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Biomedical subjects

K Miyamura

Publications and source records attributed to K Miyamura.

At least 73 records · Page 4Linked to original sources
PubMed1992

Successful aggressive treatment against multiple intra-abdominal metastases from renal cell carcinoma 18 years after nephrectomy.

The management of late metastases from renal cell carcinoma is often difficult because of multiple organ involvement. We report a case of multiple metastases from renal cell carcinoma in the duodenum, pancreas, intestine, falciform ligament and liver, 18 years after nephrectomy. The patient underwent a total pancreatectomy following a gastroduodenal arterial embolization to control duodenal bleeding, a resection of the ileum and falciform ligament at a second laparotomy and repeated hepatic arterial embolizations to control the growth of liver metastases. Aggressive treatment should be undertaken in cases of late recurrence of renal cell carcinoma after nephrectomy because of the possibly slow-growing biological character of the tumor.

Abdominal Neoplasms↗
PubMed1991

Ontogeny of surfactant apoprotein D, SP-D, in the rat lung.

Surfactant protein D (SP-D) is a collagenous surfactant-associated glycoprotein synthesized by alveolar type II cells. Antiserum against rat SP-D was raised in rabbits and an enzyme-linked immunosorbant assay (ELISA) has been developed using anti-rat SP-D IgG. In the present study we examined the developmental profile of SP-D in the rat lung compared with that of surfactant protein A (SP-A). SP-A content in the lungs increased during late gestation and reached its maximum on day 1 of neonate, and then gradually decreased until at least day 5. SP-D content during early gestation was less than 10 ng/mg protein until day 18, but on day 19 there was a 4-fold increase in SP-D (compared to that on day 18). It increased twice between day 21 and the day of birth, when it reached the adult level of 250 ng/mg protein, which is about one fourth that of the adult level of SP-A. Unlike SP-A there seemed to be no decrease in SP-D content after birth. These results demonstrate that SP-D is regulated developmentally as are the other components of surfactant, but the inconsistency in the developmental profiles of SP-A and SP-D suggests that these proteins may play different roles in lung maturation.

Animals↗
PubMed1991

Appearance of surfactant proteins, SP-A and SP-B, in developing rat lung and the effects of in vivo dexamethasone treatment.

Hydrophobic pulmonary surfactant proteins (SP-B and SP-C) promote the adsorption of phospholipids at the air/liquid interface and the addition of surfactant protein A (SP-A) enhances this function. The developmental profiles of phospholipids and SP-A in the lung have been reported, but that of SP-B and SP-C remain unknown. We recently developed an enzyme-linked immunosorbent assay (ELISA) that measures SP-B in the rat. Using ELISA for SP-A and SP-B, we measured the contents of SP-A and SP-B in lung homogenates. The developmental profiles of SP-A and SP-B during the late gestational and postnatal periods were found to be distinctly different from each other. SP-A increased during late gestation and reached its maximum on day 1 after birth. This developmental profile of SP-A in the lungs was very similar to that of disaturated phosphatidylcholine (DSPC). In contrast, the SP-B contents in fetal lungs were low and increased after birth, reaching its maximum on day 4 after birth. In vivo dexamethasone treatment resulted in significant increases of SP-A content in rat lung homogenate on day 19 and day 21 of gestation, and day 5 after birth, whereas SP-B content increased significantly only on day 19 of gestation by dexamethasone administration. SP-A synthesis may be enhanced both pre- and postnatally, but SP-B synthesis may be stimulated only during the late gestational period by in vivo dexamethasone treatment. The difference in developmental profiles and the different responses to dexamethasone treatment between SP-A and SP-B indicate that the expression of SP-A and SP-B may be regulated independently at least in developing rat lungs.

Aging↗
PubMed1991

The nucleotide sequence of 3C proteinase region of the coxsackievirus A24 variant: comparison of the isolates in Taiwan in 1985-1988.

