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Biomedical subjects

H Fujii

Publications and source records attributed to H Fujii.

At least 847 records · Page 47Linked to original sources
PubMed1989

[Serum lipoprotein abnormalities in patients with nephrotic syndrome and effects of steroid therapy].

With polyacrylamide gel electrophoresis (PAGE), we studied serum lipoprotein (Lp) abnormalities in patients with nephrotic syndrome (NS) caused by primary glomerulonephritis. Nineteen untreated nephrotic patients were studied. Seven patients of them were followed up with PAGE in the remitting course. Serum total cholesterol, triglycerides and beta-Lp concentrations were higher in untreated patients than those in normal control. Serum HDL-cholesterol concentration was lower in untreated patients than those in normal control. PAGE showed broad midband-Lp and increased pre-beta-Lp in 16 of 19 untreated patients. Those findings suggested that untreated nephrotic patients had impaired catabolism of VLDL to LDL in peripheral tissue or impaired hepatic catabolism of IDL and LDL. Furthermore, PAGE showed decreased alpha-Lp in all patients with untreated NS. Correlation was not found between histological classification of glomerulonephritis and broad midband or hyperlipidemia. After administration of prednisolone, PAGE revealed the appearance of chylomicron, and increased pre-beta-LP and alpha-Lp. After remission, broad midband-Lp and pre-beta-Lp were markedly decreased or dis appeared in all 6 patients with broad midband-Lp in untreated phase, and serum total cholesterol and beta-Lp concentrations were markedly decreased, and HDL- cholestrol was markedly increased. In the course of remission, serum total cholesterol, triglycerides and beta-Lp concentrations had negative correlation with serum albumin concentration. Furthermore, serum total cholesterol and beta-Lp concentrations were decreased along with decrease of urinary protein excretion. The results of the present study suggest that the loss of serum albumin and/or some other substances to the urine cause broad midband.

Adolescent↗
PubMed1989

[Pressure waves induced by electrical stimulation of upper pons and lower midbrain in dogs with experimental subarachnoid hemorrhage].

Neurogenic mechanisms of pressure waves were investigated by means of electrical stimulation of the upper pons and the lower midbrain of 32 dogs in which subarachnoid hemorrhage had experimentally been made. The dogs were slightly anesthetized, immobilized and artificially respired. After subarachnoid infusion of red blood cells, continuous recordings of systemic blood pressure (SBP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were made simultaneously. At the stage of increased ICP, pressure waves were induced by electrical stimulation of the upper pons and the lower midbrain from 6 to 12 mm rostral to external auditory meatus. Stimulation parameters, i.e., intensity, duration and frequency, were kept constant at 0.1 mA, 1 msec and 40-50 Hz, respectively, throughout experiments. The induced pressure waves were classified into three types: fast, slow and plateau waves. Fast waves had a duration of 10-30 sec, being associated with a marked increase in SBP. They were induced by stimulation of 41 points in various portions of the pontine and mesencephalic tegmentum. Slow waves had a duration of 30 sec to 3 min, being associated with no change or a decrease in SBP. They were induced by stimulation of 12 points in the rostral pontine reticular formation and the mesencephalic reticular formation. Plateau waves had a duration of 3 min or more, being associated with no change or a decrease in SBP. They were induced by stimulation of 2 points in the mesencephalic reticular formation 2 mm lateral to the red nucleus, where slow waves had been induced at the early stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Late cardiac events of coronary bypass surgery].

The cardiac events of 598 patients undergoing coronary bypass surgery were analyzed. The hospital and late death was 4.9% and 3.8%, respectively. The late death were caused by cardiac events in 7 patients and non-cardiac events in 16 patients. Of 7 cardiac death, 5 patients were died of acute myocardial infarction (AMI), and 2 patients were died of congestive heart failure. 5-year survival rate, 5-year event free ratio, and 5-year non-cardiac event free ratio were 88%, 70% and 91%, respectively. Of 18 patients who suffered from AMI after operation, 5 patients died. The causes of AMI were grafts occlusion in 9 patients, progression of coronary lesions in 5 patients and unknown in 4 patients. PTCR, PTCA and rebypass surgery were performed in 4, 9 and 8 patients, respectively.

Adult↗
PubMed1989

[Dynamic changes in the medial arch of the foot in childhood during walking].

