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S Nakajima

Publications and source records attributed to S Nakajima.

At least 19 recordsLinked to original sources
PubMed2006

Maternal smoking during pregnancy and genetic polymorphisms in the Ah receptor, CYP1A1 and GSTM1 affect infant birth size in Japanese subjects.

Genetic susceptibility to tobacco smoke might have relation to adverse pregnancy outcomes. To estimate the effects of maternal smoking and genetic polymorphisms on infant birth weight and length, we conducted a prospective cohort study of 293 women who delivered singleton live births in Sapporo, Japan. Birth weight and length were significantly lower among infants born to continuously smoking women having the aryl hydrocarbon receptor (AhR) wild type genotype (Arg/Arg; 211 g +/- 76 g; 1.2 cm +/- 0.4 cm, p < 0.01 and p < 0.01, respectively), the CYP1A1 variant genotype (m1/m2 + m2/m2; 170 g +/- 64 g, 0.8 cm +/- 0.3 cm, p < 0.01 and p < 0.05, respectively), or the GSTM1 null genotype (171 g +/- 58 g, 0.6 cm +/- 0.3 cm, p < 0.01 and p < 0.05, respectively). When combinations of these genotypes were considered, birth weight and length were significantly lower for infants of continuously smoking women in the AhR wild type + CYP1A1 variant group (315 g +/- 116 g; 1.7 cm +/- 0.6 cm, p < 0.01 and p < 0.01, respectively) and in the CYP1A1 variant + GSTM1 null group (237 g +/- 92 g; 1.3 cm +/- 0.5 cm, p < 0.05 and p < 0.01, respectively). These genotypes did not confer adverse effects among women who had never smoked; therefore, maternal smoking in combination with maternal AhR, CYP1A1 and GSTM1 genetic polymorphisms may adversely affect infant birth size.

Adult↗
PubMed2006

Mental health service requirements in a Japanese medical centre emergency department.

BACKGROUND: A significant number of emergency department (ED) patients in Japan may be affected by mental health problems leading to attempted suicide. This retrospective descriptive study aimed to explore mental health service needs in a Japanese medical centre ED. METHODS: Data on all inpatients were collected within 24 h of admission to the ED of a medical centre in Tokyo from 1st February 2004 to the 31st of January 2005. RESULTS: A total of 14.4% (95% CI 13.0 to 16.0) of ED visits required psychiatric services and 23.4% (95% CI 21.7 to 25.3) of inpatients had experienced psychologically traumatic events. CONCLUSIONS: Approximately 38% (95% CI 35.8 to 39.9) of patients presenting to an ED could be affected by mental health problems.

Adolescent↗
PubMed2005

ATX-S10(Na)-photodynamic therapy is less carcinogenic for mouse skin compared with ultraviolet B irradiation.

BACKGROUND: Photodynamic therapy (PDT) is available for the treatment of various skin tumours and other skin diseases. Ultraviolet (UV) irradiation induces DNA damage, cyclobutane pyrimidine dimers (CPD) (6-4) photoproducts (6-4PP) and 8-hydroxy-2'-deoxyguanosine (8-OHdG), all of which are carcinogenic for the skin. However, effects of PDT on DNA damage and carcinogenesis are unclear. OBJECTIVES: To compare the production of photoproducts and the induction of skin tumours in mouse epidermis treated with UVB or PDT. METHODS: We performed UVB irradiation or ATX-S10(Na)-PDT on the skin of 20 hairless mice, in each case, and analysed DNA damage and tumour induction. RESULTS: After a single irradiation of UVB on mouse skin, CPD, 6-4PP and 8-OHdG were detected in the nuclei of keratinocytes. In contrast, PDT-treated mouse keratinocytes showed induction of 8-OHdG, but not of CPD or 6-4PP. Skin tumours induced by UVB irradiation (3 kJ m(-2) three times weekly) were observed following 15 weeks of irradiation (mean +/- SEM tumour incidence 3.2 +/- 1.8%; tumour number 3.2 +/- 1.6 per mouse) and increased depending on irradiation times and doses. Following 30 weeks of UVB irradiation (3 kJ m(-2) three times weekly), mean +/- SEM tumour incidence and tumour number were 28.7 +/- 4.8% and 14.2 +/- 2.8% per mouse, respectively. Although skin tumours were also detected in PDT-treated mouse skin following 80 weeks of treatment (mean +/- SEM tumour incidence 9.1 +/- 1.8%; tumour number 12.2 +/- 2.3 per mouse), the number of tumours was not statistically different from untreated mouse skin (mean +/- SEM tumour incidence 4.1 +/- 3.8%; tumour number 5.2 +/- 3.3 per mouse). CONCLUSIONS: PDT induced 8-OHDG but not CPD or 6-4PP, and was shown to be a relatively safe modality following multiple applications to mouse skin.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2005

