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Biomedical subjects

K Tateishi

Publications and source records attributed to K Tateishi.

At least 55 records · Page 3Linked to original sources

[Measurement of serum and sputum eosinophil cationic protein concentrations in asthma].

Concentrations of eosinophil cationic protein (ECP) were measured in serum from patients with asthma, patients with chronic obstructive pulmonary disease (COPD), and healthy subjects. The relationships between serum ECP concentration and percent of predicted FEV1 (%FEV1), and between serum and sputum ECP concentrations were also examined in patients with asthma. Serum ECP concentration in asthma was significantly higher than those in COPD patients and healthy subjects. There was a significant inverse correlation between serum ECP concentration and %FEV1 when analysis was restricted to data from asthma patients less than 60 years old. ECP concentration in serum and in sputum were significantly correlated. These results suggest that in asthma patients, eosinophils are activated in serum, and that the degree of eosinophil activation in the airway can be estimated by measuring serum ECP to some extent. Because it does not require bronchial biopsy or bronchoalveolar lavage, measurement of serum ECP may be useful as a minimally invasive monitoring of asthma.

Adult↗

Isolation and functional expression of human pancreatic peptidylglycine alpha-amidating monooxygenase.

Pancreastatin (PST) is processed from chromogranin A and the C-terminal amide of the peptide is an absolute requirement for biological activities. Human pancreatic carcinoma cells QGP-1 which produce both chromogranin A and PST were used to isolate cDNAs encoding two forms of peptidylglycine alpha-amidating monooxygenase (PAM). The two forms are a full length bifunctional enzyme and a variant lacking the transmembrane domain-coding region. When the cDNAs of these two forms were expressed in COS-7 cells, cells transfected with the predicted soluble form released into the culture medium a very much higher amidating activity which converts human chromogranin A-(273-302) to PST-29. The optimal pH for amidating activity was 5.4 and Cu2+, ascorbate and catalase were required as cofactors for the both forms of PAM. Km values for the membrane-bound and the soluble forms of PAM were 15.7 +/- 3.1 microM and 12.4 +/- 1.6 microM, respectively. These results demonstrate that both forms of PAM can function in the posttranslational processing of chromogranin A to PST in the environment of a secretory vesicle.

Amino Acid Sequence↗

Pancreastatin-like immunoreactivity of cerebrospinal fluid in patients with Alzheimer type dementia: evidence of aberrant processing of pancreastatin in Alzheimer type dementia.

The concentrations of pancreastatin-like immunoreactivity (PST-LI) of the cerebrospinal fluid (CSF) were measured in the patients with Alzheimer type dementia (ATD) and in age-matched normal subjects. The mean PST-LI concentration in the CSF of ATD patients was significantly lower than that of normal subjects. Gel chromatographic analysis revealed that the main PST-LI peak of ATD's CSF eluted at molecular weight (MW) 13.5 kDa. However, the age-related change of the molecular forms of PST-LI in CSF was observed in normal subjects as following; PST-LI in neonatal CSF showed one peak at MW 13.5 kDa, that of 16-64-year-old showed two peaks at MW 13.5 and 5.4 kDa, however, only one main peak was shown at MW 5.4 kDa in the CSFs of 72-85-year-old. These findings suggest that the production of PST-LI was decreased and the proteolytic cleavage, which should process big PST to PST (1-52) in normal subjects, was altered to that of neonatal type in the CNS of the patients with ATD.

Aged↗

Production and secretion of chromogranin A and pancreastatin by the human pancreatic carcinoma cell line QGP-1N on stimulation with carbachol.