Acute hemorrhagic conjunctivitis caused by coxsackievirus A24 variant (CA24v) first appeared in Taiwan in October 1985, followed by two other sequential epidemics in 1986 and 1988. In order to know the evolutionary relationship of the CA24v strains isolated in Taiwan, we first determined the nucleotide sequence of the 3C proteinase (3Cpro) region of the prototype strain (EH24/70), isolated in Singapore in 1970, by molecular cloning. The nucleotide sequence of the 3Cpro region thus sequenced showed striking homology with polioviruses and coxsackievirus A21. Viral RNA of eight isolates obtained from the three epidemics was reverse transcribed, amplified by the polymerase chain reaction, and cloned into M13 phage for the production of ssDNA for nucleotide sequencing by the dideoxy chain termination method. When the number of nucleotide difference was taken as a genetic distance between isolates, all isolates showed a very similar distance from the EH24/70, the earliest isolate of CA24v, indicating that they evolved at a constant evolutionary rate. Phylogenetic analysis by the unweighted pairwise grouping method of arithmetic average (UPGMA) indicated that the six isolates collected in 1985 and 1986 were closely related, while two 1988 isolates were more distant from them. The branching time between these two groups was estimated to be May 1984, 18 months before the first recognition of the CA24v epidemic in Taiwan. This is the first report of the nucleotide sequence of CA24v genome RNA and of an evolutionary analysis of the virus using the nucleotide sequence.

3C Viral Proteases↗
PubMed1991

Sequence analysis of the 3'-end of feline calicivirus genome.

The nucleotide sequence of the 3'-end of the Japanese F4 strain of feline calicivirus (FCV) RNA was determined from a cloned cDNA of 3.5 kbp. We found three open reading frames (ORFs). The largest ORF encoded a 668-amino acid protein of 73,588 Da, which was presumably the capsid precursor protein of FCV and had significant amino acid sequence homology with the VP3 of picornaviruses. A small ORF at the extreme 3'-end was compared with that of the F9 strain of FCV, a vaccine strain originally from the U.S. Highly conserved amino acid sequences were shown, suggesting that this ORF might be functional and encode a putative 106-amino acid protein of 12,153 Da. The other ORF in the 5'-flanking region of the cDNA had consensus amino acid sequences conserved among the RNA-dependent RNA polymerases.

Amino Acid Sequence↗
PubMed1991

Herpangina surveillance in Japan, 1982-1989. A report of the national epidemiological surveillance of infectious agents in Japan.

In Japan, herpangina cases increase every summer with an incidence peak in July. During the past eight years from January, 1982 to December, 1989, a total of 3,974 viruses from herpangina cases were reported from 47 participating laboratories, and coxsackie A (CA) viruses accounted for most of them, 3,055 (76.9%). The major types associated with herpangina were, in order of frequency, CA4, 10, 5, 6, 2 and 3, representing 87.2%-80.8% of total isolations reported for each respective type in this period. Eighty-four point four percent of the total virus isolations were from children at four years of age or younger. More than 80% of total CA virus isolations were from nasopharyngeal specimens and nearly 90% of the viruses were isolated in mice.

Adolescent↗
PubMed1991

Gene amplification of Japanese non-Hodgkin lymphoma with involvement of the BCL2 gene.

Twenty cases of Japanese non-Hodgkin's lymphoma with B cell markers were studied with respect to their immunoglobulin heavy (IgH) chain gene loci on chromosome 14 and BCL2 loci on chromosome 18. All of the 20 cases showed IgH gene rearrangement on at least one of the alleles. Molecular analysis using two chromosome 18-specific DNA probes (pFL1 and pFL2) showed rearrangement of the BCL2 region in three of 20 cases. As these three samples showed the rearranged allele of the IgH gene comigrating with that of the BCL2 gene, polymerase chain reaction (PCR) was carried out to amplify the juncture between IgJH on chromosome 14 and BCL2 on chromosome 18. In all of these three cases, gene amplification between the two loci was found to occur, indicating that molecular mechanisms involved in this type of chromosomal translocation in Japan might be similar to cases in the United States (U.S.) in a limited number of cases. Furthermore, this amplification technique revealed minimal tumor cells circulating in peripheral blood, even though lymphoma cells could not be identified morphologically. Thus, the PCR technique is useful for both the detection of minimal tumor cells as well as for the determination of the molecular nature of chromosomal translocation in some of Japanese cases.

Base Sequence↗
PubMed1991

[Bone marrow transplantation for patients with Philadelphia chromosome-positive acute lymphoblastic leukemia].

We reported the results of 6 allogenic bone marrow transplantation (BMT) and 3 autologous BMT for patients with Philadelphia chromosome (Ph1)-positive acute lymphoblastic leukemia (ALL) by Nagoya BMT group. Two of six patients who received allogenic BMT have continued complete remission (CR) on +639 days and +1,597 days. Four of six patients relapsed on +134, +203, +216, and +267 days. Two patients with a disease-free survival for a long time had both acute and chronic GVHD. It is suggested that graft-versus-leukemia (GVL) effect might prevent the relapse. On the contrary, one patient who received with monoclonal antibodies plus complement-treated autologous bone marrow is free of leukemia on +439 days. Our results suggest the follows. 1) We do chromosomal analysis at initial diagnosis in all cases to do BMT in first CR. 2) We intensify the conditioning regimen for BMT. 3) We study on application of GVL effect to prevent the relapse. 4) We establish the best purging method to eradicate residual leukemic cells for autologous BMT. 5) We do allogenic BMT using HLA-matched unrelated donor for patients without related donor.

