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Biomedical subjects

Y Kuroki

Publications and source records attributed to Y Kuroki.

At least 145 records · Page 8Linked to original sources
PubMed1995

Ca(2+)-dependent binding of annexin IV to surfactant protein A and lamellar bodies in alveolar type II cells.

Surfactant protein A (SP-A), a lung-specific glycoprotein in pulmonary surfactant, is synthesized and secreted from the alveolar type II cells. It has been shown that SP-A is a Ca(2+)-binding protein with several binding sites and that the high-affinity site(s) is located in the C-terminal region of SP-A. In the present study we isolated the proteins from bovine lung soluble fraction that bind to SP-A in a Ca(2+)-dependent manner using DEAE-Sephacel and SP-A-conjugated Sepharose 4B. At least three different protein bands with molecular masses of 24.5, 32, and 33 kDa were observed on SDS/PAGE. The main protein, with molecular mass of 32 kDa, was identified as annexin IV by the partial-amino-acid-sequence analyses and an immunoblot analysis with anti-(annexin IV) antiserum. We also found from the immunoblot analysis that the cytosolic fraction of isolated rat alveolar type II cells contains annexin IV. In addition, when rat lung cytosol was loaded on to the lung lamellar body-conjugated Sepharose 4B in the presence of Ca2+, two proteins, with molecular masses of 32 and 60 kDa on SDS/PAGE respectively, were eluted with EGTA. The 32 kDa protein was shown to be annexin IV by an immunoblot analysis with the antiserum against annexin IV. The lung annexin IV augmented the Ca(2+)-induced aggregation of the lung lamellar bodies from rats. However, the augmentation of aggregation of the lung lamellar bodies by annexin IV was attenuated when the lamellar bodies were preincubated with polyclonal anti-SP-A antibodies. SP-A bound to annexin IV under conditions where contaminated lipid was removed. These results suggest that SP-A bound to annexin IV based on protein-protein interaction, though both proteins are phospholipid-binding proteins. All these findings suggest that the interaction between SP-A and annexin IV may have some role in alveolar type II cells.

Amino Acid Sequence↗
PubMed1995

Hypoglycemia in Coffin-Siris syndrome.

We describe a further patient with the Coffin-Siris syndrome who presented at 4 months with recurrent hypoglycemia attacks. Detailed examination was undertaken at 7 months but the cause of hypoglycemia was not detected. Hypoglycemia seems to be a previously undescribed finding in the Coffin-Siris syndrome.

Abnormalities, Multiple↗
PubMed1995

Epitope mapping for monoclonal antibody against human surfactant protein A (SP-A) that alters receptor binding of SP-A and the SP-A-dependent regulation of phospholipid secretion by alveolar type II cells.

Surfactant protein A (SP-A) is a lung-specific glycoprotein in pulmonary surfactant and has a collagen like sequence on its N-terminal. SP-A has been shown to function as an inhibitor of phospholipid secretion by primary culture of alveolar type II cells via cell surface receptor(s) for SP-A. In a previous report, we showed that the C-terminal non-collagen like domain of human SP-A possessed the biological activities, and that a monoclonal antibody against human SP-A, PE10, abolished the biological activity of SP-A (Murata et al. (1993) Biochem. J. 291, 71-76). In the present study, we investigated an epitope of SP-A for PE10. Western blot analysis with fragmented peptides of human SP-A generated by both lysyl endopeptidase and BrCN showed that PE10 reacted with the peptide corresponding with Glu202 to the C-terminal but that it lacked the ability to bind to the peptide corresponding with Tyr208 to the C-terminal. The antibodies against a synthetic peptide (P1) corresponding with Glu202 to Asn217 of human SP-A inhibited the binding of PE10 to SP-A, suggesting that a similar site was recognized by both PE10 and anti-P1 antibodies. Anti-P1 antibodies as well as PE10 suppressed the biological activity of SP-A. A direct interaction between P1 and rat lung membranes, or between P1 and alveolar type II cell membranes was shown from the measurement of the fluorescence emission spectra of dansyl-labeled P1. These results suggest that an area contiguous to or near the region from Glu202 to Met207 of SP-A is important for expressing the biological activities.

Amino Acid Sequence↗
PubMed1995

A novel missense mutation (C522Y) is present in the beta-hexosaminidase beta-subunit gene of a Japanese patient with infantile Sandhoff disease.

