Search PubMed⌕ Search

Biomedical subjects

T Joh

Publications and source records attributed to T Joh.

At least 55 records · Page 3Linked to original sources

The pathway of dephosphorylation of myo-inositol hexakisphosphate by phytases from wheat bran of Triticum aestivum L. cv. Nourin #61.

Phytases are the primary enzymes responsible for the hydrolysis of phytic acid, myo-inositol-1, 2, 3, 4, 5, 6-hexakisphosphate (InsP6). The pathway of hydrolysis of InsP6 by phytase from wheat bran of Triticum aestivum L. cv. Nourin #61 is proved in this study. Structures of the intermediates were established by a variety of nuclear magnetic resonance techniques (1H-, two-dimensional 1H-1H coupling-correlation spectra and two-dimensional 31P-1H correlation spectra), gas chromatography, and bioassay. On the basis of the structures identified, initial hydrolysis of the phosphate ester occurs at the D/L-4 position of InsP6 to yield D/L-Ins (1, 2, 3, 5, 6) P5. After the dephosphorylation, the pathway of dephosphorylation is divided into two routes. The main route proceeds via D/L-Ins (1, 2, 5, 6) P4, D/L-Ins (1, 2, 6) P3 and D/L-Ins (1, 2) P2, while the minor route proceeds via D/L-Ins (1, 2, 3, 6) P4, Ins (1, 2, 3) P3 and D/L-Ins (1, 2) P2. D/L-Ins (1, 2) P2 is hydrolyzed at the D/L-1 or 2-position, and finally myo-inositol is produced.

6-Phytase↗

Fas-resistance in ATL cell lines not associated with HTLV-I or FAP-1 production.

A preventive role for human T-cell leukemia virus type-I (HTLV-I) and Fas-associated phosphatase-1 (FAP-1) in Fas-mediated apoptosis has been reported in HTLV-I-infected cells. In the present study, we examined whether these molecules increased during the acquisition of Fas-resistance in adult T-cell leukemia (ATL) cell lines. SO4, ST1 and KK1 are Fas-sensitive ATL cell lines, and produce small amounts of HTLV-I in vitro. Although their subclones RSO4 and RST1 are completely Fas-resistant, they produced an equivalent amount of HTLV-I to SO4 and ST1. Moreover, FAP-1 mRNA was not detected in these cell lines irrespective of Fas sensitivity. Thus, Fas resistance in ATL cells was not directly associated with the increased production of HTLV-I or FAP-1.

Antibodies, Monoclonal↗

Total neuropathy score: validation and reliability study.

OBJECTIVE: To determine the validity and reliability of the total neuropathy score (TNS) in normal subjects and in subjects with diabetic polyneuropathy. BACKGROUND: Clinical research in peripheral neuropathy requires validated outcome measures. Multiple outcome measures have been used in clinical trials, including symptom measures, functional scales, quantitative clinical examinations, nerve conduction studies, computerized sensory examinations, and nerve biopsy. Each of these measures has its strengths and weaknesses. In two previous studies of toxic neuropathy from chemotherapeutic agents, the authors used the TNS as the outcome measure. The TNS combines information obtained from grading of symptoms, signs, nerve conduction studies, and quantitative sensory tests, and provides a single measure to quantify neuropathy. METHODS: The authors measured the inter- and intrarater reliability of the TNS and preformed a cross-sectional validation study of the TNS and its subscales with the Mayo Clinic measures of neuropathy, neuropathy symptom score (NSS), and the neurologic impairment score (NIS) in five healthy control subjects and 30 individuals with varying severities of diabetic polyneuropathy. RESULTS: Inter- and intrarater reliability of the TNS was excellent (0.966 and 0.986 respectively). The cross-sectional validation study showed excellent correlations among all measures of neuropathy. CONCLUSIONS: The total neuropathy score is a validated measure of peripheral nerve function and could be used as an end point for clinical trials of peripheral neuropathy.

Adolescent↗

Cyclin D1/PRAD1/BCL-1 alternative transcript [B] protein product in B-lymphoid malignancies with t(11;14)(q13;q32) translocation.

