Biomedical subjects

F Shimizu

Publications and source records attributed to F Shimizu.

At least 19 recordsLinked to original sources

PubMed2000

Gender differences in body fat of low- and high-body-mass children: relationship with body mass index.

The primary objective of this study was to determine gender differences in total body fat mass (TBFM) and body fat distribution (subcutaneous fat mass, SFM; and internal fat mass, IFM) in a cross-sectional sample of 280 children. Measurements of the body composition of 141 boys and 139 girls, all apparently healthy and aged 3-6 years were made using bioelectrical impedance. Determinations of impedance were made using a four-terminal impedance analyzer (TP-95K; Toyo Physical, Fukuoka, Japan). Lean body mass (LBM) was calculated using a previously published equation [Goran MI, Kaskoun MC, Carpenter WH, Poehlman ET, Ravussin E, Fontvieikke A-M (1993) Estimating body composition of young children by using bioelectrical resistance. J Appl Physiol 75: 1776-1780]. SFM was calculated using a modification of the equation derived by Skerjl [Skerjl B, Brozek J, Hunt EE (1953) Subcutaneous fat and age changes in body build and body form in women. Am J Phys Anthrop 11: 577-580] and Davies [Davies PSW, Jones PRM, Norgan NG (1986) The distribution of subcutaneous and internal fat in man. Ann Hum Biol 13: 189-192]. The main modifications of the equation in the present study were the introduction of: (1) mean thickness of adipose tissue over body surface/2, and (2) skin mass. IFM was calculated as the difference between TBFM and SFM. The body mass index (BMI; kg/m2) was calculated from the formula: body mass/height2. For each gender, the subjects in the lowest and highest 25th percentiles were designated as "low body mass" and "high body mass", respectively. In the present study, no gender differences in absolute TBFM, SFM and IFM were observed in either of these groups. In contrast, gender differences in relative TBFM (%Fat) and SFM (SFM/mass) were evident in girls. However, the four subgroups were similar in terms of relative IFM (IFM/mass). The TBFM was independently related to SFM, IFM and %Fat in both genders after adjustment for BMI; however, there was no significant association of SFM with IFM after adjustment for BMI in any group. Even after adjustment for BMI, IFM was independently related to %Fat in both genders, although SFM was not independently related to %Fat in any group except low-body-mass boys. This study shows that relative TBFM and SFM are higher in high-body-mass groups and tend to be higher in girls than in boys, and that the higher %Fat in high-body-mass girls than in high-body-mass boys appears to be associated with internal adipose tissue deposits. External adipose tissue mass does not appear to be related to the higher %Fat levels in high-body-mass girls. In addition, subcutaneous fat mass appears to be higher in low-body-mass girls than in low-body-mass boys, although this observation needs confirmation using more valid measures of subcutaneous fat such as computerized tomography and magnetic resonance imaging.

Adipose Tissue↗

PubMed2000

Revascularization using the short gastric vessels of the gastric tube after subtotal esophagectomy for intrathoracic esophageal carcinoma.

BACKGROUND: Maintaining sufficient blood flow to the substitutive organ after esophagectomy is essential to decrease the risk of anastomotic leakage. STUDY DESIGN: Forty-one patients underwent subtotal esophagectomy for intrathoracic esophageal carcinoma and reconstruction using the gastric tube. Additional vascular anastomosis between the short gastric vessels and the vessels in the neck was performed in 15 patients. Tissue blood flow was measured by laser Doppler flowmetry before and after vascular anastomosis. The incidence of anastomotic leakage in the revascularization group was compared with that in the remaining 26 patients. RESULTS: Venous anastomosis was performed in 14 patients and arterial anastomosis in 9. There was a significant increase in tissue blood flow after venous anastomosis alone (mean percent increase: 36%; p < 0.01), and after arterial and venous anastomoses (mean percent increase: 108%; p < 0.01). No anastomotic leakage was observed in the revascularization group; six patients (23.1%) in the control group had leakage (p < 0.05). Patients in the revascularization group started taking a meal 10.0 +/- 0.4 days postoperatively, compared with 15.1 +/- 1.8 days in the control group (p < 0.05). CONCLUSIONS: Additional vascular anastomosis in esophageal reconstruction after subtotal esophagectomy achieved good results. This procedure can reduce the risk of anastomotic leakage and may be useful for esophageal reconstruction.

