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Biomedical subjects

S Kodama

Publications and source records attributed to S Kodama.

At least 73 records · Page 4Linked to original sources
PubMed1999

Delayed cell death, giant cell formation and chromosome instability induced by X-irradiation in human embryo cells.

We studied X-ray-induced delayed cell death, delayed giant cell formation and delayed chromosome aberrations in normal human embryo cells to explore the relationship between initial radiation damage and delayed effect appeared at 14 to 55 population doubling numbers (PDNs) after X-irradiation. The delayed effect was induced in the progeny of X-ray survivors in a dose-dependent manner and recovered with increasing PDNs after X-irradiation. Delayed plating for 24 h post-irradiation reduced both acute and delayed lethal damage, suggesting that potentially lethal damage repair (PLDR) can be effective for relieving the delayed cell death. The chromosome analysis revealed that most of the dicentrics (more than 90%) observed in the progeny of X-ray survivors were not accompanied with fragments, in contrast with those observed in the first mitosis after X-irradiation. The present results indicate that the potentiality of genetic instability is determined during the repair process of initial radiation damage and suggest that the mechanism for formation of delayed chromosome aberrations by radiation might be different from that of direct radiation-induced chromosome aberrations.

Cell Death↗
PubMed1999

[Report of two rare cases of fungal sinusitis].

Two cases of aspergillosis of the paranasal sinuses are reported. The first case was a 30-year-old man who had a 5-month history of bilateral proptosis. Physical examination revealed nasal polyps in both middle meatus. A skin test for Aspergillus was positive. Laboratory study showed levels of serum IgE and IgE specific for Aspergillus level to be elevated significantly. Computed tomography (CT) and magnetic resonance imaging (MRI) showed pansinusitis with some bone erosion. The patient underwent bilateral Caldwell-Luc procedures and external sinus surgery (frontal, ethmoid and sphenoid sinuses). Histopathological examination showed thin septate hyphae in allergic mucin. The patient is now being treated with sinus irrigation and oral administration of fluconazole and suplatast tosilate. The second case was a 78-year-old man who had a 2-month history of nasal obstruction and a 3-week history of headaches. He also had a history of diabetes mellitus. Physical examination showed swelling of the nasal septum due to abscess. CT showed an abscess in the nasal septum and opacification of the left sphenoid sinus. There was no bone destruction. The patient underwent left sphenoid sinus surgery, and histopathological examination revealed aspergillosis of the sphenoid sinus. He presented with left visual disturbance and blepharoptosis 2 months after surgery. Ocoulusion of the internal carotid artery was revealed by MR angiography and it was thought to be caused by intracranial invasion of aspergillus. Loss of consciousness and right hemiplegia ensued despite antifungal chemotherapy. The patient died about 1 year after the onset of symptoms. Case 1 was thought to involve allergic aspergillus sinusitis, and Case 2 invasive aspergillus sinusitis. We emphasize the significance of headache, diabetes mellitus and lesion in the sphenoid sinus as a sigh of intracranial aspergillus invasion, based on our experience as well as findings reported by other clinicians in the Japanese literature.

Adult↗
PubMed1999

[Acute renal failure due to over-infusion in a child with bilateral obstruction of the pyeloureteral junction].

A 2-year-old boy was hospitalized with the chief complaint of oliguria and dyspnea. Bilateral hydronephrosis and obstruction of the pyeloureteral junction were detected by ultrasonography. Pulmonary edema was also found on chest radiographs. The clinical diagnosis was acute post renal failure due to bilateral pyeloureteral obstruction and pulmonary edema due to overtransfusion. After we performed bilateral percutaneous nephrostomy, the patient recovered from renal failure and pulmonary edema. Both nephrostomies were removed after we confirmed a non-obstructing pattern using the Whitaker test.

Acute Kidney Injury↗
PubMed1999

[Clinical evaluation of urinary leukotriene E4 levels in children with atopic dermatitis].

To evaluate the significance of peptide leukotrienes in children with atopic dermatitis, we measured urinary LTE4 levels which are thought to reflect in vivo production of peptide LTs. Urine was collected in the early morning. There was no significant difference in urinary LTE4 levels among atopic children with different severities. On the other hand, urinary LTE4 levels were significantly elevated in the patients who had severe nocturnal itches compared with the patients who had mild nocturnal itches and normal controls. These results suggested that increased production of peptide LTs may be relevant to nocturnal itch of atopic dermatitis.

Adolescent↗
PubMed1998

A novel inhibitory effect on prostacyclin synthesis of coupling factor 6 extracted from the heart of spontaneously hypertensive rats.