[Pulmonary metastasis from colorectal cancer with hepatic metastasis].

We have investigated cases where pulmonary metastasis from colorectal cancer was resected during the last 15 years, comparing a group with liver metastasis [LM (+)] to a group without liver metastasis [LM (-)]. The following are the characteristics of the LM (+) versus LM (-) groups. Gender: male 6, female 5 versus male 9, female 11, age: 61.4+/-11.4 versus 63.9+/-9.4 years, number of lung metastasis: 1.42 versus 1.29, duration of primary-lung metastasis: 1.59+/-1.02 versus 2.55+/-1.46 years, preoperative CEA: 69.3+/-71.1 versus 8.64+/-5.63 ng/ml, ratio of bilateral lung metastasis: 23.0 versus 4.8%, more than 1 ratio of pulmonary metastasis: 38 versus 19%, complete resection ratio of pulmonary metastasis: 84.6 versus 100%, ratio of thoracoscopic surgery: 69.2 versus 66.7%, and 2-year survival ratio: 63 versus 78%. There were no statistically significant differences in these values between the LM (+) and LM (-) group. A larger number of cases and follow-up duration will be required in the future; we think that the resection of pulmonary metastasis from colorectal cancer with liver metastasis can be supported for the present.

Aged↗
PubMed2004

Orexin (hypocretin) effects on constitutively active inward rectifier K+ channels in cultured nucleus basalis neurons.

Orexins are excitatory transmitters implicated in sleep disorders. Because orexins were discovered only recently, their ionic and signal transduction mechanisms have not been well clarified. We recently reported that orexin A (OXA) inhibits G protein-coupled inward rectifier K+ (GIRK) channels in cultured locus coeruleus and nucleus tuberomammillaris neurons. Other work in our laboratory revealed the existence of a novel inward rectifier K+ channel (KirNB), which is located in cholinergic neurons of the nucleus basalis (NB) and possesses unique single-channel characteristics. The mean open time is considerably shorter in KirNB than in Kir2.0 channels. Constitutive activity and a smaller unitary conductance set KirNB apart from cloned Kir3.0 channels. Previously, we found that substance P excites NB neurons by inhibiting KirNB channels. Here we show that orexins suppress KirNB channel activity, likely leading to neuronal excitation. Electrophysiological studies were performed on cultured NB neurons from the basal forebrain. OXA application decreased whole cell conductance through a pertussis toxin (PTX)-insensitive G protein. The OXA-suppressed current was inwardly rectifying with a reversal potential around E(K). Single-channel recordings of NB neurons revealed that constitutively active KirNB channels were transiently inhibited by OXA. Okadaic acid pretreatment abolished the recovery. The results suggest that OXA inhibition of KirNB is mediated by a PTX-insensitive G protein (i.e., G(q/11)), which eventually results in channel phosphorylation. Recovery from this inhibition is by dephosphorylation. These results, taken together with our previous study, suggest that orexin receptors can elicit neuronal excitation through at least two families of inward rectifier K+ channels: GIRK and KirNB channels.

