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K Saijoh

Publications and source records attributed to K Saijoh.

At least 19 recordsLinked to original sources
PubMed1997

Endogenous adenosine facilitates neurotransmission via A2A adenosine receptors in the rat superior colliculus in vivo.

The concentration of endogenous adenosine in the cerebrospinal fluid increased 2-3-fold of the original level in the area of rat superior colliculus after the intraperitoneal administration of an adenosine deaminase inhibitor, EHNA (erythro-9-(2-hydroxy-3-nonyl)adenosine, 10 mg/kg). Potentials evoked in the superior colliculus by optic tract stimulation were also facilitated by 120-160% of their initial amplitudes. A selective A1 adenosine receptor antagonist, DPCPX (8-cyclopentyl-1,3-dipropylxanthine), failed to reduce such EHNA-induced facilitation. However, a selective A2A adenosine receptor antagonist, KF17837 (8(3,4-dimethoxystyryl)-1,3-dipropyl-7-methylxanthine) completely eliminated the facilitatory effects of EHNA. Northern blot analysis demonstrated abundant expression of A1 adenosine receptor mRNA in the superior colliculus. RT-PCR analysis was able to detect the concomitant expression of A2A adenosine receptor mRNA, but at levels lower than one-tenth of the striatal expression. In the superior colliculus, A2A adenosine receptors function predominantly on the facilitatory effects of adenosine, irrespective of the ubiquitous expression of A1 adenosine receptors.

Adenine↗
PubMed1997

Human papillomavirus infection and risk determinants for squamous intraepithelial lesion and cervical cancer in Japan.

A case control design was used to investigate human papillomavirus (HPV) prevalence and risk factors associated with development of cervical squamous intraepithelial lesion (SIL) and cervical cancer (CC) in Japan. One hundred and twenty-three women with histologically confirmed SIL or CC were compared to a control group of 778 cytologically normal women. With the use of a polymerase chain reaction (PCR)-based method for detection of low-risk (types 6 and 11) and high-risk (types 16, 18, 31, 33, 35, 52 and 58) HPVs, a high prevalence of HPV infection was observed in smokers among the controls. Logistic regression analysis demonstrated that high-risk HPV infection was the most significant risk determinant for LSIL (OR=9.4, 95% CI=4.5-19), HSIL (OR=77, 95% CI=28-217) and CC (OR=97, 95% CI=35-269). It also showed that unmarried women, women married for 5 to 19 years and smokers represented high risk groups for SIL, while smokers and women with a history of many pregnancies/parities had increased risk for CC. Smoking was the only HPV infection-independent factor for CC, suggesting that smoking may have a carcinogenic effect on the cervix. Since neither history of other cancer nor family cancer history was associated with SIL or CC, genetic factors appear to play little role in cervical carcinogenesis. The risk for cervical neoplasia due to HPV infection increased after marriage in Japan, suggesting a role for husbands as carriers of HPV transmission. Protection from high-risk HPV infection may be of greatest importance for prevention of cervical cancer.

Adolescent↗
PubMed1997

Regulation of selenoprotein P mRNA expression in comparison with metallothionein and osteonectin mRNAs following cadmium and dexamethasone administration.

Selenium is recognized as an essential trace element and an antidote for carcinogens, heavy metals etc., and also as an environmental pollutant causing dysfunction of both the brain and peripheral tissues. Selenoprotein P (SelP) contains 10 selenium per molecule in the form of selenocysteines. To clarify whether SelP involved in selenium requirement and toxicity, SelP mRNA expression was compared with the expression of metallothionein (MT) and osteonectin (OST) mRNAs, the protein products of which are known to have antidote effects. MT and OST are induced by diverse forms of stress and immediately affect genes with stress promoter sequences. Cd and dexamethasone were used to examine such secondary regulation. Basal expression of SelP mRNA was high both in NRK cells and in rat kidney and brain but dexamethasone induction was observed only in NRK cells. Dexamethasone, but not Cd, decreased expression of OST mRNA in NRK cells, while OST mRNA in the kidney and brain increased after Cd administration in rats. Induction of MT mRNA was observed in response to Cd and dexamethasone in all cells and tissues examined, while the net increase was little because its basal expression was faint. Moreover, in situ hybridization indicated that SelP mRNA expression was localized to the cerebellum, one of the targets of selenium toxicity. The cerebellum is also a target for methyl-Hg intoxication, symptoms of which are ameliorated by selenium. Thus, SelP seems to be involved in both selenium homeostasis and detoxication mechanisms even though SelP mRNA is not always inducible.

