Search PubMedSearch

Biomedical subjects

H Yamamoto

Publications and source records attributed to H Yamamoto.

At least 19 recordsLinked to original sources

[Semidiscoid lateral meniscus].

We propose a new entity known as "semidiscoid lateral meniscus" of the knee. The diagnostic criteria for semidiscoid lateral meniscus is the appearance on a thin-sliced axial 3-D image of a crescent-shaped meniscus whose transverse width is within 11.6 mm to 14.3 mm on the coronal image. These numerical values were calculated by discriminant analysis. A retrospective review of MR examinations of the knees revealed 15 patients (15 knees) with this entity. These patients were our subjects. Of these 15 patients, complicated lateral meniscal tears were seen in only three cases. Nine knees were free from complications, and five were asymptomatic. Six patients were examined with MR on the contralateral side, and discoid lateral menisci were revealed in all cases. Thus semidiscoid lateral meniscus shows a cross-relationship with discoid menisci.

Adolescent

The p53 tumor-suppressor gene and ras oncogene mutations in oral squamous-cell carcinoma.

The frequencies of mutations in the p53 tumor-suppressor gene and ras proto-oncogenes were investigated systematically in surgically resected oral squamous-cell carcinomas (SCCs) using single-strand conformation polymorphism (SSCP) and/or dot-blot hybridization analysis of DNA fragments which had been amplified by the polymerase chain reaction (PCR). p53 gene mutations, within the region of exons 5 to 8, were detected in 17 out of 27 (63%) tumor specimens. The role of p53 mutations in cell-line establishment was investigated. p53 gene mutations were detected in 5 out of 6 tissue samples from which cell lines were established and in 4 out of 5 specimens from which cell lines could not be established, suggesting that the presence of p53 gene mutations is not by itself sufficient for cell-line establishment. Tumor samples were also analyzed for point mutational activation of the ras proto-oncogenes. One out of 30 (3%) tumors showed an activating point mutation in codon 12 of H-ras, this being consistent with reports from Europe and USA but not with any from India. Compared to frequencies of the other genetic changes so far reported for oral SCC, the p53 mutations have been observed most often to undergo genetic change. p53 gene mutation is thus intimately involved in the genesis of oral SCC and consequently should be useful as a marker for the diagnosis of this neoplasm.

Adult

[MR angiography enhanced by sodium acetazolamide].

We tried to use sodium acetazolamide to enhance MR angiography (MRA). Sodium acetazolamide, one of carbonic anhydrase inhibitors, has an effect to increase regional cerebral blood flow. We made a direct comparison between pre and post enhanced MRA (both 3D-TOF and 3D-PC techniques). MRA after administration of sodium acetazolamide could depict more details of cortical branches without enhancement of back-ground. So we recommend this simple method to be used widely in any examination of MR angiography.

Acetazolamide

Inhibitory effects of psychotomimetic sigma ligands on nicotine-induced K+ flux from differentiated PC12 cells.

In NGF-treated PC12 cells, nicotine-induced K+ release was measured with a K(+)-sensitive microelectrode. The K+ outflow via nicotinic ACh receptor cation channels was inhibited by various psychotomimetic sigma ligands in the sequence of PCP, dextromethorphan >> DTG, MK 801, (+)SKF10047 >> (+)3-PPP. The K+ release was not affected by the neuroleptic sigma ligand haloperidol nor by the calcium antagonist nifedipine. The results suggest that psychotomimetic sigma ligands inhibit nicotine-stimulated K+ flux by interacting with nicotinic, rather than via sigma 2 receptors.

Animals

Structure and expression of the gene encoding mouse t-complex polypeptide (Tcp-1).

The nucleotide (nt) sequence of the structural gene (Tcp-1) encoding mouse t-complex polypeptide 1 (TCP-1) has been determined. The nt sequence extending to 10,043 bp shows that the Tcp-1 gene is divided into 12 exons, 11 introns and 5'- and 3'-flanking regions. The Tcp-1 gene has a tight cluster of major transcription start points (tsp). Two GC boxes, one CCAAT box and some other possible regulatory elements are located in the region upstream from the tsp, but no TATA box was found. Extending from the 5'-flanking region to the first intron, a CpG dinucleotide-rich cluster is located. In addition, Tcp-1 gene transcripts in mouse organs, embryos and cultured cells were analyzed by Northern blotting. The Tcp-1 mRNA is enriched not only in testes, but also in early post-implantation embryos and some cultured cell lines, as compared with mouse organs other than the testis. The amount of Tcp-1 mRNA in embryos decreases during development. These results suggest that the expression of the Tcp-1 gene may be regulated spatially and temporally in embryonic and adult mice by transcriptional control or by mRNA stability.