The cyclin-D1/PRAD1 oncogene, a key regulator of the G1-phase progression of the cell cycle, has been identified as the long-sought BCL-1 oncogene in B-cell malignancies with t(11;14)(q13;q32) translocation. A novel alternative spliced cyclin-D1 transcript, called transcript[b], has been identified. The level of the variant transcript[b] was lower than that of the originally reported cyclin-D1 transcript, called transcript[a], in several human non-lymphoid cancer cell lines but the endogenous cellular expression of transcript[b] products has not yet been determined. Northern-blot analysis and reverse-transcription-polymerase-chain-reaction (RT-PCR) analysis revealed that transcript[b] mRNA is well expressed in B-lymphoid cell lines with t(11;14)(q13;q32) translocation and at much lower or undetectable levels in other cells. Western-blot analysis using a human cyclin-D1-specific monoclonal antibody, which can recognize and distinguish the products of transcripts [a] and [b], strongly suggested that the transcript [b] protein is indeed expressed in these B-cell lines. The present study provides identification of the endogenous cellular expression of the cyclin-D1-transcript[b] protein and strongly suggests that this alternative form of cyclin D1 may play a significant role in the molecular pathogenesis of B-lymphoid malignancies with t(11;14)(q13;q32) translocation.

Alternative Splicing↗

Fas gene mutation in the progression of adult T cell leukemia.

Fas antigen (Apo-1/CD95) is an apoptosis-signaling cell surface receptor belonging to the tumor necrosis factor receptor superfamily. Adult T cell leukemia (ATL) cells express Fas antigen and show apoptosis after treatment with an anti-Fas monoclonal antibody. We established the ATL cell line KOB, which showed resistance to Fas-mediated apoptosis, and found that KOB expressed two forms of Fas mRNA, the normal form and a truncated form. The truncated transcript lacked 20 base pairs at exon 9, resulting in a frame shift and the generation of a premature stop codon at amino acid 239. The same mutation was detected in primary ascitic cells and peripheral blood cells. The mutation was not detected in lymph node cells, however, although all of the primary ATL cells were of the same clonal origin. A retroviral-mediated gene transfer of the truncated Fas to Jurkat cells rendered the cells resistant to Fas-mediated apoptosis, suggesting a dominant negative interference mechanism. These results indicate that an ATL subclone acquires a Fas mutation in the lymph nodes, enabling the subclone to escape from apoptosis mediated by the Fas/Fas ligand system and proliferate in the body. Mutation of the Fas gene may be one of the mechanisms underlying the progression of ATL.

Aged↗

Establishment of an inducible expression system of chimeric MLL-LTG9 protein and inhibition of Hox a7, Hox b7 and Hox c9 expression by MLL-LTG9 in 32Dcl3 cells.

The MLL (HRX/ALL-1 gene is frequently disrupted in infantile leukemias and therapy-related leukemias and fused to various translocation partner genes. We previously showed that chimeric MLL proteins localize in the nuclei in a fashion similar to that of MLL protein even if the partner gene encodes a cytoplasmic protein and indicated the importance of the N-terminal portion of MLL common to various MLL translocations. This time we established an inducible expression system for chimeric MLL-LTG9 and truncated N-terminal MLL proteins (MLL-Zf(-)) in 32Dcl3 cells. By utilizing this system, we were able to show inhibition of Hox a7, Hox b7 and Hox c9 genes' expression by induced MLL-LTG9 and MLL-Zf(-). Up-regulation of Hox a7, Hox b7 and Hox c9 was observed when 32Dcl3 cells were cultured with granulocyte colony stimulating factor (G-CSF) in place of interleukin 3 and induction of MLL-LTG9 and MLL-Zf(-) was shown to suppress this upregulation. At the same time, expression of two mammalian Polycomb group genes, M33 and mel-18, which both reportedly affect Hox genes' expression, was not inhibited by MLL-LTG9 and MLL-Zf(-) induction. These results indicate that MLL has an important effect on the expression of at least some Hox genes in hematopoietic cells and suggest that inhibition of the proper expression of Hox genes by chimeric MLL proteins may dysregulate hematopoietic cell differentiation and proliferation, which then can lead to leukemogenesis.

Cell Differentiation↗

Efficacy of interferon treatment for patients with chronic hepatitis C: comparison of response in cirrhotics, fibrotics, or nonfibrotics.