Chromogranin A (CGA) is thought to be a precursor of pancreastatin (PST). Carbachol (Cch) stimulated the secretion of CGA and PST from QGP-1N cells derived from a human pancreatic islet cell tumor. Atropine inhibited the secretion of both. Sodium fluoride, phorbol ester, and calcium ionophore also stimulated the secretion of both. Cch (10(-5) M) stimulated inositol 1,4,5-trisphosphate production in QGP-1N cells. Stimulation with Cch increased the total amount of PST in the cells and the medium 1.7-fold and decreased the amount of CGA in the cells and medium. QGP-1N cells were labelled with [35S]methionine, and then CGA and PST in the cells and medium were immunoprecipitated with specific antisera, and separated by electrophoresis in polyacrylamide gel. Stimulation with Cch resulted in an increase in the intensity of PST-immunoreactive bands and a decrease in those of CGA-immunoreactive bands. Cch did not increase the cellular level of CGA messenger RNA. These results suggested that (1) the secretion of CGA and PST from QGP-1N cells is regulated mainly through muscarinic receptors coupled with activation of polyphosphoinositide breakdown by a G protein, with intracellular calcium ion and protein kinase C playing a role in the stimulus-secretion coupling and that (2) Cch may induce the secretion of PST and CGA and processing from CGA to PST.

Carcinoma, Islet Cell↗

Unique change of pancreastatin-like immunoreactivity in cerebrospinal fluid by aging.

Using a specific antiserum for the C-terminal glycine amide region of human pancreastatin (PST), pancreastatin-like immunoreactivity (PST-LI) was measured in cerebrospinal fluid (CSF) from 447 subjects (368 +/- 10.8 pmol/l, mean +/- S.E.M.) free from endocrine diseases. The CSF contents of PST-LI showed a mountain-shape type change which peaked at 40 years of age. The highest concentration was found in the group of ages 40-49 years old (412 +/- 22.9 pmol/l) and the lowest concentration was found in the group of ages 80-89 years old (293.2 +/- 45.2 pmol/l) among various age groups. Gel chromatographic examination revealed the presence of two major forms (MW 13,500 and 5,400) of PST-LI in CSF. Because of the character of this antibody, the large molecular form is possibly an N-terminally elongated PST and the other may be PST-52. This may be the first report on the unique age-related change of PST concentration in CSF.

Adolescent↗

Expression of the cholecystokinin precursor gene in rat tissues.

Cholecystokinin, a brain gut peptide that stimulates gall bladder contraction and pancreatic exocrine secretion, also acts as a neurotransmitter. In this study, we demonstrated that small amounts of cholecystokinin precursor mRNA were expressed in the heart, lung, and kidney, as well as in the brain and the small intestine. The nucleotide sequences of the coding regions of the cholecystokinin precursor mRNA in these tissues were identical to those of the small intestine, indicating that cholecystokinin precursor proteins produced in these tissues are identical to those in small intestine. This is the first report demonstrating that the cholecystokinin precursor gene is expressed in the heart, lung, and kidney, as well as in the gastrointestinal tract and brain.

Animals↗

Pancreastatin molecular forms in normal human plasma.

Circulating molecular forms with pancreastatin (PST)-like immunoreactivity in plasma from normal subjects were examined. An immunoreactive form corresponding to a human PST-like sequence [human chromogranin-A-(250-301)] (hPST-52) and a larger form (mol wt 15-21 kDa) were detected by gel filtration of plasma from normal subjects. On high performance liquid chromatography, predominant immunoreactive forms coeluted with the three larger forms which were purified from the xenograft of human pancreatic islet cell carcinoma cell line QGP-1N cells and with synthetic hPST-52. The fraction containing larger forms purified from xenograft of QGP-1N cells had biological activity equivalent to that of hPST-52 on the inhibition of pancreatic exocrine secretion. These results suggest that the larger molecular forms as well as hPST-52 may be physiologically important circulating forms of PST in human.

Animals↗

Quantitative characterization of insulin-glucose response in Watanabe heritable hyperlipidemic and cholesterol-fed rabbits and the effect of cilazapril.