Aged↗

PubMed2000

Cloning of rat nephrin: expression in developing glomeruli and in proteinuric states.

BACKGROUND: Nephrin is identified as a product of the gene mutated in a patient with congenital nephrotic syndrome of the Finnish type. However, its precise localization and function are not yet fully clarified. METHODS: To clone the rat homologue of nephrin, polymerase chain reaction (PCR) was employed. To elucidate the localization and expression of nephrin, immunohistological analysis with a specific antirat nephrin antibody, reverse transcription-PCR, and RNase protection assay were performed. RESULTS: Amino acid sequences of rat and human nephrin are highly homologous (82.2% identity). The domain structure of nephrin is also highly conserved between rats and humans. The rat nephrin was detected only in kidney glomeruli along glomerular capillary walls, and its localization was always identical to that of the anti-slit diaphragm monoclonal antibody (mAb) 5-1-6-recognized antigen in normal matured and fetal rat glomeruli and in the glomeruli of proteinuric states. The nephrin staining pattern was clearly distinguished from that of zonula occludens-1 (ZO-1), alpha3-integrin, or podocalyxin. mRNA expression for nephrin was first detected in the fetal rat kidneys at 18.5 embryonic days. Nephrin mRNA expression decreased just after injection of mAb 5-1-6 (47.4%) or puromycin aminonucleoside (51.2%), and the staining pattern of nephrin shifted from a linear to a granular pattern in both proteinuric states. CONCLUSIONS: Nephrin is localized in slit diaphragm in the matured glomeruli and is identical with mAb 5-1-6 antigen. Nephrin is involved in the development of proteinuria not only in mAb 5-1-6 nephropathy, but also in puromycin aminonucleoside nephropathy.

Amino Acid Sequence↗

PubMed2000

An anti-CD5 monoclonal antibody ameliorates proteinuria and glomerular lesions in rat mesangioproliferative glomerulonephritis.

BACKGROUND: Increased numbers of lymphocytes have been identified in biopsy specimens of human mesangial proliferative glomerulonephritis (GN). However, the causal relationship between infiltrating T lymphocytes and mesangial changes in mesangial proliferative GN has not been previously evaluated. In this study, we elucidated the role of lymphocytes in the development of mesangial proliferative GN. METHOD: Immunohistological and flow cytometric analyses as well as a reverse transcription-polymerase chain reaction (RT-PCR) studies were performed in monoclonal antibody (mAb) 1-22-3-induced Thy 1.1 GN. To elucidate the role of these lymphocytes, depletion studies were carried out using anti-CD8 mAb (OX-8), which depletes both CD8+ T lymphocytes and natural killer (NK) cells and anti-CD5 mAb (OX-19), which depletes both CD4+ and CD8+ T lymphocytes. RESULTS: Immunofluorescence (IF) studies revealed that NK cells and CD4+ T lymphocytes were recruited into glomeruli. Glomerular mRNA expression for interferon-gamma, interleukin-2 (IL-2), IL-10, and perforin increased after induction of GN. Increased expressions of several chemokines, which have the potential to attract lymphocytes, were also detected. Anti-CD8 mAb treatment completely prevented the recruitment of NK cells; however, it had no protective effect on proteinuria and mesangial injury. By contrast, anti-CD5 mAb treatment suppressed the recruitment of CD4+ T lymphocytes into glomeruli and reduced proteinuria (60.4 +/- 25.7 vs. 120.0 +/- 32.3 mg/day, P < 0.05) and mesangial changes evaluated by total number of cells in glomeruli (63.2 +/- 6.0 vs. 81.4 +/- 5.9, P < 0.01) and alpha-smooth muscle actin staining score (1.4 +/- 0.2 vs. 2.2 +/- 0. 4, cf2eth P < 0.01) on day 14 after induction of GN. mRNA expression for IL-2 was significantly reduced by OX-19 treatment. CONCLUSION: T lymphocytes participate in the development of mesangial proliferative GN.

