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H Yoshioka

Publications and source records attributed to H Yoshioka.

At least 109 records · Page 6Linked to original sources

[Churg-Strauss syndrome with pulmonary eosinophilia and intrapulmonary lymph nodes 2 years before the onset of vasculitis].

We report a case of a 55-year-old man who had been treated for bronchial asthma diagnosed at the age of 51. One year following diagnosis, chest X-ray films disclosed nodular shadows. Biopsy specimens obtained by video-assisted thoracoscopic surgery were histopathologically identified as intrapulmonary lymph nodes. Three years after the initial diagnosis, the patient experienced sensory disturbance of the lower extremities, low-grade fever, and weight loss. At this point he was admitted to our hospital. On admission, physical examination and clinical investigations showed peripheral eosinophilia and signs of vasculitis. Specimens obtained by transbronchial lung biopsy and bronchoalveolar lavage showed strong evidence of tissue damage with infiltration of eosinophils but no evidence of necrotizing vasculitis or extra-vascular granuloma. Churg-Strauss syndrome (CSS) was diagnosed, and treatment was initiated with prednisolone at a dose of 60 mg/day. Except for the sensory disturbances in the lower extremities, after a few days of treatment the patient's symptoms subsided and his clinical data improved. This case was clinically important because pulmonary eosinophilic infiltration into vessel walls was confirmed a year after the diagnosis of bronchial asthma, and 2 years before the patient demonstrated signs of vasculitis. Further, it was a very rare case of CSS in which intrapulmonary lymph nodes had developed beneath the visceral pleura despite the absence of a history of heavy smoking, thus suggesting continuous stimulation by some as yet unknown antigen.

Asthma↗

Pitx2, a bicoid-type homeobox gene, is involved in a lefty-signaling pathway in determination of left-right asymmetry.

Signaling molecules such as Activin, Sonic hedgehog, Nodal, Lefty, and Vg1 have been found to be involved in determination of left-right (L-R) asymmetry in the chick, mouse, or frog. However, a common signaling pathway has not yet been identified in vertebrates. We report that Pitx2, a bicoid-type homeobox gene expressed asymmetrically in the left lateral plate mesoderm, may be involved in determination of L-R asymmetry in both mouse and chick. Since Pitx2 appears to be downstream of lefty-1 in the mouse pathway, we examined whether mouse Lefty proteins could affect the expression of Pitx2 in the chick. Our results indicate that a common pathway from lefty-1 to Pitx2 likely exists for determination of L-R asymmetry in vertebrates.

Animals↗

Adenovirus-mediated p16 gene transfer prevents drug-induced cell death through G1 arrest in human glioma cells.

This study examined the effects of full-length p16 gene transfer by recombinant adenovirus on cell growth and on sensitivity to CDDP or ACNU chemotherapies. We developed a recombinant adenovirus expressing the full-length human p16 gene (AxCA-hp16) by the COS-TPC method. AxCA-hp16 was infected into the p16-null human glioma cell line, U251MG. AxCA-hp16 infection inhibited proliferation of U251MG cells. A proliferation assay employing MTT showed that AxCA-hp16 infection induced chemoresistance, preventing CDDP-induced cell death (11- to 15-fold) and ACNU-induced cell death (80- to 92-fold). In the absence of AxCA-hp16, cell death was induced with CDDP or ACNU at 3 to 5 days after treatment, as demonstrated by Trypan-blue exclusion. Flow-cytometric analysis showed that CDDP or ACNU arrested cells in the G2 phase on day 1 and that cells re-entered the cycle on day 3. However, the cells infected with AxCA-hp16 after CDDP or ACNU treatment showed G1 arrest on day 5 after re-entering the cycle from G2 arrest on day 3. The cells infected with AxCA-hp16 before CDDP or ACNU treatment showed G1 arrest over the 5 days after the infection. This study demonstrated that G1 arrest induced with p16-gene expression prevents ACNU- or CDDP-induced cell death. The cell death induced by ACNU and CDDP therefore appears to occur in the phase after the G1/S check point.

Adenoviridae↗

cDNA sequence and expression of the mouse alpha1(V) collagen gene (Col5a1).

