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C N Chuang

Publications and source records attributed to C N Chuang.

12 recordsLinked to original sources
PubMed1994

Somatostatin is released in response to cholecystokinin by activation of type A CCK receptors.

Cholecystokinin is a principal mediator of intestinal fat-induced inhibition of gastric acid secretion, indicating that it is an important physiological enterogastrone. Cholecystokinin has been shown to inhibit acid secretion by activation of type A CCK receptors and through a mechanism involving somatostatin. In the present study, we investigated the possibility that these two mechanisms are directly related such that activation of type A CCK receptors by CCK causes the release of somatostatin. We tested this hypothesis in vivo in a study of CCK-stimulated release of somatostatin in dogs and in vitro in a study of CCK-stimulated release of somatostatin from an enriched culture of canine fundic D cells. In dogs, IV infusion of CCK (50 pmol/kg/h, IV) significantly increased circulating somatostatin concentrations above basal. Further, systemic administration of somatostatin MAb F(ab)1 fragments of a somatostatin monoclonal antibody prevented most of CCK-induced inhibition of meal-stimulated acid secretion. In canine fundic D cells in culture, CCK-stimulated somatostatin release was blocked in a dose-dependent fashion by application of a type A CCK receptor antagonist. This study indicates that CCK activates type A CCK receptors to release somatostatin from canine fundic mucosal D cells, and accounts for somatostatin-dependent CCK-induced inhibition of acid secretion.

Acids↗
PubMed1993

Endogenous somatostatin inhibits histamine release from canine gastric mucosal cells in primary culture.

The effects of somatostatin on histamine release were studied using primary cultures of canine oxyntic mucosal cells in which mast cell content was reduced by density gradient. The S6 monoclonal antibody to somatostatin, but not control antibodies, enhanced gastrin-stimulated histamine release. In the presence of S6, the somatostatin analogue SMS-201-995 (10(-7) M) inhibited gastrin-stimulated histamine release by 95%. The dose producing 50% inhibition for this inhibition was approximately 3 x 10(-10) M and was completely reversed by pertussis toxin treatment. In contrast to somatostatin, epinephrine failed to inhibit this gastrin stimulation. However, the lectin concanavalin A (ConA) also stimulated histamine release from these cultures, and this response was inhibited by epinephrine but not by somatostatin. Thus somatostatin selectively inhibited the gastrin-responsive histamine pool, which presumably is stored in oxyntic mucosal endocrine cells. In contrast, epinephrine selectively inhibits histamine release from the ConA-sensitive pool, which is presumably stored in mast cells. Furthermore, enhancement of gastrin-stimulated histamine release by immunoneutralization of somatostatin indicates an important role for endogenous somatostatin as a paracrine inhibitor of non-mast cell histamine release.

Animals↗
PubMed1992

Gastrin induction of histamine release from primary cultures of canine oxyntic mucosal cells.

Using enzyme-dispersed canine oxyntic mucosal cells, we studied regulation of histamine release from fractions in which mast cells were largely removed by density gradient. Histamine-like immunoreactivity was demonstrated using peroxidase-anti-peroxidase immunohistochemistry. Histamine-containing cells in the small cell elutriator fractions (SCEF) were further separated by albumin step density gradients. Approximately 2.5% of cells in the low density fraction (LDF) contained histamine-like immunoreactivity; this fraction was largely depleted of the more dense mast cells (0.5%). These two fractions were cultured for 48-64 h on a Matrigel substrate. The cell content of histamine and release into the medium were measured by radioenzymatic assay. Gastrin, carbachol, and forskolin increased histamine release from the LDF. The induction of histamine release by gastrin was evident within 5 min and was sustained for at least 60 min. The response to gastrin was dose dependent between concentrations of 10(-11) and 10(-8) M. In contrast, in the mast cell-enriched SCEF, basal release was higher and gastrin was without effect; however, concanavalin A stimulated and epinephrine inhibited histamine release indicating that histamine-release mechanisms were intact in this fraction. Our methods provide a preparation of low density oxyntic mucosal histamine cells that demonstrate gastrin-responsive histamine release; we speculate that enterochromaffin-like cells account for this gastrin response.

