[A case of acute kidney failure complicated with rhabdomyolysis in alcoholics].
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Acute Kidney Injury↗
Biomedical subjects
H Wakasugi
Publications and source records attributed to H Wakasugi.
Simultaneous determinations of pancreatic phospholipase A2 and prophospholipase A2 in various pancreatic diseases.
Pancreatic phospholipase A2 (PLA2) is secreted into the pancreatic juice by pancreatic acinar cells as a proenzyme (proPLA2), which is activated by trypsin. Radioimmunoassays with monoclonal antibodies to PLA2 and proPLA2 were used to examine the serum PLA2 and proPLA2 levels simultaneously in patients with various pancreatic diseases. In healthy subjects, proPLA2 proved to be the major form of the enzyme. The serum PLA2 level were found to be significantly increased in patients with acute pancreatitis, the active phase of chronic relapsing pancreatitis, and the early stage of pancreatic cancer. In the terminal stage of pancreatic cancer the serum PLA2 level became low. In patients with chronic pancreatitis, significant correlations were observed between the levels of factors evaluated by the secretin test and the serum total PLA2 and proPLA2 level, but not the PLA2 level. The serum PLA2 and proPLA2 concentrations, and the proportion of proPLA2 in the total, were within normal ranges in patients with liver cirrhosis, hepatocellular carcinoma, and chronic renal failure. These results suggest that simultaneous measurements of serum PLA2 and proPLA2 are clinically useful for diagnosis and monitoring of the active phase of pancreatitis.
Acute Disease↗
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↗
Clinical implications of the serum level of CD23 in patients with undifferentiated nasopharyngeal carcinoma.
PURPOSE: In contrast with other carcinoma cells, cells from nude mice transplanted undifferentiated carcinoma of nasopharyngeal type (UCNT) release the soluble fragment of the CD23 antigen (sCD23). We sought to study the level of sCD23 in sera of untreated UCNT patients. PATIENTS AND METHODS: Pretherapeutic sera from 65 consecutive, locally advanced, initially nonmetastatic UCNT patients were assayed for sCD23. Patients were treated with a neoadjuvant chemotherapy/full-dose radiotherapy sequence. The mean follow-up duration is 50.5 months (range, 28 to 77). The Cox proportional hazards model was used to study the association between sCD23 levels and clinical signs and disease evolution. RESULTS: sCD23 levels showed an association with disease-free survival (DFS; P = .08) and overall survival (OVS; P = .08). Patients with sCD23 levels greater than a cutoff value of 0.6 ng/mL (greater cutoffs were found to be equally significant, but less sensitive), have a relative risk (RR) of relapse of 3.3 (95% confidence interval, 1.6 to 6.9; P = .002), and an RR of death of 2.9 (95% confidence interval, 1.2 to 7.3; P = .02), when taking other prognostic factors into account. CD23 does not correlate with either the response to treatment or the development of metastases, but appears to be related to local control (cutoff, 0.6 ng/mL; RR = 5.1 [95% confidence interval, 1.2 to 21.7]; P = .02). CONCLUSION: The serum level of sCD23 appears to be an independent prognostic factor for initially nonmetastatic, locally advanced UCNT patients, treated with chemotherapy and radiotherapy. Our data indicate an association between this marker and local relapses. Thus, a simple enzyme-linked immunoadsorbent assay (ELISA) could help to identify a high-risk group among nonmetastatic UCNT patients. CD23 could be a marker for two groups of UCNT tumors, with distinct biologic characteristics and clinical behaviors.
Adolescent↗
Effect of LHRH on plasma 7B2 in patients with gonadotropin-producing pituitary adenomas.
Plasma immunoreactive (IR)-7B2 was measured in four patients with gonadotropin-producing pituitary adenomas. The basal level of plasma IR-7B2 was elevated in one of the four patients. Hyperresponse of plasma IR-7B2 to LHRH or LHRH/TRH was noted in two patients tested. 7B2 was positively stained in a paraffin-embedded section of gonadotropin-producing pituitary adenoma obtained at surgery. These findings suggest that 7B2 is produced in gonadotropin-producing pituitary adenomas and secreted into the blood stream under certain conditions. 7B2 may be a useful marker for gonadotropin-producing pituitary adenomas.
Adenoma↗
Bioactivity of synthetic human cholecystokinin (CCK)-33 in vitro and in vivo.