A great deal of evidence suggests that insulin resistance, via hyperinsulinemia, contributes to hyperlipoproteinemia and coronary atherosclerosis. When Watanabe heritable hyperlipidemic (WHHL) rabbits, an animal model of familial hypercholesterolemia (FH), are compared with normolipidemic Japanese White (JW) rabbits, an elevated fasting plasma insulin level and a heightened plasma insulin response to an intravenous (i.v.) glucose challenge are found. To elucidate the mechanism behind this phenomenon, a two-compartment model of the glucose/insulin system was fitted to empirical time courses of glucose and insulin concentrations during an i.v. glucose tolerance test (IVGTT) by nonlinear least-square regression, and the model parameters such as the glucose utilization rate constant, insulin degradation rate constant, and pancreas sensitivity were determined. WHHL rabbits showed decreased values of glucose utilization and insulin degradation rate constants and slightly higher values of pancreas sensitivity. This suggests that insulin resistance occurs in extrapancreatic tissues, and that this may be attributable to insulin receptor and/or post-insulin receptor abnormalities. Cholesterol feeding did not significantly change glucose tolerance or insulin action in JW rabbits. The effects of an angiotensin-converting enzyme (ACE) inhibitor, cilazapril, on insulin resistance were also examined in WHHL and JW rabbits. A decreased insulin response to an i.v. glucose challenge and increased glucose utilization and insulin degradation rate constants were observed in WHHL rabbits that had been treated with cilazapril, indicating that cilazapril improved insulin resistance in WHHL rabbits, possibly by increasing the number of insulin receptors. No significant differences were found in glucose tolerance and insulin action in JW rabbits before and after cilazapril administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Glucagon-like peptide-1 (GLP-1) molecular forms in human pancreatic endocrine tumors resemble those in intestine rather than pancreas.

Different glucagon-like peptide-1 (GLP-1) molecular forms are produced in the pancreas and the small intestine by differential processing of proglucagon. In this report, molecular forms of GLP-1 in two human pancreatic endocrine tumors were studied and compared with those in the pancreas and small intestine. A predominant GLP-1 immunoreactive form in the pancreas was eluted at the position of GLP-1(1-36) amide, whereas a predominant immunoreactive form in the ileal mucosa was eluted at the position of GLP-1(7-36) amide. In a glucagonoma, GLP-1 immunoreactive forms corresponding to GLP-1(7-36) amide and GLP-1(7-37) were predominant and immunoreactive forms at the position of GLP-1(1-36) amide and GLP-1(1-37) were minor. In another tumor, an insulinoma, immunoreactive forms were detected at the positions of GLP-1(7-36) amide, GLP-1(7-37), GLP-1(1-36) amide and GLP-1(1-37). Thus, the pattern of GLP-1 molecules in pancreatic tumors was not a pancreatic pattern and mimicked that found in the small intestine or consisted of both the patterns found in the small intestine and the pancreas. These data suggest that neoplastic transformation of the islet cells is associated with a switching in processing phenotype from islet (A) cells to intestinal (L) cells.

Chromatography, High Pressure Liquid↗

Detection of herpes simplex virus (HSV) in the saliva from 1,000 oral surgery outpatients by the polymerase chain reaction (PCR) and virus isolation.

Herpes simplex virus (HSV) was detected by a polymerase chain reaction (PCR) in 47 (4.7%) out of 1,000 saliva samples from the outpatients of an oral and maxillofacial surgery department compared with 27 (2.7%) by conventional virus isolation. There were 20 PCR-positive, culture-negative cases but no culture-positive, PCR-negative cases. Patients younger than 10 years or older than 60 years secreted HSV more frequently than the others. Those with inflammatory diseases showed higher positivity for HSV than those with malignancy, trauma or other complaints. All 27 virus isolates were typed as HSV type 1 and none were resistant to acyclovir, arabinofuranosyl-adenine, iododeoxyuridine or phosphonoacetic acid.

Acyclovir↗

Time course of recovery from pancreatic hypertrophy during partial exclusion of bile-pancreatic juice in rats.