Adolescent↗
PubMed1991

[A case of so-called neoplastic angioendotheliosis with fever of unknown origin and temporary loss of consciousness].

A 65-year-old man was hospitalized with prolonged fever. The erythrocyte sedimentation rate was 62 mm/hour and the c-reactive protein was 5+. Serum lactic dehydrogenase was 1005 IU with elevation of isozyme types II and III. A computerized tomography scan of the abdomen showed large, bilateral adrenal masses. An aspirated specimen of the bone marrow revealed some clustered atypical cells. These findings suggested the patient had metastatic carcinoma, but the primary lesion could not be found. The patient had an episode of transient unconsciousness in mid course and died of bleeding from the gastrointestinal tract. A postmortem examination was performed. Microscopic examination showed an accumulation of neoplastic cells in the vascular system throughout the body and their extravascular proliferation in several organs. Immunohistochemical studies were performed on paraffin-embedded fixed tissues. The neoplastic cells were positive with the monoclonal antibodies LCA, LN 1, LN 2 and N 26 but did not show positive staining for factor VIII-related antigen, a marker for endothelial cells. These studies defined the neoplastic cells as being of a germinal-center B lymphocyte origin. On the basis of the above-mentioned results, we suggest that this case may be diagnosed as angiotrophic lymphoma.

Aged↗
PubMed1991

[Autologous bone marrow transplantation for acute leukemia].

Autologous bone marrow transplantation (ABMT) was performed in 20 common ALL antigen (CALLA) positive acute lymphoblastic leukemia (ALL) cases. Bone marrow cells harvested in complete remission (CR) were in vitro treated with monoclonal antibodies NL-1 (IgG2a: anti-CD10), NL-22 (IgM), HL-47 (IgM) and baby rabbit complement and cryo-preserved. Three children with high risk factor such as Ph1 chromosome were transplanted in 1st CR, 5 in 2-3 CR, 8 adults in 1st CR, 2 in 2nd CR and 2 in relapse. As conditioning of ABMT, 12 cases mostly in 1st CR were treated with 4 doses of 2 g/m2 cytarabine (CA), 2 doses of 60 mg/kg cyclophosphamide (CY) and 4 doses of 3 Gy total body irradiation (TBI). 6 cases refractory to CA/CY were treated with 3 doses of 60 mg/m2 melphalan and 4 doses of 3 Gy TBI. Disease free survival (DFS) of 11 cases in 1st CR was 81.8% at 2 years from ABMT, and 9 cases are alive in CR. DFS of 5 cases in 2nd CR was 40.0%. In one Ph1 chromosome positive case, minimal residual bcr-abl mRNA was detected by polymerase chain reaction in the 1st CR bone marrow, but disappeared after purging procedures and after 3 months from ABMT. Our results indicate that ABMT with purged bone marrow is an effective mode of therapy for high risk CALLA positive ALL.

Adolescent↗
PubMed1990

Single clonal origin of neoplastic B-cells with different immunoglobulin light chains in a patient with Richter's syndrome.

A 71-year-old man was found to have chronic lymphocytic leukemia (CLL) and diffuse large cell lymphoma (DLC) simultaneously and was diagnosed as Richter's syndrome. The CLL had mu lambda surface immunoglobulin (sIg) whereas the DLC had mu kappa sIg. However, the immunoglobulin (Ig) gene rearrangement and surface marker analysis demonstrated that both CLL and DLC had identical rearrangement patterns of the Ig heavy chain (IgH) and identical surface markers CD5+, CD19+, and CD20+. These facts imply that in this case the two malignancies are of single clonal origin initially, and that different sIg of CLL and DLC do not, therefore, necessarily indicate the biclonality of these malignancies. The origin of DLC in Richter's syndrome remains controversial. This case suggests difficulty in concluding the biclonality of these malignancies. For a conclusion on clonality to be definitive, there is a need for cloning and nucleotide sequencing of rearranged Ig genes in more patients with Richter's syndrome.

Aged↗
PubMed1990

Acute haemorrhagic conjunctivitis: seroepidemiology of coxsackievirus A24 variant and enterovirus 70 in Singapore.

