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Biomedical subjects

A Takeda

Publications and source records attributed to A Takeda.

At least 415 records · Page 23Linked to original sources
PubMed1990

An unusual form of lipid linkage to the CD45 peptide.

Some protein kinases and phosphatases are myristoylated on their amino terminus, which perhaps contributes to subcellular localization or regulation. Glycoprotein CD45, a hematopoietic tyrosine phosphatase, was examined for fatty acid content. The CD45 protein incorporated [3H]myristate, but little [3H]palmitate. The label was not metabolized and reincorporated into amino acids or saccharides, as revealed by peptide maps of CD45 labeled with [3H]myristate, 14C-labeled amino acids, [35S]methionine, or 125I, and glycosidase treatments, respectively. The myristate label was resistant to mild alkaline methanolysis and was found in fatty acid and sphingosine, indicating an unusual form of lipid attachment to CD45.

Antigens, Differentiation↗
PubMed1990

Molecular basis of tyrosinase-negative oculocutaneous albinism. A single base mutation in the tyrosinase gene causing arginine to glutamine substitution at position 59.

Tyrosinase-negative oculocutaneous albinism (OCA) is one of classical inborn errors of metabolism, characterized by a complete lack of melanin pigments in the eyes and skin. We have isolated and characterized the tyrosinase gene of one child (F. S.) affected with tyrosinase-negative OCA. Sequence analysis reveals a single-base mutation in the exon 1 (a G to A transition at nucleotide residue 312), causing the Arg (CGG) to Gln (CAG) substitution at position 59. This base change eliminates one MspI site and creates a new BstNI site in the patient's exon 1, which is invaluable for screening other OCA patients and heterozygote carriers for this mutation. We are thus able to confirm that the patient F. S. is homozygous for this OCA allele. The family members of the patient F. S. are phenotypically normal, but are shown to be heterozygote carriers. Transfection of the mutant gene fails to give rise to detectable tyrosinase activity in transient expression assays, suggesting that the mutation affects the stability or the catalytic activity of the enzyme. We therefore propose that the albino phenotype of the patient F. S. is a consequence of the Arg to Gln substitution at position 59 caused by a point mutation in the tyrosinase gene.

Albinism, Oculocutaneous↗
PubMed1990

A point mutation in the tyrosinase gene of BALB/c albino mouse causing the cysteine----serine substitution at position 85.

Murine albinism is characterized by complete lack of melanin pigments in skin and retina. In order to study the molecular basis of albinism, we have cloned and characterized the tyrosinase gene of BALB/c mice (c/c). Sequence analysis of this gene reveals a point mutation at nucleotide residue 387 (G----C transversion) causing a Cys----Ser substitution at position 85 in one of the cysteine-rich domains of the tyrosinase molecule. Since this G----C transversion creates an additional DdeI site, we were able to confirm that this mutation is actually present in BALB/c genomic DNA using DNA amplification techniques. In contrast, both C57BL/6 (C/C) and DBA/2 (C/C) mouse strains carry the G residue at the same position, suggesting that this point mutation is specific for the albino mutation at the c locus. Moreover, we were able to show that the tyrosinase containing Ser-85 is not functional in transient expression of its cDNA. We therefore suggest that a G----C transversion at nucleotide residue 387 of the tyrosinase gene could lead to the albino phenotype of BALB/c mouse.

Albinism↗
PubMed1990

Immunoreactivity of antibodies raised against synthetic peptide fragments predicted from mid portions of dystrophin cDNA.

We synthesized 3 peptide fragments predicted by residues 2354-2368 (peptide I), 2310-2324 (peptide II) and 2255-2269 (peptide III) on the mid-portion of the human dystrophin cDNA map where the most frequent intragenic deletions occurred in Duchenne muscular dystrophy. Rabbit antibodies against these peptides were raised and cryosections of 47 biopsied muscles were studied immunohistochemically. The 47 biopsied muscles included the quadriceps femoris muscles of 8 Duchenne muscular dystrophy patients, 8 child and 5 adult normal controls, 1 facioscapulohumeral dystrophy, 2 limb girdle dystrophy, 3 myotonic dystrophy, 3 polymyositis, 1 mitochondrial myopathy, 1 nemaline myopathy, 3 amyotrophic lateral sclerosis and the extensor digitorum longus muscles of 6 mdx mice (C57BL/10ScSn-mdx) and 6 normal control mice (C57BL/10ScSn). The peptide I antiserum continuously stained the myofiber surface membranes in 8 child and 5 adult normal control muscles, and in 14 other muscles from various neuromuscular diseases, but failed to stain the surface membranes in normal control mice. The surface membranes of 8 Duchenne muscles were not stained by the peptide I antiserum except for a few myofibers. Although the ELISA titers of peptide I, II and III antibodies were high, immunostaining by peptide II antiserum showed no reaction in the myofibers of any of the biopsied muscles, and immunostaining by peptide III antiserum revealed faint reactions on the myofiber surface membranes of all biopsied muscles, including the mdx control mouse muscles except for the Duchenne and mdx myofibers.

