[Reflection on the midwifery practice].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Uchida.
Explore the source record for details and available documents.
In order to clarify the erythropoiesis of complement-sensitive red cells in paroxysmal nocturnal hemoglobinuria (PNH), the proportion of complement-sensitive red cells and compositional classification of examined red cells were investigated by means of complement lysis sensitivity test in 27 patients with initial diagnosis of PNH and 17 patients with aplastic anemia-PNH syndrome, and their bone marrow nucleated cell counts were also compared. The proportion of complement-sensitive erythrocytes was 41.0 +/- 22.0% (n = 26) in PNH and 29. 5 +/- 15.0% (n = 17) in aplastic anemia-PNH syndrome, and no significant difference was recognized between them. The nucleated cell count at the time of PNH diagnosis was 19.1 +/- 12.5 X 10(4)/microliters (n = 21) in PNH and 12.6 +/- 8.8 X 10(4)/microliters (n = 12) in aplastic anemia-PNH syndrome, and no significant difference between them was apparent. These findings suggest that the erythropoiesis of complement-sensitive red cells shows a similarity between PNH at initial occurrence and aplastic anemia-PNH syndrome, once PNH has occurred.
A case of primary myelofibrosis complicated with pericardial effusion and proteinuria is described. A 66-year-old female was admitted to our hospital because of abdominal fullness and shortness of breath. On admission, hepatosplenomegaly and pericardial effusion were observed. Blood examination revealed leukoerythroblastic anemia and thrombocytosis with tear drop cells and giant platelets. Bone marrow aspiration was dry tap and its biopsy showed remarkable myelofibrosis. Urinalysis indicated severe proteinuria. Although neutrophilic alkaline phosphatase score was low, no signs of acute blastic crisis of chronic myelogenous leukemia was found. The diagnosis of an atypical type of primary myelofibrosis was obtained. Administration of MCNU was started in August 1987. Hepatosplenomegaly, pericardial effusion and proteinuria were gradually improved after the administration. The etiology of the pericardial effusion and proteinuria were not obvious, however, these facts suggest that these abnormal findings might be related to PMF itself and MCNU was effective to PNF.
Hairy cell leukemia (HCL) is characterized by slow proliferation of special mononuclear cells. Although splenectomy has been evaluated to be the most effective traditional treatment for HCL, the response of patients to splenectomy is not necessarily satisfactory. Recently, the treatment of HCL with Interferon-alpha has been reported to be effective, and we report a female case of HCL who showed marked improvement in her hematological findings with this therapy.
We observed a case of mitral valve prolapse (MVP) mimicking mitral tumor or vegetation. The patient was a 34-year-old man. He complained of palpitation and precordial oppression. Shaggy and mass echoes of the anterior mitral valve were recorded by M-mode and two-dimensional echocardiograms. The "mass" echo was confirmed to by originated in a markedly myxomatous change of the spongiosa layer of the mitral valve at operation. These problems on echocardiographic diagnosis of MVP and mitral "mass", such as mitral tumor or vegetation, were discussed in detail.
To determine the biologic activity of interleukin-6 (IL-6) on megakaryocytopoiesis and thrombocytopoiesis in vivo, the cytokine was administered intraperitoneally to mice every 12 hours at varying doses for five days or for varying time intervals, based on the kinetic analysis of IL-6 serum levels indicating the peak of 40 minutes following injection, with no detection at 150 minutes. A dose-response experiment showed that IL-6 increased platelet counts in a dose-dependent fashion at a plateau stimulation level of 5 micrograms. Administration of 5 micrograms of IL-6 reproducibly elevated platelet counts at five days by approximately 50% to 60% of increase. Moreover, a striking increase in megakaryocytic size in response to IL-6 was elicited by the treatment, but no change in megakaryocyte numbers; whereas IL-6 administration did not expand CFU-MK numbers. The in vivo studies in this manner had negligible effects on other hematologic parameters, with the minor exception of monocyte levels. These data show that IL-6 acts on maturational stages in megakaryocytopoiesis and promotes platelet production in vivo in mice, suggesting that IL-6 functions as thrombopoietin.