Animals↗
PubMed1996

Expression ratio of hepatocyte nuclear factor-1 to variant hepatocyte nuclear factor-1 in differentiation of hepatocellular carcinoma and hepatoblastoma.

BACKGROUND/AIMS: Liver-specific protein genes have multiple cis-/trans-acting elements, but those accountable for hepatocytic differentiation are unclear. An AT-rich core sequence (AT motif) is essential as a cis-acting element for the hepatic transcription. Homologous proteins hepatocyte nuclear factor-1 (HNF-1) and variant HNF-1 (vHNF-1) bind to this motif. The ratio of HNF-1 to vHNF-1 mRNA was examined in various liver tissues with respect to their differentiation. METHODS: The competitive reverse transcriptional polymerase chain reaction was employed to amplify HNF-1 and vHNF-1 mRNA simultaneously and to examine their expression ratio in total RNA extracted from frozen liver tissues of 37 patients with hepatocellular carcinoma, five patients with hepatoblastoma, and 15 non-neoplastic liver tissues. RESULTS: The ratio of HNF-1 to vHNF-1 mRNA was higher in well-differentiated cases than in poorly-differentiated and undifferentiated cases, except that one poorly-differentiated hepatoblastoma displayed a high ratio. Non-neoplastic liver tissues had low ratios similar to poorly-differentiated hepatocellular carcinoma, the reason for which remained unknown. However, chronic hepatitis and liver cirrhosis cases also demonstrated low ratios, and hence degenerative changes themselves displayed no obvious influence on such ratios. Thus, the gene expression of HNF-1 and vHNF-1 seemed to be differentially regulated in neoplastic and non-neoplastic hepatocytes. CONCLUSIONS: These results suggested that the ratio of HNF-1 to vHNF-1 mRNA correlated with histological differentiation of HCC and hepatoblastoma.

Adult↗
PubMed1995

Regional differences in expression of osteonectin mRNA after administration of cadmium to rats.

Osteonectin gene expression in relation to metallothionein mRNA expression was investigated in various tissues from Cd-treated rats. After a single 50 micromol/kg subcutaneous injection of CdCl2, Cd predominantly accumulated in the liver and metallothionein gene expression significantly increased concomitantly with Cd accumulation, but no alteration of osteonectin gene expression was observed. In the kidney and lung, both metallothionein and osteonectin mRNA increased significantly but the elevation of metallothionein mRNA levels (1 h after Cd administration) preceded that of osteonectin (3 h after administration). A significant elevation of osteonectin mRNA levels was also observed in the testis after 3 h, but that of metallothionein mRNA occurred after 6 h. Not only accumulation of Cd but also increments in both osteonectin and metallothionein mRNA were minimal in the brain, but a significant increase in gene expression was observed after 1 h for osteonectin and after 3 h for metallothionein. Since, except in the testis, metallothionein gene expression preceded osteonectin gene expression, the induced metallothionein might transpose Cd and thereby affect its levels immediately, thus reducing the levels of Cd available for accumulation in other tissues. Hence, the osteonectin-Cd interaction might be secondary to the metallothionein-Cd interaction. However, the fact that osteonectin mRNA was predominantly induced by Cd administration in the target tissues of Cd toxicity, such as the lung, kidney and testis, suggests the possible involvement of osteonectin in Cd intoxication/detoxication mechanisms.

