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Biomedical subjects

K Tateishi

Publications and source records attributed to K Tateishi.

At least 91 records · Page 5Linked to original sources

Pancreastatin producing cell line from human pancreatic islet cell tumor.

It has been characterized that cell line QGP-1 derived from human non-functioning pancreatic islet cell tumor produces human pancreastatin. Exponentially growing cultures produced 5.7 fmol of pancreastatin/10(6) cells/hr. Human pancreastatin immunoreactivities in plasma and tumor after xenografting with QGP-1 into nude mouse were 92.7 fmol/ml and 160.2 pmol/g wet weight, respectively. Immunocytochemical study revealed both chromogranin A and pancreastatin immunoreactive cells in the tumor. Gel filtrations of culture medium and tumor extract identified heterogenous molecular forms of PST-LI which eluted as large and smaller molecular species. These results suggest that plasma pancreastatin levels may be useful as a tumor marker of endocrine tumor of the pancreas, and the pancreastatin producing cell line may be useful for studies of the mechanism of secretions and processing of chromogranin A and pancreastatin.

Adenoma, Islet Cell↗

Plasma pancreastatin responses after intrajejunal infusion of liquid meal in patients with chronic pancreatitis.

The plasma concentrations of pancreastatin and cholescystokinin (CCK), exocrine pancreatic responses, and gallbladder contraction following intrajejunal ingestion of 100 kcal/hr semidigested liquid meal (Clinimeal) were simultaneously studied in six controls and six patients with chronic pancreatitis. An intrajejunal infusion of Clinimeal resulted in significant rises of pancreastatin and CCK, which paralleled the pancreatic secretion and gallbladder contraction. On the other hand, an intrajejunal infusion of Clinimeal resulted in a delayed rise of pancreastatin and no rise of CCK in chronic pancreatitis. Pancreatic secretion did not increase, and gallbladder contraction was not induced in these patients. It is suggested that pancreastatin may play an important role in the regulation of intestinal phase of exocrine pancreas. The impaired pancreastatin and CCK release in chronic pancreatitis may be due to the inappropriate stimuli in the lumen, which is attributed to pancreatic exocrine dysfunction, or to disturbed physiological regulation between the pancreas and gastrointestinal tract.

Adult↗

Pancreastatin-like immunoreactivity in urine.

The concentration and molecular form of pancreastatin-like immunoreactivity (PST-LI) in urine of normal subjects and patients with noninsulin-dependent diabetes mellitus or chronic renal failure were examined. PST-LI output (mean +/- SEM) in urine of normal subjects was 74.6 +/- 8.5 pmol/day and 87.1 +/- 11.7 pmol/g creatinine. That in patients with noninsulin-dependent diabetes mellitus was 78.1 +/- 9.0 (SEM) pmol/day and 85.6 +/- 9.0 pmol/g creatinine and was not significantly different from that in normal subjects. Gel filtration analysis showed that PST-LI molecules excreted in urine of these two groups were smaller than human pancreastatin (43-52) (hPST-10) of C-terminal fragment. The PST-LI molecular forms were deduced to be nonbioactive from the result that hPST-10 did not inhibit pancreatic exocrine secretion. PST-LI excretion in patients with chronic renal failure was 258.5 +/- 62.9 pmol/day and 713.2 +/- 219.6 pmol/g creatinine. A molecular form corresponding to hPST-52 and a larger form eluted in the high mol wt region (approximately mol wt 15 K) were detected by gel filtration of urine from these patients, indicating that PST-LI is excreted in urine without degradation in patients with chronic renal failure. These results support the suggestion that the kidney may play an important role in PST degradation or metabolism.

Chromatography, Gel↗

[Relationship between presence of Creola bodies and airway hyperresponsiveness in patients with bronchial asthma].