The time course of recovery from hypertrophied pancreas to the normal size was examined and compared with the time course of normal size pancreas getting hypertrophied in rats. The bile-pancreatic duct was cannulated and bile-pancreatic juice was partly bypassed the proximal intestine. Trypsin and bile salts disappeared from the lumen of proximal quarter of intestine during the first 7 postoperative days; however, these appeared again after the 14th postoperative day and luminal trypsin activity reached 3 to 4 times the control level during the postoperative days 14-56. Conversely, the plasma cholecystokinin (CCK) concentration significantly increased on day 7, then declined thereafter, and the mRNA level of CCK in the proximal intestinal mucosa increased and reached the maximal level on day 7. Pancreatic wet weight, as an index of size, was significantly increased and remained high on postoperative days 7-28, then returned to the control size on day 56. Therefore, it took 7 d for the pancreas to become hypertrophied by high circulating CCK, however the pancreatic size recovered to the normal size on the 56th postoperative day although the plasma CCK level decreased with the appearance of luminal bile salt and trypsin during postoperative days 14-56. In conclusion, it took longer for the hypertrophied pancreas to return to the normal size (14 or more d) than for the normal size pancreas to become hypertrophied (7d).

Animals↗

Secretion of neurotensin from a human pancreatic islet cell carcinoma cell line (QGP-1N).

Effects of various secretagogues on secretion of neurotensin from a pancreatic islet cell carcinoma cell line (QGP-1N) were examined. Carbachol stimulated secretion of neurotensin concentration-dependently in the range of 10(-6) - 10(-4) M. The neurotensin secretion stimulated with 10(-5) M carbachol was completely inhibited by atropine at 10(-5) M. Phorbol ester and calcium ionophore (A23187) stimulated secretion of neurotensin. The removal of extracellular Ca2+ suppressed the secretion through the stimulation with 10(-5) M carbachol. Fluoride, an activator of guanine nucleotide-binding (G) protein, stimulated secretion of neurotensin. Neurotensin released into culture medium through stimulation with carbachol coeluted with neurotensin 1-13 on a gel-chromatography. Our results suggest that secretion of neurotensin from QGP-1N cells is mainly regulated by acetylcholine through muscarinic receptors coupled to G protein and that an increase in intracellular Ca2+ and protein kinase C play an important role in stimulus-secretion coupling.

Calcium↗

Comparison of plasma pancreastatin and GAWK concentrations, presumed processing products of chromogranin A and B, in plasma of patients with pancreatic islet cell tumors.

Plasma pancreastatin (PST) and GAWK, peptides processed from chromogranin A and B, were elevated in patients with various neuroendocrine tumors. In the present study, we measured plasma PST- and GAWK-like immunoreactivity (LI) concentrations in 12 patients with pancreatic islet cell tumors and evaluated them as a marker for these tumors. We also performed the gel filtration of the plasma from a gastrinoma patient and investigated the processing of PST and GAWK in plasma. Elevation of plasma PST-LI was found in 4 of 12 patients (33%) and elevation of plasma GAWK-LI was found in 6 of 12 patients (50%). A significant correlation was not found between plasma PST- and GAWK-LI concentrations of the patients. In the gel permeation chromatography of the plasma from a gastrinoma patient, PST-LI composed of a single peak but GAWK-LI composed of several components with wide range molecular weights.

Adenoma, Islet Cell↗

Parallel secretion of pancreastatin and somatostatin from human pancreastatin producing cell line (QGP-1N).

In this investigation we studied pancreastatin (PST) secretion from a human PST producing cell line (QGP-1N) in response to various secretagogues. Immunocytochemical study revealed the immunoreactivity of PST and somatostatin (SMT) in the same cells of a monolayer culture. Ki-ras DNA point mutation on codon 12 was found. Carbachol stimulated secretion of PST and SMT and intracellular Ca2+ mobilization in the range of 10(-6)-10(-4) M. The secretion and Ca2+ mobilization were inhibited by atropine, a muscarinic receptor antagonist. Phorbol ester and calcium ionophore (A23187) stimulated secretion of PST and SMT. The removal of extracellular calcium suppressed both secretions throughout stimulation with 10(-5) M carbachol. Fluoride, a well-known activator of guanine nucleotide binding (G) protein, stimulated intracellular Ca2+ mobilization and secretion of PST and SMT in a dose-dependent manner in the range of 5-40 mM. Also, 10(-5) M carbachol and 20 mM fluoride stimulated inositol 1,4,5-triphosphate production. However, cholecystokinin and gastrin-releasing peptide did not stimulate Ca2+ mobilization or secretion of the two peptides. These results suggest that secretion of PST and SMT from QGP-1N cells is regulated mainly by acetylcholine in a parallel fashion through muscarinic receptors coupled to the activation of polyphosphoinositide breakdown by a G-protein and that increases in intracellular Ca2+ and protein kinase C play an important role in stimulus-secretion coupling.