Chronic hepatitis C patients (472 patients) were treated with consensus interferon (CIFN) or interferon (IFN) alfa-2b for 6 months in a large multicenter trial. Efficacy was assessed by clearance of hepatitis C virus (HCV) RNA using reverse transcription polymerase chain reaction (RT-PCR) (<100 copies/mL), normalization of serum alanine aminotransferase (ALT), and histological improvement. The purpose of these analyses was to compare these efficacy parameters in nonfibrotics, fibrotics, and cirrhotics. Patients with chronic HCV and cirrhosis showed the same benefit from IFN treatment as noncirrhotic patients when efficacy was assessed by clearance of serum HCV RNA or by histological benefit. Sustained HCV RNA response rates were similar when measured among nonfibrotic (11%), fibrotic (13%), and cirrhotic (11%) patients. Improvement in histologic activity index (HAI) scores was noted among all 3 groups. Cirrhotic patients had a lower sustained ALT response rate (12%) than did nonfibrotic patients (23%). Ninety percent of nonfibrotics, but only 71% of fibrotics and 67% of cirrhotics, who sustained a virological response normalized their ALT. This suggests that cirrhotic patients may clear the hepatitis C virus without normalization of ALT levels. The pattern of both HCV RNA clearance over time and ALT decrease was similar among nonfibrotics, fibrotics, and cirrhotics. Tolerability to IFN therapy was similar among the 3 groups except that more cirrhotics required dose reduction because of thrombocytopenia. In patients with cirrhosis, ALT levels may be a less appropriate endpoint in the measurement of response to therapy. We conclude that liver cirrhosis should not be a reason for excluding patients from therapy because both cirrhotic and fibrotic HCV patients benefit from IFN therapy not only by clearance of virus but by improvements in liver histology.

Adult↗

Racial differences in responses to therapy with interferon in chronic hepatitis C. Consensus Interferon Study Group.

The likelihood of a sustained response to a course of interferon in patients with chronic hepatitis C correlates with several clinical and viral factors, including age, viral genotype and initial levels of hepatitis C virus (HCV) RNA in serum. The role of race and ethnicity has not been assessed. We evaluated the association of race with response to interferon in a large randomized, controlled trial using either consensus interferon (9 microg) or interferon alfa-2b (3 million units) given three times weekly for 24 weeks. African-American patients participating in the study were similar to white patients in mean age (43 vs. 42 years) and baseline levels of HCV RNA (3.6 vs. 3.0 million copies/mL) but had lower rates of cirrhosis (5% vs. 12%) and more frequently had viral genotype 1 (88% vs. 66%: P =.004). Most strikingly, the rates of end-of-treatment and sustained virological responses were lower among the 40 African-American patients (5% and 2%) than among the 380 white patients (33% and 12%) (P =.04 and.07). Rates of response among Hispanic and Asian-American patients were not statistically different than non-Hispanic white patients. Median viral levels decreased by week 24 of therapy by 2.5 logs in white patients (from 3.0 to 0.012 million copies/mL) but by only 0.5 logs among African- American patients (from 3.6 to 1.8 million copies/mL). Thus, there are marked racial differences in virological responses to interferon in hepatitis C that must be considered in assessing trials of interferon therapy and in counseling patients regarding treatment. The differences in response rates are as yet unexplained.

Adolescent↗

Injurious effect of Helicobacter pylori culture fluid to gastroduodenal mucosa, and its detoxification by sucralfate in the rat.

BACKGROUND: Helicobacter pylori plays an important role in the pathogenesis of peptic ulcer. Although several cytotoxins related to H. pylori have been reported, their effects on gastroduodenal mucosa have not been well evaluated in vivo. AIM: To investigate the effects of the combination of acid and toxic substances derived from H. pylori on gastroduodenal mucosa, and to observe the effect of sucralfate on such factors in the rat. METHODS: Male Sprague-Dawley rats were fasted overnight and anaesthetized. The pylorus was ligated, and a double-lumen cannula was inserted into the forestomach for gastric luminal perfusion. In other animals, a cannula was inserted to perfuse the proximal duodenum. 51Cr-EDTA was administered intravenously and mucosal integrity was monitored by measuring the blood-to-lumen 51Cr-EDTA clearance. After 72 h of culture of H. pylori (NCTC11637 and Sydney strain 1), Brucella broth containing 3% FBS was filtered to remove the bacteria (supernate of H. pylori culture fluid; HPsup). HPsup was acidified (pH=2.0) with HCl, and tested for its injurious action on gastric or duodenal mucosa by luminal perfusion. HPsup was incubated with sucralfate for 30 min. The supernate was collected by centrifugation and the pH was readjusted to 2.0. This sucralfate-treated HPsup was used to test the effect of sucralfate against H. pylori-related mucosal injurious factors. RESULTS: Non-acidified and acidified HPsup did not cause any detectable injury to the gastric mucosa. Non-acidified HPsup did not cause injury in the duodenal mucosa. However, acidified HPsup induced a significantly greater increase in 51Cr-EDTA clearance and greater histological damage than in controls. Sucralfate completely reversed this. CONCLUSION: These results suggest that an H. pylori-related toxic substance may aggravate duodenal acid injury by acting on luminal surfaces, and that the detoxification of this substance by sucralfate may contribute to its anti-ulcer action.