Several overlapping cDNA clones corresponding to the entire coding sequence of the mouse alpha1(V) collagen gene (Col5a1) were isolated. The conceptual amino acid translation indicated a high degree of sequence identity (94%) with the human alpha1(V) chain. All of the important structures previously noted in the human alpha1(V) chain were also conserved in the mouse chain. The alpha1(V) transcripts were easily detected in mouse embryos as early as 11 days post coitum (d.p.c.). The transcripts were widely distributed in non-cartilaginous and cartilaginous tissues. Finally, we calculated the ratio of transcripts of alpha1(V):alpha2(V):alpha1(XI) in the calvaria and tongue of 18 d.p.c. embryos using the competitive reverse transcription-polymerase chain reaction (RT-PCR) technique. The results raised the possibility that there are at least two different kind of types V/XI collagen heterotrimers in mouse embryonic tissues.

Amino Acid Sequence↗

Material analysis end-station of the Hyogo-ken beamline at SPring-8.

Plans to construct surface-analysis equipment which will be placed on beamline BL24XU of SPring-8 are presented. There are three experimental hutches in BL24XU, which are available simultaneously by using diamond monochromators as beam splitters. The purpose of the surface-analysis equipment is the simultaneous measurement of fluorescent and diffracted X-rays in grazing-incidence geometry. The instrument is equipped with a solid-state detector (SSD) and a flat position-sensitive proportional counter (PSPC) combined with analysing crystals for X-ray fluorescence (XRF) analysis. A curved PSPC and the goniometer that mounts the SSD used for XRF are also installed for X-ray diffraction. X-ray fluorescence holography and polarized X-ray emission spectroscopy modes are available, so three-dimensional images of atomic configurations and also the anisotropic structure of materials will be studied.

Journal Article↗

Two genes, COL4A3 and COL4A4 coding for the human alpha3(IV) and alpha4(IV) collagen chains are arranged head-to-head on chromosome 2q36.

We first isolated and characterized genomic DNA fragments that cover the 5' flanking sequences of COL4A3 and COL4A4 encoding the human basement membrane alpha3(IV) and alpha4(IV) collagen chains, respectively. Nucleotide sequence analysis indicated that the two genes are arranged head-to-head. To determine transcription start site for COL4A4 gene, we performed RACE and RNase protection assays, indicating that there are two alternative transcripts presumably derived from two different promoters. Interestingly, one transcription start site (from exon 1') of COL4A4 is only 5 bp away from the reported transcription start site of COL4A3, whereas the other transcript (from exon 1) starts 373 nucleotides downstream from the first one, generating the two kinds of transcripts that differ in the 5' UTR regions. Expression of these two transcripts appears tissue-specific; exon 1 transcript was expressed predominantly in epithelial cells, while exon 1' transcript showed rather ubiquitous and low expression. The nucleotide sequence of the promoter region is composed of dense CpG dinucleotides, GC boxes, CTC boxes and a CCAAT box but no TATA box. These results provide information to delineate the promoter activity for the tissue-specific expression of the six type IV collagen genes and basement membrane assembly in different tissues and organs.

Alternative Splicing↗

Induction chemotherapy is associated with an increase in the incidence of locoregional recurrence in patients with carcinoma of the oral cavity: results from a single institution.

BACKGROUND: This study was conducted to determine long term survival rates and the pattern of failure in patients with carcinoma of the oral cavity treated with induction chemotherapy or preoperative radiotherapy followed by surgery. METHODS: A retrospective analysis was performed of 141 eligible patients with Stage II-IV International Union Against Cancer (UICC) staging system squamous cell carcinoma of the oral cavity at the study department between 1985 and 1994. These patients received one of three treatments: surgery with or without peplomycin chemotherapy (Group A; n = 49); preoperative radiotherapy with or without concomitant peplomycin chemotherapy followed by surgery (Group B; n = 59); and induction chemotherapy followed by surgery (Group C; n = 33). Induction chemotherapy was comprised of two cycles of cisplatin, vincristine, peplomycin, with or without mitomycin C. RESULTS: When all 141 patients were analyzed, there was no significant difference in overall survival or disease free survival. However, a statistically significant increase in the incidence of neck recurrence in Group C was observed compared with Group A (P = 0.002). Within 79 patients with N0 disease, a statistically significant disadvantage was detected for Group C in terms of disease free survival compared with Group A (P = 0.038). In patients with Stage II disease (50 patients), there was a significant difference in disease free survival, with Group C inferior to both Group A (P = 0.04) and Group B (P = 0.066). CONCLUSIONS: Induction chemotherapy was associated with a significant increase in regional failure for patients with carcinoma of the oral cavity with N0 disease and those with Stage II disease.