A case of chronic myelogenous leukemia (CML) of 10-year survival in described. A 44-year old male was admitted to our hospital because of general malaise, abdominal fullness and fever in February, 1977. On physical examination, giant splenomegaly and hepatomegaly were detected. Peripheral blood examination revealed leukocytosis without hiatus leukemia , normochromic macrocytic anemia and thrombocytosis. NAP rate and score were 16% and 22. Cytogenetic analysis of PB without stimulator revealed 46, XY, Ph1. Then he was diagnosed as having a typical type of Ph1-positive CML. He had been successfully treated over 9 years by intermittent administration of busulfan. However, anemia suddenly progressed in February, 1986 followed by leukopenia and thrombocytopenia. Hemorrhage was not detected by the examination. Though he had been received blood transfusion, the anemia progressed rapidly. He was died of cachexia on 4th of August, 1987. The postmortem examination revealed bone marrow aplasia with no signs of blast crisis nor myelofibrosis. Secondary hemochromatosis was seen in the liver, spleen, pancreas and some other organs.
To clarify the genesis of a high-pitched diastolic rumble in mitral stenosis, 51 patients with mitral stenosis were studied. They were subdivided into two groups based on the pitch of a rumble; six patients with a high-pitched rumble and 45 patients with an ordinary low-pitched rumble. Phonocardiography, and M-mode and two-dimensional (2-D) echocardiography were performed in all patients. Color and continuous wave Doppler echocardiography were performed in four patients with a high-pitched rumble and in 13 with a low-pitched rumble. Results obtained were as follows: 1. Points of the maximum intensity of a rumble: A low-pitched rumble was best heard at the apex in all patients. A high-pitched rumble was best heard at the mesoapical area, except in one patient who had an oval mitral orifice by 2-D echocardiography. 2. Correlation between the pitch of rumble and the shape of the mitral orifice: In five of the six patients with a high-pitched rumble, the mitral orifice had a tadpole-shaped deformity, in which commissural fusion and valvular thickening were more marked anterolaterally than posteromedially. Among 45 patients with oval, slit or pinhole-like valve orifices, only one had a high-pitched rumble. 3. Direction of the left ventricular (LV) inflow jet as observed by color Doppler echocardiography: On the short-axis view at the level of the papillary muscles, the inflow jet was directed toward the medial portion of the LV cavity in the patients with a high-pitched rumble. However, it was directed towards the central portion of the LV cavity in all patients with a low-pitched rumble. On the apical long-axis view, no distinct difference was detected in the direction of the LV inflow jet between the two groups. 4. Other findings: There were no significant differences between the two groups in the mitral orifice area, the peak velocity of LV inflow, fractional shortening of the LV, dimension of the left atrium, Wells' index and the degree of organic change in the subvalvular structures. These results suggest that the deformity of the mitral valve and resultant changes in the direction of the LV inflow jet may play an important role in the mechanism of producing a high-pitched diastolic rumble in mitral stenosis.
By Southern blot hybridization, the state of hepatitis B virus (HBV) in the liver was investigated by utilizing needle biopsy specimens of 59 patients with hepatitis B surface antigen-positive noncarcinomatous liver disease. The tissue HBV DNA revealed a replicative form in 23 patients with chronic active hepatitis (48%) and an integrated form in 23 (48%) of these 48 patients. A liver with a replicative form was more frequently associated with hepatitis Be antigen (HBeAg), serum HBV DNA, and expression of hepatitis B core antigen than one without it. Integration of HBV DNA was more common in the anti-hepatitis Be phase or in the absence of necroinflammatory activity, and its frequency of occurrence roughly paralleled progression of liver disease: early, 21%; advanced, 56%; and cirrhotic stage, 61%.
A 49-year old man was admitted with a complaint of syncopal attack. Transient A.V block was detected and permanent pacemaker (DDD) was implanted. Five months later he was re-admitted because of dyspnea and palpitation. Infective endocarditis with aortic regurgitation and mycotic aortic valve aneurysm was diagnosed by echocardiography and cineangiography. The aortic valve and valve aneurysm were resected and AVR was performed using Björk-Shiley disc valve (23A) in the usual manner. But 6 months later he suffered from acute cardiac failure due to perivalvular leakage. He died in spite of re-AVR with translocation method.
