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Biomedical subjects

T Maeda

Publications and source records attributed to T Maeda.

At least 631 records · Page 35Linked to original sources
PubMed1995

Posttranscriptional inhibition of mouse placental lactogen-II secretion by transforming growth factor beta 1: synergistic effects with epidermal growth factor and interleukin-6.

We studied the effect of transforming growth factor beta 1 (TGF beta 1) on mouse placental lactogen (mPL)-I and mPL-II secretion by primary cultures of placental cells from Days 7, 9, and 12 of pregnancy. We also studied the effects of co-incubation of epidermal growth factor (EGF) or interleukin-6 (IL-6) with TGF beta 1 on mPL-I and mPL-II secretion. TGF beta 1 at 10 ng/ml did not affect mPL-I secretion by cells from Days 7 or 9 of pregnancy or mPL-II secretion by cells from Day 7 of pregnancy but significantly inhibited mPL-II secretion by cells from Days 9 or 12 of pregnancy. The lowest concentration of TGF beta 1 that significantly inhibited mPL-II secretion by cells from Days 9 or 12 of pregnancy was 1 ng/ml. Immunocytochemistry for mPL-II indicated that treatment of placental cells from Day 12 of pregnancy with 10 ng/ml TGF beta 1 significantly reduced the number of mPL-II-containing cells. Inhibition of mPL-II secretion by TGF beta 1 was eliminated completely by addition of an anti-TGF beta 1 antibody. Northern analysis showed that steady state levels of mPL-II mRNA were not reduced by incubation of placental cells from Day 12 of pregnancy with 10 ng/ml TGF beta 1 for 5 days. EGF at 10 ng/ml significantly inhibited mPL-II secretion by cells from Day 7 of pregnancy, and addition of 10 ng/ml TGF beta 1, which did not itself inhibit mPL-II secretion by those cells, enhanced the inhibition by EGF of mPL-II secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Small hepatocellular carcinomas undetected on two-phased incremental computed tomography. Angiographic and clinicopathologic findings.

RATIONALE AND OBJECTIVES: To elucidate the characteristic clinicopathologic features of hepatocellular carcinomas (HCCs) undetected on two-phased incremental computed tomography (CT). METHODS: Computed tomographic scans of 115 surgically resected small (< or = 3 cm) HCCs from 83 patients were performed 45 seconds and 6 minutes after the administration of contrast material. These scans were compared with corresponding angiographic and histopathologic findings. RESULTS: Eighty HCCs (70%) were depicted on the early images; 73 (63%) on the delayed images; and 89 (77%) using two-phased incremental CT. The small HCCs undetected on the early images but seen histologically had the following characteristics: (1) absence of a fibrous capsule, (2) well-differentiated tumor, (3) replacing growth patterns of the tumors, (4) lack of fatty metamorphosis and/or clear cell changes, (5) hypovascular on angiography. Those not seen on delayed images had the following characteristics: (1) absence of a fibrous capsule, (2) replacing growth patterns, and (3) presence of portal tracts in the tumors. CONCLUSIONS: The replacing growth pattern and the presence of portal tracts correlate with the undetectability on CT. For HCCs undetected on CT, treatment methods must be considered carefully, because the HCCs may be receiving transsinusoidal and portal blood supplies.

Adult↗
PubMed1995

The primary cytotoxicity in ultraviolet-a-irradiated riboflavin solution is derived from hydrogen peroxide.

The cytotoxic action of near-ultraviolet (UVA) radiation on cultured mammalian cells is dependent upon oxygen, suggesting that reactive oxygen species are involved in the cellular action of the radiation. Flavins are thought to be an important chromophore for photo-induced skin injury. Irradiation of riboflavin with UVA radiation is known to produce singlet oxygen, superoxide anions, and triplet-state riboflavin radicals, which, however, are immediately quenched by many constituents of the human skin. If the chemical produces a long-lived reactive oxygen species, hydrogen peroxide (H2O2), after UVA radiation, its deleterious effect is not limited to its generation site. Thus, we investigated whether H2O2, is produced in UVA-irradiated riboflavin solution and whether it plays an important role in the cytotoxic action of the solution. The solution showed a marked cytotoxic effect when placed on human fibroblasts, and cytotoxicity was retained in the solution for at least 40 min after radiation. Most of the toxicity appeared to be derived from H2O2 produced in the solution, because the solution lost its cytotoxicity as a result of catalase treatment, and the resultant restoration of survival was almost complete. Under our conditions, two molecules of riboflavin were calculated to produce one molecule of H2O2 after UVA radiation.

