[A case of accessory mitral valve documented by two-dimensional and pulsed Doppler echocardiography].
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Biomedical subjects
Publications and source records attributed to T Baba.
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Active ion transport by the airway epithelium plays an important role in maintaining the effective defense mechanisms of the airway by regulating the volume and composition of the airway fluid. We investigated the abilities of adrenergic agents, cholinergic agents, and chemical mediators to modulate ion transport in canine tracheal epithelium, using Ussing-type chambers. Transepithelial electric potential difference (PD), resistance (R), and short circuit current (SCC) of the tracheal epithelium were measured before and during exposure to a drug or after a change in the perfusate composition. The mean values and S.E. (N = 41) of PD, R, and SCC during the control period were -18 +/- 4 mV (luminal negative to submucosa), 240 +/- 42 omega.cm2, and 50 +/- 5 microA/cm2, respectively. Ouabain (10(-4) M), an inhibitor of Na+-K+-ATPase, in the mucosal bath abolished PD and SCC. Replacement of luminal Na by choline reversibly reduced PD and SCC. These findings suggest that PD and SCC of the tracheal epithelium are maintained by the transcellular transport of luminal Na toward the mucosa. Isoproterenol (10(-5) M), epinephrine (10(-4) M), and norepinephrine (10(-4) M) markedly increased both PD and SCC. Acetylcholine (10(-4) M) and histamine (10(-4) M) did not alter SCC significantly. Prostaglandin E1 (10(-6) M) and F2 alpha (10(-5) M) slightly increased PD and SCC. These results indicate that adrenergic and cholinergic agents induce different patterns of effect on ion transport (adrenergic-dominant) in the tracheal epithelium. Thus, the effects of autonomic agents and chemical mediators on ion transport may explain, in part, the pathogenesis of airway disorders observed in many respiratory diseases.
We reported 2 patients treated with Methotrexate (MTX)-Fluorouracil (5-FU) sequential therapy combined with Doxifluridine (5'-DFUR). The method of administration was as follows: MTX 60 mg was given intravenously (iv) followed by 5-FU 600 mg iv 2 hours later in colon cancer and 5 hours later in gastric cancer. Leucovorin 20 mg was administered 3 times every 6 hours beginning 6 hours after 5-FU infusion. This cycle was repeated once a week for 5 weeks. 5'-DFUR 1,200 mg was given orally daily and continued after MTX.5-FU therapy. Patient 1 was a 60-yr-old female with recurrent colon cancer developed four years after sigmoidectomy. She was referred to our hospital for further examinations of elevated serum carcinoembryonic antigen (CEA). The enlarged intraabdominal lymph nodes due to recurrence were demonstrated on computer tomography and the chemotherapy was performed as described above. The swelling of lymph nodes showed marked reduction in size and CEA value was normalized. Patient 2 was a 59-yr-old man with advanced gastric cancer accompanied by giant liver metastasis. Both primary and metastatic lesion responded favorably to this regimen. There was no remarkable side effect in either patient. These results suggest that this method is worth performing in further clinical trials for cancer patients.
The contact sensitivity evaluated by the ear swelling test and the dynamic changes of epidermal Ia+ dendritic cells (Ia+DECs) and Thy-1+ dendritic cells (Thy-1+DECs) were studied in trinitrochlorobenzene (TNCB) sensitized different age group C3H/He mice after challenge. A significant increase of ear swelling was observed between 6 h and 10 days of both 8-10 week (wk) and 40-48 wk groups; the ear swelling indices of 8-10 wk group were significantly higher than those of 40-48 wk group from 18 h to 5 days. A significant decrease of the densities of Ia+DECs from 18 h to 48 h, followed by a gradual increase reaching significant increase of the densities of Ia+DECs from 5 days to 21 days in both 8-10 wk and 40-48 wk groups, was observed; the densities of Thy-1+DECs significantly decreased from 18-48 h, followed by a gradual increase reaching a significant increase from 5 days to 21 days in both 8-10 wk and 40-48 wk groups. In the normal control groups, a significant decline of both Ia+DECs and Thy-1+DECs in the 40-48 wk group was observed. Results suggest that contact allergy may be diminished in aged mice. On the other hand, like Ia+DECs, Thy-1+DECs seem to be involved in the process of contact allergy.