Animals↗
PubMed2004

Immunocytochemical localization of monoamine oxidase type B in enterochromaffin-like cells of rat oxyntic mucosa.

We used immunohistochemistry to identify the localization of monoamine oxidase type B (MAOB) in the rat oxyntic mucosa. At light microscopic levels, MAOB-immunopositive cells were mostly located in the basal half of the oxyntic mucosa. By a double-labeling immunofluorescence method, it was shown that MAOB immunoreactivity was localized in almost all of histidine decarboxylase (HDC)-positive cells. Only a few MAOB-positive cells were negative for HDC. At electron microscopic levels, immunohistochemical reaction products of MAOB were detected on the mitochondrial outer membranes in cells that showed morphological characteristics of enterochromaffin-like (ECL) cells. These findings indicate that ECL cells contain MAOB in the rat. We provide a hypothesis that MAOB is involved in the inactivation mechanism of histamine that is released from ECL cells and activates parietal cells to secrete gastric acid.

Animals↗
PubMed2004

Fluorescence detection of a new photosensitizer, PAD-S31, in tumour tissues and its use as a photodynamic treatment for skin tumours in dogs and a cat: a preliminary report.

We describe here the detection by fluorescence of a new photosensitizer, PAD-S31, in tumours in dogs and cats and the effect of photodynamic therapy (PDT) by using PAD-S31 for skin tumours in two dogs and one cat. PAD-S31 is a hydrophilic photosensitizer that has two peaks at absorption wavelengths 406 and 665 nm in distilled water. In a preliminary experiment in mice transplanted with SCCVII and colon 26, PAD-S31 was retained in tumour tissues rather than in other organs. The tumours resected from dogs and cats after intravenous administration of PAD-S31 at a dose of 15 mg/kg emitted strong red fluorescence under light illumination of 402 nm wavelength. Animals given PAD-S31 showed no cutaneous photosensitivity under room light illumination. Irradiation at laser light 670 nm wavelength (fluence rate 150 mW/cm2 and total light dosage 150 J/cm2) on cutaneous mast cell tumours in dogs ( n=2 ) and a cutaneous basal cell tumour in a cat induced complete remission. These results suggest PAD-S31 could be a promising photosensitizer for use in a small animal veterinary practice.

Animals↗
PubMed2004

Amino-acid change on the antigenic region B1 of H3 haemagglutinin may be a trigger for the emergence of drift strain of influenza A virus.

Sera from 27 children and eight older persons, which had been collected in 1998 and 1999 and showed haemagglutination-inhibition (HI) activity against influenza A/Sydney/5/97 (H3N2) strain, were characterized with a binding assay using chimeric haemagglutinin (HA) proteins between A/Aichi/2/68 (A/AI/68) and A/Sydney/5/97 (A/SD/97) strains. Sera from the young children had a tendency to recognize only the antigenic site B1 of the HA1 region. On the other hand, sera of the older individuals were fully reactive to all antigenic sites of HA1 except antigenic site D. Recent epidemic strains, A/Panama/2007/99 (A/PM/99)-like viruses have differences in amino acids in antigenic sites A, C, and B2 but not B1. However, human antisera obtained even from young children had HI activity to Panama-like viruses. The limited epidemic of A/PM/99-like viruses may have been due to the existence of antibody against B1, which had been produced in response to infection by the A/SD/97-like viruses.

Adolescent↗
PubMed2004

Histological aspects and role of mast cells in Helicobacter pylori-infected gastritis.