It has recently been suggested that epithelial damage participates in the development of bronchial hyperresponsiveness. In this study we investigated the relationship between the presence of clusters of desquamated respiratory epithelial cells (Creola body. CrB) in sputum and airway responsiveness. Sputa were collected from asthmatic patients and acetylcholine inhalation tests were performed to assess airway responsiveness. Smears of 100 microliters of sputum were spread in pairs of two glass slides. One slide was stained with Papanicolaou's stain, the other with Giemsa stain. CrBs were detected on the whole glass slide stained with Papanicolaou's stain and the CrB score was determined by summing up the points given to each CrB on a glass slide according to the number of epithelial cells composing one CrB. The CrB score was significantly higher in patients with CrBs than in patients without CrBs. The patients with higher CrB score (CrB score greater than or equal to 6) had significantly greater number of eosinophils in sputa than the patients without CrBs. These results suggest the participation of damage to the respiratory epithelium in the development of airway hyperresponsiveness in bronchial asthma. The detection of CrBs is easy and we consider it clinically useful in the estimation of airway hyperresponsiveness.

Acetylcholine↗

Isolation and characterization of a tumor-derived human pancreastatin-related protein.

A protein with pancreastatin-like immunoreactivity has been isolated and purified from liver metastasis of a patient with insulinoma. NH2-terminal sequence analysis in conjunction with the use of antibodies specific for the C-terminal structure of pancreastatin identified this protein as a 186-amino acid residue protein corresponding to human chromogranin A-116-301. Using a sensitive radioimmunoassay it was found that serum from the patient with insulinoma contains two peptide species; one comigrates with the 186-amino acid residue pancreastatin and the other the 48-residue pancreastatin.

Amino Acid Sequence↗

Central pressor actions of neurokinin B: increases in neurokinin B contents in discrete nuclei in spontaneously hypertensive rats.

The regional distributions of neurokinin B-like immunoreactivity and substance P-like immunoreactivity in the central nervous system in spontaneously hypertensive rats (SHRs) and normotensive Wistar Kyoto rats (WKYs) were examined. The distribution of neurokinin B-like immunoreactivity in WKYs was not exactly the same as that of substance P-like immunoreactivity. The neurokinin B-like immunoreactivity contents of the supraoptic nucleus of the hypothalamus and the caudal part of the nucleus tractus solitarii were higher in SHRs than in WKYs. Injections of selective neurokinin B receptor peptides, senktide (suc-[Asp6,Me-Phe8]-substance P6-11) and [Pro7]-neurokinin B, into the lateral brain ventricle of the normotensive rats caused dose-dependent increases in the blood pressure, and blockade of peripheral vascular vasopressin receptors reduced these pressor responses, but did not affect the substance P-induced pressor response. These findings suggest that the novel tachykinin peptide, neurokinin B has an important role in central pressor action in rats.

Animals↗

Cardiovascular roles of tachykinin peptides in the nucleus tractus solitarii of rats.

Unilateral removal of the afferent fibers of the IXth and Xth cranial nerve (nodose ganglionectomy) caused significant decrease in the content of substance P-like immunoreactivity (SP-LI) and neurokinin A-like immunoreactivity (NKA-LI) in the nucleus tractus solitarii (NTS) of rats. Microinjection of SP (1 ng) or NKA (10-100 ng) into the NTS caused prompt, transient hypotension and bradycardia, suggesting that SP and NKA may be neurotransmitters of the baroreceptor reflex in the NTS. NKB-like immunoreactivity (NKB-LI) was also detected in the NTS of rats by radioimmunoassay, but its content in the NTS was not affected by unilateral nodose ganglionectomy. The microinjection of 1-10 ng of suc-[Asp5, Me-Phe8]-SP(6-11) (senktide, a selective neurokinin B receptor peptide) into the NTS caused long-lasting hypertension and tachycardia. These results indicate that NKB may also be a neuromodulator on cardiovascular responses in the NTS.

Animals↗

Bioactivity of human pancreastatin and its localization in pancreas.

Synthetic human pancreastatin and its C-terminal fragment were first evaluated with respect to the biological activity on the insulin secretion in the isolated rat islets. Both these pancreastatins inhibited glucose-stimulated insulin secretion at a concentration of 100 nM. The relative molar potency of human pancreastatin compared to that of porcine pancreastatin was equivalent. The pancreastatin-reactive cells were widely located in the islets of Langerhans, and not observed in exocrine acinar cells by immunocytochemistry using human pancreastatin C-terminal specific antibody. These results suggest that human pancreastatin may modulate endocrine function of the pancreas, especially insulin secretion.