Amino Acid Sequence

Mutations in genes for acetylcholinesterase intensify lethality by acrylamide in Caenorhabditis elegans.

Acrylamide inhibits growth and results in death in the nematode Caenorhabditis elegans. The lethargic effect is marked in the mutants defective in genes for acetylcholinesterase (AChE) and the effect is approximately parallel with the decrease in AChE activity by mutations. Although neither the activity nor the localization of the enzyme is affected by acrylamide, the acetylcholine level was significantly elevated.

Acetylcholinesterase

Polyclonal and monoclonal antibodies monospecific to MMTV LTR orf protein produced in E. coli.

Monoclonal and polyclonal antibodies specific to an open reading frame of the mouse mammary tumor virus long terminal repeat were generated using an open reading frame-beta-galactosidase fusion protein produced in E. coli. Both antibodies reacted with the open reading frame-beta-galactosidase fusion protein but not with beta-galactosidase alone using an immunoblotting technique. It is concluded that these antibodies were specific for the protein encoded by the open reading frame of the mouse mammary tumor virus long terminal repeat.

Antibodies, Monoclonal

Glycoprotein-binding site of dystrophin is confined to the cysteine-rich domain and the first half of the carboxy-terminal domain.

Dystrophin, a protein product of the Duchenne muscular dystrophy gene, is thought to associate with the muscle membrane by way of a glycoprotein complex which was co-purified with dystrophin. Here, we firstly demonstrate direct biochemical evidence for association of the carboxy-terminal region of dystrophin with the glycoprotein complex. The binding site is found to lie further inward than previously expected and confined to the cysteine-rich domain and the first half of the carboxy-terminal domain. Since this portion corresponds well to the region that, when missing, results in severe phenotypes, our finding may provide a molecular basis of the disease.

Amino Acid Sequence

Simian immunodeficiency virus-specific cytotoxic T lymphocytes are present in the AIDS-associated skin rash in rhesus monkeys.

An infiltration of CD8+ lymphocytes in the dermis and epidermis underlies the skin rash that commonly occurs as a primary manifestation of an AIDS virus infection. These cutaneous lymphocytes were characterized in simian immunodeficiency virus of macaques (SIVmac)-infected rhesus monkeys. Skin rash-associated lymphocytes exhibited greater lysis of SIVmac-expressing target cells and a higher cloning efficiency for SIVmac-specific effector T cells than PBL. Moreover, both SIVmac envelope- and gag-specific CTL could be readily cloned from these skin rash-associated lymphocytes. In fact, the skin rash-associated CTL exhibited the same MHC restriction and epitope specificity as those CTL derived from PBL. These studies, therefore, demonstrate that the cutaneous infiltrating CD8+ lymphocytes in SIVmac-infected rhesus monkeys include SIVmac-specific CTL. Thus, whereas virus-specific CTL are likely to represent an important mechanism for controlling AIDS virus infections, they also may play a role in the pathogenesis of the skin lesions that occur after this infection.

Animals

Direct activation of purified Go-type GTP binding protein by tricyclic antidepressants.

A growing body of evidence suggests that tricyclic antidepressant agents (TCAs) interact with GTP binding proteins (G proteins). We have investigated if TCAs directly alter the function of the purified Go protein which is specifically expressed in neuronal tissue. Several TCAs markedly enhanced the GTPase activity of Go protein in a pertussis toxin-susceptible manner, whereas MAO-inhibitor and anxiolytic agent did not. This enhancing effect of TCAs on Go function may be due to an increase in the GDP-GTP exchange reaction occurring on Go. Thus, it is very likely that TCAs can modify various signal transduction by directly interacting with G proteins in brain cells.

Animals

Causes of oral tongue cancer treatment failures. Analysis of autopsy cases.