Animals↗

Limitations of imaging diagnosis for small hepatocellular carcinoma: comparison with histological findings.

BACKGROUND AND AIMS: The purpose of this study was to clarify the value and limitation of imaging modalities for diagnosing small hepatocellular carcinoma (HCC). METHODS: Nodules (n = 207) with diameters of 20 mm or less detected by periodic ultrasonography and computed tomography in 139 patients with chronic liver disease were investigated with digital subtraction angiography (DSA) and magnetic resonance imaging (MRI). These findings were compared with histological findings. RESULTS: Histological diagnoses were adenomatous hyperplasia (AH, n = 27), well-differentiated HCC (n = 99), moderately differentiated HCC (n = 79) and poorly differentiated HCC (n = 2). We compared two groups: group A (n = 62), nodules of 10 mm diameters or less; and group B (n = 145), nodules 11-20 mm. Adenomatous hyperplasia accounted for approximately 30% of group A, but was difficult to diagnose with imaging modalities alone. We diagnosed those nodules showing hypervascular staining on DSA or hyperintensity on MRI T2-weighted images as HCC. Imaging alone was sufficient to diagnose HCC in 58% of the well-differentiated nodules and 87% of the moderately and poorly differentiated nodules (P < 0.01). It was possible to diagnose HCC by imaging alone in 60% of all nodules or 45% of group A and 68% of group B (A vs B, P < 0.005). CONCLUSIONS: With decreasing differentiation and increasing diameter of nodules, the use of imaging modalities to diagnose HCC improved. Tumour biopsy was required to diagnose 55% of the cases in group A and 32% of the cases in group B.

Adenoma, Liver Cell↗

Role of complement regulatory membrane proteins in ischaemia-reperfusion injury of rat gastric mucosa.

BACKGROUND: The role of complement in ischaemia-reperfusion injury has not been well investigated. 5I2 is a monoclonal antibody (mAb) directed against a rat membrane inhibitor of the C3 convertase step, which is the rat counterpart of mouse Crry/p65. 6D1 is a mAb against rat CD59 which inhibits the formation of membrane attack complexes. METHODS: We visualized the tissue distribution of these membrane inhibitors in rat gastrointestinal tract by immunohistochemical staining with the appropriate mAb. Then, we tested the hypothesis that complement regulatory proteins protect rat gastric mucosa against ischaemia-reperfusion stress by using these mAbs. Gastric mucosal integrity was continuously monitored by measuring the blood-to-lumen clearance of [51Cr]-labelled ethylenediaminetetraacetic acid (EDTA) under control conditions, during ischaemia and after reperfusion. RESULTS: Rat 6D1 and 5I2 antigens were both widely distributed and predominantly expressed on smooth muscle and endothelial cells in gastrointestinal tracts. Blockade of complement regulatory proteins with 5I2 and 6D1 mAbs resulted in a significant increase in [51Cr]-EDTA clearance after reperfusion. CONCLUSIONS: These findings support the hypothesis that endogenous complement regulatory proteins may act as important protective factors against ischaemia-reperfusion stress in rat gastric mucosa.

Animals↗

The therapeutic effect of proton pump inhibitors on Helicobacter pylori-positive gastric ulcers.

