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Biomedical subjects

N Iwamoto

Publications and source records attributed to N Iwamoto.

At least 73 records · Page 4Linked to original sources
PubMed1994

Persistence of affected T lymphocytes in long-term clinical remission in paroxysmal nocturnal hemoglobinuria.

Long-term clinical remission of more than 10 years is rarely seen in paroxysmal nocturnal hemoglobinuria (PNH). Affected blood cells in PNH lack glycosylphosphatidylinositol (GPI)-anchored membrane proteins such as decay-accelerating factor (DAF) and CD59. We performed a flow cytometric analysis of circulating blood cells obtained from two patients with PNH who had been in clinical remission for more than 10 and 25 years, respectively. Affected cells with the PNH phenotype were demonstrated only among T-lymphocytes. Persistent affected T cells were negative for the CD52 protein only, this protein being a GPI-anchored lymphocyte marker without complement regulatory activity. The persistence of the affected T cells may be explained either by an inherently long life span after the disappearance of the PNH stem cell or by insidious production at a subclinical level by affected stem cell. In either event, detection of affected T cells, especially CD52-negative T cells, may be useful for the evaluation of long-term clinical remission in PNH.

Adrenal Cortex Hormones↗
PubMed1994

Demonstration of CRP immunoreactivity in brains of Alzheimer's disease: immunohistochemical study using formic acid pretreatment of tissue sections.

C-reactive protein (CRP) is a well-known serum protein which increases during inflammation and deposits in damaged tissues. To establish whether CRP appears in brain of Alzheimer's disease (AD), we immunohistochemically investigated tissue sections which were pretreated with formic acid. Positive immunostaining by anti-CRP antibodies was clearly recognized in senile plaques (SP) in the pretreated tissue sections, with very weak immunostaining in non-treated sections. These findings may suggest that the formation process of SP includes an acute-phase inflammatory state.

Aged↗
PubMed1994

Interleukin-2-dependent T-cell lines established from paroxysmal nocturnal hemoglobinuria patients.

Peripheral blood T lymphocytes obtained from two patients with paroxysmal nocturnal hemoglobinuria (PNH) were immortalized with human T-lymphotropic virus type 1 (HTLV-1). These cells showed interleukin-2 (IL-2)-dependent cell growth in culture. Cell surface analysis showed that they had the phenotype of a helper/inducer T subset that was positive for CD2, CD3, and CD4, but negative for CD8, similar to adult T-cell leukemia cells induced by HTLV-1. These cell lines lacked glycosylphosphatidylinositol (GPI)-anchored proteins, CDw52, CD55 (decay-accelerating factor; DAF), and CD59 on the cell surface, whereas intracellular DAF protein was detected. These T-subset cell lines with a PNH phenotype did not synthesize GPI anchor, whereas a control cell line, similarly prepared from the T cells of a healthy volunteer, produced the anchor. The control cells expressed CDw52, DAF, and CD59 on the cell surface and showed the phenotype of a helper/inducer subset. Southern blot analysis confirmed the clonality of each cell line. These CD4+ T-cell lines with a PNH phenotype and a subset-matched control counterpart could be a useful model for PNH investigation.

Antigens, CD↗
PubMed1994

Amyloid-P-component-like immunoreactivity in beta/A4-immunoreactive deposits in Alzheimer-type dementia brains.

An immunohistochemical study using the mirror-image technique was performed in order to establish whether amyloid P component is involved in the mechanism of deposition of amyloid fibrils in senile plaques (SPs) in Alzheimer-type dementia (ATD). Ninety percent of beta/A4 protein-immunoreactive SPs were also stained by the anti-amyloid P component immunohistochemistry, and this applied to all of the diffuse, primitive and classical types of beta/A4 deposits. These findings may suggest an involvement of amyloid P component in the formation of amyloid fibrils in senile plaques in ATD brains.

Alzheimer Disease↗
PubMed1994

A new method of purification and sensitive bioassay of platelet-activating factor (PAF) in human whole blood.

There is no satisfactory assay procedure of PAF in human whole blood in terms of sensitivity, reproducibility and simplicity. This is due to coexisting lipids from plasma and cellular membranes which inhibit measurement of PAF in various assay procedures, including bioassay. In the present study, an attempt was made to eliminate these interfering lipid inhibitors from blood samples. Lipids in human whole blood were extracted according to the method of Bligh & Dyer and the organic layer was dried under a stream of nitrogen. Then, the dried organic layer was dissolved in diethyl-ether and the solution was kept at -20 degrees C which was then centrifuged. The resulting supernatant was then applied to an anion-exchange column and the PAF fraction was obtained by step-wise gradient elution. The fraction was further purified by normal phase HPLC. Then PAF in the final sample was determined by sensitive bioassay using rabbit platelets containing fibrinogen and epinephrine. The recovery rate of PAF throughout this procedure was constant and satisfactory (37.4 +/- 9.7%), which was confirmed using [3H]-PAF. The lower limit of the present assay was estimated to be 5pg in 1 ml of blood and it was sensitive enough to detect PAF in blood samples from healthy volunteers and patients with sepsis or liver cirrhosis. Furthermore, attempts were made to compare the sensitivity and the recovery of our method with these of a commercially available radioimmunoassay (RIA) kit for PAF. However, it was not possible to detect any amount of authentic PAF added to whole blood.

Animals↗
PubMed1994

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↗
PubMed1994

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↗
PubMed1994

Effects of amino acid variations in recombinant Der fII on its human IgE and mouse IgG recognition.