Adult↗

Evaluation of argyrophilic nucleolar organizer region and proliferating cell nuclear antigen in colorectal cancer.

BACKGROUND AND OBJECTIVES: Information on cellular proliferation is gaining importance for predicting prognosis in several cancers. To clarify the clinicopathological significance of argyrophilic nucleolar organizer region (AgNOR), proliferating cell nuclear antigen (PCNA), and DNA ploidy pattern, we studied their correlations with clinicopathological factors in colorectal cancer. METHODS: Fifty-two patients with colorectal cancer were examined by AgNOR staining, immunohistochemical study of PCNA expression, and DNA flow cytometry. RESULTS: The AgNOR score and the PCNA labeling rate (PCNA LR) were significantly higher in patients with deep invasion (P = 0.0072, P = 0.0355), liver metastasis (P = 0.0022, P = 0.0001), and Dukes D classification (P = 0.0002, P = 0.0001) than in patients without these factors. In patients with high AgNOR score (>3.83) or with high PCNA LR (>48.8), prognosis was significantly worse (P = 0.0002, P = 0.0123) than in those with low AgNOR score (<3.83) or in those with low PCNA LR (<48.8), respectively. No significant association was observed between AgNOR score and PCNA LR. Combined analysis revealed that the survival curve for patients with high AgNOR score and high PCNA LR was significantly lower (P = 0.0156) than that for patients with high AgNOR score and low PCNA LR. There was no significant correlation between DNA ploidy pattern and clinicopathological findings. CONCLUSIONS: PCNA LR and AgNOR score were correlated not only with local progression but also with metastasis. Their determination provided useful prognostic information, and these parameters are probably independent. Their simultaneous determination was useful for accurate evaluation of prognosis. The value of DNA ploidy pattern was uncertain.

Aged↗

Prospective randomized controlled trial comparing percutaneous acetic acid injection and percutaneous ethanol injection for small hepatocellular carcinoma.

To assess whether ultrasound-guided percutaneous acetic acid injection is superior to percutaneous ethanol injection in the treatment of small hepatocellular carcinoma (HCC), 60 patients with one to four HCCs smaller than 3 cm were entered onto a randomized controlled trial. Thirty-one and 29 patients, respectively, were treated by percutaneous acetic acid injection using 50% acetic acid or by percutaneous ethanol injection using absolute ethanol. There were no significant differences in age, sex ratio, Child-Pugh class, size of tumors, or number of tumors between the two groups. When there was no evidence of viable HCC from biopsy, plain and helical dynamic computed tomography, or angiography, the treatment was considered successful and was discontinued. All original tumors were treated successfully by either therapy. However, 8% of 38 tumors treated with percutaneous acetic acid injection and 37% of 35 tumors treated with percutaneous ethanol injection developed a local recurrence (P < .001) during the follow-up periods of 29 +/- 8 months and 23 +/- 10 months, respectively. The 1- and 2-year survival rates were 100% and 92% in percutaneous acetic acid injection and 83% and 63% in percutaneous ethanol injection (P = .0017). A multivariate analysis of prognostic factors revealed that treatment was an independent predictor of survival. The risk ratio of percutaneous acetic acid injection versus percutaneous ethanol injection was 0.120 (range, 0.027-0.528; P = .0050). In conclusion, percutaneous acetic acid injection is superior to percutaneous ethanol injection in the treatment of small HCC.

Acetic Acid↗

Spontaneous disappearance of a middle cranial fossa arachnoid cyst after suppurative meningitis.

