Fever and persistent pulmonary infiltrate in a one-month-old infant.
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Biomedical subjects
Publications and source records attributed to Y Fukuda.
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We treated three asthmatic children diagnosed as typical cryptomeria pollen asthma (Cryptomeria japonica). Wheezing started from one to four years after onset of pollinosis. Asthmatic attacks occurred one or several days after pollen counts increased. We could find asthmatic attacks in the years when the pollen counts were higher than in average years. In the laboratory findings, only specific IgE antibody to cryptomeria with its high titer of over 17.5 PRU/ml was detected in these three cases. Allergen inhalation tests were performed with positive results in the two cases, suggesting that these three cases were typical child cryptomeria pollen asthma.
A case of adenoid cystic carcinoma (ACC) with polymorphous features and an unknown differential diagnosis was presented. It appeared, without any pain, in the right maxillary sinus of a 47 year-old man. A variety of histopathological patterns were found, including glandular, cribriform, tubular and solid ones. However, the typical features of ACC, such as cribriform pattern associated with pseudocyst and tubular formations were rather scarce. A single cell strand appearance, so-called "Indian file arrangement", and papillary cystic formation were also noted, which are often associated with polymorphous low-grade adenocarcinoma (PLGA). Immunohistochemistries of EMA, CEA and musclespecific actin showed also similar staining patterns to those of PLGA in some areas. Our case could not be regarded as PLGA; but this case with features of PLGA as well as those of ACC might suggest an entity of transitional type between ACC and PLGA.
In order to obtain MoAbs against N-domain or domain III of carcinoembryonic antigen (CEA), mice have been immunized with a recombinant deleted CEA which was devoid of most of domains I and II. Of the nineteen MoAbs established, ten MoAbs were reactive with the N-domain of CEA, and others recognized the domain III. All Fab fragments of the MoAbs against the N-domain significantly inhibited homophilic cell adhesion mediated by CEA, whereas that of normal mouse IgG or control MoAb (anti-HLA class II) did not. Among the Fab fragments of MoAbs against the domain III, three inhibited the cell adhesion slightly, while five enhanced and one had no effect. These findings suggest that the N-domain of CEA plays an important role in the cell adhesion, and that the domain III is also involved in the binding. The MoAbs described in this study will be useful to elucidate the functional roles of the domains of CEA molecule.
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Acetylcholine could induce the incurvation of neural retina to form a cup-structure by muscarinic receptors in vitro. Neural retinae isolated from chick embryos were cup-shaped, but, it soon became flat in a normal bath solution. Then addition of acetylcholine caused an incurvation of the retina remaking the initial cup-structure. Ca2+ was involved in this movement since a calcium ionophore A23187 could also induce the folding of neural retina. Acetylcholine caused a rise in cytoplasmic Ca2+ concentration even in a Ca(2+)-free bath solution as measured with Fura-2. Atropine completely blocked both of the Ca2+ rise and the incurvation of neural retina by acetylcholine. It was suggested that the Ca2+ mobilization from intracellular reservoirs triggered the contractile movement to fold the embryonic neural retina.
Effect of recombinant human interleukin-11 (rhIL-11) on the expression of transcripts encoding microsomal heme oxygenase (HO), the rate-limiting enzyme in heme catabolism, and haptoglobin (Hpt), a major acute-phase protein, were examined in human HepG2 hepatoma cells. Treatment of HepG2 cells with rhIL-11 elicited an increase in HO mRNA in a dose- and a time-dependent fashion. The dose response curve, its magnitude of response and its time course were similar to those observed with recombinant human interleukin-6 (rhIL-6). In contrast, rhIL-11 had a far smaller effect on the level of Hpt mRNA than did rhIL-6. These findings demonstrate that the two cytokines are similar in regulating heme catabolism, while markedly different in inducing certain acute-phase proteins.
Bilateral cooling of the parapyramidal region in the rostral ventral medullary surface (VMS) elicited a reduction in respiratory frequency and phrenic inspiratory activity in halothane anesthetized rats. A distinct cluster of neurons (nucleus parapyramidalis superficialis) was found in a superficial layer (10-15 microns from the surface) just beneath the area where cooling produced suppression of respiration. The rat VMS layer contains neural substrates which regulate the respiratory rhythm generation and inspiratory neural output.