The aim of the present study was to elucidate the risk factors that could delay gastric ulcer healing when either a proton pump inhibitor or an H2-receptor antagonist is used for gastric ulcer treatment. Endoscopically-diagnosed gastric ulcer patients (216 men and 96 women, mean age: 57+/-13 years) were investigated. All patients were consecutively recruited and randomly assigned to receive H2-receptor antagonist (n = 196) or proton pump inhibitor (n = 116) treatment for eight weeks. Chi-squared tests and multivariate analysis to determine factors influencing ulcer healing were used to analyse the patients profiles, endoscopic findings, and Helicobacter pylori-infection status. In the H2-receptor antagonist group, the most important risk factor was a large ulcer size (> 2 cm diam.), followed by a linear shape of the ulcer, undermining tendency of ulcer, previous history of gastric ulcer, and H. pylori infection. In the proton pump inhibitor group, linear shape of the ulcer was the only significant risk factor for slow ulcer healing; other factors, including H. pylori infection, were insignificant. These results indicate that ulcer morphology may be the most important information for predicting ulcer healing, and that H. pylori infection does not delay gastric ulcer healing when proton pump inhibitor treatment is used.

2-Pyridinylmethylsulfinylbenzimidazoles↗

[Pronounced progression of interstitial pneumonia in a precious metal worker].

A 43-year-old man who had been engaged in the precious-metal processing industry for 18 years was admitted to our hospital because of shortness of breath on exertion. Chest roentgenograms disclosed ground glass opacities and annular-nodular shadows in the basal area of the right lung field and almost all of the left lung field. A video-assisted thoracoscopic lung biopsy was performed, and histologic examination disclosed usual interstitial pneumonia (UIP). Mineral analysis revealed high modes of silicon and aluminum, two elements consistent with the materials used in the patient's factory. The histopathological findings indicated interstitial pneumonia caused by the inhalation of dust particles. After corticosteroid therapy, computed tomographic scans disclosed that the ground glass opacities had subsided, but that honeycomb shadows remained. A chest roentgenogram taken 2 years earlier demonstrated only minute granular lesions in the basal area of right lung field. The interstitial shadows had progressed significantly over the intervening 2-year span. The findings in this case should be of value to the etiologic study of UIP.

Adult↗

A small deletion in the 3'-untranslated region of the cyclin D1/PRAD1/bcl-1 oncogene in a patient with chronic lymphocytic leukemia.

The cyclin DI/PRAD1 oncogene, a key regulator of the G1 phase of the cell cycle, has been incriminated in the pathogenesis of human neoplasia. Cyclin D1 was also demonstrated to be identical to the long-sought bcl-1 oncogene in B-cell malignancies with the t(11;14)(q13;q32) translocation. We report here a small deletion in the 3'-untranslated portion of the cyclin D1 gene in leukemia cells of a patient diagnosed with B-chronic lymphocytic leukemia (CLL), associated with overexpression of the corresponding cyclin D1 mRNA. During a Northern blot survey of B-cell malignancies, we identified a patient whose CLL cells showed a marked increase in 1.5-1.6 kb cyclin D1 mRNA species. Subsequent Southern blot analysis showed that genomic DNA from the patient's cells contained an extra band in the EcoRI digest, suggesting that one allele of the cyclin D1 gene may be altered. Polymerase chain reaction (PCR) analysis of the genomic DNA and direct DNA sequencing clearly disclosed that one allele of the cyclin D1 gene was deleted in the 3'-untranslated region, which would contribute to an increased stability of its mRNA. Reverse transcription-polymerase chain reaction (RT-PCR) analysis and direct DNA sequencing revealed that the cyclin D1 mRNA was deleted at the corresponding region. This finding provides further evidence for a critical role of cyclin D1 in the pathogenesis of B-cell malignancies and highlights a novel mechanism, a small deletion in the 3'-untranslated region, responsible for deregulation of the cyclin D1 gene in oncogenesis.

Base Sequence↗

Lymphoma arising in mucosa-associated lymphoid tissue of the duodenal bulb.

We report a case of low-grade B-cell lymphoma of the duodenal bulb arising from mucosa-associated lymphoid tissue. A barium swallow and an endoscopic examination showed multiple elevated, irregularly contoured lesions limited to the duodenal bulb. Endoscopic biopsy specimens were highly suggestive of non-Hodgkin's lymphoma. The resected specimen showed a gyriform mucosal elevation measuring 3 x 2cm in extent, with multiple small polypoid elevations scattered around it. Histologically, the small lymphocytes constituting the tumor infiltrated the duodenal mucosa and submucosa. The neoplastic centrocyte-like cells tended to grow around reactive lymphoid follicles and to invade epithelial structures, forming characteristic lymphoepithelial lesions. Monoclonal proliferation of the lymphoid tissue was demonstrated by the polymerase chain reaction method. The histologic appearance and the demonstration of monoclonality fulfilled the criteria for malignant lymphoma arising from mucosa-associated lymphoid tissue, which is extremely rare in the duodenum.