Animals↗

PubMed2000

Severe proteinuria, sustained for 6 months, induces tubular epithelial cell injury and cell infiltration in rats but not progressive interstitial fibrosis.

BACKGROUND: Sustained proteinuria is reported to be very harmful to the tubulointerstitium, leading to severe interstitial injury. However, it remains unclear whether sustained proteinuria itself is responsible for severe interstitial injury because, in the previously reported models, the development of factors other than proteinuria in tubulointerstitial lesions could not be excluded completely. METHODS: After treatment to induce immune tolerance to mouse immunoglobulin, 20 rats were injected with anti-rat slit diaphragm monoclonal antibody (mAb) 5-1-6 twice a week for 6 months and were then sacrificed. RESULTS: mAb 5-1-6 induced massive proteinuria in 11 rats. In nine rats with mild proteinuria, no histological alteration could be detected with light microscopy and immunofluorescence. In nephrotic rats, light microscopy showed minor glomerular abnormalities, with interstitial oedema, tubular epithelial cell degeneration and interstitial cell infiltration. Immunofluorescence revealed increased expression of vimentin and an increased number of OX1-, OX19- and ED1-positive cells. However, we could not detect any accumulation of type I and IV collagen or laminin in the tubulointerstitium. RT-PCR showed that the expression of mRNA for type I collagen was not increased, compared with that in control rats. CONCLUSIONS: We succeeded in developing a model of persistent nephrosis without severe glomerular abnormalities, nephrectomy or other manoeuvres known to induce disturbed haemodynamics, using an agent without tubulointerstitial toxicity, and considered it to be suitable for investigating the direct toxicity of proteinuria. In this model, isolated massive proteinuria induced interstitial injury. However, the degree of injury was suggested to be much less than that observed in other previously developed models.

Animals↗

PubMed2000

Simultaneous separation of lysophospholipids from the total lipid fraction of crude biological samples using two-dimensional thin-layer chromatography.

A novel solvent system for two-dimensional thin-layer chromatography was shown to simultaneously separate lysophospholipid standards, including lysophosphatidylcholine, lysophosphatidylethanolamine, lysophosphatidylserine, lysophosphatidylinositol, lysophosphatidylglycerol, lysophosphatidic acid, lysosphingomyelin (sphingosylphosphorylcholine), and sphingosine-1-phosphate from diradylphospholipids, glycosphingolipids, and neutral lipids. Lysophospholipids contained in the total lipid fraction of activated platelets were also well separated by the same system. The present system is a useful tool for the metabolic and structural analysis of lysophospholipids in biological samples.

Animals↗

PubMed1999

Use of the Harmonic Scalpel in open abdominoperineal surgery for rectal carcinoma.

We describe a technique of open abdominoperineal resection with the use of the Harmonic Scalpel in seven patients. Using this instrument we dissected all pelvic vessels, including the middle hemorrhoidal artery, with no subsequent bleeding. In addition, we divided the levator ani muscles completely in the abdominal procedure alone.

Abdomen↗

PubMed1999

Additional microvascular anastomosis in reconstruction after total esophagectomy for cervical esophageal carcinoma.

BACKGROUND: Maintaining sufficient blood flow to the substitute organ after total esophagectomy is essential for decreasing the risk of anastomotic leakage. Additional venous, or arterial and venous, anastomoses between the vessels of the gastric tube and the vessels in the neck after total esophagectomy are described for 11 patients with cervical esophageal carcinoma. METHODS: The tissue blood flow was measured by laser Doppler flowmetry before and after anastomosis. Venous anastomosis was performed for all 11 patients, and arterial anastomosis was added for 7 patients. RESULTS: A significant increase in tissue blood flow was observed after venous anastomosis alone (mean, 19%; P < 0.05) and after arterial and venous anastomoses (mean 43%; P < 0.01). There was no anastomotic leakage or hospital death. CONCLUSIONS: This procedure may reduce the risk of anastomotic leakage especially in the case of pharyngogastrostomy following total esophagectomy.