Epidemics of acute haemorrhagic conjunctivitis caused by a variant of coxsackievirus A24 (CA24v) and enterovirus 70 (EV70) have occurred periodically in Singapore. A seroepidemiological survey conducted before the CA24v epidemic in 1985 and in the midst of the EV70 epidemic in 1983 showed a neutralising antibody prevalence (greater than or equal to 1:4) of 19.1% and 66.9% to CA24v and EV70, respectively. The seropositivity rate to both viruses was highest in children 10-14 years of age, but no sex or ethnic difference was noted. It appears from the data that an epidemic could be triggered when the herd immunity of the population falls below a critical level. There was a significant correlation in seroprevalence between CA24v and EV70 (P = 7.75 x 10(-3).

Adolescent↗
PubMed1990

Evolutionary study on the Coxsackievirus A 24 variant causing acute hemorrhagic conjunctivitis by oligonucleotide mapping analysis of RNA genome.

The evolution of the variant of Coxsackievirus A 24 (CA 24 v) which causes acute hemorrhagic conjunctivitis was explored. Using 15 isolates obtained from Southeast Asia during the period 1970-1986, the genetic distance between isolates was estimated from pairwise comparison of nucleotide changes deduced from common spots on oligonucleotide maps of the isolates. From regression analysis of the genetic distance and the time of isolation of the isolates, the evolutionary rate of CA 24 v was estimated to be 3.44 x 10(-4)/nucleotide/month. The phylogenetic relationship of these isolates was explored using the neighbor-joining method and the modified unweighted pair group method using arithmetic averages (UPGMA). The phylogenetic tree constructed indicates that CA 24 v appeared from one focal place in July 1968 +/- 25 months, very close to the time of the first world epidemic of, then newly recognized, acute hemorrhagic conjunctivitis.

Asia, Southeastern↗
PubMed1990

Expression of HTLV-I envelope protein fused to hydrophobic amino-terminal peptide of baculovirus polyhedrin in insect cells and its application for serological assays.

The envelope of human T-cell leukemia virus type I (HTLV-I) consists of two glycoproteins gp46 and p20E. Recombinant envelope proteins were produced by using an expression vector derived from insect baculovirus, Bombyx mori nuclear polyhedrosis virus. Polyhedrin fusion proteins C182, N147, and N287 contained whole region p20E, C-terminal half of gp46, and almost whole region gp46, respectively. N147 and N287 were suggested to be processed forms resulting from internal cleavage by cellular enzymes. In cultured cells and the insect larvae, C182 and N147 were produced abundantly enough to be purified to homogeneity; however, N287 was produced poorly and not purified. The purified proteins were recognized by HTLV-I-infected human sera and shown to be highly specific antigens for blood screening systems.

Amino Acid Sequence↗
PubMed1990

Serum type IV collagen concentrations in diabetic patients with microangiopathy as determined by enzyme immunoassay with monoclonal antibodies.

In long-term diabetes mellitus, thickening of basement membrane in capillaries and small vessels is a characteristic lesion and plays an important role in the progression of diabetic microangiopathy. We have developed a sandwich enzyme immunoassay for human serum type IV collagen peptide with monoclonal antibodies. Previous studies suggested that collagen levels reflect the activity of fibrogenesis in basement membrane. Serum type IV collagen levels were measured in 137 non-insulin-dependent diabetic patients (aged 50-75 yr) with or without clinical signs of retinopathy, nephropathy, and/or neuropathy and 110 healthy subjects (aged 50-75 yr) without serological abnormality. Serum concentrations of type IV collagen were significantly higher (P less than 0.01) in diabetic patients (mean +/- SE 124.1 +/- 4.1 ng/ml) than in healthy subjects (73.9 +/- 2.2 ng/ml) and were increased with the prevalence or incidence of diabetic complications. In the patients with diabetic microangiopathy, serum type IV collagen levels became higher as clinical signs worsened. Especially in the patients with diabetic nephropathy, serum type IV collagen levels became higher with elevation of blood urea nitrogen, serum creatinine, and serum beta 2-microglobulin but not urinary excretion of beta 2-microglobulin and N-acetyl-beta-glucosaminidase. These observations indicated that elevation of serum type IV collagen in diabetic nephropathy was related to glomerular filtration dysfunction rather than renal tubular dysfunction. However, the antigen, which can be detected by our assay system, did not exist in urine specimens of healthy subjects, and an intimate relationship was not observed between serum type IV collagen level and serum creatinine level.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