A 33-year-old woman noticed recurrent and sudden attacks of subcutaneous swelling of the extremities and face since the age of 4 years. Sometimes the attacks involved colicky abdominal pain. Her mother and younger sister had episodes of recurrent swelling of the extremities as well. Complement studies revealed low CH50, C1q, C4, and C1 inhibitor levels, with normal C3 and C5 levels. Similar reductions of CH50 C4 and C1 inhibitor levels were observed in her mother, older, and younger sisters. Therefore, she was diagnosed as hereditary angioneurotic edema. In addition, she was diagnosed as having a butterfly rash at the age of 20 years and had a history of solar sensitivity. Histologically the facial lesion showed liquefaction degeneration of the basal cell layer. Direct immunofluorescent staining of the affected skin lesion showed basement membrane-zone staining of IgG and IgM. Laboratory studies revealed lymphopenia and positive ANF. On the basis of the above findings, hereditary angioneurotic edema associated with systemic lupus erythematosus was diagnosed.
Compounds in beechwood creosote were analyzed by gas chromatography-mass spectrometry, and 22 major constituents were identified. Of these, 19 were phenolic compounds, i. e., guaiacol, phenol, two cresol isomers, four methylguaiacol (creosol) isomers, six xylenol isomers, two trimethylphenol isomers, 4-ethylguaiacol, 4-ethyl-5-methylguaiacol, and 4-propylguaiacol. The remaining three were hitherto unpredicted five-membered ring compounds, i. e., 3-methyl-2-hydroxy-2-cyclopenten-1-one, 3,5-dimethyl-2-hydroxy-2-cyclopenten-1-one, and 3-ethyl-2-hydroxy-2-cyclopenten-1-one. The relative quantities of these compounds were also compared with those obtained by high-resolution high-performance liquid chromatography. This report probably represents the first extensive analysis of beechwood creosote.
Parent B16 melanoma and B16-F1 cell lines express a third actin (Ax) in addition to beta- and gamma-actin. It has the same molecular mass (43,000 daltons) and a more acidic isoelectric point (pI = 5.2) than the latter two actins (pI = 5.3) (Taniguchi, S., Kawano, T., Kakunaga, T., and Baba, T. (1986) J. Biol. Chem. 261, 6100-6106). We constructed a cDNA library from poly(A)+ RNA of B16-F1 and then isolated Ax actin candidate clones. According to the nucleotide sequencing analysis for one of the candidate clones, pMA 30, the predicted amino acid sequence was composed of 375 amino acids and was similar to that of beta-actin, but differed at the 28th amino acid in that leucine replaced the arginine of beta-actin. When RNA synthesized from the clone pMA 30 with the SP6 transcription system was translated in vitro using reticulocyte lysate, we identified a polypeptide which had the same isoelectric point and molecular weight as Ax actin; the polypeptide had binding activity to DNase I, a common characteristic of native actin. These observations provide evidence that the clone pMA 30 encodes the mRNA for Ax actin. In the nucleotide sequence of the Ax cDNA, there are: 1) one base change in the coding region which causes a loss of the SmaI site and an amino acid exchange, as mentioned above; 2) four deletion sites in the 3'-noncoding region; 3) one insertion site in the 3'-noncoding region; and 4) one base change in the 5'-noncoding region, as compared with hitherto known mouse beta-actin cDNA. These differences between Ax and beta-actin cDNA indicate that the Ax actin is encoded by an unique gene set, independent of beta-actin.
A D-mannose 6-phosphate receptor was isolated from total membranes of porcine testis, and its interaction with ligands was examined. The receptor was a glycoprotein comprised of several 36-kDa sub-units with an isoelectric point (pI) of 6.1. The binding of the receptor to the insoluble phosphomannan core occurred in the absence of divalent cations, but was selectively stimulated by MnCl2 and effectively inhibited by D-mannose 6-phosphate, D-fructose 1-phosphate, and pentamannosyl monophosphate. The phosphate group and HO-2 of D-mannose 6-phosphate are important in the receptor-ligand interaction, HO-4 probably contributes to a lesser extent, and HO-1 seems to have no interaction.