Adenoma, Islet Cell↗

[A case of congenital atrial flutter associated with atrial septal defect].

We report the case of a 8-month-old boy with atrial septal defect associated with congenital atrial flutter. He was operated on for ASD successfully. Atrial flutter in infants has been reported to be uncommon and to have a poor prognosis when associated with underlying cardiac disease. Therefore, early surgical intervention may improve the prognosis.

Atrial Flutter↗

[Multicenter study of the effects of sulbactam/cefoperazone on bacterial infections in the fields of internal medicine focused mainly on respiratory infections in Tochigi Prefecture].

Clinical effects of sulbactam/cefoperazone (SBT/CPZ) was studied on variety of bacterial infections in the fields of internal medicine focused mainly on respiratory infections. The total 135 infections were consisted of 103 respiratory infections, 15 urinary tract infections, 4 sepsis, 7 biliary tract infections, and 6 other infections, of which 86 patients had underlying diseases. The daily doses of SBT/CPZ were 2 to 6 g divided into 2 to 3 times i.v. or d.i.v., and the duration of administration was from 3 to 35 days. The clinical effects were judged by the attending doctors based on the changes in fever, cough, rales, chest rentogenograms, white blood cell counts, CRP values, ESR, etc. The total efficacy rate was 76.9%, and 69.0% of the isolated organism was eradicated by SBT/CPZ. The side effect was noted in 1 case, and the abnormal laboratory findings were noted in 1 case, however it was difficult to determine whether they were due to SBT/CPZ. These results suggest that the clinical usefulness of SBT/CPZ for the infections in the fields of internal medicine.

Adult↗

Soluble interleukin-2 receptor in sputum from patients with bronchial asthma.

To evaluate the activation of T-lymphocytes in the airways of patients with asthma, we attempted to measure the concentration of soluble interleukin-2 receptor (sIL-2R) in sputum extracts from asthma patients with acute attacks or in remission. The large amount of alkaline phosphatase in the sputum extracts excluded the use of an ELISA kit. Measurement was attempted by radiolabeling the second antibody in the ELISA kit. sIL-2R was detectable in 10/23 (43%) of the sputum extracts from patients with acute asthma attacks, but not in those from patients in remission (n = 12, p < 0.02). These observations suggest that T-lymphocyte activation takes place in the airways of patients with acute asthma attacks.

Acute Disease↗

Interaction between phosphoinositide turnover system and cyclic AMP pathway for the secretion of pancreastatin and somatostatin from QGP-1N cells.

It is found that secretion of pancreastatin and somatostatin from QGP-1N cells is regulated through muscarinic receptor-mediated activation of phosphatidylinositide hydrolysis system. In this report, whether the cAMP pathway interacts with the phosphoinositide turnover system for the secretion of pancreastatin and somatostatin from QGP-1N cells through muscarinic receptors was studied. Stimulation of QGP-1N cells with carbachol increased intracellular cAMP levels. The carbachol-induced increase in cAMP levels was inhibited by atropine. Calcium ionophore (A23187) and phorbol 12-myristate 13-acetate increased cAMP synthesis. Dibutyryl cAMP, forskolin and theophylline stimulated secretion of pancreastatin and somatostatin. When either dibutyryl cAMP, forskolin or theophylline was added in culture medium with A23187, phorbol ester or carbachol, a synergistic effect was found on pancreastatin and somatostatin secretion. These results suggest that interaction between the phosphoinositide turnover system and the cAMP pathway occurs in QGP-1N cells through muscarinic receptor stimulation for the secretion of pancreastatin and somatostatin.

Adenoma, Islet Cell↗