Amino acid sequencing of the major mite allergen Der fII purified from mite body extract revealed that it is a mixture of at least two variants. Substitutions were found only at positions in which amino acid variations were predicted from the nucleotide sequences of three cloned cDNAs. When cDNAs corresponding to the three variants were expressed in Escherichia coli, Der fII proteins were produced as inclusion bodies. Denaturation and renaturation with urea converted recombinant Der fII into a protein with three intramolecular disulfide bonds (Cys8-Cys119, Cys21-Cys27, and Cys73-Cys78), which were identical to those previously identified in native Der fII. All the variants, including native Der fII, were equally recognized by human IgE antibodies from 14 different sera of mite-allergic patients. These results suggested that recombinant Der fII proteins assumed a conformation identical to that of the native Der fII and that all the Der fII variants acted as allergens. This result also suggested that IgE antibody binds to the region where there were no amino acid variations. The binding ability of the monoclonal antibody (mAb) 18G8 for the variant clones 1, 2, and 11 Der fII was almost the same. However, mAb 15E11 bound to clone 1 Der fII more efficiently than to clones 2 and 11, whereas mAb 13A4 recognized clone 2 Der fII as the most preferable antigen. This suggested that these antibodies recognized the region of amino acid variations. The stability of Der fII variants was analyzed by measuring their IgE antibody binding activity after heating, freezing, or acid treatment, and was analyzed by resistance to trypsin digestion.(ABSTRACT TRUNCATED AT 250 WORDS)

Allergens↗
PubMed1993

Selective loss of calbindin D28K-immunoreactive neurons in the cortical layer II in brains of Alzheimer's disease: a morphometric study.

To investigate the relationship between neuronal death and intracellular calcium homeostasis in brains from patients with Alzheimer's disease (AD), we quantitatively analyzed morphological changes of calbindin-immunoreactive neurons. Neuronal counts were made in the autopsy brains from 6 control and 6 AD patients. Calbindin-immunoreactive neurons were mainly distributed in cortical layer II and were selectively lost in the AD brains. Further, the number of calbindin-immunoreactive neurons showed a negative correlation with age in the control group. These findings strongly suggest that age-related reduction of calbindin-immunoreactive neurons may be exaggerated in AD brains and change in calcium homeostasis may be involved in the pathogenesis of AD.

Age Factors↗
PubMed1993

Impaired glycosylation of glycosylphosphatidylinositol-anchor synthesis in paroxysmal nocturnal hemoglobinuria leucocytes.

Metabolic labeling with [3H]sugars in vivo or [3H]sugar nucleotides in vitro of glycosylphosphatidylinositol (GPI)-anchor precursors in peripheral blood granulocytes and cultured T lymphocytes of paroxysmal nocturnal hemoglobinuria (PNH) patients showed a synthetic defect in the GPI-anchor. Among the GPI-anchor precursors, phosphatidylinositol (PI) was normally synthesized, while the synthesis of glucosaminylphosphatidylinositol (GlcN-PI) and subsequent mannosylation of GlcN-PI were inhibited in affected cells. The defect in the GPI-anchor synthesis in PNH is thus attributed to interrupted glycosylation at plural sites in the synthesis of the common carbohydrate structure of the anchor.

Carbohydrate Sequence↗
PubMed1993

Morphological evaluation of amyloid-laden arteries in leptomeninges, cortices and subcortices in cerebral amyloid angiopathy with subcortical hemorrhage.

To investigate the relationship between cerebral amyloid angiopathy and subcortical (lobar) hemorrhage, we examined the severity of amyloid deposition in the leptomeningeal, cortical and subcortical arteries in 28 autopsied elderly patients with cerebral amyloid angiopathy with subcortical hemorrhage, deep cerebral hemorrhage or without hemorrhage. The severity was evaluated in terms of the frequency of amyloid-laden arteries and the degree of amyloid deposition within the arteries. The frequency of amyloid-laden arteries, especially among arteries over 200 microns in diameter, was higher in subcortical hemorrhage group than in the deep hemorrhage group and the non-hemorrhage group, and when the degree of amyloid deposition in the arteries was divided into four grades (none, mild, moderate or severe), the severity was higher in the subcortical hemorrhage group than in the deep cerebral hemorrhage group and the non-hemorrhage group. These results suggest that severe cerebral amyloid angiopathy is related to non-traumatic subcortical hemorrhage in elderly persons.

Aged↗
PubMed1993

Ultrasound imaging for stereotactic evacuation of hypertension-associated intracerebral hematomas with aqua-stream and aspiration.

Stereotactic aqua-stream and aspiration (SASA) has been used for the evacuation of intracerebral hematomas. The authors have introduced ultrasound imaging (US) to monitor the evacuations of the hematoma during the surgical procedure. Hematomas were reproduced in an agar hematoma model which showed that if air collected in the hematoma cavity, it produced a strong artifact, and the hematoma could not be monitored. In the clinical trial, hematomas were visualized, and the surgical procedures were monitored in real time. The needle of the SASA and the air that collected in the hematoma cavity produced only weak artifacts, and the SASA water jet showed as a hyperechoic region on US, so that the procedure could be monitored in real time. In all cases, the average amount of evacuated hematoma exceeded 92%, as calculated from the preoperative and postoperative computed tomography images. The level of consciousness improved from a preoperative level of 1-20 (Japan Coma Scale) to 0-3 postoperatively. The addition of US monitoring to computed tomography guided stereotactic evacuation of hematomas with SASA enabled hypertension-associated intracranial hematomas to be evacuated more safely and more completely than has been achieved hitherto.

Agar↗