Anastomosis, Surgical↗

PubMed1999

Ultrastructural localization of megalin in the rat cochlear duct.

Megalin is an endocytic receptor predominantly expressed in the kidney proximal tubule cells. In the present study, localization of megalin was examined using a post-embedding immunogold method in the rat cochlear duct. Marginal cells of the stria vascularis were labeled on the apical surface, but not on the basolateral surface. This localization pattern resembles kidney proximal tubule cells. Immunoreactivity was also detected on various other cells, including epithelial cells of the spiral prominence and epithelial cells of Reissner's membrane. In contrast, virtually no gold particles were seen on intermediate cells and basal cells of the stria vascularis, mesothelial cells of Reissner's membrane or fibrocytes in the lateral wall. Also unlabeled were cells in the tympanic wall of the cochlear duct, including sensory cells and supporting cells of the organ of Corti. The present findings show the involvement of megalin in endocytosis of marginal cells and are suggestive of different uptake mechanisms for aminoglycosides in the kidney proximal tubule cells and in the cochlear sensory cells.

Animals↗

PubMed1999

Blocking angiotensin II ameliorates proteinuria and glomerular lesions in progressive mesangioproliferative glomerulonephritis.

BACKGROUND: The renin-angiotensin system is thought to be involved in the progression of glomerulonephritis (GN) into end-stage renal failure (ESRF) because of the observed renoprotective effects of angiotensin-converting enzyme inhibitors (ACEIs). However, ACEIs have pharmacological effects other than ACE inhibition that may help lower blood pressure and preserve glomerular structure. We previously reported a new animal model of progressive glomerulosclerosis induced by a single intravenous injection of an anti-Thy-1 monoclonal antibody, MoAb 1-22-3, in uninephrectomized rats. Using this new model of progressive GN, we examined the hypothesis that ACEIs prevent the progression to ESRF by modulating the effects of angiotensin II (Ang II) on the production of transforming growth factor-beta (TGF-beta) and extracellular matrix components. METHODS: We studied the effect of an ACEI (cilazapril) and an Ang II type 1 receptor antagonist (candesartan) on the clinical features and morphological lesions in the rat model previously reported. After 10 weeks of treatment with equihypotensive doses of cilazapril, cilazapril plus Hoe 140 (a bradykinin receptor B2 antagonist), candesartan, and hydralazine, we examined systolic blood pressure, urinary protein excretion, creatinine clearance, the glomerulosclerosis index, and the tubulointerstitial lesion index. We performed a semiquantitative evaluation of glomerular immunostaining for TGF-beta and collagen types I and III by immunofluorescence study and of these cortical mRNA levels by Northern blot analysis. RESULTS: Untreated rats developed massive proteinuria, renal dysfunction, and severe glomerular and tubulointerstitial injury, whereas uninephrectomized control rats did not. There was a significant increase in the levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III in untreated rats. Cilazapril and candesartan prevented massive proteinuria, increased creatinine clearance, and ameliorated glomerular and tubulointerstitial injury. These drugs also reduced levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III. Hoe 140 failed to blunt the renoprotective effect of cilazapril. Hydralazine did not exhibit a renoprotective effect. CONCLUSION: These results indicate that ACEIs prevent the progression to ESRF by modulating the effects of Ang II via Ang II type 1 receptor on the production of TGF-beta and collagen types I and III, as well as on intrarenal hemodynamics, but not by either increasing bradykinin activity or reducing blood pressure in this rat model of mesangial proliferative GN.

Angiotensin II↗

PubMed1999

Role of mesangial cell damage in progressive renal disease.