Amino Acid Sequence↗

High plasma pancreastatinlike immunoreactivity in a patient with malignant insulinoma.

High levels of pancreastatinlike immunoreactivity were detected in the plasma (2.9 pmol/ml, greater than 200-fold the normal level), pancreas (2.9 nmol/g wet wt, greater than 450-fold the normal level), and liver (1.6 nmol/g wet wt) of a patient with pancreatic insulinoma with metastasis to the liver by a sensitive and specific radioimmunoassay for human pancreastatin. Antiserum was produced against the C-terminal fragment of human pancreastatin-(24-52), which was synthesized according to the sequence of human chromogranin A corresponding to that of pancreastatin. With the antiserum, intense immunocytochemical staining was detected in the tumors. Sephadex G-50 gel filtration showed that the tumors and plasma contained two molecular forms of pancreastatinlike immunoreactivity--a molecular form coeluted with synthetic human pancreastatin-52 and a larger molecular form (Mr approximately 12,000-15,000). The smaller form eluted in the same position as synthetic human pancreastatin-52 on reverse-phase high-performance liquid chromatography.

Adenoma, Islet Cell↗

Establishment of highly specific radioimmunoassays for neurokinin A and neurokinin B and determination of tissue distribution of these peptides in rat central nervous system.

Highly specific radioimmunoassays (RIAs) for neurokinin A (NKA) and neurokinin B (NKB) were developed. Antisera were produced by the procedure which involved immunization with NKA or NKB, both conjugated with keyhole limpet hemocyanin, and treatments with a tolerogenic conjugate of kassinin and a copolymer of D-glutamic acid and D-lysine (D-GL) to inhibit the production of cross-reactive antibodies against common C-terminal region of tachykinins. Cross-reactivities of anti-NKA antiserum (R704), thus produced, with NKB, kassinin, eledoisin were 12.6%, 10.6% and 11.5%, respectively. This was in sharp contrast with those of antiserum obtained from the rabbit not treated with kassinin-D-GL, these values corresponding to 129.0%, 42.5% and 94.4%, respectively. The cross-reactivities of R704 with substance P and physalaemin were 0.3% and 1.5%, respectively. This antiserum also bound 35.6% of neuropeptide K which contains NKA at its C-terminal. More importantly, anti-NKB antiserum (R707) obtained by the above tolerizing regimen was highly specific for NKB and the cross-reactivities with NKA, neuropeptide K, kassinin and other tachykinins were all less than 0.001%. RIAs using these specific antisera allowed us to measure directly NKA and NKB in tissue extracts without their fractionation by chromatography prior to RIAs. Measurements of immunoreactive NKA and NKB in different rat brain regions and spinal cord revealed that they are present with various ratios (NKA/NKB: 1.1-9.9) depending on the region.

Amino Acid Sequence↗

Marked depression of brain cholecystokinin and vasoactive intestinal polypeptide levels in Eck fistula dogs.

Cholecystokinin-like immunoreactivity (CCK-LI) and vasoactive intestinal polypeptide-like immunoreactivity (VIP-LI) were measured in the brain of Eck fistula dogs and dimethylnitrosamine (DMN)-treated dogs which were prepared as experimental models of hepatic encephalopathy (HE). Significant reduction of CCK-LI was observed in all cortical regions of Eck fistula dogs, especially in parietal and occipital cortex (approximately 40% of control values). In DMN dogs, CCK-LI was reduced in the temporal, parietal and occipital cortex (65%, 47% and 51% of control values, respectively). Significant reduction of VIP-LI was also observed in the occipital cortex of both Eck fistula and DMN dogs (75% and 70% of control values, respectively). These data were compared with the concentrations of tyrosine and phenylalanine, precursors of false neurotransmitters suggested as causing HE. Phenylalanine was significantly increased in all areas of cortex of both models. Tyrosine was also significantly increased in frontal, parietal and occipital cortex of Eck fistula dogs, and in temporal, parietal and occipital cortex of DMN dogs. However, reduced amounts of these peptides did not correlate with increased amounts of the aromatic amino acids in these models. The results imply that reduced levels of CCK and VIP may be elicited by a mechanism distinct from that inducing increase of false neurotransmitters.