The relative potencies of synthetic human cholecystokinin (h-CCK)-33, porcine CCK-33 (p-CCK-33) and CCK-8 were examined by measuring pancreatic secretion in the conscious rat (in vivo) and amylase release from rat pancreatic acini using a perifusion study (in vitro). The increments of protein output during an 1-hr infusion of 100 pmol/kg/hr of h-CCK-33, p-CCK-33 and CCK-8 were 27.0 +/- 2.9 mg/hr (M +/- SE), 19.3 +/- 2.8 and 14.0 +/- 1.8 mg/hr, respectively. H-CCK-33 and p-CCK-33 showed significantly higher responses of protein output than CCK-8 in a same molar ratio, in vivo. In vitro, the stimulation with 10(-10) M h-CCK-33, p-CCK-33 and CCK-8 led to a similar biphasic amylase release in a perifusion study. Twenty-five microM CR-1409, an antagonist for CCK receptor, completely inhibited the 10(-10) M h-CCK-33-stimulated amylase release. Although it was found that h-CCK-33 and p-CCK-33 were more potent than CCK-8 in vivo, 10(-10) M CCK-8, h-CCK-33 and p-CCK-33 were equipotent on rat pancreatic acini in vitro. It is suggested that the discrepancy in potencies of the large molecular form and small molecular form of CCK in vivo and in vitro may be attributed to the delay of degradation of the large molecular form of CCK in vivo.
Amylases↗
7B2, a possible marker for nonfunctioning pancreatic islet cell tumor.
Plasma 7B2 was measured in 13 patients with pancreatic islet cell tumors, 11 with pancreatic adenocarcinoma and 31 normal subjects as a control. The mean (+/- SD) concentrations of plasma 7B2 in the normal subjects and the patients with pancreatic islet cell tumors were 67 +/- 10 and 1041 +/- 1786 pmol/l, respectively, and the value in the patients with pancreatic islet cell tumors was significantly higher than that in the normal subjects (p less than 0.01). Elevation of plasma 7B2 over the normal range, defined as less than the mean + 3SD value of those in the normal subjects, was found in 10 of 13 patients with pancreatic islet cell tumors including 4 with nonfunctioning tumor. Plasma 7B2 dropped into the normal range postoperatively in 3 patients with nonfunctioning tumor. Plasma 7B2 concentrations in the patients with pancreatic adenocarcinoma remained in the normal range. These results raise a possibility that 7B2 is a useful marker for pancreatic islet cell tumors, in particular nonfunctioning tumor.
Adenoma, Islet Cell↗
Clinical usefulness of serum phospholipase A2 determination in patients with pancreatic diseases.
A new kit for radioimmunoassay of serum phospholipase A2 (PLA2) with monoclonal antibody (S-0932, Shionogi, Osaka, Japan) was used to examine PLA2 levels in patients with various diseases. Patients with acute pancreatitis showed significantly increased serum PLA2 levels. In patients with chronic pancreatitis, significant correlations were observed between the levels of factors evaluated by the secretin test and serum PLA2 levels. In patients with pancreatic cancer, serum PLA2 levels varied with disease severity. Serum PLA2 concentrations were within the normal range in patients with other malignant tumors, diabetes mellitus, and chronic liver diseases but were increased in patients with chronic renal failure. S-Sepharose column analysis of sera showed a small peak of pro-PLA2 and a large peak of PLA2 in sera from patients with severe acute pancreatitis, but a large peak of pro-PLA2 in healthy controls and patients with other diseases. On G-100 gel filtration, high-molecular-weight PLA2 immunoreactivity was detected in sera of patients with chronic renal failure, whereas a single peak of PLA2 immunoreactivity coinciding with that of standard PLA2 was detected in sera of patients with acute pancreatitis. These results suggest that (a) measurement of serum PLA2 is clinically useful for diagnosis and monitoring of pancreatitis, (b) active PLA2 in the circulation is dominant in severe acute pancreatitis, and (c) the kidney may be the main site of PLA2 degradation or excretion.
Acute Disease↗
Acetylcholine regulates pancreastatin secretion from the human pancreastatin-producing cell line (QGP-1N).
Studies were made of pancreastatin (PST) secretion from a human PST-producing cell line (QGP-1N) in response to various secretagogues. Cells with immunoreactivity for PST were observed in monolayer cultures of QGP-1N cells. Carbachol stimulated PST secretion and the intracellular Ca2+ mobilization concentration dependently in the range of 10(-6)-10(-4) M. The PST secretion and Ca2+ mobilization induced by carbachol were inhibited by atropine. The calcium ionophore (A23187) stimulated PST secretion. However, cholecystokinin and gastrin-releasing peptide did not stimulate either PST secretion or Ca2+ mobilization. Secretin also did not stimulate PST secretion. The glucose concentration in the culture medium had no effect on PST secretion. These results suggest that PST secretion is mainly regulated by acetylcholine through a muscarinic receptor, and that an increase in intracellular Ca2+ plays an important role in stimulus-secretion coupling in QGP-1N cells.