Eighty-three autopsy cases of squamous cell carcinoma of the oral tongue were reviewed to identify retrospectively the causes of treatment failure. The cure rate for the primary cancers at autopsy was 48.2% (40 of 83). Regional lymph node metastases were found in 71.1% (59 of 83). Regional metastases and/or juxtaprimary recurrence frequently spread continuously and diffusely, forming bulky neck tumors in 38.6% (32 of 83). The incidence of distant lymph node metastasis (below the clavicle) and hematogenous metastasis was 35.4% (29 of 82) and 58.5% (48 of 82), respectively. The lung was the most common site of hematogenous metastases (52.4%, 43 of 82). Hematogenous metastasis occurred more frequently in the younger age group (less than 40 years of age; P = 0.03). Distant lymph node metastases were identified in the lung hilar, bifurcation, and paratracheal nodes in 89.7% (26 of 29) and had a statistically significant association with lung hematogenous metastasis. Univariate analysis revealed that gross appearance, tumor stage, clinical stage, presence of cervical lymph node metastasis, and interval from N0 to NX were significant predictors of survival time (duration from initial treatment to death). Rupture of the neck vessels was fatal in eight patients (9.6%), and hypercalcemia was seen in six (7.2%). Pulmonary infection was the direct cause of death in 33.7% of patients (28 of 83). Secondary malignant lesions occurred in 22.9% (19 of 83).

Adult

Significant existence of deleted mitochondrial DNA in cirrhotic liver surrounding hepatic tumor.

To understand the role of mitochondria in carcinogenesis, we compared the amount of deleted mtDNAs between human hepatic tumors and surrounding cirrhotic portion of the liver of ten patients by using polymerase chain reaction (PCR). Multiple mtDNA deletions were detected in cirrhotic portion, but no deletions were detected in the tumor portion. Direct sequencing of the fragments revealed a 7,079-bp deletion (nucleotide position 8,992-16,072) involving no direct repeated sequences and a 7,436-bp deletion (position 8,649-16,084) involving a 12-bp directly repeated sequence of 5'-CATCAACAACCG-3' exists in both the ATP6 gene and the D-loop region. These mtDNA mutations could be one of the endogenous factors that induce somatic mutations in nuclear genome and etiologically contribute to human carcinogenesis.

Adenoma, Bile Duct

Changes in thrombomodulin level in plasma of endotoxin-infused rabbits.

Changes in the plasma thrombomodulin (TM) level were examined in endotoxin-infused rabbits. The plasma TM level in normal rabbits was 143.8 +/- 8.4 ng/ml (n = 67) and the molecular weight of the major TM was about 55 kd. Endotoxin (lipopolysaccharide, LPS, E. Coli B8:0127) was intravenously infused. LPS infusion increased the plasma TM level dose-dependently between 0.2 mg/kg and 5 mg/kg. When 5 mg/kg LPS was infused, the plasma TM level started to increase immediately and was 2.3 times higher than the control value within 1 hr. The molecular weight of the major TM was about 75 kd. This rapid increase in TM occurred before the decrease in fibrinogen content and the prolongation of prothrombin time. To examine the effect of circulating leukocytes on the TM increase in endotoxin-infused rabbits, 5 mg/kg LPS was infused into rabbits with leukocytopenia induced by X-ray irradiation. The maximum plasma level of TM was significantly lower than in the untreated rabbits given LPS. These data suggest that the increase in plasma TM is caused by LPS-stimulated leukocyte's prior to hemostaseological changes. It is well known that endothelial cells can be injured by stimulated leukocytes, so this increase in plasma TM probably reflects the deterioration of endothelial cells. This deterioration decreases the ability of endothelial cells to inhibit thrombosis, which would, in turn, contribute to the development of disseminated intravascular coagulation in endotoxin-infused rabbits.

Animals

Relative effect of steroid hormone receptors on the prognosis of patients with operable breast cancer. A univariate and multivariate analysis of 3089 Japanese patients with breast cancer from the Study Group for the Japanese Breast Cancer Society on Hormone Receptors and Prognosis in Breast Cancer.