Animals↗
PubMed1991

Gastrin-histamine interactions: direct and paracrine elements.

The receptors mediating the physiologic actions of gastrin on acid secretion and growth have thus far not been localized to specific cells or fully characterized. Studies in canine fundic mucosa indicate that gastrin receptors are present on several cell types, including parietal cells and somatostatin cells. There is also increasing evidence for a gastrin-inducible pool of histamine in the fundic mucosa which is presumably stored in histamine-enterochromaffin-like cells. From the vantage point of studies in the canine fundic mucosa, the issue is no longer which cell type has the gastrin receptor but to sort out the mechanisms by which the effects of the gastrin receptors on endocrine/paracrine (histamine and somatostatin) cells and exocrine (parietal) cells are integrated to regulate secretory function and mucosal growth and differentiation.

Animals↗
PubMed1990

Complete agenesis of the dorsal pancreas--a case report and review of the literature.

A case of agenesis of the dorsal pancreas associated with diabetes mellitus and dilated biliary trees was reported. Preoperative diagnosis was made by endoscopic retrograde cholangiopancreatography and computed tomography. Laparotomy revealed a normal head of the pancreas but complete agenesis of the body and tail. Biopsy specimens removed from the head showed normal pancreatic tissue but only fat tissue from the presumed body and tail. This anomaly has rarely been reported in the literature. A thorough review of the literature was made and consideration of differential diagnosis was discussed.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed1985

Early detection of hepatocellular carcinoma by real-time ultrasonography. A prospective study.

For early detection of hepatocellular carcinoma (HCC), real-time ultrasonography (US) was performed prospectively in 528 patients, including 236 with cirrhosis, 81 with chronic hepatitis, 168 asymptomatic hepatitis B surface antigen carriers, and 43 with a family history of HCC. Simultaneous measurement of serum alpha-fetoprotein (AFP) level was also done. In addition, 233 patients had regular controls at 3- to 6-month intervals, with an average follow-up period of 1.4 years. On initial screening, a total of 17 patients were found to have HCC: 13 in the cirrhotic group, 3 in the HCC family group, and 1 in the asymptomatic carriers. Of these HCCs, 7 were smaller than 3 cm, 6 were between 3 to 5 cm, and 4 were larger than 5 cm. In patients with tumors smaller than 5 cm, the AFP levels were normal in 46.2%, between 20 to 400 ng/ml in another 46.2%, and only 7.6% were over 400 ng/ml. On follow-up, another seven patients, all in the cirrhotic group, were found to have HCCs varying from 1.6 to 4.7 cm; three of them had normal serum AFP level. The authors conclude that real-time US is more sensitive than AFP assay in early detection of HCC, and the high-risk subjects should receive this procedure at regular intervals.

Adolescent↗
PubMed1985

Growth rate of asymptomatic hepatocellular carcinoma and its clinical implications.

The growth rate of 31 asymptomatic hepatocellular carcinomas (diameter less than or equal to 5 cm) discovered in 28 patients by a prospective screening program was determined by real-time ultrasonography over 36-860 days. Except for one tumor that shrank on follow-up, the doubling time ranged from 29 to 398 days, with a median of 117 days, an arithmetic mean of 136 days, and a geometric mean of 110 days. In 17 tumors with more than two measurements, the growth rate remained exponential in nine, declined in growth in seven, and showed an initial lag period in one. Doubling time correlated with initial tumor diameter but was independent of the patient's age, sex, hepatitis B surface antigen status, tumor location, liver function tests, stage of liver cirrhosis, histologic type, or grade of malignancy. Although initial alpha-fetoprotein levels did not correlate well with growth rate, in 14 patients with an exponential increase of serum alpha-fetoprotein, the alpha-fetoprotein doubling time was closely related to the tumor doubling time. Based on the above data, the median detectable subclinical period of hepatocellular carcinoma was deduced to be 3.2 yr, and the suitable screening interval for its early detection in our area was 4-5 mo.