BACKGROUND: Spontaneous disappearance of an arachnoid cyst is very rare, particularly after suppurative meningitis. CASE REPORT: A 2-month-old boy with a high fever was diagnosed with suppurative meningitis by cerebrospinal fluid examination. Computed tomography disclosed a large arachnoid cyst in the left middle cranial fossa. Two months later, the meningitis was cured. The arachnoid cyst disappeared with long-term antibiotic therapy alone. CONCLUSION: Although an infected arachnoid cyst may disappear with antibiotic treatment alone, careful observation and individualized patient management are essential.

Arachnoid Cysts↗

Immunoadsorption therapy in Guillain-Barré syndrome.

A 12-year-old boy rapidly developed Guillain-Barré syndrome (GBS) after Campylobacter jejuni enteritis. Electrophysiologic studies suggested that demyelination was dominant, and serum anti-C. jejuni and both IgG and IgM anti-GM1 antibodies were significantly elevated. The patient was treated three times with immunoadsorption therapy using a tryptophan-immobilized column. The volume of treated plasma in each session was about 2 L. His blood pressure was maintained within normal range with the use of 5% albumin preparations and etilefrine hydrochloride. His clinical and electrophysiologic findings began to recover shortly after therapy, with a decrease in the levels of serum IgG and IgM anti-GM1 antibodies. This immunoadsorption therapy should be considered for anti-GM1 antibody-associated GBS.

Antibodies, Bacterial↗

Transformation of rat glioma cells with the M-CSF gene inhibits tumorigenesis in vivo.

Macrophage colony-stimulating factor (M-CSF) is a potent stimulator of the effector cells such as monocytes and macrophages. To evaluate the effect of M-CSF on malignant gliomas, we transfected the rat gliosarcoma cell line (9L) with human M-CSF expression vector (pCEF-MCSF) by a liposome method. Transfectants were selected using G418-containing medium. As a control, 9L cells transfected with pRc/CMV and selected by G418 were used. The effects of M-CSF gene transfection on tumor cell proliferation in vitro and in vivo were examined. All growth rate did not change in vitro. While the control 9L cells formed progressively enlarging masses, 9L cells transfected with the M-CSF gene did not develop into tumors after the injection into rats. On the other hand, in rats receiving anti-asialo GM1 antibody, 9L cells transfected with M-CSF gene developed into tumors, though at a slower rate than control 9L cells. Histologic examination after transplantation of 9L cells transfected with M-CSF gene disclosed intense infiltration of macrophages in the tumor. Thus M-CSF gene transfection into glioma cells stimulates an antitumor effect.

Animals↗

Autocrine effects of transforming growth factor-alpha on the development of preimplantation mouse embryos.

PURPOSE: We wished to explore the role of transforming growth factor (TGF)-alpha in mouse embryonic development. METHODS: We examined the gene expression of TGF-alpha and epidermal growth factor receptor (EGFR) in mouse blastocysts by the reverse transcription-polymerase chain reaction and evaluated the effects of TGF-alpha on the development of preimplantation mouse embryos using TGF-alpha antisense oligodeoxynucleotide. Mouse teratocarcinoma F9 cells were also a subject of this study. RESULTS: Gene transcripts of TGF-alpha and EGFR were present in both blastocysts and F9 cells. TGF-alpha significantly stimulated the rate of blastocoel expansion in early-cavitating blastocysts and the proliferation of F9 cells. Northern blot analysis showed that TGF-alpha gene expression in F9 cells was markedly suppressed in the presence of TGF-alpha antisense oligodeoxynucleotide. TGF-alpha antisense oligonucleotide significantly reduced the rate of blastocoel expansion and the growth of F9 cells. The inhibitory effects of TGF-alpha antisense oligonucleotide on blastocysts and F9 cells were reversed by the addition of TGF-alpha. CONCLUSIONS: The present observations suggest that TGF-alpha acts as an autocrine factor in the development of preimplantation mouse embryos.

Animals↗

A novel method to immobilize bioactive substances on hydrophobic surfaces using a polymerizable cationic lipid.