Catalase↗
PubMed1995

Chronological difference in walking impairment among Japanese group A xeroderma pigmentosum (XP-A) patients with various combinations of mutation sites.

Almost all Japanese group A xeroderma pigmentosum (XP-A) patients have nonsense and/or nonsense codon-leading mutations in the XP group A (XPA) gene, and develop neurological abnormalities. Walking ability is one of the most important neuromuscular functions of the patients, because it determines their daily activities. We studied the correlation between the various combinations of mutations found by PCR-RFLP in Japanese XP-A patients and their chronological walking impairment. We classified these patients into six groups. Group I: A patient who was homozygous for the mutation at codon 116 in exon 3 (Type 1 mutation) could never walk unaided. Group III: Typical patients who were homozygous for the mutation at intron 3 (Type 2 mutation) could walk unaided till 7-16 years of age. Group V: Patients who were compound heterozygous for Type 2 mutation and for the mutation at codon 228 in exon 6 (Type 3 mutation) began to develop some walking difficulty at 5-13 years of age and became unable to walk at 25-28 years of age. Group VI: A patient who was homozygous for Type 3 mutation could walk unaided without any difficulty till the age of 21. The walking ability of group II and IV patients is not known yet.

Adolescent↗
PubMed1995

Humoral and cellular immune responses to dihydrolipoamide dehydrogenase (E3): lack of specificity for primary biliary cirrhosis.

Immune responses to dihydrolipoamide dehydrogenase, the E3 subunit which is a common component of 2-oxoacid dehydrogenase complexes, have been suggested to be associated with the etiology of primary biliary cirrhosis (PBC). However, since an antibody to E3 could be detected in Caucasian patients with PBC, but was not specific for the disease, the proposal is not evident at the antibody level. We have identified the antibody also in Japanese patients with PBC by immunoblotting with sera at a 1:100 dilution and have assessed cellular immune responses to E3 by proliferation assay of peripheral blood lymphocytes. Anti-E3 antibody was detected more frequently in 25 of 43 PBC (58.1%) than in normal controls (p < 0.01) and in chronic liver diseases (p < 0.05), but the antibody was not specific for PBC as reported in Caucasian PBC. Anti-E3 antibody-positive sera of PBC patients or normal controls and their IgG fraction did not inhibit the enzyme activity of E3. Lymphocyte blastogenesis to E3 in PBC was significantly greater than normal controls (p < 0.05), but was not significant as compared with chronic liver disease or non-hepatic autoimmune diseases. Thus, these data do not support the hypothesis that the immune response to the E3 subunit is associated with etiology of PBC.

Autoantibodies↗
PubMed1995

The arterial ketone body ratio and serum alpha-fetoprotein level in patients with acute hepatic failure.

Hepatocyte regeneration is essential for recovery in acute hepatic failure, although it requires a large amount of energy. The ratio of acetoacetate to beta-hydroxybutyrate in arterial blood has been reported to reflect the cellular energy charge of hepatocytes, and we proposed that the recovery of the ratio in the early days of acute hepatic failure is essential for survival. However, there is no report on any marker of regeneration to confirm this hypothesis. In this study, we have assessed this ratio and the serum alpha-fetoprotein level sequentially in 26 patients with acute hepatic failure. Ten patients recovered and 16 died. The arterial blood ketone body ratio 3 days after the onset of hepatic encephalopathy of grade II or more was below 0.6 in 15 of the 16 nonsurvivors, whereas that in the 10 survivors was above 0.6. There was a positive correlation between the arterial blood ketone body ratio and the maximal concentration of alpha-fetoprotein (r = 0.465, p < 0.02 by Student's t-test). These data indicate that the arterial blood ketone body ratio is a marker for the capacity of the liver to regenerate and for the prognosis in patients with acute hepatic failure: effective hepatocyte regeneration may be impossible if these metabolic changes in acute hepatic failure impair the hepatocyte energy charge severely.

3-Hydroxybutyric Acid↗
PubMed1995

Role of excitatory amino acid-mediated ionic fluxes in traumatic brain injury.