BACKGROUND: Mast cells are one of the main pro-inflammatory cells, while their knowledge in Helicobacter pylori infection has not been summarized. METHODS: We reviewed studies on mast cells in H. pylori infection, and summarized the histological aspects and roles. RESULTS: The density of mast cells is greater in H. pylori-infected than in non-infected subjects. Increased mast cell density in infected gastritis significantly decreases after eradication. On electron microscopy, mast cells in infected gastric mucosa show degranulation. Some experimental studies demonstrate that mast cells are degranulated with H. pylori-derived products. CONCLUSIONS: Mast cells are actively involved in the pathogenesis of H. pylori-infected gastritis. The possible roles are to initiate and promote the formation of oedema through degranulated and secreted mediators, and to release multiple chemotactic factors, which induce inflammatory cells to infiltrate to the site of oedema, showing acute inflammatory changes. Mast cells also stimulate the degradation of pericellular matrices and the growth of cells in their vicinity, and thereby promote tissue turnover. In chronic H. pylori infection, these reactions continue until the bacteria are eradicated. Mast cells may act both to maintain gastritis and to repair tissue damage in H. pylori-infected chronic gastritis.

Cell Division↗
PubMed2004

Oesophageal adenocarcinoma or gastric cancer with or without eradication of Helicobacter pylori infection in chronic atrophic gastritis patients: a hypothetical opinion from a systematic review.

BACKGROUND: As chronic atrophic gastritis is a precancerous condition for gastric cancer and the eradication of Helicobacter pylori infection halts chronic gastritis, eradication of infection may prevent gastric cancer. However, as chronic atrophic gastritis is a risk factor for reflux oesophagitis after eradication of infection, the risk of oesophageal adenocarcinoma may also increase. METHODS: We systematically reviewed papers and estimated the expected annual incidence of oesophageal or gastric cancer with and without eradication of H. pylori infection in patients with chronic atrophic gastritis. RESULTS: The expected annual incidence of gastric cancer in patients with corpus atrophy with persistent infection was at least 5.8-fold higher than that for oesophageal adenocarcinoma after the eradication of infection at all ages. Even for patients with accompanying reflux oesophagitis or Barrett's oesophagus, the expected incidence of either gastric or oesophageal adenocarcinoma with persistent infection was higher than that of oesophageal adenocarcinoma after eradication of infection. CONCLUSION: If eradication of infection lowers the incidence of gastric cancer, it should be recommended for patients with corpus atrophy at all ages irrespective of the presence of reflux oesophagitis or Barrett's oesophagus, especially in populations having a high prevalence of gastric cancer.

Adenocarcinoma↗
PubMed2003

A gene for a Class II DNA photolyase from Oryza sativa: cloning of the cDNA by dilution-amplification.

Ultraviolet radiation induces the formation of two classes of photoproducts in DNA-the cyclobutane pyrimidine dimer (CPD) and the pyrimidine [6-4] pyrimidone photoproduct (6-4 product). Many organisms produce enzymes, termed photolyases, which specifically bind to these lesions and split them via a UV-A/blue light-dependent mechanism, thereby reversing the damage. These photolyases are specific for either CPDs or 6-4 products. Two classes of photolyases (class I and class II) repair CPDs. A gene that encodes a protein with class II CPD photolyase activity in vitro has been cloned from several plants including Arabidopsis thaliana, Cucumis sativus and Chlamydomonas reinhardtii. We report here the isolation of a homolog of this gene from rice (Oryza sativa), which was cloned on the basis of sequence similarity and PCR-based dilution-amplification. The cDNA comprises a very GC-rich (75%) 5; region, while the 3; portion has a GC content of 50%. This gene encodes a protein with CPD photolyase activity when expressed in E. coli. The CPD photolyase gene encodes at least two types of mRNA, formed by alternative splicing of exon 5. One of the mRNAs encodes an ORF for 506 amino acid residues, while the other is predicted to code for 364 amino acid residues. The two RNAs occur in about equal amounts in O. sativa cells.

Amino Acid Sequence↗
PubMed2003

Effects of orexin (hypocretin) on GIRK channels.