The signal sequence of simian virus 40 (SV40) large T-antigen for translocation into the nucleus is composed of positively charged amino acids Lys-Lys-Lys-Arg-Lys. Rabbit antibodies to a synthetic peptide containing the negatively charged amino acid sequence Asp-Asp-Asp-Glu-Asp were obtained. Indirect immunofluorescence of the antigens recognized by the antibody was punctate at the nuclear rim or the nuclear surface, depending on the plane of focus. The antibody blocked transport of nuclear proteins into the nucleus. The antigens recognized by the antibody were predominantly localized to the nuclear pores.
Immunoblot analysis of WEHI-231 B lymphoma cell homogenates revealed that both type II, a major component, and type III, a minor component, protein kinase C (PKC) were present. Northern blot analysis of PKC mRNA showed a higher level of beta II and beta I mRNA (encoding type II PKC) than of alpha mRNA (encoding type III PKC). Short term (3 min) treatment with phorbol 12-myristate 13-acetate (PMA) caused a rapid loss of PKC in cytosol and a concomitant increase in the particulate fraction. After prolonged (24 hr) exposure, the level of both PKC isozymes were decreased. However, the corresponding mRNA levels remained intact. PMA did not inhibit the anti-IgM-mediated increase in [Ca2+]i in PKC-depleted cells.
The 3'----5' exonuclease activity of the Klenow fragment operates in 3'-end labeling of DNA fragments. In the presence of excess deoxyribonucleoside 5'-triphosphates (dNTPs), the 5'----3' polymerase activity is dominant over the exonuclease activity. However, in the presence of a small amount of dNTPs, the exonuclease activity removed deoxyribonucleoside 5'-monophosphate (dNMP) incorporated in the 3'-end of a DNA strand by the polymerase activity. We found that the radioactivity of incorporated dNMP decreased remarkably in the course of 3'-end labeling by the Klenow fragment. On the other hand avian myeloblastosis virus (AMV) reverse transcriptase also possesses the polymerase activity. The decline of the incorporated radioactivity was not observed, indicating that the enzyme has neither exo- nor endonuclease activities. Furthermore, the level of the incorporated radioactivity was the same as that obtained by the Klenow fragment. We conclude that AMV reverse transcriptase is easier to use than the Klenow fragment for labeling the 3'-end of a DNA fragment.
The hamster elongation factor 2 gene was isolated from genomic libraries of diphtheria toxin- and Pseudomonas aeruginosa exotoxin A-resistant cells containing non-ADP-ribosylatable elongation factor 2, and its structure was determined by a combination of restriction endonuclease mapping and DNA sequence analysis. The entire gene is about 6 kilobases long and has 13 exons. Almost all the introns are about 90-200 bases long, except the first and third, which are about 1 kilobase and 400 bases long, respectively. The first exon is processed just after the initiation codon for translation. The promoter of this gene was also characterized. As this gene contains the mutation conferring resistance to diphtheria toxin and P. aeruginosa exotoxin A, introduction of this gene into mammalian cells results in expression of toxin resistance. Using this characteristic, gene expression by deletion mutants of the 5'-flanking region were examined, and results showed that about 60 base pairs upstream of the TATA sequence were most efficient for expression of the elongation factor 2 gene.