Duodenal Neoplasms↗

Expression of mRNA for heregulin and its receptor, ErbB-3 and ErbB-4, in human upper gastrointestinal mucosa.

Expression of mRNA for heregulin (HRG), a member of the epidermal growth factor (EGF) family and its receptors, ErbB-3 and ErbB-4, were evaluated in human upper gastrointestinal (GI) mucosa. Multi-target reverse-transcriptase polymerase chain reaction (RT-PCR) analysis using capillary electrophoresis and laser-induced fluorescence allowed us to quantify the minute amounts of mRNA from one biopsy specimen with high sensitivity. HRG, ErbB-3 and ErbB-4 mRNA were detected in esophagus, stomach and duodenum and the highest expression was found in duodenum. In gastric cancer, mRNA for ErbB-4 was significantly overexpressed. Immunoreactivity of ErbB-4 in carcinoma cell membrane was also confirmed. These findings suggest that HRG and its receptors, ErbB-3 and ErbB-4 may be physiologically significant in the human upper GI mucosa, especially in duodenum, and that ErbB-4 may contribute to the growth of gastric cancer.

ErbB Receptors↗

Effect of dietary linoleate/alpha-linolenate balance on experimentally induced gastric injury in rats.

Rats were fed diets containing different ratios of linoleate (18:2 n-6) to alpha-linolenate (18:3 n-3), and the severity of gastric injury induced by ethanol, ischemia/reperfusion and water-immersion stress was compared. On decreasing the 18:2 n-6/18:3 n-3 ratios in the diets, the proportion of arachidonic acid (20:4 n-6) decreased and that of eicosapentaenoic acid (20:5 n-3) increased in the phospholipids of the gastric mucosa, which was associated with decreased mucosal prostaglandin E2 content. Mucosal injury in all the three experimental models was exacerbated significantly in the diet group fed 18:2 n-6/18:3 n-3 ratio of 0.25 (perilla oil) as compared with the groups fed dietary oils with 18:2 n-6/18:3 n-3 ratios of 2.7 (mixture of perilla and safflower oils) and 127 (safflower oil). This adverse effect induced by perilla oil diet was not observed when rats were pretreated with a mild irritant (20% ethanol) prior to challenge with a strong irritant (absolute ethanol). Furthermore, an 18:2 n-6/18:3 n-3 ratio of as low as 1 was found to be in a safe range in the water-immersion stress ulcer model. Thus, oils with very low n-6/n-3 ratios, for example perilla oil, could be used without the risk of the observed adverse effects on experimental gastric injury in people of industrialized countries ingesting foods with n-6/n-3 ratios of above 4. A decrease in the n-6/n-3 ratios to 2 or below is still recommended for the prevention of chronic diseases in the elderly related to atherosclerosis and inflammation.

Animals↗

Regulatory mechanism of pepsinogen gene expression in monolayer cultured guinea pig gastric chief cells.

We have investigated the effects of dibutyryl cAMP, forskolin, carbamylcholine chloride (carbachol), ionomycin, and 12-O-tetradecanoylphorbol-13-acetate (TPA) on the expression of guinea pig pepsinogen mRNA in monolayer cultured gastric chief cells. After exposure of the cells to each of these compounds for 4 to 24 hr, and at 48 hr after primary culture, total cellular RNA was isolated using acid guanidium-phenol-chloroform and then was reverse transcribed to cDNA. Obtained cDNA was amplified by polymerase chain reaction (PCR) using primers detecting guinea pig pepsinogen mRNA and human beta-actin mRNA as an internal standard. The PCR products were separated and quantified using capillary electrophoresis. Dibutyryl cAMP and forskolin significantly increased pepsinogen mRNA, but carbachol, ionomycin, and TPA failed to increase that. These findings suggested that pepsinogen gene expression was up-regulated by intracellular cAMP, but not by intracellular calcium or protein kinase C in guinea pig chief cells.

Animals↗