Orexins (hypocretins) are recently discovered excitatory transmitters implicated in arousal and sleep. Yet, their ionic and signal transduction mechanisms have not been fully clarified. Here we show that orexins suppress G-protein-coupled inward rectifier (GIRK) channel activity, and this suppression is likely to lead to neuronal excitation. Cultured neurons from the locus coeruleus (LC) and the nucleus tuberomammillaris (TM) were used, as well as HEK293A cells transfected with GIRK1 and 2, either human orexin receptor type 1 (OX1R) or type 2 (OX2R), mu opioid receptor and GFP cDNAs. In GTPgammaS-loaded cells, orexin A (OXA, 3 microM) inhibited GIRK currents that had previously been activated by somatostatin (in LC cells), nociceptin (TM cells), or the mu opioid agonist DAMGO (HEK cells). In guanosine triphosphate (GTP)-loaded HEK cells, in which GIRK currents were not preactivated, OXA induced a biphasic response through both types of orexin receptors: an initial current increase and a subsequent decrease to below resting levels. Current-voltage (I-V) relationships revealed that both the OXA-induced and suppressed currents are inwardly rectifying with reversal potentials around EK. The OXA-induced initial current was partially pertussis toxin (PTX) sensitive and partially PTX insensitive, whereas the OXA-suppressed current was PTX insensitive. These data suggest that orexin receptors couple with more than one type of G-protein, including PTX-sensitive (such as Gi/o) and PTX-insensitive (such as Gq/11) G-proteins. The modulation of GIRK channels by orexins may be one of the cellular mechanisms for the regulation of brain nuclei (e.g., LC and TM) that are crucial for arousal, sleep, and appetite.

Analgesics, Opioid↗
PubMed2003

Intraoperative three-dimensional reconstruction of power Doppler vascular images.

We have developed a simple method for reconstructing a three-dimensional (3D) image in the operating room from sequentially scanned intraoperative two-dimensional (2D) power Doppler images using a personal computer and commercially available software. During three operations, 2 for cerebral aneurysm and 1 for cerebral tumor, intracranial vessel images were digitally transferred to a personal computer by freehand scanning over the dura mater or surface of the brain with a 7.5-MHz linear probe. A series of 2D images were converted to a smaller file, and 3D image was reconstructed with volume-rendering software. It took about 15 minutes to reconstruct of the initial 3D image. In the cases of cerebral aneurysm, the vessels connected to the lesion or running nearby were easily identified on the image. In the tumor case, the anatomical relation between the vascular structures and the tumor was clear. This simple 3D reconstruction method provides spatial information about intracranial vascular structures that is useful in intraoperative surgical planning.

Aged↗
PubMed2002

Two different inward rectifier K+ channels are effectors for transmitter-induced slow excitation in brain neurons.

Substance P (SP) excites large neurons of the nucleus basalis (NB) by inhibiting an inward rectifier K(+) channel (Kir). The properties of the Kir in NB (KirNB) in comparison with the G protein-coupled Kir (GIRK) were investigated. Single-channel recordings with the cell-attached mode showed constitutively active KirNB channels, which were inhibited by SP. When the recording method was changed from the on-cell to the inside-out mode, the channel activity of KirNB remained intact with its constitutive activity unaltered. Application of Gbeta(1gamma2) to inside-out patches induced activity of a second type of Kir (GIRK). Application of Gbeta(1gamma2), however, did not change the KirNB activity. Sequestering Gbeta(1gamma2) with Galpha(i2) abolished the GIRK activity, whereas the KirNB activity was not affected. The mean open time of KirNB channels (1.1 ms) was almost the same as that of GIRKs. The unitary conductance of KirNB was 23 pS (155 mM [K(+)](o)), whereas that of the GIRK was larger (32-39 pS). The results indicate that KirNB is different from GIRKs and from any of the classical Kirs (IRKs). Whole-cell current recordings revealed that application of muscarine to NB neurons induced a GIRK current, and this GIRK current was also inhibited by SP. Thus, SP inhibits both KirNB and GIRKs. We conclude that the excitatory transmitter SP has two types of Kirs as its effectors: the constitutively active, Gbetagamma-independent KirNB channel and the Gbetagamma-dependent GIRK.