Amino Acid Sequence↗
PubMed1995

Molecular cloning of cDNA encoding a bovine selenoprotein P-like protein containing 12 selenocysteines and a (His-Pro) rich domain insertion, and its regional expression.

When cDNA containing proteins enriched in the bovine cerebellar cortex were cloned, a clone which seemed to encode a selenoprotein P-like protein was isolated. The coding nucleotide sequence of its cDNA insert displayed high homology to rat and human selenoprotein P cDNA but contained 12 rather than 10 TGAs (12 rather than 10 selenocysteines in deduced amino acids), a tandem repeat of one CACTCC (His-Ser) and seven CATCCCs (His-Pro), and a 3' untranslated region approximately 890 bases shorter than that of rat liver selenoprotein P. RT-PCR using a set of primers flanking to the repeat displayed the existence of mRNA without the repeat. The tandem repeat and its adjacent region consisted of a similar motif of CAC/TCC/AC/T. Thus, these proteins included a (His-Pro) rich domain with a slightly negative free energy change irrespective of having the tandem repeat or not. Such His-Pro repeats reportedly exist in the segmentation gene paired or homeobox protein Om(1D) of Drosophila. Moreover, both this selenoprotein P-like protein mRNA and selenoprotein P mRNA were expressed in all the areas of the brain but most prominently in the cerebellar cortex, hippocampus, and olfactory bulb. These findings suggest the possibility that these selenoproteins are major selenium carriers in the brain and play a role in the morphological response of nerve or glial cells.

Amino Acid Sequence↗
PubMed1995

[Serotonin].

Explore the source record for details and available documents.

Humans↗
PubMed1994

Calcitonin directly acts on mouse osteoblastic MC3T3-E1 cells to stimulate mRNA expression of c-fos, insulin-like growth factor-1 and osteoblastic phenotypes (type 1 collagen and osteocalcin).

The present study was performed to examine whether calcitonin directly acted on mouse osteoblastic MC3T3-E1 cells to stimulate the mRNA expression of insulin-like growth factor-1 (IGF-1) and c-fos, followed by an increase in their proliferation and differentiation. Eel calcitonin increased [3H]thymidine incorporation and alkaline phosphatase activity as well as the mRNA expression of type 1 collagen and osteocalcin which were characteristic of osteoblasts. Eel calcitonin (10(-8)M) induced c-fos mRNA transiently after its addition, followed by gene expression of IGF-1, an important autocrine/paracrine growth factor in the regulation of osteoblastic proliferation. We first demonstrated that calcitonin directly acted on osteoblasts to stimulate transcription of c-fos and IGF-1 genes as well as functional phenotypes including type 1 collagen and osteocalcin.

Animals↗
PubMed1993

Effects of methylmercury on protein kinase A and protein kinase C in the mouse brain.

The effects of methylmercury administration on adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase (protein kinase A) and protein kinase C were investigated by determining their second messenger bindings ([3H]cAMP binding for protein kinase A and [3H]PDBu for protein kinase C) and enzymatic activities in the brains of methylmercury-treated mice. After single administrations of methylmercury (10 mgHg/kg, sc), no neurological symptoms were observed, while the mercury concentration in the brain reached 5.6 ppm. Neither second messenger bindings nor enzymatic activities of either protein kinase displayed significant changes. When methylmercury was administered repeatedly (10 mg Hg/kg x 5), the mercury concentration was 11.7 ppm and the enzymatic activity of protein kinase C was reduced to 75% of the control level without significant change in [3H]PDBu binding. Significant change has not been observed in either [3H]cAMP binding or enzymatic activity of protein kinase A. The reduction of enzymatic activity of protein kinase C was reversed by the simultaneous administration of selenite (0.5 mgSe/kg x 5). However, the fact that selenite administration alone displayed not a significant but about a 20% increase in [3H]PDBu binding suggested that selenite itself could affect the level of protein kinase C despite having no apparent effects on protein kinase C in vitro. Further investigation is necessary to assess whether protein kinase C is involved in the detoxication mechanism of selenite with respect to methylmercury. Since the mercury concentration in the brain was higher than the IC50s for both protein kinase A and protein kinase C observed in vitro even after single administration, methylmercury might inhibit both protein kinases, which might impair intracellular signal transduction. This might in part conceal the symptoms during the early stages of methylmercury toxicity.