The purpose of this study was to estimate the period of gait maturation from the viewpoint of changes of the medial arch of the foot. Gait studies are performed on normal children between the ages of seven and twelve years and compared with those of normal adults. The first peak of lengthening of the medial arch of the foot, caused mainly by the vertical force on the foot, is shortened with age and becomes almost the same as the adult at nine years of age. In the late stage of the stance phase, the pattern of the medial arch becomes almost the same as the adult at twelve years of age. It is suggested that the medial arch of the foot during walking is well established at the age of nine years in foot flexibility, and finally transformed into an adult pattern at the age of twelve years in relation to foot flexibility and muscle force.

Aging↗
PubMed1989

[Ph1 positive acute lymphoblastic leukemia with DIC after operation of colon and lung cancer].

We reported a rare case of triple cancers with acute lymphoblastic leukemia (ALL) associated with disseminated intravascular coagulopathy (DIC) after the operations of colon cancer and primary lung cancer. A 78-year-old Japanese male, who had been operated upon for colon cancer (adenocarcinoma) on March 1981, metastatic brain tumor (adenocarcinoma) on December 1986, and primary lung cancer (squamous cell carcinoma) on February 1987, was admitted to our hospital because of severe general malaise on December 6 1987. On admission, he had mild hepatosplenomegaly and hemorrhage diathesis such as purpura. Serum LDH increased to 2,515 mU/ml. The white blood cell count was 6,210/microliters with 53% leukemia cells, and the platelet count was 12,000/microliters. A bone marrow was infiltrated with 96.0% leukemia cells. The leukemia cells stained positively for PAS and negatively for peroxidase. Immunological examination of leukemia cells showed that HLA-DR, TdT, B1 and J5 were positive and cytoplasmic Igmu and surface Ig were negative, indicating common ALL. The coagulation studies revealed that the activated partial thromboplastin time was prolonged to 42.0 seconds, FDP increased to 79.9 micrograms/ml, and antithrombin-III decreased to 62%. Chromosome analysis showed a 48, XY, +2, +21q-, t(9;22) karyotype. He was diagnosed as having Ph1 positive ALL associated with DIC. He was treated with vindesine, prednisolone, L-asparaginase, and adriamycin and complete remission (CR) was achieved after two months. But on August 1988, 8 months after CR, ALL and brain tumor relapsed and he died of pneumonia on September 19, 1988.

Adenocarcinoma↗
PubMed1988

Human M2-type pyruvate kinase: cDNA cloning, chromosomal assignment and expression in hepatoma.

Two overlapping clones, covering the entire coding sequence of human M2-type pyruvate kinase (PK) cDNA, were isolated and sequenced. Nucleotide sequencing results showed that they contained the 109-bp 5'-untranslated region, the 1593-bp coding region and the 585-bp 3'-untranslated region. Nucleotide sequence homology was 90% and 69% with rat M2-type and L-type PK cDNA, respectively. In situ hybridization using the human M2-type PK cDNA probe disclosed that the gene for M2-type PK is located at band q22 on chromosome 15. Northern blot analysis with RNA from human hepatoma demonstrated that M2-type PK was predominantly expressed in hepatoma cells, whereas L-type PK was preferentially expressed in the non-tumor portion of the liver.

Amino Acid Sequence↗
PubMed1988

Fulminant clonal expansion of large granular lymphocytes. Characterization of their morphology, phenotype, genotype, and function.

A 39-year-old woman exhibited abrupt malignant transformation of the large granular lymphocytes (LGL) after a chronic course of T gamma-lymphoproliferative disease (T gamma-LPD). The T gamma-lymphocytes were CD2+, CD3-, CD8-, CD16+, Leu7-, and Leu19+ with morphologic characteristics of LGL. Newly appearing LGL were much larger and had more prominent azurophilic granules. Although fundamentally they had the same phenotype as the LGL in chronic stage, they showed increased Ia-like antigen and decreased CD16 antigen expressions. Immunoglobulin (Ig) G-kappa type monoclonal component was detected in the patient's serum. The LGL showed a germ-line configuration for T-cell receptor (TCR) beta and gamma chain genes, whereas the clonal chromosomal abnormalities indicated the neoplastic nature of the LGL. The LGL exhibited competent natural killer (NK), interleukin 2 (IL2) activated killer (AK), and antibody-dependent cell-mediated cytotoxicity (ADCC) activities. The LGL may have derived from NK cells at their mature stage with prethymic phenotype and may have influenced the homeostasis of the patient's humoral immune response.

