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Biomedical subjects

L D Wang

Publications and source records attributed to L D Wang.

17 recordsLinked to original sources
PubMed1995

Inhibition of N-nitrosomethylbenzylamine-induced esophageal tumorigenesis in rats by green and black tea.

In this study, we investigated the effects of green tea and black tea, when given either during or after carcinogen treatment, on esophageal tumorigenesis in male Sprague-Dawley rats. Rats were treated with N-nitrosomethylbenzylamine (NMBzA) (2.5 mg/kg, s.c., twice weekly) for 5 weeks; 39 weeks after the initial dose of NMBzA, 65% of the rats had esophageal tumors with an average of 1.4 +/- 0.3 tumors per rat. In the groups of rats receiving 0.6% of decaffeinated green tea (DGT) or decaffeinated black tea (DBT) (6 mg tea solids/ml) as the sole source of drinking fluid during the NMBzA-treatment period, esophageal tumor incidence and multiplicity were reduced by approximately 70%. When the tea preparations were given after the NMBzA treatment period, the esophageal papilloma incidence and multiplicity were reduced by approximately 50%. The volume per tumor was much smaller in rats that received black tea after the carcinogen treatment period. In a second experiment, NMBzA was given to rats at a dose of 3.5 mg/kg (s.c., twice weekly) for 5 weeks; after 16 weeks, the tumor incidence was 82% and tumor multiplicity was 6.7 +/- 1.2 tumors per rat. In the groups of rats receiving 0.9% regular green tea (RGT) or DGT after the NMBzA treatment period, tumor multiplicity was decreased by > 55%. The volume per tumor was reduced by approximately 60% in the rats receiving 0.9% RGT. Histological analysis indicated that both the incidence and multiplicity of esophageal carcinoma was decreased by either RGT or DGT. The blood and urine levels of green tea polyphenols due to tea administration were determined in rats, and the levels were comparable to those in humans after tea ingestion. The above results indicate that both green tea and black tea can inhibit the tumorigenic action of NMBzA during the period of carcinogen treatment and the subsequent molecular events important for esophageal tumorigenesis.

Animals↗
PubMed1994

Changes in p53 and cyclin D1 protein levels and cell proliferation in different stages of human esophageal and gastric-cardia carcinogenesis.

The objective of this study was to quantify the changes in p53 and cyclin D1 protein levels in different stages of human esophageal and gastric cardia carcinogenesis in a high-risk population in Henan, China. Immunoreactivity of p53, cyclin D1 and proliferating-cell nuclear antigen (PCNA) was observed in the cell nuclei of esophageal and gastric cardia biopsies. The number of p53-immunostaining-positive cells was low in normal epithelia, slightly increased in basal-cell hyperplasia (BCH), markedly increased in dysplasia (DYS) (10-fold), and further increased in squamous-cell carcinoma (SCC) (40-fold). This pattern of change was similar to that of cell proliferation as indicated by PCNA immunostaining. On the other hand, the number of cyclin D1-immunostaining-positive cells did not increase from BCH to DYS, although a slight increase from DYS to SCC was noted. In the gastric cardia, again, the pattern of change of p53-positive cells in different stages of lesions paralleled the pattern of cell proliferation. The number of p53-positive cells was very low, much lower than that of PCNA-positive cells, in normal, chronic superficial gastritis (CSG) and chronic atrophic gastritis (CAG); therefore, the increase of p53-positive cells from CAG to DYS was more dramatic (100-fold). From DYS to adenocarcinoma (AC), the p53-positive and the PCNA-positive cells increased 4-fold. On the other hand, the number of cyclin D1-positive cells did not increase in pre-cancerous lesions, but increased slightly in AC. This study demonstrates that p53 protein accumulation increased with the progression of pre-cancerous lesions, especially in the genesis of dysplasia, both in the esophagus and in the gastric cardia. Our approach of quantitative immunohistochemistry sheds light on the mechanisms of genesis of esophageal and gastric-cardia cancers, which frequently occur together in many high-incidence areas.

Adenocarcinoma↗
PubMed1992

Molecular basis for the interaction of histamine with the histamine H2 receptor.