Adult↗
PubMed1990

Tumor accumulation mechanism of 99mTc-DL-homocysteine, a model compound for the development of tumor-imaging radiopharmaceuticals.

To elucidate the tumor accumulation mechanism of 99mTc-DL-homocysteine (99mTc-Hcy), the role of mercaptalbumin, a carrier protein of 99mTc-Hcy in blood, was studied. 99mTc-Hcy bound to serum mercaptalbumin was carried to tumor tissue, efficiently adsorbed onto the cell surface, released from albumin, and taken up by the cells. An enlarged capillary permeability observed in tumor tissue played an important role in the transport process.

Animals↗
PubMed1990

FcR-mediated enhancement of HIV-1 infection by antibody.

Although CD4 is a major receptor for human immunodeficiency virus (HIV) infection of cells, studied by ourselves and others clearly show that the Fc receptor (FcR) also plays a role in infection, perhaps in conjunction with other surface receptors. IgG antibodies to HIV-1 will enhance infectivity in cells (such as monocyte-macrophages) that have surface Fc receptors; F(ab')2 fragments of antibodies did not enhance, and blocking of FcR inhibited enhancement. The high-affinity FcR for IgG (Fc gamma RI) appeared to be functional. Sera from HIV-1-infected patients had neutralizing activity at high concentrations, but enhanced infection at low concentrations (i.e., high dilutions). Our studies show that the CD4 receptor is required for antibody-mediated enhancement of infection, as enhancement can be blocked by recombinant soluble CD4 and by Leu3 antibody. Although enhancement can be demonstrated in vitro, the in vivo importance of enhancing antibodies remains to be defined in HIV-1 infection.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Factors that preclude the successful use of monopharmacy in the medical treatment of patients with epilepsy.

A neurologist conducted research efforts for more than 12 years as a step toward the establishment of monotherapy for epilepsy. Of 406 patients with epilepsy, seizures could be controlled for more than one year in 72% and for more than 3 years in 54%. Monotherapy was given to 57% of all the patients with a success rate of 54%. Factors that were found likely to interfere with a reduction in antiepileptic drug therapy to one drug modality included: symptomatic etiology, prolonged duration of illness, low age at onset and secondary generalized epilepsy with a large number of seizures in combination, for generalized epilepsies; symptomatic etiology, prolonged duration of illness, low age at onset, other than occipital lobe origin, complex partial seizure with secondary generalization, temporal lobe epilepsy with associated automatisms, elementary sensorimotor seizure and high frequency of seizures, for partial epilepsies. In addition to these factors relevant to the nature of epilepsies, other factors apparently unrelated to the disease process, e.g., liability of polypharmacy to produce side effects precluding dosage elevation, patient's rejection to reduce drug and the inability of a physician to treat the patient properly for want of information, were also recognized to exist.

Adult↗
PubMed1990

Two receptors are required for antibody-dependent enhancement of human immunodeficiency virus type 1 infection: CD4 and Fc gamma R.

Evidence of antibody-dependent enhancement of human immunodeficiency virus type 1 (HIV-1) infection via Fc receptor (FcR) was published previously (A. Takeda, C. U. Tuazon, and F. A. Ennis, Science 242:580-583, 1988). To define the entry mechanism of HIV-1 complexed with anti-HIV-1 antibody, we attempted to determine the receptor molecules responsible for mediating enhancement of HIV-1 infection of monocytic cells. Monoclonal antibodies to FcRI for immunoglobulin G substantially blocked antibody-dependent enhancement of HIV-1 infection. Furthermore, we demonstrate a requirement for the CD4 molecule in antibody-enhanced HIV-1 infection via FcR. Soluble CD4 prevented infection by HIV-1 antibody-treated virus, and enhancement of infection of virus-antibody complexes was abrogated by a monoclonal antibody to CD4 (anti-Leu3a antibody). Treatment of human macrophages with an anti-CD4 antibody also inhibited antibody-enhanced HIV-1 infection of macrophages, supporting our contention that antibody-dependent enhancement of HIV-1 infection via FcR requires CD4 interaction with the virus glycoprotein.

Antibodies, Monoclonal↗
PubMed1990

Acquired radioresistance after low dose X-irradiation in mice.

Low doses (2.5-15 cGy) of X-irradiation two months prior to a second exposure to a sublethal dose enhanced the survival rate in mice. Optimal and significant increase was observed with 5-10 cGy. Endogenous spleen colony counts (endo-CFUs) after 7 Gy increased by a factor of about 1.7 in mice pre-irradiated with 5-10 cGy, while the number of blood forming stem cells (CFUs) in the pre-irradiated group did not exceed that in the sham-irradiated control group at the period of the second exposure (two months after irradiation with 5 cGy). The low dose exposure seems to stimulate recovery of blood forming stem cells after the second irradiation and favors a decrease in the incidence of bone marrow death.

Animals↗
PubMed1990

[Castleman disease in the pelvic retroperitoneum].