Pentamannosyl monophosphate, derived from Hansenula holstii O-phosphomannan, was conjugated to bovine serum albumin by reductive amination. The conjugate inhibited the binding of the porcine testis mannose 6-phosphate receptor to the insoluble phosphomannan core. A mannose 6-phosphate receptor with a molecular weight of 200,000 was purified from porcine liver membranes, using an affinity matrix of the conjugate attached to Sepharose 4B. Rabbits were immunised with the conjugate, and the antisera were purified on a phosphomannan core-Sepharose 4B column in order to give an antibody which was specific for the 6-phosphate group and the equatorial HO-4 of D-mannose 6-phosphate. On Western blot analysis using the purified antibodies, ovalbumin, which contained a typical high-mannose type of oligosaccharide, was not recognised. However, a testicular glycoprotein fraction formed an immunostaining band. These results indicate the effectiveness of the conjugate as a ligand for mannose 6-phosphate receptors. The antibodies highly specific for mannose 6-phosphate may be used to detect or purify lysosomal enzymes.
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The effect was investigated of combinations of cytokines known to be cytostatic for some tumor cells, namely interleukin 1 alpha (IL-1 alpha), interferon-beta (IFN-beta), and tumor necrosis factor (TNF), on the growth and differentiation of the mouse myeloid leukemic cell line, M1, cells. IL-1 alpha, IFN-beta, and TNF by themselves are antiproliferative for M1 cells. Treatment of cells with a mixture of any two of the three cytokines resulted in at least additive growth inhibition. None of these cytokines by themselves induced differentiation of M1 cells as assessed by increased expression of Fc receptors (FcR), stimulation of phagocytic activity and by morphologic criteria. However, as little as 1 U/ml IL-1 alpha in conjunction with IFN-beta or TNF increased FcR expression, phagocytic activity and morphologic changes in addition to inhibiting the growth of M1 cells. The combination of IFN-beta and TNF did not induce differentiation, although the growth of the cells was markedly inhibited. Both TNF and lipopolysaccharide (LPS) induced the in vitro production of IFN activity by M1 cells. Furthermore, the induction of differentiation of M1 cells by a combination of IL-1 alpha with either IFN-beta, TNF, or LPS was inhibited by antibody against mouse IFN-beta. Therefore, it appears that IFN-beta provides one of the two required signals for differentiation of M1 cells by these combinations of stimulants, the other being IL-1. Furthermore, the cytostatic effect of TNF by itself on M1 cells was also partly blocked by anti-IFN-beta antibody, suggesting that IFN-beta is also involved in the growth inhibitory effect of TNF for M1 cells. In contrast, the cytostatic effect of IL-1 on M1 cells was not blocked by anti-IFN-beta antibody. In conclusion, both the cytostatic and differentiative effect of TNF appear to be mediated by IFN-beta. Thus, the combination of IL-1 and IFN-beta or inducers of IFN-beta resulted in terminal differentiation of M1 cells. Northern blot analysis using cDNAs for murine IFN-beta1 or human IFN-beta2 showed an increased expression of mRNA for IFN-beta1 but not for IFN-beta2 by stimulation with TNF or LPS, strongly suggesting that IFN-beta 1 rather than IFN-beta 2 is responsible for TNF or LPS effects.
The hepatic granulomas in experimental cryptococcosis were analyzed by peroxidase (PO) cytochemistry. Cryptococcus neoformans was inoculated intravenously into rats (group A), and some rats were administrated with dextran sulphate to suppress Kupffer cell functions before inoculation (group B). All rats were sacrificed 7 days after inoculation. The livers were examined PO cytochemically. In addition, the liver, spleen, lungs, kidneys and brain were also examined histopathologically. The hepatic granulomas consisted of the following four type cells; exudate macrophages (type I), PO-negative macrophages (type II), Kupffer cells (type III), and other inflammatory cells (type IV) such as neutrophils and lymphocytes. The percentages of the granuloma-composing cells in group A were 10.3% (type I), 27.3% (type II), 52.9% (type III) and 9.5% (type IV), respectively. In contrast in group B, type II cells outnumbered type III cells by a ratio of 5:3. In group B, necrosis and hemorrhage were observed in the granuloma. The lesions in the lungs changed from granulomatous to cystic ones after suppression of the Kupffer cell functions. These results suggest that resident macrophages such as Kupffer cells may play an important role in the formation of cryptococcal lesions.
