Search PubMed⌕ Search

Biomedical subjects

H Baba

Publications and source records attributed to H Baba.

At least 433 records · Page 24Linked to original sources

Conjugal acquisition and stable maintenance of Ent plasmids in nontoxigenic wild-type strains of Escherichia coli.

In spite of the ability of the genetic determinants for enterotoxin production to be conjugally transferred, mobilized or transposed, enterotoxigenic Escherichia coli (ETEC) isolated from diarrheal patients is restricted to certain serotypes. Four conjugative enterotoxigenic plasmids (Ent plasmids) encoding either a heat-labile enterotoxin or a heat-stable enterotoxin or both and belonging to one of three incompatibility groups IncFI, IncHl, or IncX, were examined for their transferability to and stability in 157 nonenterotoxigenic Escherichia coli strains belonging to various serotypes and 89 clinical isolates nonenterotoxigenic but belonging to those serotypes in which ETEC from diarrheal patients are usually found. The serotypes of the strains to which Ent plasmids were efficiently transferred and in which they were maintained stably were not always the serotypes in which ETEC had usually been found and vice versa. The frequencies of transfer of four Ent and two R plasmids to each of the 157 recipients were correlated with each other, indicating that the frequency of transfer of the plasmid is not determined by a resident plasmid, if there is one, but by a recipient factor which commonly affects transferability to all donors. These results have led to the conclusion that the reason why only certain serotypes are found among ETEC isolated from diarrheal patients is not the ability of these strains specifically and preferentially to acquire and maintain the Ent plasmids.

Conjugation, Genetic↗

Production and characterization of monoclonal antibodies against myelin-associated glycoprotein.

Monoclonal antibodies against myelin-associated glycoprotein were generated by fusing mouse myeloma cells with spleen lymphocytes from BALB/c mice immunized with human myelin-associated glycoprotein purified from CNS myelin. Three groups of antibodies were identified: IgG antibodies recognizing the polypeptide moiety and IgG and IgM antibodies recognizing the carbohydrate moiety of the intact molecule. Properties of these antibodies were examined with sodium dodecyl sulfate-polyacrylamide gel electrophoresis and the immunostaining technique using human CNS and peripheral nerve myelin, and ganglioside fractions isolated from human brain and peripheral nerve, and with immunohistochemical staining of human peripheral nerves. Part of human peripheral blood mononuclear cells was stained with the antibodies against the carbohydrate moiety, but not with IgG antibodies recognizing the polypeptide moiety. Natural killer activity was partially reduced after treatment of human peripheral blood lymphocytes with an IgM antibody and complement in vitro. The possibility that anti-myelin-associated glycoprotein antibodies might play a role in the pathogenesis of demyelinating diseases through modification of natural killer activity is discussed.

Animals↗

Anti-myelin-associated glycoprotein antibody in sera from patients with demyelinating diseases.

An enzyme-linked immunosorbent assay (ELISA) was developed for quantitating anti-myelin-associated glycoprotein (MAG) IgM antibody in human sera. Absorbance values of anti-MAG antibody were higher than 0.2 at 1:80 of serum dilution in sera from some patients with demyelinating diseases of the central or peripheral nervous systems including multiple sclerosis, subacute sclerosing panencephalitis, Guillain-Barré syndrome, chronic relapsing polyradiculoneuritis and carcinomatous polyneuropathy and also some patients with autoimmune diseases such as collagen diseases and myasthenia gravis. However, absorbance values of anti-MAG antibody in sera from control individuals and patients with some other neurological diseases were less than 0.2 and considered as negative. Because of the reported existence of a cross antigenicity between MAG and lymphocyte, and especially natural killer cells, the possibility of the functional importance of anti-MAG antibody on cellular immunity is discussed with particular reference to the demyelinating diseases.