One major event taking place at the moment of traumatic brain injury in neuronal cells is the occurrence of massive ionic fluxes across the plasma membrane, which can be referred to as traumatic depolarization (TD). Unlike spreading depression, TD can occur over wide brain areas simultaneously. Furthermore, recovery from TD often takes far longer than recovery from ionic perturbation elicited by the passage of a single wave of spreading depression. Neuronal cell damage caused by ischemic brain injury is also initiated by massive ionic fluxes, termed anoxic depolarization. The occurrence of similar ionic events in these two forms of brain injury may account for the genesis of diffuse ischemia-like damage without actual episodes of hypoxia or ischemia in traumatic brain injury. We review the data indicating that excitatory amino acids (EAA) may play a vital role in producing TD, and that such EAA-mediated ionic perturbation is responsible for a number of posttraumatic events including subcellular metabolic dysfunction and cellular responses such as microglial activation and astrocytic transformation. TD may represent one of the most important mechanisms of diffuse neuronal cell dysfunction and damage associated with traumatic brain injury.

Animals↗
PubMed1995

Uneven fatty replacement of the pancreas: evaluation with CT.

PURPOSE: To determine the computed tomographic (CT) features of uneven fatty replacement of the pancreas and clarify their radiologic and clinical importance. MATERIALS AND METHODS: CT scans from 80 patients with uneven fatty replacement of the pancreas were reviewed. Uneven fatty replacement of the pancreas was classified into two types. In type 1, the posterior aspect of the head of the pancreas was spared from intense fatty replacement. In type 2, the focal area around the common bile duct (CBD) was spared from fatty replacement. Each type was divided into two subgroups on the basis of whether the body and tail of the pancreas showed intense fatty replacement (type a = negative for intense fatty replacement, type b = positive for intense fatty replacement). Findings from endoscopic retrograde cholangiopancreatography performed in five patients, histopathologic examination in one patient, and clinical examination in all 80 patients were also evaluated. RESULTS: Twenty-eight patients (35%) had type 1a replacement, 29 (36%) had type 1b replacement, nine (11%) had type 2a replacement, and 14 (18%) had type 2b replacement. In all patients, the anterior aspect of the head of the pancreas showed distinctly lower attenuation at CT. CONCLUSION: Fatty replacement is more severe in the anterior aspect of the head of the pancreas. The posterior aspect of the head of the pancreas and the area around the CBD tended to be spared.

Adult↗
PubMed1995

Acute progressive and extensive metastatic calcifications in a nephrotic patient following chronic hemodialysis.

We report on a 46-year-old female patient with a 5-year history of refractory nephrotic syndrome who rapidly developed extensive metastatic calcifications in lung, bone, blood vessels, skin, uterus and other soft tissues following maintenance hemodialysis. She was admitted for controlling anasarca. On admission, she suffered from severe nephrotic syndrome and chronic renal failure, showing 1.3 g/dl of serum albumin and 4.6 mg/dl of serum creatinine. She received bicarbonate dialysis combined with extracorporeal ultrafiltration to control anasarca. Following hemodialysis, she was treated with alfacalcidol and an increasing dose of calcium carbonate. Although anasarca was controlled, her nephrotic state remained unchanged. After 3 months of dialysis, roentgenograms of the body disclosed multiple metastatic calcifications. At this time, though the calcium-phosphorous product in serum was almost normal, the free calcium index was confirmed to have been high for 4 weeks. We considered that administration of calcium carbonate and alfacalcidol as well as an influx of free calcium from a dialysate resulted in increased serum ionized calcium which may be unable to be bound to serum protein because of lack of total protein, leading to ectopic deposition of calcium and phosphate. Our findings suggested that intensive care is needed to prevent metastatic calcification when uremic patients with severe nephrosis are treated with bicarbonate hemodialysis.

Acute Disease↗
PubMed1995

Plasma plasminogen activator inhibitor-1, tissue plasminogen activator and serum lipoprotein(a) after reperfusion therapy in acute myocardial infarction: comparison between sequential and direct percutaneous transluminal coronary angioplasty.

