus-exercise interventions were associated with 31% (P < 0.03), 46% (P < 0.0005), and 42% (P < 0.005) reductions in risk of developing diabetes, respectively. CONCLUSIONS: Diet and/or exercise interventions led to a significant decrease in the incidence of diabetes over a 6-year period among those with IGT.

Adult↗
PubMed1997

Protection of ebselen against anoxic damage of cultured neurons of cerebral cortex.

AIM: To study the protective effect of ebselen on anoxic damage of brain cells. METHODS: On d 10 after plating of the cortical neurons from 1-d-old rat, cultures were placed under 95% N2 + 5% CO2 for 2-6 h. Lactate dehydrogenase (LDH) in supernatant, thiobarbituric acid reactive substance (TBARS) and glutathione peroxidase (GSH-Px) activity of neurons were determined. RESULTS: Under anoxia, efflux of LDH and TBARS from cultured neurons increased while GSH-Px activity decreased. Ebselen reduced the efflux of LDH and TBARS in a dose-related manner and increased the total GSH-Px activity. CONCLUSION: Ebselen can protect neurons from anoxic damage.

Animals↗
PubMed1997

[Protection of ebselen on oxygen free radical-induced lipid peroxidation damage of cultured rat cortical neuron and cortical mitochondria].

Ebselen (2-phenyl-1, 2-benzisoselenanzol-3 (2H) one, C13 H9NOSe) is a seleno-organic anti-oxidant compound. In this study, the effect of ebselen on lipid peroxidation damage induced by O2.- and .OH in vitro, of cultured rat cortical neuron and cortical mitochondria was studied. When neuron was exposed to hypoxanthine/xathine oxidase system and vitamin C/CuSO4 system, obvious damage was detected: lactic dehydrogenase(LDH) was released and TBARS content increased. Ebselen (10, 25, 50 mumol.L-1) reduced LDH efflux induced by O2.- and .OH in a dose-dependent manner. As for the TBARS content, from 5 mumol.L-1 to 50 mumol.L-1, ebselen negated its increase, also dose-dependently. Furthermore, ebselen lowered TBARS content of cortical mitochondria treated with O2.- and .OH in a dose-related manner. But ebselen showed no activity of scavenging O2.- and .OH. This suggests that ebselen has direct anti-oxidant activity on neuron and its activity is not achieved by scavenging oxygen free radical.

Animals↗
PubMed1991

[Effects of econazole and clotrimazole on TXB2 and PGE2 production in calcimycin-stimulated neutrophils and arachidonic acid-stimulated platelets].

The effects of econazole and clotrimazole which are used as antifungal agents, on TXB2 and PGE2 production in calcimycin (A-23187)-stimulated rat pleural neutrophils and arachidonic acid (AA)-stimulated washing rabbit platelets were examined by radioimmunoassay. Econazole and clotrimazole 0.05-100 mumol.L-1 inhibited TXB2 production both in rat pleural neutrophils and in rabbit platelets with a dose-dependent manner. The most potent inhibition was found in rabbit platelets. At the concentration of 50 mumol.L-1, econazole and clotrimazole were sufficient to inhibit TXB2 production in rabbit platelets by up to 99% and 98% respectively. Econazole and clotrimazole 0.05-5 mumol.L-1 also increased PGE2 biosynthesis in rabbit platelets. But econazole and clotrimazole 50 mumol.L-1 reduced the PGE2 production in rabbit platelets to 11% and 37% of the amounts of 5 mumol.L-1 econazole and clotrimazole respectively. The results suggest that econazole and clotrimazole at lower concentration may have a selective inhibitory effect on thromboxane synthetase, at higher concentration they also inhibit cyclooxygenase.

Animals↗
PubMed1991

Radioimmunolocalization of human malignant tumors with In-111 labeled monoclonal antibody.

An anti-human colon carcinoma monoclonal antibody 2C10 was radiolabeled with In-111 and studied in 15 patients with gastrointestinal and ovarian carcinoma. The labelling efficiency approached 100% and immunoactivity of the labeled antibody was over 75%. 2-3 mCi (1 mg) In-111-2C10 was given to the patients intravenously and scintigraphy was performed 72 hours after administration with a gamma camera. Specimens were also scanned in some of the patients. The resected tumors and remote margin were examined immunohistochemically. Positive scintigraphic images were obtained in 12/15 patients with colorectal cancer (10) and ovarian cancer (2). Negative results were seen in the two patients with gastric cancer. The scintigraphic results of 10 patients were confirmed surgically and pathologically. The remaining 5 were confirmed by endoscopy, B-ultrasonography or X-ray CT. Most patients had been definitely diagnosed before imaging except one patient with metastatic focus from ovarian cancer to colon and one with recurrent colon cancer were first detected with RIAD, showing the unique advantage the latfer. The high background radioactivity in the liver, however, is a conspicuous problem to be solved.