Acetylcholine↗
Role of calcium on interleukin-1 production by monocytes: its relevance during T cell proliferation.
T cell proliferation, in the presence of monocytes, triggered either by an anti-CD3 monoclonal antibody (mAb) or by a mitogenic pair of anti-CD2 mAbs was inhibited either by the calcium chelator EGTA or the calcium channel blocker nifedipin. Antibodies against interleukin-1 (IL-1) inhibited T cell proliferation in both mitogenic systems. However inhibition achieved by anti-IL-1 beta Ab was greater than by anti-IL-1 alpha Ab while the combination of both anti-rIL-1 alpha Ab + anti-rIL-1 beta could completely inhibit the CD3-triggered T cell proliferation. On the other hand, IL-1 production by LPS-stimulated monocytes was strongly decreased both by EGTA and nifedipin. Northern blot analysis showed that this inhibition paralleled a decrease of IL-1 alpha and beta messenger RNA (mRNA) expression only in the presence of EGTA but not in the presence of nifedipin. These results indicate that EGTA acted at the transcriptional level while nifedipin acted at a yet undefined posttranscriptional level. Thus, it is suggested that the impairment of T cell proliferation by calcium inhibitors could result not only from an effect on Ca2+ influx in T cells but also from interfering with the function of accessory cells, such as the production of IL-1.
Antibodies, Monoclonal↗
A case of transient elevation of the serum carcinoembryonic antigen and associated with severe malnutrition and low T3, T4 syndrome.
A patient with a transient elevation of the serum carcinoembryonic antigen (CEA) associated with a benign disease was reported. The elevation of CEA was noted in the patient with low T3, T4 syndrome associated with malnutrition due to malabsorption syndrome induced by post-gastrectomy and chronic pancreatitis. Mild liver dysfunction and diabetes mellitus were also noted. The CEA level decreased as T3, T4 level and malnutrition were improved by administration of a massive digestive enzyme preparation. This inverse correlation between the serum CEA and serum T3, T4 levels suggested that high levels of the serum CEA can be found in the patient with malnutrition.
Biomarkers, Tumor↗
Elevated plasma levels of pancreastatin (PST) in patients with non-insulin-dependent diabetes mellitus (NIDDM).
Pancreastatin (PST) is known as the peptide which inhibits first phase of glucose-stimulated insulin secretion. Fasting plasma PST levels and responses of PST after oral glucose ingestion in patients with non-insulin-dependent diabetes mellitus (NIDDM) were studied with human PST-specific radioimmunoassay. Fasting plasma PST in NIDDM patients was not different from healthy controls, although a slightly higher level of PST was observed in patients treated with sulfonylurea among NIDDM patients. No significant increase in plasma PST was observed after a glucose ingestion in healthy controls. In contrast, plasma PST levels in NIDDM patients rose significantly after glucose ingestion. These results suggest a possible pathophysiological role for PST in NIDDM.
Administration, Oral↗
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↗
Quinolone-induced differential modification of IL-1 alpha and IL-1 beta production by LPS-stimulated human monocytes.
We previously reported that ciprofloxacin (Cip), a quinoline-derivative antibiotic, decreases the biological activity of IL-1 released by LPS-stimulated monocytes after 24 hr of culture without affecting cell-associated IL-1 activity. To analyze further the effects of Cip on LPS-induced IL-1 alpha and IL-1 beta synthesis, each species was measured in the supernatants and cell lysates of monocyte cultures over a 4-day period using IL-1 alpha and IL-1 beta-specific ELISA methods. Cip had a post-transcriptional differential effect on the production of IL-1 alpha and IL-1 beta, reducing the total amount of IL-1 beta produced by LPS-stimulated monocytes, while that of IL-1 alpha was unaffected. In addition, the production of both species was delayed. These findings explain the discrepancy between the Cip-induced alteration of extracellular IL-1 activity and the preservation of cell-associated activity. Cip is, to our knowledge, the first pharmacological agent found to have a differential effect on the synthesis of IL-1 alpha and IL-1 beta. It may form the basis for new pharmacological agents capable of selectively reducing the systemic effects of IL-1 without affecting local activity.