Animals↗
PubMed2002

Antiproliferative activity induced by the somatostatin analogue, TT-232, in human pancreatic cancer cells.

Somatostatin analogues have been developed as antiproliferative agents, but their administration as general antitumour agents is limited, mainly because of the wide distribution of somatostatin receptors throughout the human body. TT-232, a new somatostatin structural analogue, was reported to have tumour-selective antiproliferative activity without an antisecretory action. We examined whether TT-232 had antiproliferative activity in human pancreatic cancer cell lines, and compared its antiproliferative activity with that of RC-160 and other TT-232 derivatives. TT-232 inhibited the growth of all of the cell lines used in this study and induced apoptotic cell death. RC-160 showed no such growth inhibition. TT-232 also inhibited tumour formation in a xenograft model. A competitive binding assay was performed using the cell membrane fraction and 111In-DTPA-TT-232 in order to show the existence of a specific binding site on the cells. A specific binding site was detected in MIAPaCa-2 cells. It has been shown that the activation of protein tyrosine phosphatase (PTPase) is one of the main intracellular pathways responsible for somatostatinergic inhibition of cell growth. We found a significant PTPase stimulation after TT-232 administration using an immunoblot analysis assessing the level of protein tyrosine phosphorylation, and also a direct measurement of the PTPase activity. We also demonstrated that PTPase stimulation by TT-232 was involved in its antiproliferative activity as this activity was reversed by the addition of sodium orthovanadate, a PTPase inhibitor. Our results indicate that TT-232 could be a potentially useful therapeutic agent if these data are translated into clinical practice.

Antineoplastic Agents↗
PubMed2002

Leukotriene receptor antagonist, montelukast, can reduce the need for inhaled steroid while maintaining the clinical stability of asthmatic patients.

BACKGROUND: Oral leukotriene receptor antagonists have been shown to have efficacy in chronic asthma. OBJECTIVE: To determine whether the addition of montelukast could lead to a reduction in inhaled corticosteroid dose without a significant decrease in peak expiratory flow rate (PEFR). METHODS: After a 4-week run-in period, 191 moderate-to-severe asthmatic patients whose asthma had been well controlled with daily inhaled corticosteroid therapy (beclometasone dipropionate 800 to 1600 micro g/day), were randomly assigned to one of two treatments - placebo (n = 98) or montelukast 10 mg once daily (n = 93) - for a 24-week, multicentre, double-blind, treatment period. At the beginning of the active treatment period, the daily dose of inhaled corticosteroid was halved in all of the patients. In addition, the inhaled corticosteroid dose was subsequently titrated every 8 weeks, based on PEFR, asthma symptoms and beta-agonist use. RESULTS: After 8 weeks of a 50% reduction in inhaled corticosteroid use, morning PEFR increased by 5.3 +/- 32.3 L/min from baseline in patients receiving montelukast and significantly decreased by 6.9 +/- 29.0 L/min in those receiving placebo (P = 0.035). In addition, evening PEFR significantly decreased by 9.8 +/- 28.5 L/min (P = 0.003) in the placebo group, but was maintained in the montelukast group. In spite of a subsequent 50% reduction in the inhaled corticosteroid dose every 8 weeks, morning and evening PEFRs were maintained over the 24-week treatment period in the montelukast group; PEFR significantly decreased in the placebo group. There was a significant difference between the two groups with regard to morning PEFR, therapy score and asthmatic score at weeks 8, 16 and 24, as well as evening PEFR at week 8. However, the symptom scores were not significantly different between the two groups or within each group. CONCLUSION: These data suggest that montelukast reduces the need for inhaled corticosteroids while maintaining asthma control over a 24-week period. Therefore, montelukast may be useful for long-term treatment in patients with asthma who require high doses of inhaled corticosteroids.

Acetates↗