The possible presence of an unknown prostacyclin synthesis inhibitory substance has been reported in some strains of rats. We purified the inhibitory substance from the heart of spontaneously hypertensive rats by collecting active fractions after gel-filtration column chromatography and two steps of reverse-phase high performance liquid chromatography. The amino acid composition and automated gas-phase sequencing of the full-length substance and fragments cleaved by AspN indicated that the prostacyclin-inhibitory peptide was identical to coupling factor 6. Recombinant rat coupling factor 6, which was synthesized using a cleavable fusion protein strategy, attenuated base-line and bradykinin (10(-6) M)-induced prostacyclin synthesis and [3H]arachidonic acid (AA) release in human umbilical vein endothelial cells in a dose-dependent manner (10(-9)-10(-7) M). Exogenous AA- and prostaglandin H2-induced prostacyclin synthesis were unchanged even after treatment with 10(-7) M recombinant coupling factor 6. Base-line and bradykinin-induced [3H]AA release were suppressed by arachidonyltrifluoromethyl ketone, a relatively specific inhibitor of cytosolic phospholipase A2 at 40 microM, and simultaneous administration of coupling factor 6 showed no further effect. Neither oleyloxyethyl phosphorylcholine at 1 microM nor bromoenol lactone at 1 microM affected AA release. Preincubation (1 min) with 10(-7) M recombinant coupling factor 6 had no influence on adenosine diphosphate- and collagen-induced platelet aggregations. We conclude that coupling factor 6 possesses a novel function of prostacyclin synthesis inhibition in endothelial cells via suppression of Ca2+-dependent cytosolic phospholipase A2, although it is unclear whether coupling factor 6 functions in normal conditions or only in pathophysiological states.

Adenosine Triphosphatases↗
PubMed1998

Failure to complement abnormal phenotypes of simian virus 40-transformed Werner syndrome cells by introduction of a normal human chromosome 8.

The Werner syndrome (WS) gene (WRN) was isolated by positional cloning, based on mapping to chromosome 8p12, and the WRN protein was recently shown to encode an active helicase. To examine functional complementation of WS phenotypes by expression of the WRN gene, we introduced a normal human chromosome 8 into a SV40-transformed WS fibroblastoid cell line (WS780) by microcell fusion and studied several cellular phenotypes associated previously with WS cell lines, including cell growth rate, 4-nitroquinoline-1-oxide (4NQO) sensitivity, and spontaneous mutation rate and type of mutation at the hypoxanthine-guanine phosphoribosyl transferase locus. The WRN gene was expressed in two of three microcell hybrids introduced with chromosome 8. We failed to observe a difference between normal and WS cell lines in terms of growth rates and spontaneous mutation rates. However, we found that the WS cell line was highly sensitive to 4NQO-induced cytotoxicity and showed an unusually high proportion of deletion mutations at the hypoxanthine-guanine phosphoribosyl transferase locus as compared to a control cell line, as shown previously. Here, we report that these phenotypes were not corrected by introduction of the WRN gene, although the WRN protein was expressed. Our results suggest that the hypersensitivity to 4NQO and the extensive deletion mutations observed in the WS cell line are caused by a defect that is secondary to the WRN gene mutation, possibly a repair gene defect that controls the phenotypes of hypersensitivity to carcinogen(s) and/or the extensive deletion mutations.

4-Nitroquinoline-1-oxide↗
PubMed1998

Radiation-induced long-lived radicals which cause mutation and transformation.

Using electronic spin resonance (ESR), we found a new type of radical with a long life-time in cells (T1/2>20 h) and which may play a more important role in the induction of mutation and transformation than either the active, short-lived, H, or OH radicals. When cells were treated with dimethyl sulfoxide (DMSO) and l-ascorbic acid (AsA) just before irradiation, the short-lived radicals were well-scavenged. On the other hand, if cells were treated with the scavengers 20 min after irradiation, then AsA scavenged the long-lived radicals, but DMSO did not. AsA treatment 20 min after the start of irradiation drastically reduced both the frequencies of mutation at the hypoxanthine guanine phosphoribosyl transferase (HGPRT) locus in human cells and morphological transformations in mouse m5S cells, but DMSO treatment did not. In addition, AsA treatment 20 h after irradiation also reduced the mutation frequency in human cells. These results suggested that mutations and morphological transformation are probably caused by the presence of long-lived radicals in the cells, rather than by short lived radicals, and that AsA reacts efficiently with long-lived radicals, resulting in a decrease of the mutations and transformations induced.

Animals↗
PubMed1998

Nasal immune system: distinctive Th0 and Th1/Th2 type environments in murine nasal-associated lymphoid tissues and nasal passage, respectively.