The effects of oral dilevalol (an R, R-isomer of labetalol), a new beta-adrenoceptor blocker with beta 2-receptor stimulating and alpha-recepter blocking properties on blood pressure, renal function, plasma renin activity (PRA) and plasma aldosterone have been studied in 15 patients with mild-to-moderate essential hypertension treated with it for 6 weeks. Two patients with apparent treatment failure and one patient who developed muscle pain and cramps, and had an elevated creatine phosphokinase level, were excluded from the study. Dilevalol monotherapy 100 mg once daily for 6 weeks significantly lowered both the systolic and diastolic blood pressure compared to placebo. Total renal vascular resistance was significantly reduced, and RBF and GFR remained unchanged. Dilevalol significantly decreased PRA. The results suggest that prolonged daily treatment with dilevalol preserves renal function and produces a concomitant hypotensive action in patients with mild-to-moderate essential hypertension. The ancillary pharmacological properties of dilevalol rather than PRA suppression may be relevant to its renal effects.
Thin layer chromatographic and gas chromatographic separation and mass spectrometric identification of mycolic acid subclasses and molecular species from eight strains of Mycobacterium smegmatis were established. Two major adjacent spots and a lower minor one were detected on silica gel thin layer chromatograms of methyl esters. The most abundant subclass showing the highest Rf value on TLC was that of alpha-mycolic acids (M1), the second was that of alpha-mycolic acids (M1), a shorter homologue than alpha-mycolates, and the third was the hydroxy mycolic acids (M4) derived from epoxy mycolic acids. They were identified by gas chromatography-mass spectrometry as their trimethylsilylether derivatives. alpha'-Mycolic acids were monoenoic acids ranging from C60 to C66 and possessing an alpha-unit of C24:0. Such profiles of alpha'-mycolic acids were common in eight strains. alpha-Mycolates were dienoic acids ranging from C75 to C79 and possessing an alpha-unit of C24:0. In most strains, the major molecular species of alpha-mycolates were odd-carbon-numbered, centering at C77 and C79, possessing a methyl branch in the even-carbon-numbered straight chain. The average carbon number of alpha-mycolates, from seven strains examined, was about 78, but that of the Takeo strain was 76.3. The profiles of epoxy mycolic acid molecular species composition from eight strains ranging from C75 to C81 were very similar to their M1 subclass profiles.
A 34-year-old man with acromegaly was observed, and the clinical course and various endocrinological deficiencies occurring before, during and after the development of pituitary apoplexy were evaluated. Following the attack, the patient experienced acute reductions in growth hormone (GH) and other pituitary hormones, adrenohypophyseal insufficiency and transient diabetes insipidus which appeared subsequent to glucocorticoid therapy. The level of growth hormone in serum and cerebrospinal fluid (CSF) was measured synchronously, and the respective regressions of GH levels in serum and CSF were observed. The results demonstrated the utility of measuring hormonal levels in CSF in the clinical evaluation of pituitary apoplexy in a patient with a functioning pituitary tumor.
To determine whether or not human pancreatic secretory trypsin inhibitor (PSTI) is an acute phase reactant released from hepatocytes, we investigated the effects of various cytokines on the release of PSTI from cultured human hepatoblastoma cells. PSTI was synthesized in human hepatoblastoma cells and released on stimulation with various cytokines: interleukin-1, tumor necrosis factor and interferon-beta.
Seventeen patients with primary or metastatic malignancy in the liver were treated with 'two-route chemotherapy' (TRC). One course of this TRC consisted of hepatic artery infusion of cisplatin, 120 mg/m2, in combination with concurrent intravenous administration of sodium thiosulfate, its neutralizing agent, at a dose of 9.0 g/m2 by a rapid push, followed by 1.2 g/m2/h by continuous infusion for 6 h. Five of 11 (45%) hepatocellular carcinoma and two of six (33%) metastatic tumors achieved partial response. Although almost all patients experienced nausea or vomiting, severe side-effects, including nephrotoxicity, peripheral neuropathy or ototoxicity, were not encountered. Myelosuppression was observed in one patient after seven courses of this TRC. The results indicate that TRC may be relatively effective against hepatic malignancies in patients without severe toxicity.