Adult↗
PubMed1991

Effects of CI-930 on hemostasis, thrombosis, and AA-induced hemodynamic reaction.

In mice, CI-930 0.5-2 mg.kg-1 ip not only prolonged the tail bleeding time but also protected the mice from sudden thromboembolic death induced by arachidonic acid (AA, 100 mg.kg-1, i.v.) or TXA2/PGH2 mimetic U46619 (200 micrograms.kg-1, i.v.). CI-930 0.625 and 2.5 mg.kg-1 i.v. exhibited a dose-dependent inhibitory effect on thrombus formation in rat arteriovenous shunt. All these effects of CI-930 were more potent than those of dazoxiben, a known antiplatelet drug. In rabbit, AA 0.75 mg.kg-1 i.v. caused a rapid and marked increase in pulmonary vascular resistance and a concomitant sharp decrease in cardiac output and carotid arterial pressure. CI-930 itself 0.5 mg.kg-1 i.v. resulted in a long-lasting fall in carotid arterial pressure, systemic vascular resistance, and a slight decrease in cardiac output. In addition, CI-930 protected rabbit from all the harmful hemodynamic responses to the occlusion of pulmonary microcirculation, which was induced by AA. The results suggest that CI-930 possess a potent anti-hemostatic, antithrombotic, and probably antihypertensive effects on experimental animals.

Animals↗
PubMed1990

Effects of CI-930, a novel phosphodiesterase III inhibitor, on platelet aggregation and arachidonic acid metabolism.

In the platelet-rich plasma of rabbits, 4,5-dihydro-6-[4-(1H-imidazol-1-yl)phenyl]-5-methyl-3(2H)-pyridazinone (CI-930) inhibited platelet aggregation triggered by AA, U-46619, ADP, collagen and PAF, with the IC50 values of 0.91, 0.73, 2.12, 2.35 and 7.15 mumols/L, respectively. The inhibitory effect of CI-930 on AA-induced aggregation was potentiated by PGE1, an adenylate cyclase activator, and antagonized by SQ-22536, an adenylate cyclase inhibitor. The contents of cAMP in washed rabbit platelets were increased by CI-930 5-50 mumols/L. In the concentration range of 0.5-500 mumols/L, CI-930 reduced the synthesis of TXB2 by either washed rat or rabbit platelets or rat pleural neutrophils. At the same time, CI-930 induced a dose-dependent increase of PGE2, PGF2a, and PGD2 biosynthesis by rat platelets and had no significant influence on the formation of 6-keto-PGF1a by the neutrophils. It is showed that CI-930 is an anti-platelet agent with a wide-spectrum activity and its anti-aggregating action may be exerted by dual mechanisms, both increasing cAMP contents and selectively inhibiting TXA2 synthesis in platelets.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

[Selective inhibition of CI-914 on the production of TXA2 and HHT].

The effects of CI-914, a novel cardiotonic agent, on AA metabolism in rat neutrophils and platelets in vitro were investigated. Using washed rat platelets, the formation of HHT (measured by HPLC), a product of AA metabolism via cyclooxygenase and TXA2 synthetase, was found to be inhibited by the agent in a dose-dependent manner, with IC50 value of 78.6 mumol/L. Only at higher concentration (500 mumol/L) of CI-914, was the production of 12-HETE (measured by HPLC), a lipoxygenase product in platelets, shown to be inhibited. These indicate that CI-914 mainly inhibits the metabolism of AA via cyclooxygenase and TXA2 synthetase rather than via lipoxygenase. In rat platelets and A23187-stimulated pleural neutrophils, CI-914 caused a dose-related decrease of TXA2 production (measured by RIA), with IC50 values of 28.6 and 51.3 mumol/L, respectively. Meanwhile, significant increases of PGE2 synthesis in the platelets and 6-keto-PGF1 alpha synthesis in the pleural neutrophils were observed when CI-914 was preincubated with these cells. It is suggested that CI-914 might selectively inhibit the activity of TXA2 synthetase in rat platelets and pleural neutrophils.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

[Inhibition of release of prostaglandins and leukotrienes from calcimycin-induced mouse peritoneal macrophages and bovine aorta endothelial cells by anisodamine].