Mesangial cell proliferation and matrix accumulation are considered to contribute to the development of glomerulosclerosis. To investigate the pathological role played by mesangial cell damage in progressive renal disease appropriate progressive models initiated by a mesangial cell injury should be developed. Monoclonal antibody (mAb) 1-22-3 (IgG3) recognizes a critical epitope of the Thy-1.1 molecule on the mesangial cell surface, binding of which induces more severe mesangial cell injury than in the case of OX-7, a commercially obtainable anti-Thy-1.1 mAb. The mAb 1-22-3 has enabled us to develop irreversible models of renal damage induced by two consecutive injections, by a single injection into unilaterally nephrectomized rats, or by a single simultaneous injection with another mAb, in addition to the corresponding reversible model. Detailed examinations using the combination of both types of models, all of which are initiated by an immune mechanism directed against the identical epitope on the Thy-1.1 molecule, are expected to provide new insights into mechanisms of irreversible renal injury initiated by mesangial cell damage and also to develop novel and rational therapeutic approaches to progressive, primarily mesangial diseases.

Animals↗

PubMed1999

Expression of the molecule detectable by anti-propolypeptide of von Willebrand factor antibody in rat mesangial cells in anti-Thy 1.1 mAb 1-22-3 induced glomerulonephritis: A marker of injured mesangial cells.

We have previously reported that propolypeptide of von Willebrand factor (pp-vWF) binds to collagen with an affinity comparable to that of mature vWF, inhibits collagen-induced platelet aggregation, is cross-linked with laminin, and also serves as a ligand for very-late antigen 4 integrin. These observations from in vitro experiments suggest that pp-vWF is incorporated in the extracellular matrix and affects the cell-matrix interaction and that pp-vWF functions in leukocyte recruitment to inflammatory and vascular injury sites. We, therefore, hypothesize that pp-vWF might be involved in the induction and/or progression of mesangial proliferative glomerulonephritis. To test this hypothesis, we examined the kinetics of the immunostaining of the molecule detectable by an affinity-purified anti-pp-vWF antibody in rat glomeruli in monoclonal antibody 1-22-3 induced glomerulonephritis. Immunostaining by pp-vWF antibody was observed in the nuclear rim of mesangial cells in monoclonal antibody 1-22-3 induced glomerulonephritis. Positive staining first appeared on day 10 after monoclonal antibody injection, when mesangial cell proliferation and mesangial matrix expansion had already begun. Staining was still detected on day 56, when morphologic alterations observed by light microscopy had been normalized. The pp-vWF antibody recognized molecule appeared later than alpha-smooth muscle actin or collagen type I. Positive staining was not detected in cultured mesangial cells. It should be noted that the positive staining by pp-vWF antibody in mesangial cells was still detected in previously injured glomeruli that have almost recovered normal morphology. These observations indicate that positive staining by pp-vWF antibody could be a very useful marker for identifying a past episode of injury in mesangial cells.

Animals↗

PubMed1999

Nephritogenic mAb 5-1-6 is directed at the extracellular domain of rat nephrin.

mAb 5-1-6 identifies an antigen on rat podocyte slit-diaphragms and induces severe proteinuria when injected into rats. Nephrin, an Ig-like transmembrane protein that is mutated in congenital nephrotic syndrome of the Finnish type, has been localized to the slit-diaphragm on human podocytes. Here we document that the mAb 5-1-6 antigen is rat nephrin. After incubation of rat glomeruli with this mAb, the antibody/antigen complex was chemically cross-linked, extracted, and immunoprecipitated, prior to Western analysis. By mass spectrometry and 2D gel electrophoresis, we identified several peptides with complete identity to human nephrin. In addition, the 185-kDa protein immunoprecipitated by mAb 5-1-6 from rat glomerular extracts reacts with a rabbit anti-mouse nephrin antibody. Finally, nephrin and the mAb 5-1-6 antigen have identical glomerular localization patterns on immunofluorescence of rat kidney. These results demonstrate that the nephritogenic mAb 5-1-6 identifies the extracellular domain of nephrin, thereby documenting the importance of the slit-diaphragm and its component, nephrin, in the regulation of glomerular permselectivity.