To determine which reperfusion therapy for acute myocardial infarction (AMI) is advantageous to avoid subsequent thrombotic coronary occlusion, 8 patients with AMI were studied. Four of them (group S) underwent sequential PTCA following unsuccessful intracoronary thrombolysis and the others (group D) direct PTCA. Serial changes in plasma plasminogen activator inhibitor-1 (PAI-1), plasma tissue plasminogen activator (t-PA) antigen and serum lipoprotein(a) levels were compared between the two groups. In group S, plasma PAI-1 levels showed no significant serial change after PTCA. However, in group D, plasma PAI-1 levels increased significantly 4-24 h after PTCA. We suggest that more attention should be focused on the prevention of thrombotic coronary closure as well as mechanical abrupt occlusion after direct PTCA.

Angioplasty, Balloon, Coronary↗
PubMed1995

Immunopathological mechanisms of human T cell lymphotropic virus type 1 (HTLV-I) uveitis. Detection of HTLV-I-infected T cells in the eye and their constitutive cytokine production.

The immunopathology of human T cell lymphotropic virus type 1 (HTLV-I) uveitis was addressed by using T cell clones (TCC) established from the intraocular fluid of patients with HTLV-I uveitis. Proviral DNA of HTLV-I was identified in 55 out of 94 (59%) or 13 out of 36 (36%) TCC from the ocular fluid or the peripheral blood of these patients, respectively. Most of HTLV-I-infected TCC had a CD3+ CD4+ CD8- phenotype. HTLV-I infection on TCC was confirmed by analysis of the viral mRNA, nucleotide sequence, virus-associated proteins, and virus particles. HTLV-I-infected TCC, but not HTLV-I negative TCC, constitutively produced high amounts of IL-6 (1,336 +/- 1,050 pg/ml) and TNF-alpha (289 +/- 237 pg/ml) in the absence of any stimuli. HTLV-I-infected TCC from the ocular lesion also constitutively produced high amounts of IL-1 alpha (12,699 pg/ml), IL-2 (61 pg/ml), IL-3 (428 pg/ml), IL-8 (1,268 pg/ml), IL-10 (28 pg/ml), IFN-gamma (5,095 pg/ml), and GM-CSF (2,886 pg/ml). Hydrocortisone, a drug effective in vivo for the treatment of HTLV-I uveitis, severely depressed cytokine production in vitro in most cases. In summary, the results demonstrated direct evidence of HTLV-I infection of the eye and suggest that cytokines produced by HTLV-I-infected T cells are responsible for the intraocular inflammation in patients with HTLV-I uveitis.

Adult↗
PubMed1995

Cyclic adenosine-3',5'-monophosphate stimulates mouse placental lactogen-I (mPL-I) secretion but inhibits mPL-II secretion at midpregnancy.

To determine whether cAMP regulates mouse placental lactogen-I (mPL-I) and mPL-II secretion at midpregnancy in vitro, mouse placental tissue from day 9 of pregnancy was dispersed with collagenase, cells were fractionated on a Percoll gradient, and the purified trophoblast cells were plated in a serum-free medium. The cells were then incubated with various agents that increased the intracellular cAMP level for 5 days. 8-Bromo-cAMP stimulated mPL-I secretion, but inhibited mPL-II secretion in a time- and dose-dependent manner without changing the amount of newly synthesized trichloroacetic acid-precipitable proteins. Cholera toxin and forskolin, which increase intracellular cAMP accumulation, also regulated mPL-I and mPL-II secretion in the same manner. 8-Bromo-cAMP increased the intracellular mPL-I concentration, decreased the intracellular mPL-II concentration, and increased the immunoprecipitable newly synthesized mPL-I concentration in both the medium and cells. 8-Bromo-cAMP increased the expression of mPL-I messenger RNA and decreased the expression of mPL-II messenger RNA. The sequential reverse hemolytic plaque assay and double immunocytochemistry indicated that 8-bromo-cAMP regulates the subpopulation of giant cells containing and releasing mPL. These findings suggest that an increase in intracellular cAMP stimulates mPL-I secretion, but inhibits mPL-II secretion by changing the subpopulation of giant cells containing and releasing mPL.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1995

Cyclic adenosine 3',5'-monophosphate stimulation of placental proliferin and proliferin-related protein secretion.