A novel missense mutation (1565G-->A) was identified in the cDNA and genomic DNA coding for the beta-hexosaminidase beta-subunit of a Japanese patient with infantile Sandhoff disease. The patient was homozygous for this mutation, which should result in a cysteine-to-tyrosine substitution at codon 522. Computer-assisted analysis of this amino acid substitution predicted alteration in the secondary structure in the region of a highly conserved sequence. An immunofluorescence study revealed the accumulation of GM2 ganglioside in cultured fibroblasts from the patient with this mutation.

Base Sequence↗
PubMed1995

Rieger syndrome with de novo reciprocal translocation t(1;4) (q23.1;q25).

We report on a boy with Rieger syndrome, who had an apparently balanced reciprocal translocation between chromosomes 1 and 4. The clinical manifestations of this patient were characterized by irregular shaped pupils with a prominent Schwalbe line and an umbilical hernia. On cytogenetic studies, he was found to have a de novo reciprocal translocation 46,XY,t(1;4) (q23.1;q25), without visible deletion. His parents had normal chromosomes. A review of both cytogenetic and genetic linkage analyses with Rieger syndrome showed that chromosome 4q was involved. This and other previous reports suggested that the gene for Rieger syndrome is mapped to the 4q25-->4q26 segment adjoining the breakpoint.

Abnormalities, Multiple↗
PubMed1995

Autosomal dominant inheritance in Setleis syndrome.

Setleis syndrome is characterized by bitemporal skin depressions resembling forceps marks, abnormalities of the eyelashes, and "leonine" facial appearance. The cause is unknown, although autosomal recessive inheritance has been proposed. Recently, two families were reported in which one of the parents of a patient with Setleis syndrome showed mild manifestations, suggesting autosomal dominant inheritance. We describe a 9-month-old Japanese boy with typical Setleis syndrome. His father, who has normal intelligence, has bitemporal focal dermal dysplasia but a normal face. His paternal second cousin also has Setleis syndrome. This family shows autosomal dominant inheritance including father-to-son transmission of Setleis syndrome with variable expressivity and reduced penetrance. Careful examination of the relatives of patients with Setleis syndrome is recommended.

Adult↗
PubMed1995

EDA-containing fibronectin is synthesized from rheumatoid synovial fibroblast-like cells.

OBJECTIVE: To identify the cells that synthesize EDA-containing fibronectin (FN) and examine the role of EDA+FN in the pathogenesis of rheumatoid joint lesions. METHODS: Localization of EDA+FN and c-Fos protein in rheumatoid joints was studied immunohistochemically by utilizing antibodies for EDA+FN and c-Fos. Expression of EDA+FN was studied by immunoelectron microscopy and in situ hybridization. The amount of EDA+FN was measured by enzyme-linked immunosorbent assay. RESULTS: EDA+FN was specifically localized in the synovial lining layer of synovium with active rheumatoid arthritis (RA) (n = 17), but not in that with osteoarthritis (n = 4) or with inactive fibrous RA (n = 2). EDA+FN messenger RNA was localized in the synovial lining layer. EDA+FN was immunoelectron microscopically localized in the synovial lining fibroblast-like (type B) cells. EDA+FN was also detected at the cartilage-pannus junction and on the surface of RA cartilage. Double staining showed that EDA+FN colocalized with c-Fos protein in the rheumatoid synovial lining layer. Quantification of EDA+FN showed that it was highly concentrated in rheumatoid synovial fluids. CONCLUSION: EDA+FN is synthesized by the synovial lining fibroblast-like (type B) cells in situ in rheumatoid synovium, and appears to be expressed in association with activated or transformed states of synovium.

Animals↗
PubMed1995

Competition between c-fos and 1,25(OH)2 vitamin D3 in the transcriptional control of type I collagen synthesis in MC3T3-E1 osteoblastic cells.

Interaction between c-fos and 1,25(OH)2 vitamin D3 (VD) on the type I collagen synthesis was studied. VD inhibited collagen synthesis and type I collagen mRNA expression in MC3T3-E1 osteoblastic cells. In contrast, VD reversed the inhibition of collagen synthesis and mRNA expression of the c-fos transfectants that overexpressed c-fos gene to a comparable level as those of the control transfectants. The gel shift assay showed the vitamin D receptor (VDR) complex binding to vitamin D responsive element (VDRE) was inhibited under constitutively expressed c-fos gene, suggesting that c-fos gene product, c-Fos, may inhibit the binding of VDR complex to VDRE by making a c-Fos-VDR complex. The result suggests the existence of a fine tuning between c-fos and VD in the bone metabolism which may be relevant to the pathogenesis of rheumatoid bone lesion.

3T3 Cells↗
PubMed1995

Histological comparison of patellar cartilage degeneration between chondromalacia in youth and osteoarthritis in aging.