We undertook these studies to characterize the molecular basis of the interaction of histamine with the H2 receptor. Key areas of homology in the structures of the histamine H2 and beta 2 adrenergic receptor suggested specific transmembrane amino acids that might be important for binding of histamine. A third transmembrane aspartic acid of the histamine receptor (Asp98), thought to serve as a counter anion that interacts with the cationic amine moiety of histamine, was mutated to Asn98, and the mutated receptor was expressed in Hepa cells. Removal of the negatively charged amino acid abolished both binding of the H2 receptor antagonist [methyl-3H]tiotidine and histamine stimulated increases in cellular cAMP content. Mutation of a fifth transmembrane aspartic acid (Asp186) to Ala186 or Asn186 by itself or in conjunction with mutation of another fifth transmembrane amino acid (Thr190 to Ala190) resulted in a loss of [methyl-3H] tiotidine binding, although the generation of cAMP in response to histamine was maintained. The histamine receptor with only a Thr190 to Ala190 or Cys190 mutation retained the ability to bind [methyl-3H]tiotidine, but both the affinity and efficacy of binding were reduced. These data lead us to propose a model for histamine binding in which Asp98 is essential for histamine binding and action, Asp186 defines H2 selectivity, and Thr190 is important in establishing the kinetics of histamine binding, but is not essential for H2 selectivity.

Amino Acid Sequence↗
PubMed1992

[Preliminary study on nutrition and precancerous lesions of the esophagus in the adolescents].

This paper reports the prevalence of chronic esophagitis and nutritional status among 538 persons 15-26 years old in the high-risk area of esophageal cancer. 166 subjects were from households with history of esophageal cancer while 372 from households without. The frequency of chronic esophagitis among male and female adolescents in the high risk areas (37.6% and 36%) was significantly, higher than that in the low risk areas. Furthermore, the frequency of chronic esophagitis in the adolescents in households with history of esophageal cancer was also higher than that without history of this cancer. There was a positive correlation between avitaminosis C and chronic esophagitis. Suffering from avitaminosis C and B2, these people are prone to develop chronic esophagitis which, in turn, may serve as an early phase in the carcinogenesis of esophageal epithelium.

Adolescent↗
PubMed1991

Sucrose octasulfate stimulates gastric somatostatin release.

To explore the mechanisms of the effects of sucralfate on the stomach, we investigated the action of sucrose octasulfate (SOS), a constituent of sucralfate, on the function of canine gastric parietal cells and somatostatin cells and in the isolated perfused intact rat stomach. Somatostatin cells from the canine gastric fundus were isolated by EDTA-collagenase dispersion and counterflow elutriation, and somatostatin-like immunoreactivity (SLI) release in response to SOS was measured by radioimmunoassay. Similar methods were used to isolate gastric parietal cells, in which gastric acid secretion was measured by uptake of a radiolabeled weak base, [14C]aminopyrine. SLI release by the intact rat stomach was examined in an isolated vascularly perfused rat stomach model. SOS, either alone or co-administered with epinephrine or gastrin heptadecapeptide (G17), dose-dependently stimulated SLI release by isolated canine fundic D-cells. At the highest doses, SOS potentiated the effect of epinephrine but not G17. Similarly, SOS potentiated the stimulating effect of dibutyryl cyclic adenosine 3',5'-monophosphate (DBcAMP), but not 12-O-tetradecanoylphorbol 13-acetate (TPA). The effect of SOS on SLI release could be inhibited by octreotide, a somatostatin analogue. SOS did not alter acid secretion by cultured canine parietal cells either in the basal state or when coadministered with acid secretagogues. In isolated perfused rat stomach studies, SOS produced a significant (60% greater than basal) increase in SLI secretion. There was a similar effect when SOS was perfused against a background of isoproterenol. SOS stimulates SLI release from gastric somatostatin cells and from the isolated perfused stomach but has no direct effect on gastric parietal cells. These actions of SOS may mediate in part the apparent ability of sucralfate to enhance gastric mucosal defense.

Aminopyrine↗
PubMed1990

Labeling index and labeling distribution of cells in esophageal epithelium of individuals at increased risk for esophageal cancer in Huixian, China.