In an attempt to determine the effect of aflatoxin B1 (AFB) intoxication on livers with duck hepatitis B virus (DHBV) infection, domestic ducks were given 0.1 mg of AFB/kg body weight twice a week for a maximum period of 54 weeks employing various experimental designs. The ducks were infected with DHBV by i.v. inoculation of DHBV-positive sera within 24 h posthatch. The livers were examined histologically, immunohistochemically, and ultrastructurally, and the livers and sera were examined by molecular hybridization for DHBV DNA. AFB administration induced hepatocellular necrosis and marked biliary cell proliferation of the periportal areas, and finally liver cirrhosis. On short-term administration, the hepatocytes of DHBV-infected livers revealed a marked increase in incomplete particles of DHBV by immunostaining and electron microscopy, as compared to those without its administration. Long-term AFB administration provoked frequent nodular or cirrhotic changes. There was no significant increase in frequency of these changes in DHBV-positive ducks as compared to DHBV-negative ones. AFB administration induced hepatocellular carcinoma (HCC) in one DHBV-positive duck and in two DHBV-negative ducks. The HCC and cirrhotic livers revealed extrachromosomal but no integrated form of DHBV DNA by Southern blot hybridization analysis. Immunostaining demonstrated a heterogeneous distribution of DHBV from area to area in nodular and cirrhotic livers. Thus, AFB intoxication provoked various liver disorders independent of DHBV infection, and neither a cocarcinogenic effect of AFB and DHBV nor integration of viral DNA into the genome of neoplastic and nonneoplastic tissues was observed in the present experiments. Generally speaking, DHBV infection did not appear to accelerate hepatic disorders induced by AFB intoxication. However, AFB administration altered the DHBV in the liver in terms of its amount and distribution.
In order to evaluate geographical differences in the liver pathology of ducks infected with duck hepatitis B virus (DHBV), ducks in Chiba and Shimane, Japan, and Shanghai, China, were investigated. The numbers (DHBV positive/negative) and the maximum age of the ducks examined were 18/10 at 19 mo, 15/1 at 3 yr 4 mo, and 72/27 at 18 mo, respectively. DHBV infection was induced experimentally in ducks from Chiba and Shimane but was present congenitally in those from Shanghai. Ducks were examined regarding liver function tests, conventional histology, immunohistology, electron microscopy, and molecular hybridization for DHBV DNA in the serum and liver. There was no significant difference between DHBV-positive and -negative ducks in bilirubin and transaminase and alkaline phosphatase activities in the sera. Histologically, while the livers of ducks from Chiba and Shimane did not show necroinflammatory (hepatitis) activity, those from Shanghai frequently did (52.5%). Necroinflammatory activity of the Shanghai ducks was present almost equally in both DHBV-positive and -negative livers. The livers of Shanghai ducks but not the other two areas often (8.3%) had ground-glass inclusions which corresponded ultrastructurally to numerous virus particles in the dilated cisternae of the proliferated endoplasmic reticulum. No advanced liver disease, such as cirrhosis or hepatocellular carcinoma, was observed. There was no significant difference in the amount of DHBV DNA in the sera or in its pattern in the liver tissue among ducks of the three areas. In addition, the livers of Chiba ducks frequently had amyloidosis, while those of Shanghai ducks were contaminated with parasites. In conclusion, DHBV infection did not appear to provoke significant hepatitis activity or advanced liver disease in the examined ducks of all three areas, and the DHBV-positive livers from Shanghai ducks showed a different morphological appearance from those of the other two areas. This variation might reflect the difference in the strain of ducks, subtypes of DHBV, environmental factors, or a combination of these influences.
A method for determination of serum glycated albumin by high-performance liquid chromatography is presented. The system involves anion exchange chromatography to separate albumin and consecutive boronate affinity chromatography to separate glycated and nonglycated albumin. The method is rapid (20 min), precise (coefficient of variation, 0.7-4.9%), requires only a small sample (5 microliters), and can be automated. Assay of glycated albumin by this method is not influenced by the protein concentration of the sample or the presence of glucose. The variation in glycated albumin values in consecutive samples obtained within a day from diabetic patients (coefficient of variation, 2.02 +/- 0.65%) was significantly smaller (p less than 0.001) than that of values for fructosamine (coefficient of variation, 4.33 +/- 2.0%). The values of glycated albumin in normal subjects (20.2 +/- 1.6%) were clearly less than those in diabetic patients [39.6 +/- 5.4% in 40 Type 1 (insulin-dependent) and 39.4 +/- 5.9% in 25 Type 2 (non-insulin-dependent) patients]. The serum glycated albumin level was well correlated with HbA1c in 65 diabetic patients (r = 0.60). Because the life span of albumin in the circulation is short, measurement of glycated albumin should be useful as a short-term index of glycaemic control.
A 78-year-old female with hepatocellular carcinoma and high serum levels of carcinoembryonic antigen is reported. Using a immunohistochemical technique, CEA was demonstrated within the cytoplasm of the tumor cells.