The nasal mucosa, an important arm of the mucosal immune system, is the first site of contact with inhaled antigens to induce an IgA response. A major aim of this study was to characterize the Th1 and Th2 cytokine expression of mucosal T cells residing in nasal-associated lymphoid tissue (NALT) and nasal passages (NP) as IgA inductive and effector sites, respectively, at the transcription and cellular levels. An application of single-cell reverse transcription-PCR for analysis of Th1 (IFN-gamma) and Th2 (IL-4 and IL-6) cytokine-specific mRNA revealed the presence of CD4+ T cells with a Th0 profile in NALT, while high numbers of Th2 cytokine-specific mRNA expressed by CD4+ T cells were noted in NP followed by Th1-type cells. NALT CD3+ CD4+ T cells of Th0 type have the capacity to become Th1- and/or Th2-type cells since their activation via the TCR-CD3 complex resulted in the expression of an array of Th1 and Th2 cytokines. CD3+ CD4+ T cells from NP, but not NALT, provide a helper function for the induction of antibody-forming cells including IgA isotype in B cell cultures. These findings suggest that NALT is characterized by a Th0 environment which can gain a Th1 and/or Th2 phenotype. In contrast, NP is considered to be a Th2 dominant site with some Th1 cells that can support the induction of IgA-producing cells.

Animals↗
PubMed1998

Enhancement of nasal clearance of nontypeable Haemophilus influenzae by oral immunization with outer membrane proteins.

BALB/c mice were orally immunized with liposomes containing outer membrane proteins (OMPs) isolated from nontypeable Haemophilus influenzae (NTHi) and GM-53 as an adjuvant daily for 14 days. Anti-OMP IgA antibody titers in nasal wash, saliva, and fecal extract were significantly increased after the immunization. Although anti-OMP IgM and IgG antibodies were detected in serum, serum IgA antibodies specific to OMPs were not found. Enzyme-linked immunospot assay showed an increased number of OMP-specific IgA-secreting cells in nasal passages, intestinal lamina propria lymphocytes, and the spleen. Following oral immunization, a suspension of live NTHi was injected into the nose; nasal washes were collected 12 h after the inoculation. The number of NTHi in nasal washes was significantly reduced in mice immunized with liposomes containing OMPs and GM-53 compared to that in mice immunized with liposomes containing GM-53 alone. There was a significant negative correlation between the number of NTHi and anti-OMP IgA antibody titers in nasal washes. These findings suggest that antigen-specific IgA responses in the nose can be induced by oral immunization with OMPs and might be associated with the ability to clear NTHi from the nose.

Adjuvants, Immunologic↗
PubMed1998

Paraneoplastic cerebellar degeneration with anti-Purkinje cell antibody associated with primary tubal cancer.

In patients with paraneoplastic cerebellar degeneration (PCD) due to gynecologic malignancies, a high titer of anti-Purkinje cell antibody (anti-Yo) has been found. Most patients, however, have limited oncologic disease at the time of onset of neurologic symptoms. We describe 2 cases of PCD due to tubal cancer with anti-Yo antibody. The onset of PCD occurred 4 and 14 months before the detection of cancer, respectively, and the presence of anti-Yo antibody facilitated early laparotomy in both cases. These patients, whose neurologic symptoms have not progressed, have survived without evidence of disease for 81 and 30 months since surgery, respectively. The presence of the anti-Yo antibody in patients with PCD warrants an aggressive approach to diagnosis and treatment of the underlying gynecologic cancer.

Adenocarcinoma↗
PubMed1998

Recurrent T354P mutation of the Na+/I- symporter in patients with iodide transport defect.

Iodide transport defect (ITD) is a rare disorder causing congenital hypothyroidism. We previously reported that homozygous T354P mutation in the sodium/iodide symporter (NIS) gene caused ITD. To clarify the prevalence of this mutation, artificial substitution introducing PCR followed by restriction enzyme analysis was developed as a rapid screening method to detect the T354P mutation. Three apparently unrelated families with ITD, one patient with low thyroidal 99mTc pertechnetate (99mTcO4-) uptake and 52 healthy controls (104 alleles) were analyzed for this mutation. All families with ITD harbored the mutation, suggesting that T354P is a recurrent mutation and a major cause of ITD. This was not a widespread mutation, because it was not detected in the 52 unrelated normal controls. Because two cases with homozygous T354P mutation developed multinodular goiters within their second decade of life though they had been maintained in euthyroid state, homozygous T354P mutation alone and/or low intrathyroidal iodide and high serum TSH level in early life might account for tumorigenesis. The patient with low thyroidal 99mTcO4- uptake did not harbor the T354P mutation. Because familial hypocalciuric hypercalcemia was also present in this family, a possibility of the combined abnormality of TSH receptor and calcium functions, which includes an abnormality around the G protein, may be examined further.