Blotting, Northern↗
Role of ATL-derived factor (ADF) in the normal and abnormal cellular activation: involvement of dithiol related reduction.
HTLV-I transformed T cells not only express a large number of interleukin-2 receptors (IL-2R/p55(Tac], but also produce an IL-2R/Tac inducer named ATL-derived factor (ADF). We have cloned the ADF cDNA and found that ADF production in human lymphocytes can be enhanced by cellular activators such as mitogens or phorbol esters. Recombinant ADF produced by E. coli was shown to have growth-promoting activity in combination with interleukin-2 or suboptimal mitogenic stimuli on several lymphoid cells including human PBMCs, besides the originally reported IL-2R/Tac inducing activity. Homology analysis revealed an unexpected structural relationship between ADF and dithiol-reducing enzyme, thioredoxin, which had been characterized originally in prokaryotic system. Recombinant ADF also has a reducing activity, suggesting the presence of still unknown features of ADF action in vivo. The requirement of dithiol reduction in the biological activities of ADF, together with the possible involvement of ADF production in the normal and abnormal activation of human cells are discussed.
Amino Acid Sequence↗
Adult T-cell leukemia-derived factor/thioredoxin, produced by both human T-lymphotropic virus type I- and Epstein-Barr virus-transformed lymphocytes, acts as an autocrine growth factor and synergizes with interleukin 1 and interleukin 2.
Interleukin 1 (IL-1) has been obtained from the Epstein-Barr virus-infected B-lymphoblastoid cell line 3B6 and shown to be involved in autocrine growth of 3B6 B cells. Independently, adult T-cell leukemia-derived factor (ADF) was purified from human T-lymphotropic virus I-infected leukemic T-cell line (ATL-2) and reported as an interleukin 2 (IL-2) receptor-inducing factor. We have previously reported the same molecular mass, pI, and NH2-terminal amino acid sequence for both 3B6-derived IL-1 and ADF. cDNA cloning of ADF demonstrated high homology with the prokaryotic disulfide reducing enzyme thioredoxin. We show here that ADF and 3B6-derived IL-1 are identical. By RNA blot, 3B6 and ATL-2 cells were shown to contain high levels of 0.6-kilobase mRNA corresponding to ADF. Such message was not detected in resting peripheral blood lymphocytes but could be weakly induced by lymphocyte activation. Antibodies have been raised against synthetic peptides corresponding to the NH2 terminus and the COOH terminus of ADF. Immunoblotting and sequential immunoprecipitation with these antibodies revealed the same 13-kDa protein in 3B6 and ATL-2 cells. Recombinant ADF could sustain growth of 3B6 and ATL-2 cells at low cellular concentration without fetal calf serum; ADF, thus, appears involved in their autocrine growth. Similarly, recombinant ADF could enhance growth of other B-cell lines, including the Epstein-Barr virus-negative Burkitt lymphoma line BL41 and the lymphoblastoid cell lines CRAG8, CRB95, and 1G8. Finally, recombinant ADF exhibits marked synergism with other cytokines, such as IL-1 and IL-2, allowing virally infected lymphocytes to respond to suboptimal amounts of a variety of growth factors.
B-Lymphocytes↗
Structure and regulation of the blast-2/CD23 antigen in epithelial cells from nasopharyngeal carcinoma.
Undifferentiated nasopharyngeal carcinoma (NPC) is tightly associated with the Epstein-Barr virus (EBV) and very heavily infiltrated with T lymphocytes. We demonstrated recently that NPC epithelial cells produce immuno-regulatory molecules, including the Blast-2/CD23 antigen, which is induced in B lymphocytes upon infection by EBV. We demonstrate here that CD23 expression is a non-constant but highly specific feature of epithelial cells from NPC. The C15 and C17 NPC tumor cells express mainly the b form of CD23, which is known to be non-lineage-specific and IL-4-inducible. C17 cells were found also to weakly express the a form of CD23, which has been described as B cell-specific. In addition, several factors potentially released in vivo by tumor infiltrating lymphocytes (TILs) are able to regulate CD23 expression in NPC cells. In particular, we found that IL-4 was a potent inducer of CD23 expression in C15 cells, as shown at both the protein and the mRNA levels. These results, together with the already reported expression of class II MHC antigens and the release of IL-1 by NPC cells, suggest that the interactions between TILs and malignant cells are a key factor in NPC pathogenesis and development.
Animals↗