Autoantibodies↗

Identification of parathyroid hormone messenger ribonucleic acid in an apparently nonfunctioning parathyroid carcinoma transformed from a parathyroid carcinoma with hyperparathyroidism.

mRNA coding for pre-pro-PTH, a precursor of PTH, was sought in an apparently nonfunctioning parathyroid carcinoma that had transformed from one that was previously functioning. Total poly(A+) RNA was prepared by phenol-chloroform-isoamyl alcohol extraction and oligo-dT-cellulose affinity chromatography from the tumor tissue and bovine parathyroid glands. In the rabbit reticulocyte lysate cell-free translation system, total poly(A+) RNA from the tumor as well as that from bovine parathyroid glands directed the translation of a product which was specifically precipitated by an anti-PTH serum and which migrated at the same position as pre-pro-PTH on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. These results indicated the presence of mRNA coding for pre-pro-PTH (PTH mRNA) in an apparently nonfunctioning parathyroid carcinoma, suggesting that PTH synthesis is not always absent in parathyroid carcinomas which are not accompanied by hyperparathyroidism.

Animals↗

Chronic T cell leukemia with a NK phenotype reacting with anti-myelin-associated glycoprotein (MAG) mouse monoclonal antibody.

We describe a patient demonstrating chronic T cell leukemia with a natural killer (NK) phenotype. The leukemic cells could be stained by OKT 3 (T cells), anti-Leu-7 and anti-myelin-associated glycoprotein (MAG) (NK cells) but not anti-Leu-11 monoclonal mouse antibody (activated NK cells). Fresh mononuclear cells showed a very low NK activity, although this activity returned to normal levels after 18 days incubation with interleukin-2 and some stimulants. It was not known why the NK activity of fresh mononuclear cells was low. This report is the first on leukemia characterized by anti-MAG monoclonal antibody.

Antibodies, Monoclonal↗

Parathyroid hormone-degrading enzyme of high molecular weight in the cytosol of rat renal cortical cells.

Using unlabeled bovine parathyroid hormone (b-PTH) as the substrate, the PTH-degrading activity in the 100,000 x g supernatant of rat renal cortex was examined. The PTH-degrading activity showed the highest peak at pH 7.25, along with 3 minor peaks at pH 4.5, 6.0 and 8.5. The neutral PTH-degrading activity of the 100,000 x g supernatant (pH 7.25) was eluted at V0 in Sephadex G-200 gel filtration corresponding to a high molecular weight. The neutral PTH-degrading activity was inhibited by ATP and calcium, but the acid PTH-degrading activity (pH 4.5) was slightly activated by ATP and was uninfluenced by calcium. The cytosolic neutral PTH-degrading activity was not inhibited by PMSF, trypsin inhibitor, E-64, chymostatin, leupeptin or pepstatin, whereas the acid PTH-degrading activity was inhibited by pepstatin, leupeptin, trypsin inhibitor and chymostatin. The neutral and acid PTH-degrading activities most probably depend on different enzymes. The neutral PTH-degrading enzyme is unlike any of the PTH-degrading enzymes so far reported.

Adenosine Triphosphate↗

Antitumor polysaccharide-induced tumor-regressing factor in the serum of tumor-bearing mice: purification and characterization.

Marked tumor-regressing activity was induced in the serum of S180 tumor-bearing mice by injection of an antitumor polysaccharide, CM-TAK [carboxymethylated beta(1-3)glucan]. Maximal activity was induced 7-14 days after the tumor transplantation and 10-12 h after CM-TAK treatment. A quantitative assay for the activity was established on the basis of the initial decrease in the number of the tumor cells within 24 h. The factor with tumor-regressing activity was purified 10,000-fold by the series of hydroxylapatite chromatography, ammonium sulfate precipitation, anion-exchange chromatography, gel filtration, and boronate-mediated affinity chromatography. The molecular weight was estimated to be 250,000 by gel filtration. The activity was proteinase K sensitive, but relatively resistant to trypsin. Neuraminidase did not affect the activity. It is believed that the tumor-regressing factor is different from the tumor necrosis factor.