Amino Acid Sequence↗

PubMed1998

Altered anionic GBM components in monoclonal antibody against slit diaphragm-injected proteinuric rats.

BACKGROUND: We previously reported that monoclonal antibody (mAb) 5-1-6 bound to renal filtration slits induces massive proteinuria without causing ultrastructural changes in the glomerulus. This study evaluated the underlying mechanisms of the increase in glomerular permeability. METHODS: The distribution of endogenous albumin and IgG in the glomerular basement membrane (GBM) was studied in in situ drip-fixed glomeruli of Munich-Wistar rats by use of immunogold immunocytochemistry in the presence and absence of mAb 5-1-6. The density of foot process glycocalyx components was estimated by labeling with Limax fluvus lectin- or Helix pomatia lectin-gold complexes. Anionic sites in the GBM were examined by labeling with cationic gold at pH 2.0 or 7.4. Carboxyl groups, which also furnish an anionic charge to the GBM, were examined by specific biotinylation and colloidal gold probe methods. In addition, the infusion-staining of anionic sites was performed by use of ruthenium red in both Munich-Wistar and Wistar rats. RESULTS: The urinary excretion of albumin and IgG was increased markedly in the treated rats, indicating a non-selective barrier defect. In the control rats, albumin and IgG molecules were mainly located along the inner half of the GBM, and to a lesser degree in the lamina rara externa. In the treated rats, the albumin and IgG moieties were more equally distributed throughout the width of the GBM. Newly appearing, small dense peaks at the outer side of the GBM were evident, indicating a barrier function of outer zone of the GBM and/or epithelial cell layer. No intergroup differences in the density of lectin binding sites on foot processes were seen. The reduction in the number of ruthenium red-positive anionic sites and cationic gold (pH 2. 0)-labeled anionic sites in the lamina rara externa was significant in the treated rats at day 3, indicating a possible alteration of charged proteoglycan in the lamina rara externa. No such changes were seen with cationic gold (pH 7.4)-labeled anionic sites in the GBM. The density of labeled carboxyl groups was significantly reduced in the treated rats relative to the controls. CONCLUSIONS: These results show that the injection of mAb 5-1-6 induced a perturbation of the charge- and probably the size-selective glomerular filtration barrier. The observed reduction in the levels of various negatively charged substances resulted in massive proteinuria, implying that alteration of target antigens can affect the integrity of the GBM constituents maintaining the normal barrier function.

Albuminuria↗

PubMed1998

Comparative nephritogenicity of two monoclonal antibodies that recognize different epitopes of rat Thy-1.1 molecule.

The pathophysiological role of the Thy-1.1 molecule expressed on rat mesangial cells with regard to mesangial cell dysfunction and injury remains unknown. The mechanism of Thy-1.1-associated injury has now been investigated with two monoclonal antibodies, 1-22-3 and OX7, that recognize different epitopes of Thy-1.1. Mesangiolysis and mesangial cell proliferation were more marked in rats injected with 1-22-3 than in those treated with OX7. Immunostaining for rat complement component C3 and also C9 was similar in the kidneys of rats 1 h after injection of either antibody. Alpha smooth muscle actin was first detected 3 days after injection of 1-22-3 and peaked on day 5; type I collagen staining showed a mesangial pattern on days 5 and 10. The staining for alpha smooth muscle actin and type I collagen was less intense in OX7-treated rats than in the 1-22-3-injected rats. The amounts of mRNAs encoding collagen types I and III peaked 5 days after injection of 1-22-3 and 10 days after injection of OX7. Rats injected with 1-22-3 developed proteinuria that was already marked on day 1 and peaked at 150 mg/day on day 3, whereas OX7 induced a low grade of proteinuria with large interindividual variability on day 3. Immunostaining for rat C3 in the normal rat kidneys, incubated in vitro with 1-22-3 or OX7 followed by incubation with normal rat fresh serum as a complement source, as well as the levels of serum complement activity, CH50, 30 min after injection of 1-22-3 or OX7 were similar, suggesting that the difference in the nephritogenicity of these two antibodies is not attributable to a difference in their complement-fixing activities, but rather may result from the difference in epitope specificities. The epitope recognized by 1-22-3 thus appears to be important in the initiation and progression of antibody-induced nephritis.