[3H]Arachidonic acid (AA)-prelabeled mouse peritoneal macrophages were stimulated by calcium ionophore A-23187 to release [3H]AA metabolites. The major labeled products which were co-chromatographed with the authentic PG and LT standards by TLC and determined by liquid scintillation were 6-keto-PGF1 alpha, PGE2, LTC4, and LTB4. Anisodamine (Ani) significantly inhibited the A-23187-induced release of PG and LT from mouse macrophages in a dose-dependent manner. In the presence of Ani at 0.5 mmol/L, the A-23187-induced release of 6-keto-PGF1 alpha, PGE2, LTC4 and LTB4 was reduced by 57%, 20%, 53% and 49%, respectively. A-23187-induced release of 6-keto-PGF1 alpha measured by RIA from bovine aorta endothelial cells was also significantly inhibited by Ani in a dose-dependent manner. These results indicate that the calcium-antagonistic effects of Ani may not only play a significant role in its inhibiting release of PG and LT, but also contribute to its salutary effects in the treatment of septic shock.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

[Effects of imazodan and dazoxiben on cAMP levels and PGI2 production in cultured bovine aortic endothelial cells].

We have investigated the effects of imazodan, a potent inhibitor of phosphodiesterase III (PDE III) and dazoxiben, a selective inhibitor of thromboxane synthetase on cAMP levels and PGI2 production in cultured bovine aortic endothelial cells by radioimmunoassay. When cultured endothelial cells were incubated with imazodan, intracellular levels of cAMP were increased in a dose-dependent manner. PGI2 production induced by arachidonic acid (AA) was not affected by imazodan 0.1-10 mumol/L. But imazodan 100 mumol/L caused a 35% inhibition of PGI2 production. In the presence of AA, dazoxiben could also elevate intracellular levels of cAMP. Furthermore, dazoxiben 1-10 mumol/L caused a marked increase in PGI2 production, but 1000 mumol/L inhibited PGI2 production.

Animals↗
PubMed1987

[Biologic effects of hyperthermia and radiation on gastric cancer cells (SGC-7901) in vitro. II. Ultrastructural changes of cells].

Different characteristic damages of the SGC-7901 gastric adenocarcinoma cells were studied by electron microscopy 1, 36, 72, 96 and 120 hours after heating and radiation in vitro. The visible damages, such as the enlarged mitochondria, increase of lysosomes and perichromatin granules could be shown 1 hour after heating (43 degrees C for 30 min) but no visible damages of the cells were shown until 36 hours following radiation (500 rad). In order to study the ultrastructural changes of the gastric cancer cells in mitosis after heating and radiation, we have used the new method of ultrastructural research in selecting and observing the M cell in vitro and found loosened structure of chromosome and disappearance of microtubules 1 hour following hyperthermia. At the same time, no apparent abnormalities of the mitotic cells were observed after radiation. It is the chief cause of division delay in heat injured cells. However, the chromosomes and microtubules of the new mitotic cells could recover 36 hours after heating (43 degrees C for 30 min). After radiation, the giant cells and abnormal morphologic changes of cells gradually increase and the living cells decrease. Unexpectedly, the division of a few giant cells is observed 72 hours after heating and radiation.

Adenocarcinoma↗
PubMed1987

[Biologic effects of hyperthermia and radiation on gastric cancer cells (SGC-7901) in vitro--I. Influence on cell growth curve, number of colonies and mitosis].

Biologic effects of hyperthermia (42 degrees-44 degrees C) and radiation on SGC-7901 were studied quantitatively and morphologically. Action of hyperthermia and radiation on the population and subpopulation of cells was monitored by cell growth curve and colony counts. The results show that both hyperthermia (43 degrees C for 30 min) and radiation (500 rad) can cause the cell kill and growth curve decrease but the cells still tend to proliferate. The synergistic action of heat plus radiation is demonstrated when they are given in the interval of 30 min. The thermal enhance rate was 1.27 and 1.37 for survival rate down to 2% and 5%. The concentration of potassium ions in the media is increased with cell kill after heat and radiation. The damage from heating appears like a direct kill or immediate death, the damage from radiation reveals delayed or metabolic death. Partial and transitory redistribution of cell cycle occurs following heating or radiation. Delayed division is more marked following heating than radiation. The synchronization effect may be used to hit the cycling tumor cells in the most radiosensitive phase.

Cell Count↗
PubMed1986

[Prostaglandin E (PGE) and gastric carcinoma].

Since 1984, an experimental and clinical study on the relation between PGE and gastric carcinoma has been performed by determining PGE content in the bioptic gastric mucosa and plasma. It is found the PGE content in the gastric mucosa and plasma is increased in all patients with gastric cancer, especially with signet ring cell carcinoma. It is higher in the regional lymph node metastasis than in the early cancer, extensive metastases and normal subjects. The PGE content in the plasma is reduced obviously 7-10 days after operation but is increased markedly in recurrent patients. There is no significant difference in extensive metastases, relapse free and normal subjects. The PGE content in the plasma is significantly higher in gastric carcinoma than in chronic atrophic gastritis, but no difference is present between chronic atrophic gastritis and normal subjects.

Adenocarcinoma↗