The pattern of proliferation of epithelial cells in esophageal epithelium was studied by means of [3H]deoxythymidine labeling of esophageal epithelium in subjects from Huixian, Henan Province, China, a high-risk geographical region for esophageal cancer. Comparisons were made among patterns of cell proliferation observed in normal esophagus, in hyperplasia, in mild dysplasia, and in moderate dysplasia in a total of 118 subjects. The amount of cell proliferation observed was lowest in normal esophageal epithelium and increased progressively in subjects having hyperplasia, mild dysplasia, and moderate dysplasia. The location of proliferating cells was limited mainly to the base of the esophageal epithelium in normal esophagus, but expanded toward the surface of the esophageal lining in individuals with hyperplasia and dysplasia. The larger total numbers of proliferating cells in the esophageal epithelium and the progressive expansion of the proliferative compartment toward the epithelial surface found in hyperplasia and in dysplasia could both facilitate the screening of subjects for esophageal cancer risk and serve as intermediate biomarkers in prophylactic dietary or pharmacological intervention studies.

Cell Count↗
PubMed1990

[Inhibitory effect of secretin on gastric motility in isolated vascular perfused rat stomach].

Effect of secretin on gastric motility was studied on the preparation of isolated vascular perfused rat stomach. The results showed: (1) Secretin markedly inhibited spontaneous as well as pentagastrin stimulated antral motility. (2) Antisecretin serum completely abolished the inhibitory effect of secretin on antral motility. (3) Antisomatostatin serum and indomethacin blocked the inhibitory effect on antral motility induced by secretin. The results indicated that the inhibitory effect of secretin might be produced through direct action of secretin on secretin receptors and mediated partially by the local somatostatin and prostaglandin in gastric antrum.

Animals↗
PubMed1990

[Effect of added dietary calcium on human esophageal precancerous lesion in the high risk area for esophageal cancer--a randomized double blind intervention trial].

A randomized double blind intervention trial was carried out in Huixian County Henan Province, a high risk area for esophageal cancer, to observe the effect of oral calcium supplementation on esophageal precancerous lesions. Two hundred and fourteen cases with basal cell hyperplasia and 40 with dysplasia of the esophagus aged 25-75 randomly received daily oral supplementation of 600 mg calcium or placebo for 7 months. In the calcium supplementation group, the basal cell hyperplasia and dysplasia of the esophagus were significantly improved and the profile of esophageal epithelial proliferation cells labeled with 3H-TdR approached that of the normal subjects in low risk area for esophageal cancer. The results indicate that calcium supplementation can inhibit basal cell hyperplasia and dysplasia of the esophageal epithelium in high risk area for esophageal cancer. The mechanism of interruption of esophageal precancerous lesions by calcium is discussed.

Adult↗
PubMed1989

[Inhibition of gastric acid secretion by vascularly perfused secretin and somatostatin in isolated rat stomach].

Effects of secretin and somatostatin on acid secretion and its relation to prostaglandin E, I2 release in the totally isolated vascularly perfused rat stomach were studied. The results showed: (1) Secretin and somatostatin both markedly inhibited acid secretion stimulated by pentagastrin. Indomethacin could reverse the inhibitory effects of acid secretion by secretin and somatostatin. (2) Secretin increased PGE and PGI2 metabolite 6-Keto-PGF1 alpha release significantly. Somatostatin only increased PGE release. Indomethacin could block stimulatory affects of secretin on PGE, 6-Keto-PGF1 alpha release and somatostatin on PGE release. These results indicated that: (1) inhibition of acid secretion by secretin was mediated by PGI2 and PGE release; (2) inhibition of acid secretion by somatostatin was mediated only by PGE release.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Possible contribution from epidemiological studies.

The problem of chemically contaminated water supplies are in general terms followed by a description of three examples of water supply problems in China. A large-scale prospective epidemiological study, now in the early planning stages, to be carried out in China is also described.

China↗
PubMed1981

Synthesis and vasodepressor screen of a series of 2-(2-alkylaminoalkylamido)-3-carbamyl-4-methyl-5-benzylpyrroles.

A series of 2-(2-alkylaminoalkylamido)-3-carbamyl-4-methyl-5-benzylpyrroles was synthesized and screened for vasoactivity. The compounds were administered intraperitoneally as a suspension to approximate the oral route of administration and intravenously when solubilization could be affected with suitable solvents. The most active compound following intravenous or intraperitoneal administration lowered blood pressure 73 and 35.5 mm Hg at doses of 4 mg/kg iv and 100mg/kg ip, respectively. It also exhibited the longest duration of vasodepressor activity (25 min). Several other compounds exhibited vasodepressor activity following intraperitoneal administration. Several hydrochloride salts appeared to be more potent vasoactive agents than the corresponding bases.

Animals↗