Carrier Proteins↗
PubMed1998

Establishment and characterization of a hypocatalasemic mouse cell strain.

Contact-inhibited catalase-deficient fibroblast cell strain has been established from the homozygous hypocatalasemic C3H/Csb mutant mouse. This cell strain has low level of catalase enzyme activity and has normal level of enzyme activities of both glutathione peroxidase and superoxide dismutase. Catalase-deficient C3H/Csb mutant cell strain is markedly more sensitive to the toxicity of hydrogen peroxide compared to wild-type C3H/Csa cell strain. In addition, mutant cell strain is sensitive to X-rays and near-UV compared to wild-type cell strain, but shows the same sensitivities to topoisomerase II inhibitors, adriamycin and 4'-(9-acridinylamino) methanesulfon-m-anisidide (m-AMSA), and the DNA cross-linking agents, cisdiamminedichloroplatinum (II) (cis-Pt) and trans-diamminedichloroplatinum (II) (trans-Pt). These cell strains will be of use in the study of the roles which catalase plays in the intracellular prevention of DNA damage induced by oxidative stress.

Acatalasia↗
PubMed1998

Extension of in vitro life-span of gamma-irradiated human embryo cells accompanied by chromosome instability.

We studied the effect of repeated irradiation with a low dose rate (about 0.0012 cGy per min) of 60Co gamma-rays on the in vitro life-span of human embryo (HE) cells. HE cells were cultured in an incubator that was set in a 60Co gamma-ray-irradiation room, and the irradiation was repeated throughout the life-span of the HE cells (for about 150 to 160 days) on every day base. During this period, the cells accumulated 106 to 123 cGy. The life-span of the irradiated cells prolonged 1.14 to 1.35 times when compared to that of non-irradiated cells. The incidence of cells with chromosome bridge and micronuclei significantly increased in the irradiated cells. Although the number of chromosomes gradually changed with repetition of culture in both non-irradiated and irradiated cells, the frequencies of aneuploid cells in irradiated cells were about two times higher than that in non-irradiated cells. These results indicate that repeated irradiation with a low dose of gamma-rays produces chromosome instability, and it may be a cause of numerical chromosome abnormalities and life-span extension of irradiated cells.

Aneuploidy↗
PubMed1998

Telomerase activity, telomere length, and chromosome aberrations in the extension of life span of human embryo cells induced by low-dose X-rays.

We examined whether the shortening of telomere structure is related to in vitro cellular aging after multiple low-dose irradiation. We used three strains of HE cells (HE23, HE31, and HE40) exhibiting different levels of telomerase activity and irradiated these cells twice a week with a dose of 2 cGy or 4 cGy of X-rays until they senesced. The cells were in total exposed to doses of 52-208 cGy of X-rays. Only the HE31 cells, which had no telomerase activity, experienced an increase in the number of cell divisions, reaching a maximum of 120-124% of the non-irradiated controls. However, in two strains which did exhibit telomerase activity in an early passage in culture, no extension of cell life span was found. Telomerase-positive cells completely lost all telomerase activity when the cells were subcultured several times without irradiation. In the HE31 cells where the life span was extended, the ratio of cell having a long telomere was higher than those of the other two cells (HE23 and HE40). Cytogenetic analysis revealed that the life span extension due to multiple low-dose irradiation which was observed in HE31 cells did not correlate with specific chromosome alterations. Our results suggest that the telomerase activity remaining in the cells at an early passage does not correlate with the extension of life span in vitro by X-irradiation. The factor other than telomerase activity may play an important role in the regulation of telomere length and the extension of life span.

Cell Division↗
PubMed1998

[Evaluation of theophylline in children hospitalized with asthma attack].

The purpose of this study is to determine whether theophylline provides clinical benefits in the hospitalized children with asthma attack. Aminophylline was intravenously given to the 50 patients (Group A) who were admitted 1994. A small dose of aminophylline compared to that of Group A was given to the 44 patients (Group B1) who were admitted 1998. On the other hand, aminophylline was not given to the 12 patients (Group B2) who were admitted 1998. However, there were no differences among those groups in the duration of admission, in the total dose of intravenously given methylprednisolone, and in the improvement of clinical score of asthma. These results suggested that there was no clinical benefit in using theophylline for treatment to hospitalized children with asthma attack combined high fever.

Aminophylline↗