To identify factors that regulate proliferin (PLF) and PLF-related protein (PRP) secretion by the mouse placenta, placental cells from day 9 of pregnancy were cultured for up to 5 days, and PLF and PRP release into the medium was assessed by RIA. Transforming growth factor-alpha, interleukin-1 alpha, and interleukin-6 did not regulate either PLF or PRP secretion. However, treatment of primary placental cell cultures with 8-bromo-cAMP, cholera toxin, or forskolin resulted in 2- to 3-fold increases in the percentages of PLF- and PRP-producing cells in the population and corresponding increases in both PLF and PRP messenger RNA and secreted protein. The increase in the number of PLF-producing cells was accompanied by an increase in the number of cells expressing both PLF and mouse placental lactogen-I. These data suggest that cAMP levels can regulate trophoblast giant cell differentiation and, consequently, the amount of PLF and PRP secretion.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1995

Extraction of water-soluble vitamins from pharmaceutical preparations using AOT (sodium di-2-ethylhexyl sulfosuccinate)/pentane reversed micelles.

Reversed micelles can be used to concentrate water-soluble materials in the water pool. In this study, the extraction of water-soluble vitamins into reversed micelles was attempted, and a flow system was used to determine the time-course of the vitamin extraction. The efficiency of extraction was strongly affected by the extraction temperature and the concentration of reversed micelles, and the selectivity depended on the size of micelles. Water-soluble vitamins could be efficiently and rapidly extracted. The selective extraction of a model mixture of vitamins from pharmaceutical preparations was also attempted. Moreover, the usefulness of the proposed method for the determination of vitamins in various commercial tablets was also demonstrated. Using of this method, the surfactant remains mixed with the extracted compounds, and so we attempted to remove the surfactant from the extract by supercritical fluid extraction. Supercritical carbon dioxide containing 7.5% ethanol as entrainer was found to be the most efficient solvent for removing residual surfactant from the extract.

Ascorbic Acid↗
PubMed1995

Electrocardiographic abnormalities in patients with Cushing's syndrome.

The electrocardiograms in 8 patients with Cushing's syndrome and 4 with Cushing's disease were studied. The patients were divided into group A with electrocardiographic abnormalities and group B without. The mean age was significantly higher in group B than in group A. However, blood pressure, mean heart rate and the plasma adrenocorticotropic hormone level showed no significant differences between the two groups. In group A, the plasma concentration of cortisol had a tendency to be higher than in group B (A vs. B: 281 +/- 100 ng/ml, 188 +/- 9 ng/ml, respectively). Echocardiography performed on three of four patients in group A revealed cardiac hypertrophy. While, in group B, echocardiography performed on two patients showed no hypertrophic findings. As a result, it seems that the electrocardiographic changes are correlated with the plasma level of cortisol via myocardial hypertrophy.

Adrenocorticotropic Hormone↗
PubMed1995

Primary hypoparathyroidism in Turner's syndrome.

A case of hypoparathyroidism accompanied with Turner's syndrome is reported. On admission, a 44-year-old woman had facial dystonia, deafness, and primary amenorrhea. Laboratory examinations showed a decrease in serum PTH and mosaicism of 45,X and 46,XX(6:34). A brain CT revealed marked calcification in the basal ganglia, cerebellum and periventricular area. Antiparkinsonian drugs were found to be effective for the dystonia. This case therefore suggests that some relationship may exist between intracranial calcification and Turner's syndrome.

Adult↗
PubMed1995

Effects of salivary immune response to Streptococcus mutans on caries occurrence and caries development in mice with autoimmune disease.

MRL/l strain mice, which possess a lymphoproliferative gene inducing swelling of systemic lymph nodes, develop a SLE (systemic lupus erythematosus)-like syndrome at around 8 w of age. MRL/n mice, which carry 99.6% of the genes of MRL/l mice, lack the gene for lymphoproliferation and exhibit only a slight degree of lymph node swelling late in life. This study investigated whether the salivary immune response caused by Streptococcus mutans(S. mutans) infection prevented dental caries in MRL/l and MRL/n mice after 8 w of age. A total of 10 MRL/l mice and 10 MRL/n mice were fed a commercial pellet diet without sucrose until 74 d of age, and then fed Diet 2000 containing 56% sucrose ad libitum from 75 to 130 d of age. On d 75, both strains of mice were inoculated with S. mutans JC-2 for 7 d. At 130 d of age, saliva samples were collected and caries scores were assessed. The results obtained suggested that the salivary immune response was one of the most important factors regulating caries occurrence.

Animals↗