About 50% of the cases with Castleman disease firstly described by Castleman in 1956 occur in the thoracic cavity. The pelvic cavity is a rare location affected by the disease; there are only 7 reports. Herein, a case of Castleman disease of the pelvic cavity is reported. A 41-year-old man complaining of microscopic hematuria consulted us. Drip intravenous pyelography and computerized tomography showed a solitary mass at the pelvic retroperitoneum. Abnormal laboratory findings were as follows; glucose tolerance test (GTT), erythrocyte sedimentation rate, alpha 2-globulin level, CRP titer and hematuria. With the diagnosis of a pelvic retroperitoneal tumor, pelvic exploration was performed. The resected tumor was encapsulated, elastic hard and 4x3x2 cm in size. The cut surface was homogeneously granular and yellowish white in color. Histological diagnosis was the plasma cell type of Castleman disease. Within three weeks after the operation, laboratory abnormalities diminished except for GTT and microscopic hematuria. The patient is free from the disease with no signs of recurrence for 2 years postoperatively.

Adult↗
PubMed1990

[Anesthetic care of a patient intoxicated with thinner].

This is a report of a 28 year old male who underwent emergency laparotomy. He had a history of asthma and chronic abuse of thinner (toluene), and he stabbed himself after acute intoxication by the drug. Anesthesia was induced and maintained by halothane and oxygen. Vecuronium was used for muscle relaxation. Abnormal EKG was seen during perioperative period: A-V dissociation and incomplete RBBB. After emergence from anesthesia, so called "flash back" phenomenon was observed but this was controlled by diazepam. Since the chronic abuse of toluene causes organic changes in many vital organs, we must take special precautions when we anesthetize a patient with thinner intoxication: (1) toluene has a negative inotropic effect and also delays the S-A and A-V conduction rate, which may potentiate the cardiac effect of inhalation anesthetics; (2) toluene causes liver damages; and (3) the patient may experience "flash back" phenomenon.

Adult↗
PubMed1990

[Interaction of halothane and PGE1 on ICG excretion].

We performed ICG-test during surgery to study the effect of halothane on ICG excretion in humans. We also evaluated the effect of PGE1 on ICG excretion concomitantly used during halothane anesthesia. A significant decrease in ICG clearance occurred in the patients who received only halothane to reduce the systolic arterial pressure (SAP) to 70% of the preoperative value. The reduction in SAP induced by PGE1 together with halothane, however, did not decrease the ICG clearance rate. We conclude that halothane may decrease the hepatic blood flow, but PGE1 may neutralize the effect of halothane, and maintain the hepatic blood flow in man.

Adult↗
PubMed1989

Human oculocutaneous albinism caused by single base insertion in the tyrosinase gene.

Tyrosinase-negative oculocutaneous albinism (OCA) is an inborn error of metabolism, characterized by a complete lack of melanin pigments in the eyes and skin. We have isolated and characterized the tyrosinase gene of one affected child (S.S.) with tyrosinase-negative OCA. Sequence analysis reveals a single-base insertion in the exon 2 that shifts the reading frame and introduces a premature termination signal (TGA codon) after the amino acid residue 298. Functional analysis of the mutated gene indicates that such a truncated tyrosinase lacking one potential copper-binding region is catalytically inactive. We therefore conclude that the albino phenotype of the patient S.S. is a consequence of the inactive tyrosinase caused by the nonsense mutation in the tyrosinase gene.

Albinism↗
PubMed1989

Functional analysis of the cDNA encoding human tyrosinase precursor.

The DNA segment harboring the promoter region and the exon 1 of the human tyrosinase gene has been cloned and characterized. Sequence analysis reveals the amino-terminal half of tyrosinase molecule including a signal peptide, of which six amino acid residues are not represented in the tyrosinase cDNA, pHT gamma 1 [Shibahara et al. (1988) Tohoku J. Exp. Med. 156, 403-414]. We therefore constructed the expression plasmid containing the human tyrosinase precursor cDNA, and introduced it into mouse amelanotic melanoma cells. Both tyrosine hydroxylase and dopa oxidase activities were expressed only in the cells transfected with such a full-length cDNA, providing direct evidence that tyrosinase actually possesses a dual catalytic activity.

Amino Acid Sequence↗
PubMed1989

Chemical form of tumor-tropic 99mTc-DL-homocysteine.

Analyses of the chemical forms of 99mTc-complexes provide important information for the development of a new tumor-tropic 99mTc-labeled radiopharmaceutical. We attempted to determine the chemical form of 99mTc-DL-homocysteine (99mTc-Hcy) which was previously reported to be tumor-tropic. By analyzing the functional residues of Hcy in the 99mTc-Hcy molecule, it was estimated that the sulfhydryl and amino residues participated in the chelate formation. Gel filtration analysis of 99mTc-Hcy indicated that its molecular size was bigger than that of 99mTc-penicillamine monomer. The analysis also indicated that 99mTc-Hcy complex seemed to be a relatively small oligomer. Although an uncertainty remains on the valency of Tc in 99mTc-Hcy molecule and the accurate molecular size of this complex, its putative chemical form is described.

Adsorption↗