In a retrospective multicenter study to investigate the correlation between estrogen (ER) and/or progesterone receptors (PgR) in primary breast cancer with patient prognosis, 3118 patients with operable breast cancer (International Union Against Cancer Stages I, II, and III) were investigated from ten hospitals in Japan who underwent surgery from October 1972 to December 1982; 3089 were evaluable. The ER-positive and PgR-positive cancers were found in 56% and 34% of patients, respectively. The positivities decreased as the tumor size increased but were independent on lymph node metastasis. There were no significant differences in relapse-free survival (RFS) in relation to receptor status (median follow-up, 89 months [ER], 84 months [PgR]). However, in patients with four or more positive nodes, those with PgR-positive cancer had a longer RFS. The patients with ER-positive cancer survived significantly longer than ER-negative ones, with the greatest difference seen in those with four or more positive nodes. There was a significantly longer postrelapse survival (PRS) for patients with ER-positive cancer because of the different distribution of the major metastasis and better responses to first-line and subsequent treatments. Cox's multivariate analysis showed that overall survival but not PRS was affected by ER (and more weakly by PgR) because of the longer PRS in patients with ER-positive cancer.

Adult

Correlation between photodynamic efficacy of differing porphyrins and membrane partitioning behavior.

The ability of a photosensitizer to partition into membrane is determined by its structure and physical properties. Partitioning behavior can be quantitated as the partition coefficient (Kp) for a particular drug. This property may be an important determinant of cytocidal efficacy in photodynamic therapy. The Kp of five photoactive drugs--13,17-ditetraammonium protoporphyrin (PH1008), photofrin II (PII), hematoporphyrin (Hp), benzoporphyrin derivative monoacid (BPD-MA), coproporphyrin (Cp), and uroporphyrin (Up)--was determined using a simple liposome system composed of sonicated egg phosphatidylcholine single bilayer vesicles. The cytocidal efficacy of each drug was compared by determining the concentration of drug resulting in 50% maximal lysis (C50) obtained by measuring the hemoglobin absorbance at 414 nm released from lysed human red blood cells. The percentage lysis at 1 microM final drug concentration was also determined. An argon-dye laser was used to administer light of 630-nm wavelength for a total exposure of 5 J/cm2. Porphyrins with a greater tendency to partition into phosphocholine bilayer membranes demonstrated a greater lytic efficacy in the rbc system utilized. The comparison of physical properties with lytic ability may be useful in understanding the mechanism by which PDT exerts its effects and in predicting the clinical efficacy of different drugs.

Cell Membrane

Autoantibodies to 64,000-M(r) islet cell protein in long-term type 1 (insulin-dependent) diabetic patients.

Autoantibodies to the 64,000-M(r) (64K) islet cell protein, identified as glutamic acid decarboxylase, were assayed in 46 Type 1 (insulin-dependent) diabetic patients with a disease duration of more than 5 years. Of 46 Type 1 diabetic patients, 18 (39.1%) were found to be positive for 64K antibodies and 12 of these patients had been diagnosed with autoimmune thyroid disease. Serum C-peptide levels were not detectable in 15 of 18 patients positive for 64K antibodies. The samples were also tested for titres of islet cell antibodies. Islet cell antibodies were detected in 15 (32.6%) of the 46 patients and all the islet cell antibody positive patients were also found to be positive for 64K antibodies. Furthermore, of these 15 patients 12 had previously been diagnosed with autoimmune thyroid disease. A correlation between levels of 64K antibodies and islet cell antibody titre revealed that higher levels of 64K antibodies were observed in patients who had higher islet cell antibody titre. These results demonstrate that most long-term Type 1 diabetic patients with 64K antibodies were also positive for islet cell antibodies complicated by autoimmune thyroid disease.

Adult

Heterologous supersensitization between serotonin2 and alpha 2-adrenergic receptor-mediated intracellular calcium mobilization in human platelets.

Recent reports suggest that serotonin (5-HT)2 receptor-mediated second messenger systems are enhanced in platelets of affective disorders. To make the mechanism of the enhanced response clear, we investigated 5-HT2 and alpha (alpha) 2-adrenergic receptor-induced intracellular calcium (Ca2+) mobilization in platelets of healthy volunteers, using fura-2. 5-HT2 and alpha 2-adrenergic receptor-mediated Ca2+ mobilization was enhanced by prior exposure to the other type of agonist, so called "heterologous supersensitization." The supersensitization was due to the enhancement of maximal response without change in agonist affinity. Chelating extracellular Ca2+ did not diminish the supersensitization. This enhancement of Ca2+ mobilization was not inhibited by H-7, an inhibitor of protein kinase C. However, this supersensitization was inhibited by pretreatment with sodium fluoride which directly activates guanine nucleotide binding regulatory proteins (G proteins). These results suggest that the supersensitization was caused from intracellular Ca2+ storage sites through a G protein-coupled pathway.

Blood Platelets