Animals↗
PubMed1991

Recent status of the medical examiner system in Japan: demographic variation of medicolegal deaths in Hyogo Prefecture and uncertainty in medicolegal investigations conducted by medical practitioners.

The medical examiner system has been steadily abolished in Japan. Instead, medicolegal investigations are entrusted by the police to medical practitioners, who are not permitted to perform autopsies. The necessity for the medical examiner system was assessed through inquest records in Hyogo, one of the three prefectures which still have medical examiner systems. Standardized mortality ratios (SMRs) for accidents and suicides were negatively associated with population density, being high in rural areas with a large proportion of elderly citizens, while the SMR for natural deaths was high in urbanized areas and associated with the proportion of inquests to total resident deaths. The high proportion of inquests, however, did not always mean that inquest records were of good quality. Significant differences in the quality of medicolegal investigations seemed to exist between medical examiners and medical practitioners. That is, in order to certify the cause-of-death, medical examiners performed autopsies in about half of their cases, while only 2% of medical practitioner cases were subjected to autopsies. Medical practitioners, who certified the cause-of-death as "heart failure" without advising an autopsy, were regularly entrusted with inquests. It is likely that the causes-of-death for medicolegal cases may be questionable since more than 85% of all medicolegal deaths were investigated by medical practitioners, which may cause inaccuracy in at least 3-7% of mortality statistics. It is necessary to educate medical practitioners concerning the importance of mortality statistics and ICD and on the validity of autopsies, in order to obtain accurate mortality statistics from medicolegal cases.

Accidents↗
PubMed1991

Action of mercurials on 3H-cAMP binding to the regulatory subunit-II of cAMP-dependent protein kinase.

Binding of the regulatory subunit type II (RII) of adenosine 3',5'-cyclic monophosphate (cAMP) dependent protein kinase was inhibited by Hg2+ with an IC50 value of 0.31 microM. Methyl mercury, p-chloromercuribenzoic acid (PCMB), and 5,5'-dithiobis-2-nitrobenzoic acid (DTNB) also inhibited cAMP binding with IC50 values of 70-80 microM for organic mercurials and 130 microM for DTNB. Addition of 1 mM 2-mercaptoethanol and 1 M cysteine to the assay mixture reversed these inhibitions. N-ethylmaleimide (NEM) showed little effect on the binding. On the other hand, Hg2+ and methyl mercury markedly suppressed enzymatic activity of the catalytic subunit. The IC50 value was 0.13 microM for Hg2+ and 0.15 microM for organic mercurials. Scatchard plots of kinetic analysis data for the cAMP binding revealed a noncompetitive type of inhibition by mercurials and DTNB. It is suggested that blockade of sulfhydryl groups resulted in the inhibition of cAMP binding to the RII subunit, which might result in preserving the association of the RII subunit and the catalytic subunits and in preventing further inactivation of the catalytic subunit by Hg2+.

Animals↗
PubMed1991

Mortality in medicolegal deaths in Hyogo Prefecture (1986-88).