Adult↗
PubMed1985

Hepatocellular carcinoma: US evolution in the early stage.

To study the sonographic evolution of hepatocellular carcinoma (HCC) in its early stage, 26 HCCs in 24 patients were observed regularly with real-time ultrasound for a period of 90 to 691 days. In the beginning, 21 tumors were hypoechoic, two isoechoic, and three diffusely hyperechoic. On follow-up, two of the 21 initially hypoechoic HCCs remained the same echodensity, 12 increased in internal echoes but were still hypoechoic, one became isoechoic, four changed to hyperechoic, and the remaining two shifted from hypoechoic to isoechoic and then to hyperechoic. The two initially isoechoic HCCs also gained echogenicity and became hyperechoic. By contrast, the three initially hyperechoic HCCs kept the same echo patterns. The "acquired" hyperechoic HCCs were inhomogeneous in echodensity and larger in size whereas the three originally hyperechoic HCCs were homogeneous and smaller. It is concluded that most small HCCs evolve progressively from hypoechoic to isoechoic and then to inhomogeneously hyperechoic patterns as they grow; a few HCCs have diffusely high echogenicity from the beginning and retain the same features thereafter.

Adult↗
PubMedDate not supplied

Regulation of histamine release from oxyntic mucosa.

The regulation of histamine release from oxyntic mucosa is complex because of two potential sources of histamine: mast cells and enterochromaffin-like (ECL) cells. A gastrin-responsive histamine pool was identified in the rat oxyntic mucosa two decades ago, but these ECL cells from the rat have not yet been isolated or characterized in vitro. In vivo studies in canine and human mucosa have been more difficult because of the high content of histamine in mast cells. Using enzyme-dispersed canine oxyntic mucosal cells, we have studied regulation of histamine release from a mast cell-depleted fraction prepared by sequential elutriation and density gradient. Histamine-like immunoreactivity was demonstrated, using peroxidase-anti-peroxidase immunohistochemistry. After short-term culture, histamine was released in response to gastrin, cholecystokinin, carbachol, and forskolin. Somatostatin potently and effectively inhibited the response to gastrin. The cultures used for these studies also contained somatostatin cells, and, furthermore, the response to gastrin was enhanced by incubation with monoclonal antibodies to somatostatin. The latter findings suggested that somatostatin was acting in these cultures by a paracrine route. This pattern contrasts with that obtained in previous studies of canine oxyntic mucosal mast cells.

Animals↗
PubMedDate not supplied

The pathways regulating acid secretion: the view from the isolated cell.

Although many aspects of the regulation of acid secretion at the cellular level among different species remains controversial, certain concepts have emerged that span the differences between species, model systems and investigators. The paracrine, endocrine, neural and autocrine pathways mediate acid secretion by acting both directly on the parietal cell and indirectly via modulation of mucosal paracrine cell function. Studies with cells isolated from the acid secreting canine oxyntic mucosa indicate that gastrin and cholinergic receptors are present on parietal cells, somatostatin cells, and the histamine-enterochromaffin-like cell (ECL). Subtypes of these receptors are clearly important; the gastrin receptor on the ECL cell and parietal cell are "B" type CCK/gastrin receptors, whereas the receptor on the somatostatin cell is an A type CCK receptor. From the vantage point of studies in the canine oxyntic mucosa, the challenge is no longer to determine whether parietal, histamine or somatostatin cells have gastrin or muscarinic receptors but to establish the physiologic relevance of the specific actions (secretory, trophic or differentiative) of these receptor subtypes. Furthermore, the mechanisms integrating these paracrine, exocrine and neural elements require elucidation.

Animals↗