The histological findings of the patellar cartilage were compared between cases of chondromalacia, which occurs predominantly in young persons (22 patients, average age 19.8 years) and cases of osteoarthritis, which is common among the elderly (21 patients, average age 65.4 years). The histological findings of cartilage in the chondromalacia were characterized by increased density and vigorous fibrous metaplasia of chondrocytes. These findings may be considered to represent a reactive change in the chondrocyte. Cartilage degeneration in osteoarthritis, by contrast, is regressive and presents a clearly different histological picture from that of chondromalacia patellae. We conclude that chondromalacia does not easily lead to osteoarthritis. On the other hand, the cartilage was characteristically softened, as observed by gross inspection, and showed rarefaction of the cartilage matrix. It should be noted that the change was not observed in aging, but showed a pattern of cartilage degeneration peculiar to young patients with chondromalacia patellae.

Adolescent↗
PubMed1995

Anal atresia: effect of smoking and drinking habits during pregnancy.

Using data compiled from 216,707 births from the population-based Kanagawa Birth Defects Monitoring Program (KAMP), we conducted a case-control study to evaluate the effect of maternal smoking and/or drinking during pregnancy on the risk of infants' anal atresia in 1989-1994. The frequency of maternal smoking (including passive smoking) and/or maternal drinking during pregnancy among 84 infants with anal atresia was compared with 174 matched controls. The 84 anal atresias include 49 cases of isolated anal atresia and 35 cases of syndromal anal atresia. Our findings suggest that maternal drinking during early pregnancy is associated with an increased risk of isolated anal atresia (OR = 4.8, 95% CI 1.2 to 19.1, p < 0.05). A slightly increased trend was also observed in the association of maternal smoking during pregnancy with both in the pooled groups of anal atresia (OR = 1.4, 95% CI 0.5 to 3.6).

Adult↗
PubMed1995

Shwachman syndrome associated with de novo reciprocal translocation t(6;12)(q16.2;q21.2).

We describe a de novo apparently balanced reciprocal translocation t(6;12)(q16.2; q21.2) in an 18 month old girl with Shwachman syndrome, characterised by exocrine pancreatic insufficiency and bone marrow dysfunction. The cause of this syndrome is unknown, although autosomal recessive inheritance has been proposed. The translocation breakpoints in the present patient may be candidate regions for a gene responsible for Shwachman syndrome.

Abnormalities, Multiple↗
PubMed1995

Aberrant appearance of lung surfactant protein A in sera of patients with idiopathic pulmonary fibrosis and its clinical significance.

Pulmonary surfactant protein A (SP-A) is known to be a major phospholipid-associated glycoprotein in pulmonary surfactant, which is specific to the lung. In this study, the SP-A concentrations in sera of patients with various lung diseases were determined using an enzyme-linked immunosorbent assay. Patients with idiopathic pulmonary fibrosis (IPF) and pulmonary alveolar proteinosis (PAP) exhibited prominently high concentrations of serum SP-A compared to those of other lung diseases and healthy volunteers, although there were significant increases in serum SP-A concentrations in patients with pulmonary tuberculosis, chronic pulmonary emphysema, diffuse panbronchiolitis and bacterial pneumonia compared to those of healthy volunteers. Successive measurement in 2 patients with IPF showed that serum SP-A levels reflect the disease activity of IPF. In patients with IPF, serum SP-A concentrations were significantly correlated with those of serum lactate dehydrogenase, whereas there were no significant correlations of serum SP-A concentrations with erythrocyte sedimentation rate, arterial oxygen saturation, vital capacity and carbon monoxide diffusing capacity. Determination of serum SP-A will contribute to diagnosing IPF and PAP, and may reflect the disease activity of IPF.

Biomarkers↗
PubMed1995

Pulmonary surfactant protein D in sera and bronchoalveolar lavage fluids.