The role of inorganic metals and metalloporphyrins in the induction of mRNAs for haem oxygenase and heat-shock protein 70 (hsp70), the two heat-shock proteins, was examined in human HepG2 and Hep3B hepatoma cells. SnCl2, but not Sn-protoporphyrin, was found to be a potent inducer of both haem oxygenase and hsp70 mRNAs. In contrast, CoCl2, ZnCl2 and FeCl2 caused little induction of haem oxygenase and hsp70 mRNAs, whereas the porphyrin complexes of these metals strongly induced haem oxygenase mRNA, without influencing the level of hsp70 mRNA. The induction process was largely transcriptional, as judged by the inhibition of induction by actinomycin D, but not by cycloheximide, and by increased transcription demonstrated by nuclear run-off analysis. Since CoCl2 is a potent inducer of haem oxygenase in vivo in animals, the possibility of the biosynthesis of Co-protoporphyrin was examined in human hepatoma cells by incubating them with CoCl2 and protoporphyrin, or delta-aminolaevulinate (ALA), the precursor of protoporphyrin. Both types of treatment led to a potent induction of haem oxygenase mRNA. Co-protoporphyrin formation was also spectrally demonstrated in cells incubated with the metal and ALA. The results of this study indicate that certain metals, e.g. SnCl2, may directly induce haem oxygenase mRNA, whereas with other elements, incorporation of the metal into the porphyrin macrocycle is necessary for induction. Therefore CoCl2, like haemin, may activate the haem oxygenase gene via a haem-responsive transcription factor, whereas SnCl2 may exert its effect via a metal-responsive transcription factor.
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The mutational spectrum of the p53 gene was analyzed in 53 hepatocellular carcinomas. Somatic mutations of the p53 gene were detected in 17 cases (32%). Among these 17 mutations, 9 were missense mutations; the mutations in the other 8 cases were nonsense mutations, deletions, or mutations at the intron-exon junctions. These mutations were found in a wide region stretching from exon 4 to exon 10 without any single mutational hot spot. G:C to T:A transversions were predominant, suggesting the involvement of environmental mutagens in the mutagenesis of the p53 gene in a subset of the hepatocellular carcinoma cases. Mutations of the p53 gene occurred frequently in advanced tumors, although several tumors in the early stages also showed mutations. A deletion map of chromosome 17 was constructed by using 10 polymorphic probes and was compared with the p53 gene mutation in each case. Loss of heterozygosity (LOH) on chromosome 17p was observed in 49% of the cases (24 of 49), and two commonly deleted regions were detected (around the p53 locus and at 17p13.3 to the telomere). Sixteen of the 17 cases with p53 gene mutations showed LOH around the p53 locus, and mutations were rare in hepatocellular carcinomas without LOH. However, no mutations were detected in 8 cases with LOH on 17p, suggesting the possibility that an unidentified tumor suppressor gene(s) located on 17p may have also been involved in hepatocarcinogenesis.
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The properties of calcium channels were studied at the period of neurogenesis in the early embryonic chick retina. The whole neural retina was isolated from embryonic day 3 (E3) chick and loaded with a Ca(2+)-sensitive fluorescent dye (Fura-2). The retinal cells were depolarized by puff application of high-K+ solutions. Increases in intracellular Ca2+ concentrations were evoked by the depolarization through calcium channels. The type of calcium channel was identified as L-type by the sensitivity to dihydropyridines. The Ca2+ response was completely blocked by 10 microM nifedipine, whereas it was remarkably enhanced by 5 microM Bay K 8644. Then we sought a factor to activate the calcium channel and found that GABA could activate it by membrane depolarization at the E3 chick retina. Puff application of 100 microM GABA raised intracellular Ca2+ concentrations, and this Ca2+ response to GABA was also sensitive to the two dihydropyridines. Intracellular potential recordings verified clear depolarization by bath-applied 100 microM GABA. The Ca2+ response to GABA was mediated by GABAA receptors, since the GABA response was blocked by 10 microM bicuculline or 50 microM picrotoxin, and mimicked by muscimol but not by baclofen. Neither glutamate, kainate, nor glycine evoked any Ca2+ response. We conclude that L-type calcium channels and GABAA receptors are already expressed before differentiation of retinal cells and synapse formation in the chick retina. A possibility is proposed that GABA might act as a trophic factor by activating L-type calcium channels via GABAA receptors during the early period of retinal neurogenesis.