Only three medical examiner offices are undertaking inquests on medicolegal deaths and no coroner system exists in Japan. Medical practitioners are also entrusted to hold such inquests. Certificates filed by the medical examiners of Hyogo Prefecture were compared with those filed by medical practitioners. Medical examiners certified deaths as "heart failure" only when no pathological changes were found after an autopsy. Of 2,622 deaths caused by diseases, 1,707 were certified as "heart failure" by medical practitioners without performing an autopsy. The term "heart failure" seems likely to be misused for deaths of which causes are unknown. Although the age-adjusted mortality rate for "heart disease" in Japan (98.7 per 100,000 population) showed a higher rate than for "cerebrovascular disease" (84.2), it included 53.9 for "heart failure". The misuse of the term "heart failure" seems to have introduced serious bias into the recent mortality statistics of Japan. This inaccuracy is due to ignorance about the importance of mortality statistics and ICD. Improvement in the reliability of mortality statistics is necessary for disease prevention projects through clinical medicine and public health means.

Cause of Death↗
PubMed1991

Sequence and expression of a neuropeptide Y receptor cDNA.

The polymerase chain reaction was used to isolate novel GTP-binding protein (G protein)-coupled receptors from bovine locus coeruleus (LC), a brain region enriched in the neuropeptide Y (NPY) system, using degenerate primers derived from the third and sixth transmembrane domains of known G protein-coupled receptors. Partial sequence analysis revealed that the polymerase chain reaction cDNA fragments were homologous to other G protein-coupled receptors. One of these cDNA fragments was used to isolate a full length cDNA clone, referred to as LCR1, from an LC cDNA library. LCR1 is 1.7 kilobases in length and encodes a predicted protein of 353 amino acids, with a membrane topology similar to that of other G protein-coupled receptors. Expression of LCR1 in mammalian cells revealed saturable and specific high affinity binding for 125I-NPY but not for any of the other ligands tested. Northern blot analysis revealed that labeled LCR1 DNA hybridized with a predominate mRNA transcript of approximately 1.7 kilobases, which was found to be most abundant in LC, cerebellum, and pons, intermediate in dorsal raphe, substantia nigra, and thalamus, and lowest in cerebral cortex and neostriatum. Significant levels of LCR1 mRNA were also present in heart, kidney, lung, and liver. This cDNA clone will be useful for studies of the regulation and function of NPY receptors, as well as for the isolation of related NPY receptor subtypes.

Amino Acid Sequence↗
PubMed1989

Neurochemical effect of lead exposure: a study on catecholamine metabolism.

In an attempt to examine the neurochemical changes of lead exposure, a study was conducted on 106 lead workers and a control group of 25 nonexposed workers. The urinary excretion of major catecholamine metabolites, homovanillic acid (HVA), and vanillylmandellic acid (VMA) were measured. Workers exposed to lead had a mean blood lead concentration of 43.2 micrograms/100 ml, whereas the concentration for workers not exposed to lead was 12.7 micrograms/100 ml. Urinary HVA was significantly elevated in the exposed group when compared with controls (p less than 0.01). HVA was also found to be associated with an increase of lead in blood. Although not statistically significant, the VMA excretion was also noted to be moderately elevated; however, it is recognized that the present study was unable to establish a highly significant dose-response relationship between lead exposure and HVA excretion, as has been reported earlier in lead-poisoned children.

Adult↗
PubMed1989

The interaction of aluminium with soluble protein kinase C from mouse brain.

The interaction of aluminium ion species with soluble protein kinase C, Ca2+/phospholipid-dependent protein kinase, from mouse brain has been examined in vitro. The activity of protein kinase C was increased by addition of Ca2+ displaying an EC50 value of 10.3 +/- 1.1 x 10(-6) M. The A1 species inhibited the activity with an IC50 values of 8.6 +/- 0.5 x 10(-5) M and 2.7 +/- 0.3 x 10(-5) M in the presence of 0.5 mM Ca2+ and absence of Ca2+, respectively. Concerning the EC50 for Ca2+ activation, this was increased by the A1 species in a dose-dependent manner. Moreover, the inhibition was of a non-competitive type with respect to H1 histone and of a mixed type with respect to ATP. It is likely that the inhibition was caused by 1) the blocking of Mg2+ binding to ATP, 2) the blocking of CA2+ binding to protein kinase C. Our results suggested that protein kinase C was involved in neurotoxicity of A1.

Aluminum↗