Pulmonary surfactant protein D (SP-D) is a hydrophilic glycoprotein with a reduced molecular mass of 43 kDa and a member of the C-type lectin superfamily, along with mannose-binding proteins and surfactant protein A (SP-A). We have recently prepared monoclonal antibodies against human SP-D and developed an enzyme-linked immunosorbent assay (ELISA). In this study, the levels of SP-D in sera and bronchoalveolar lavage (BAL) fluids of patients with lung diseases were determined by ELISA, using human recombinant SP-D as a standard. We demonstrated that the concentrations of SP-D in sera are prominently increased in patients with idiopathic pulmonary fibrosis (IPF), interstitial pneumonia with collagen disease (IPCD), and pulmonary alveolar proteinosis (PAP). Patients with IPF, IPCD, and PAP exhibited levels of serum SP-D 5.1-fold, 7.2-fold, and 7.0-fold, respectively, of those in healthy volunteers; 91.5% of the patients with IPF, 81.3% with IPCD, and 100% with PAP exhibited serum SP-D levels that exceeded the cut-off value (mean + 2 SD of control value). Serum SP-D levels appeared to reflect the disease activity of IPF and IPCD and the disease severity of PAP. High levels of SP-D in BAL fluids were shown in patients with PAP, but not with IPF and IPCD. We conclude that measurement of SP-D in sera can provide an easily identifiable and useful clinical marker for the diagnosis of IPF, IPCD, and PAP, and can predict the disease activity of IPF and IPCD and the disease severity of PAP.

Adult↗
PubMed1995

Lung surfactant protein-A and carcinoembryonic antigen in pleural effusions due to lung adenocarcinoma and malignant mesothelioma.

Lung surfactant protein-A (SP-A) is a major phospholipid-associated glycoprotein in surfactant, and is a useful immunohistochemical marker for lung adenocarcinoma. Carcinoembryonic antigen (CEA) has not been immunohistochemically detected in mesothelioma. In pleural effusions due to malignant mesothelioma, very low concentrations of SP-A and CEA can be expected. We studied the value of combined determinations of CEA and SP-A in pleural fluid to distinguish between lung adenocarcinoma and mesothelioma. SP-A and CEA concentrations were measured in pleural effusions from 78 patients with lung adenocarcinoma and 10 with malignant mesothelioma. SP-A concentrations in pleural effusions due to lung adenocarcinoma and mesothelioma were 516 +/- 140 and 16.9 +/- 3.6 ng.ml-1 (mean +/- SEM), respectively. CEA concentrations in pleural effusions due to lung adenocarcinoma and mesothelioma were 239 +/- 92.4 and 1.7 +/- 0.3 ng.ml-1, respectively. SP-A values did not exceed 100 ng.ml-1 in any of 10 mesotheliomas, whilst in 37 of 78 lung adenocarcinomas they did. CEA values did not exceed 10 ng.ml-1 in any of 10 mesotheliomas, whilst in 53 of 78 lung adenocarcinomas they did. Increased values of SP-A and/or CEA were found in pleural effusions from 67 of 78 lung adenocarcinomas. It is concluded that a combination of CEA and SP-A assays in pleural effusions will be helpful for discriminating lung adenocarcinoma from mesothelioma.

Adenocarcinoma↗
PubMed1995

Immunocytochemical localization of estrogen and progesterone receptors (ER & PgR) in breast cancer.

The localization of estrogen receptors (ER) and progesterone receptors (PgR) in human breast cancer was examined light and electron microscopically by using specific monoclonal antibodies. Among the breast cancer patients, ER-positive (ER[+]) cases were shown by enzyme immunoassay (EIA) to account for 58.9% (63/107), and 63.5% of these cases were women in the postmenopausal state. The PgR-positive (PgR[+]) rate was 50.5% (54/107), with 44.4% of these positive cases being postmenopausal women. The rates of ER(+) and PgR(+), ER negative (ER[-]) and PgR negative (PgR[-]), and ER(+) and PgR(-) cases were 43.9% (47/107), 34.6% (37/107) and 15.0% (16/107), respectively. Although ER(-) and PgR(+) cases were in few number, they were found (6.5%, 7/107). These results correlated well with those obtained by the immunocytochemical method. In either case, i.e anti-ER or anti-PgR reaction, positive nuclei and negative nuclei were found intermingled with each other in a given visual field. In electron microscopy, both anti-ER and anti-PgR antibodies bound to sites in the euchromatin area of the nucleus.

Antibodies, Monoclonal↗
PubMed1995

Osteodysplastic primordial dwarfism: a case with features of type II.

We describe a 22-month-old Japanese girl with severe microcephaly with a prominent nose and a receding chin, developmental delay, marked intrauterine and postnatal dwarfism with limb shortening and brachydactyly, and distinctive radiological changes of the skeleton. The radiological findings include hypoplasia of the short tubular bones, multiple pseudoepiphyses in the bases of the metacarpals, coxa valga, a wide pelvis with iliac flaring, thoracolumbar scoliosis, and disharmonious ossification delay. The clinical and radiological features are somewhat different from those of previously reported cases with osteodysplastic primordial dwarfism. The clinical and radiological manifestations of osteodysplastic primordial dwarfism are reviewed and compared with those in our patient.

Dwarfism↗