Animals↗

PubMed1998

Immunohistochemical identification of type B intercalated cells in the rat kidney by a monoclonal antibody.

We recently produced monoclonal antibodies using macrophagic cells derived from cultured rat glomeruli as the antigen. One of the antibodies, named OS-3, was found to detect a cell population scattered in collecting ducts of the rat kidney as well as macrophages in various tissues. The present study deals with the cellular and subcellular localization of immunoreactivities with OS-3 in the kidney and other organs of rats. Double immunostaining using OS-3 and an anti-serum against either calbindin or epidermal cytokeratin showed that OS-3-immunoreactive cells exist exclusively in both the connecting segment and cortical collecting duct, and differ from calbindin- or cytokeratin-positive epithelial cells. Ultrastructurally, OS-3-immunoreactive cells appeared spherical in shape with few cytoplasmic microprojections on the narrow apical surface. Their relatively dark cytoplasm contained numerous mitochondria and a developed tubulo-vesicular system. The intense immunoreactivity was selectively localized in the basolateral membrane exhibiting shallow but complicated infoldings. Distribution and ultrastructural properties of the OS-3-immunoreactive cells showed that they were type B intercalated cells, which are engaged in the regulation of the acid-base balance mainly by secreting HCO3-. Another positive staining with OS-3 was found in the macula densa and some epithelial cells of Bowman's capsule, the former monitoring Cl- concentrations in the urine. Immunoblotting of extracts from the rat kidney demonstrated a protein band immunoreactive to OS-3 at a molecular weight of 43 kDa. Aside from the kidney, a specific and intense immunoreactivity with OS-3 was also found in the epithelial cells of the pancreatic excretory duct and in the secretory cells of the salivary, pyloric and duodenal glands, all of which are HCO3- -secreting cells. These immunohistochemical findings imply that OS-3 is useful for the detection of type B intercalated cells and recognizes a functional molecule involved in the production/secretion of HCO3- or transport of Cl-.

Animals↗

PubMed1998

[Chronic pancreatitis, acute pancreatitis].

MRCP has been recognized as a safe and noninvasive diagnostic method. In the present study we evaluated the usefulness of MRCP in diagnosis of chronic and acute pancreatitis. Two-dimensional fast asymmetric spin-echo (FASE) MRCP was performed in 40 patients with chronic pancreatitis and 13 with acute pancreatitis. In 29 patients (72.5%) with chronic pancreatitis and 9 (66.7%) with acute pancreatitis, main pancreatic duct (MPD) was visualized entirely. MRCP could demonstrate the characteristic findings of chronic pancreatitis such as dilatation and irregularity of MPD in most cases. In acute pancreatitis, MRCP indicated that MPD was normal in diameter, but irregular in configuration compared with that of the control group. MRCP may facilitate the diagnosis of chronic and acute pancreatitis.

Acute Disease↗

PubMed1997

Isolation and expression of a cDNA for human brain fatty acid-binding protein (B-FABP).

We have isolated and sequenced a novel 754-bp human fetal brain cDNA encoding a fatty acid-binding protein (FABP). The cDNA contains an open reading frame of 396 nucleotides (132 amino acids). Northern analysis revealed small amounts of a 1.2-kb transcript in adult human brain and a shorter transcript in skeletal muscle, but no message was detected in other tissues examined. On the other hand, it was abundantly expressed in fetal brain but not in fetal lung, liver or kidney tissues. The elevated level of transcript at immature stages and its subsequent decline In adult brain indicate that the encoded protein may be essential for development of the human brain.

Adult↗