Alcaligenes↗

Rapid tumor regression caused by antitumor polysaccharide and induction of tumor-regressing factor in the serum of tumor-bearing mice.

The antitumor polysaccharide CM-TAK [carboxymethylated beta(1-3)glucan] caused immediate and rapid loss of viable tumor cells from S180 solid tumors in ICR mice if it was given after a week of tumor growth. We found marked tumor-regressing activity in the serum of mice with S180 tumors undergoing CM-TAK-induced regression. When injected intravenously into S180-bearing mice, 0.1 ml of serum/mouse induced complete regression of day-14 tumors. However, in vitro cytotoxic activity against L929 and S180 cells was not detected. After the injection of CM-TAK or serum, along with the rapid decrease in tumor cells there was a marked increase in polymorphonuclear leukocytes. The serum was also active against fibrosarcoma Meth A in BALB/c mice, inducing partial regression or significant decrease in growth of the tumor. The properties of the factor in the serum seem to be different from those reported for tumor-necrotizing factor and other endogenous cytotoxic substances.

Animals↗

[Experimental study of spinal cord evoked potentials in cats].

Assessment of function of the spinal cord utilizing spinal cord evoked potentials (SEP) has become a useful diagnostic tool. In the present study, various aspects of characteristics of SEP were analyzed. The basic waveform of conductive SEP consisted of two major components, namely, N1 and N2, whose conduction velocities along the dorsal surface of the cord were 74 m/s and 55 m/s, respectively. Halothane inhalation caused reduction of N2 amplitude, whereas asphyxia caused latency delay of N2. Significant amplitude reduction of N1, N2 (p less than 0.005) and considerable latency delay of N1 were noted in ventral epidural recording. Although there was no relationship between severity of injury and the appearance of positive potentials, N2 tended to be positive-going in heavy injury. Findings of positive potentials showed that N1 originated in the area of ventral gray matter through the ventro-lateral column and N2 through the dorsal column.

Anesthesia, Inhalation↗

Human natural killer cell activity is reduced by treatment of anti-myelin-associated glycoprotein (MAG) monoclonal mouse IgM antibody and complement.

Human mononuclear cells could be stained by anti-myelin-associated glycoprotein (MAG) monoclonal mouse IgM antibody. The remaining human natural killer (NK) cell activity examined by using K-562 cells at 20:1 as effector:target ratio after treatment of anti-MAG monoclonal mouse or anti-Leu-7 (HNK-1) antibody and complement revealed 13.4% and 15.1%, respectively (untreated NK activity was 40.8%). However, human NK activity could be abrogated by anti-Leu-11 and complement. The remaining NK activity shown as lytic units after treatment with anti-MAG, anti-Leu-7 or anti-Leu-11 and complement was 6.1, 5.3 and below 1.0, respectively (untreated NK cells showed 15.4). When NK activity was examined in another target cell, MOLT-4, the remaining activity shown as lytic units was also decreased with anti-MAG antibody (4.3) or with anti-Leu-7 (3.0) (untreated NK activity was 8.3). Our findings suggest that NK cells may be influenced by anti-MAG antibody if it is found in the sera as anti-lymphocytotoxic antibody.

Animals↗

EEG changes 24 hours after myelography with metrizamide.

A prospective study of EEG changes following metrizamide myelography was made on 34 patients aged 17-79 years. EEGs were recorded just before and 22-26 hours after myelography. Usually 8-10 ml of metrizamide was injected by either lumbar or lateral cervical puncture. The concentration of metrizamide was relatively high. EEGs were abnormal in 15 out of the 20 patients whose baseline EEGs were normal. EEGs deteriorated in 10 of the 14 patients whose control tracings were abnormal. High voltage delta activity and/or a great deal of theta activity were common abnormalities. Three patients showed triphasic waves. No relationships were found between the EEG changes and clinical variables. But central nervous system involvements by metrizamide tended to be accompanied by a severe EEG slowing.

Adolescent↗