Amino Acids↗

Plasma pancreastatin-like immunoreactivity in various diseases.

Plasma pancreastatin (PST)-like immunoreactivity in normal subjects and patients with various diseases was estimated by a RIA, using antiserum raised against a synthetic C-terminal peptide of human PST deduced from the sequence of human chromogranin-A. The mean level +/- SEM was 13.2 +/- 0.6 pmol/L in normal subjects, but was significantly higher in patients with chronic renal failure (526.7 +/- 48.5). An immunoreactive form corresponding to a human PST-like sequence [human chromogranin-A-(250-301)] and a larger form were detected by gel filtration of plasma from these patients, suggesting accumulation of the larger molecular form in these patients. A significant increase in PST-like immunoreactivity was also found in patients with liver cirrhosis (20.8 +/- 3.0 pmol/L), but not in patients with noninsulin-dependent diabetes mellitus, chronic pancreatitis, or pancreatic cancer. Elevated levels were found in 16 of the 21 patients with small cell lung carcinoma examined. High levels were also found in 3 of 11 patients with islet cell tumor.

Adenoma, Islet Cell↗

[A successful arterial switch operation for the transportation of the great arteries with posterior aorta--with special reference to its anatomical features and possibility of the indication of the Jatene procedure].

A five months old infant with the transposition of the great arteries with posterior aorta undergoing arterial switch operation is reported. A pre-operative diagnosis of the transposition of the great arteries with posterior aorta, subarterial ventricular septal defect, anterior pulmonary artery, bilateral conus and fibrous continuity between aortic and mitral valve was made. This diagnosis was confirmed by the open heart surgery. The ventricular septal defect was subaortic from the transected aortic aspect, and the infundibular and trabecular septum was aligned. For these reasons, this subarterial ventricular septal defect was easily closed transaortically. The right coronary artery arose from the left sinus and the left coronary artery from the posterior sinus, so the coronary arterial pattern of this patient was a Shaher type 9. And in addition, another small ostium located in the left sinus gave rise to an additional small branch. Translocation of the coronary arteries was performed. The new pulmonary trunk was reconstructed to the right pulmonary artery so as not to compress the coronary artery and distort the great arteries. This patient was restudied three months after the repair. The right to left ventricular systolic pressure ratio was 0.42 and no pressure gradient was present between the right ventricle and the right pulmonary artery. But a moderate aortic regurgitation was detected. This was caused by deformity of the aortic sinus of valsalva. Only 28 patients with the transposition of the great arteries with posterior aorta were reported in the literature, but there were no reports on the successful surgical treatment for its rare anomaly, to our knowledge.(ABSTRACT TRUNCATED AT 250 WORDS)

Aorta↗

[Analysis with immunoreactive CCKs and bioactive CCKs in rat duodenum and brain].

We extracted immunoreactive CCKs from rat duodenum and brain. We fractionated these samples by gel-filtration and analyzed with immunoreactivity and bioactivity of each fraction. 1) Elution profile of CCKs in duodenum and brain was well corresponding to that of bioactive CCKs. 2) Contents of CCKs determined by both RIA and Bioassay in each fraction were well correlated with each other. 3) Apparent molecular weights of CCKs of duodenum calibrated in column chromatography were approximately 2200, 1000 and 800. 4) Apparent molecular weight of CCK of brain seemed to be 1000.

Animals↗

Gastrin-releasing peptide stimulates cholecystokinin secretion in perfused rat duodenum.