We have successfully developed a novel method to stably immobilize bioactive substances that have anionic groups, such as heparin and succinylated collagen (SC), on hydrophobic surfaces through ionic complexation using a polymerizable cationic lipid, diallyl(dioleyl)ammonium bromide (DADOA). It is composed of a hydrophobic part consisting of long hydrocarbon chains and a hydrophilic head with double bonds which render it polymerizable. Analysis of the modification with DADOA and heparin suggested that the modification formed a thin layer, roughly 60 nm in thickness, as a result of the spontaneous deposition of DADOA and heparin dissolved in water, through the hydrophobic interaction between DADOA and the surface and the ionic complexation between DADOA and heparin. The heparin deposition and its rate of release in plasma were 1.5 microg/cm2 and 0.0017 U/cm2/min, respectively. Cytotoxicity test results showed that the polymerization of the deposited DADOA rendered the modified surface stable and noncytotoxic. Further, antithrombogenicity and cell attachability test results demonstrated that heparin and SC were effectively immobilized on hydrophobic surfaces through ionic complexation. This method has proved useful for the modification of the hydrophobic surfaces of medical devices because the modification process can be performed under aqueous conditions without the use of organic solvents which induce crazing/cracking of plastic casings.

Allyl Compounds↗

Topoisomerase I and II consensus sequences in a 17-kb deletion junction of the COL4A5 and COL4A6 genes and immunohistochemical analysis of esophageal leiomyomatosis associated with Alport syndrome.

Diffuse esophageal leiomyomatosis (DL), a benign smooth-muscle-cell tumor, is characterized by abnormal cell proliferation. DL is sometimes associated with X-linked Alport syndrome (AS), an inherited nephropathy caused by COL4A5 gene mutations. COL4A5 is tightly linked, in a head-to-head fashion, to the functionally related and coordinately regulated COL4A6 gene. No X-linked AS cases are due to COL4A6 mutations, but all DL/AS cases are always associated with deletions spanning the 5' regions of the COL4A5/COL4A6 cluster. Unlike the COL4A5 breakpoints, those of COL4A6 are clustered within intron 2 of the gene. We identified a DL/AS deletion and the first characterization of the breakpoint sequences. We show that a deletion eliminates the first coding exon of COL4A5 and the first two coding exons of COL4A6. The breakpoints share the same sequence, which, in turn, is closely homologous to the consensus sequences of topoisomerases I and II. Additional DNA evidence suggested that the male patient is a somatic mosaic for the mutation. Immunohistochemical analysis using alpha-chain-specific monoclonal antibodies supported this conclusion, since it revealed the absence of the alpha5(IV) and alpha6(IV) collagen chains in most but not all of the basement membranes of the smooth-muscle-cell tumor. We also documented a similar segmental staining pattern in the glomerular basement membranes of the patient's kidney. This study is particularly relevant to the understanding of DL pathogenesis and its etiology.

Adult↗

Analysis of loss of heterozygosity in small adenocarcinomas of the lung.

BACKGROUND: Despite the many studies of genetic alterations in advanced lung carcinomas, few reports have analyzed early stage adenocarcinoma of the lung. METHODS: We focused on small pulmonary adenocarcinomas, classified according to recently proposed histological criteria (Noguchi M., et al. Cancer 1995;75:2844-52) which divided adenocarcinomas 2 cm or less in diameter into two groups; one showing replacing growth of the pulmonary alveolar structure [A, localized bronchioloalveolar carcinoma (LBAC); B, LBAC with alveolar collapse; C, LBAC with active fibroblastic proliferation] and the other showing non-replacing growth (D, poorly differentiated adenocarcinoma). Ninety-four small pulmonary adenocarcinomas, including 40 of type A and B, 30 of type C and 24 of type D, were examined for loss of heterozygosity (LOH) using microsatellite markers. RESULTS: The frequencies of LOH were 19.8% in types A and B, 26.8% in type C and 32.7% in type D tumors. There were no significant differences in the frequency of LOH on chromosomes 2p, 3p, 9p and 17q among tumor types. However, on 17p, the frequency of LOH was significantly lower for types A and B than for type C or D. Three out of six type C tumors which were positive for LOH at several loci showed different LOH patterns in two areas (central and peripheral regions). CONCLUSIONS: Allelic losses were detected in very early adenocarcinomas and the frequency of LOHs on chromosome 17p increased during malignant progression of the tumor. Heterogeneous genetic alterations were demonstrated even in small pulmonary adenocarcinomas.

Adenocarcinoma↗