We report herein our experience of two cases of spontaneous hemopneumothorax in which the source of bleeding was found to be aberrant vessels. Both patients were successfully treated by early thoracotomy. Case 1 was a 23-year-old female in whom chest X-ray revealed an air-fluid line and a bulla with a narrow restiform shadow connecting the pleural cupola. Angiography clearly visualized aberrant vessels branching from the costocervical trunk, distributed in and around the bulla in the apex of the lung, being the possible source of bleeding. These aberrant vessels were confirmed at surgery and resected. Case 2 was a 56-year-old male who underwent thoracotomy for persistent bleeding. At surgery, a continuously bleeding vessel from the pleural cupola was seen and ligated. The remnant of the vessel was located in the apex of the lung, and resected with the bulla. Thus, the rare entity of a congenital aberrant vessel lying concealed as a possible source of bleeding should be borne in mind.
Since specific treatment has not yet been decided on for Crohn's disease, the immediate target is the induction of remission and its maintenance. We examined the effects of an elemental diet (ED) in Crohn's disease with special reference to the maintenance of remission. Eighty-four patients received total enteral nutrition with the ED (35 to 40 kcal/kg ideal body weight/day) and/or conventional drug treatment for induction of remission. Sixty-one patients in remission were then followed-up with prolonged ED therapy (home elemental enteral hyperalimentation, HEEH) and/or drugs. During the follow-up periods the course of patients receiving HEEH was better than those of patients without HEEH, namely the cumulative continuous remission rates after one, 2 and 4 years were, 94%, 63% and 63% in the group receiving HEEH, 75%, 66% and 66% in the group receiving HEEH and drugs, 63%, 42% and 0% in the group receiving drugs, and 50%, 33% and 0% in the group receiving no maintenance therapy, respectively. In particular, when more than 30 kcal/kg ideal body weight/day of the ED was given, the maintenance of remission was successful in 95% of the patients. These results indicated that ED therapy was effective not only for the induction of remission but also for the maintenance of remission in Crohn's disease.
PURPOSE: We have demonstrated that colony-stimulating factor (CSF)-producing tumor cell lines produce not only CSF but also interleukin-1 (IL-1) and interleukin-6 (IL-6). Clinically, we have observed that patients bearing such tumors present with liver dysfunction and fever in addition to marked leukocytosis. The purpose of this study was to determine whether or not the liver damage was specifically related to CSF-producing tumors. PATIENTS AND METHODS: Clinicopathologic examinations were performed in six autopsied patients with CSF-producing tumors. We also transplanted two tumor cell lines (KHC287 and CHU-2), which produce granulocyte (G)-CSF, IL-1, and IL-6, to nude mice. RESULTS: Of the six patients, five had G-CSF- and one had granulocyte/macrophage (GM)-CSF-producing tumors. IL-1 and IL-6 concentrations in plasma or culture supernatant were elevated in these patients. Biochemical examinations revealed high serum enzyme levels of the biliary system in contrast to normal or slight increases in transaminase levels in all patients studied. Serum direct bilirubin was elevated in five of the six patients. Three common pathologic changes of the liver were found: (1) focal necrosis associated with neutrophil infiltration in the centrilobular zones, (2) fibrous change and enlargement of the portal area associated with neutrophil infiltration, and (3) intrahepatic cholestasis. The same pathologic changes, except for cholestasis, were reproduced in the liver of mice transplanted with KHC287 or CHU-2. CONCLUSION: These results indicate that patients with CSF-producing tumors have characteristic liver damage, and suggest a new paraneoplastic syndrome of leukocytosis and liver damage.
In adult golden hamsters (Mesocricetus auratus), the optic nerve was bilaterally sectioned with one side grafted with the sciatic nerve to make a bridge to the ipsilateral superior colliculus. Shuttle-box avoidance was tested using light as the conditioned stimulus. Three of the five transplanted animals revealed statistically significant increase in percentages of avoidance. A significant increase in the avoidance scores was also observed in 15 normal hamsters, but none of 13 blind hamsters showed such an increase. Intertrial responses, which represent spontaneous responses, did not show significant changes. We conclude that some of the transplanted animals can discriminate between light and dark, probably through their restored visual pathway.