We examined the effect of porcine gastrin-releasing peptide (GRP-27) and other analogous neuropeptides on cholecystokinin (CCK) secretion from the isolated perfused rat duodenum. GRP-27 stimulated CCK secretion in a monophasic pattern and in a dose-dependent manner ranging from 10(-9) M to 10(-6) M, and 10(-7) M of GRP-27 led to an increment of 442 +/- 120.8 fmol/3 min. The stimulatory effect of GRP-27 on CCK was not inhibited by 10(-5) M of atropine. 10(-7) M of neuromedin C and B, analogs of GRP, stimulated CCK secretion to increments of 382 +/- 64.1 and 289 +/- 47.2 fmol/3 min, respectively. Carbachol (10(-9) to 10(-6) M), VIP (10(-9)M), secretin (10(-9)M) and glucose (11 mM) did not stimulate CCK secretion, and the addition of atropine (10(-5)M) to them led to no significant changes. These results suggest that GRP may directly stimulate CCK secretion from the duodenum and work as a non-cholinergic, peptidergic neurotransmitter.

Animals↗

Reduced somatostatin-28-(1-12)-like immunoreactivity in cerebral cortex of dogs with an Eck fistula and somatostatin molecular forms in brain.

Somatostatin-28-(1-12)-like immunoreactivity (S28(1-12)LI) in brains of Eck fistula dogs, prepared as an experimental model of hepatic encephalopathy, was measured. Significant reductions of S28(1-12)LI were observed in all cortical regions of Eck fistula dogs. The reductions of S28(1-12)LI were significantly correlated with decreases in somatostatin-14-like immunoreactivity (S14LI) in the cortical region. The ratios of S28(1-12)LI to S14LI in all cortical regions were not different between Eck fistula and normal dogs. Additionally, no difference in gel chromatographic profiles of S28(1-12)LI and S14LI was observed between Eck fistula and normal dogs. These results imply that reduced somatostatin immunoreactivity in hepatic encephalopathy may be caused not by altered degradation but by reduced production of prosomatostatin. Our S28(1-12)LI assay system could detect prosomatostatin(1-76) and S28(1-12) and the S14LI system prosomatostatin, S28 and S14. S28(1-12)LI/S14LI ratios in cortex were 0.64-0.83 and these were significantly different from those (1.02-1.36) in thalamus, midbrain and medulla. Relative proportions of prosomatostatin (20%) and S28 (23-24%) in cortex were larger than those (6-7% and 5-7%, respectively) in thalamus, midbrain and medulla. The differential distribution of these molecular forms suggests that processing of prosomatostatin in cortex may be different from that in thalamus, midbrain and medulla.

Acute Kidney Injury↗

An aspect of the organizational principle of the gamma-aminobutyric acidergic system in the cerebral cortex.

The possibility of the colocalization of a Ca2+-binding protein, parvalbumin (PV), with peptides, cholecystokinin (CCK) and somatostatin (SS), all of which are known to be contained gamma-aminobutyric acidergic neurons in the cerebral cortex, was tested in the rat visual cortex by means of immunohistochemistry using the adjacent section technique. No PV immunoreactive (PV-I) neurons showed CCK-like immunoreactivity, and almost none (932 out of 934 PV-I neurons examined) showed SS-like immunoreactivity. These observations suggest that the GABAergic system of the cerebral cortex may consist of some distinct subsystems with different chemical and presumably physiological characteristics.

Animals↗

Diurnal profile of pancreatic exocrine secretion and plasma levels of gut hormones (cholecystokinin and pancreatic polypeptide).

We examined diurnal changes of pancreatic exocrine secretion and plasma levels of cholecystokinin (CCK) and human pancreatic polypeptide (hPP) in men with postoperative transient external pancreatic drainage (3 with pancreatico-jejunostomy: PJ, and 5 with pancreato-duodenectomy:PD). Plasma CCK levels increased and the pancreatic exocrine secretion showed a corresponding increase after meals in both groups. In the PJ group hPP levels increased after meals and there was a significant correlation between the plasma levels of CCK and hPP. In the PD group the plasma hPP levels were not detectable throughout the study and there was a better correlation between the exocrine secretion and the plasma CCK levels than in the PJ group. Plasma CCK levels showed rhythmic changes associated with pancreatic exocrine secretion, with no significant changes in plasma glucose and insulin in the night (24:00-07:00). These results suggested that (1) the resection of the pancreatic head which is rich in hPP contents led to a complete loss of anti-CCK effects on CCK, and that (2) fluctuation in plasma CCK levels, in the fasting state, might initiate pancreatic exocrine secretion.

Aged↗