Adult↗
PubMed1988

Establishment of a peripheral T-cell lymphoma cell line showing amplification of the c-myc oncogene.

A new T-cell lymphoma cell line, designated T34, was established from freshly isolated lymph node tumor cells of a patient with non-Hodgkin's diffuse large cell lymphoma. The T34 cells, as well as the parental lymphoma cells, showed mature helper/inducer immunophenotypes in that they formed spontaneous sheep erythrocyte rosettes and reacted with OKT-3 and OKT-4 monoclonal antibodies. They were negative for OKT-6, OKT-8, terminal deoxynucleotidyl transferase, WT-1, and HLA-DR antigens. Molecular analysis revealed that the T34 cells contained 8- to 16-fold amplified c-myc DNA. The same genetic change was observed in parental lymphoma cells, indicating that the c-myc amplification had occurred in vivo. There was no gross rearrangement of the c-myc DNA. The c-myc gene of the T34 cell line was actively transcribed into normal-sized c-myc mRNA. Cytogenetic analysis showed that both the T34 and the parental lymphoma cells had a near-triploid karyotype with multiple structural chromosome changes. The terminal end of the long arm of chromosome No. 8, the chromosomal locus of single-copy c-myc, was elongated (8q+ chromosome), perhaps reflecting the site of c-myc amplification. These data suggested that amplification of the c-myc oncogene played some role in progression and proliferation of this peripheral T-cell neoplasm.

Aged↗
PubMed1988

Effects of phentolamine and atropine on angina pectoris induced by handgrip test in patients with variant angina.

In 19 patients with variant angina, handgrip test as an isometric exercise was performed in 3 conditions on different successive days in the early morning: in the control, after administration of phentolamine (0.3 mg/kg) and after administration of atropine sulfate (0.04 mg/kg). Angina associated with ST-segment elevation on the electrocardiogram was induced in 5 patients (26%) in the control condition, in 14 (74%) after phentolamine and in 5 of 16 (31%) after atropine. All anginal events but 1 occurred after the cessation of the exercise and were not associated with the significant increase of rate-pressure products. These attacks were considered to be due to coronary spasm. The frequency of the induction of angina was significantly higher after phentolamine than in the other 2 conditions (p less than 0.01). It is concluded that the attack can be induced by the handgrip exercise in a sizable number of patients with variant angina, and that the administration of phentolamine increases the incidence of angina induced by handgrip exercise. The mechanism or mechanisms by which coronary spasm is induced by handgrip exercise remains to be elucidated.

Adult↗
PubMed1988

Genotypic analysis using a Y-chromosome-specific probe following bone marrow transplantation.

To monitor successful engraftment after bone marrow transplantation, we performed Southern hybridization analysis or dot blot analysis of DNA in a set of sex-mismatched cases using a Y-chromosome-specific DNA probe (pHY10). This method was extremely sensitive and rapid for checking which cells contain the Y-chromosome. Using this probe, analysis of cells from peripheral blood and bone marrow after transplantation demonstrated the usefulness of confirming engraftment of donor cells and of detecting mixed lymphohematopoietic chimerism.

Adult↗
PubMed1988

Elevated erythrocyte adenosine deaminase activity in a patient with primary acquired sideroblastic anemia.

We report a case of primary acquired sideroblastic anemia (PASA) associated with elevated erythrocyte adenosine deaminase (ADA) activity. The patient was an 85-year-old Japanese male. Analysis of the peripheral blood revealed pancytopenia, and the bone marrow findings showed marked ringed sideroblasts and chromosomal deletion (46XY, 11q-). The erythrocyte ADA activity was 17 times higher than that of normal control, the leukocyte ADA activity was within the normal range, and the plasma ADA activity was 2 times higher than the normal mean. The adenine nucleotides in the patient's erythrocytes were within normal range. According to starch gel electrophoresis, ADA isozyme of the patient was ADA 1. Western blotting showed an increased amount of ADA protein in the patient's erythrocytes. Southern blotting revealed no gene amplification or large structural change. Dot blot analysis of the reticulocyte mRNA showed no increase in the amount of ADA mRNA in the patient's reticulocytes compared with those of reticulocyte-rich controls. We considered that the mechanism of elevated ADA activity in this acquired defect was similar to that found in hereditary hemolytic anemia associated with ADA overproduction.

Adenine Nucleotides↗