Search PubMed⌕ Search

Biomedical subjects

M Iwasaki

Publications and source records attributed to M Iwasaki.

At least 109 records · Page 6Linked to original sources

Functional organisation of anterior thoracic stretch receptors in the deep-sea isopod Bathynomus doederleini: behavioural, morphological and physiological studies.

The relationship between segmental mobility and the organisation of thoracic stretch receptors was examined in the deep-sea isopod Bathynomus doederleini, which shows a developed adaptive behaviour during digging. The movements of segments during digging were analysed from video recordings, which showed that a large excursion occurred in the anterior thoracic segments. Dye-fills of axons revealed four types of thoracic stretch receptor (TSR): an N-cell type (TSR-1), a differentiated N-cell type (TSR-2), a muscle receptor organ (MRO)-type with a long, single receptor muscle (TSR-3) and an MRO-type with a short, single receptor muscle (TSR-4 to TSR-7). Physiologically, TSR-1 and TSR-2 are tonic-type stretch receptors. TSR-3 to TSR-7 show two kinds of stretch-activated responses, a tonic response and a phasico-tonic response in which responses are maintained as long as the stretch stimulus is delivered. Both TSR-2, with a long muscle strand, and TSR-3, with a single, long receptor muscle, have a wide dynamic range in their stretch-activated response. In addition, TSR-2 is controlled by an intersegmental inhibitory reflex from TSR-3. These results suggest that, although TSR-1 has no receptor muscle and TSR-2 has a less-differentiated receptor-like muscle, they are fully functional position detectors of segmental movements, as are the MRO-type receptors TSR-3 to TSR-7.

Animals↗

Carboxy-PTIO increases the tetrahydrobiopterin level in mouse brain microvascular endothelial cells.

The aim of the present study was to characterize the increase in tetrahydrobiopterin (BH4), which is a cofactor for nitric oxide synthase (NOS), by carboxy-PTIO, a scavenger of nitric oxide (NO), in vascular endothelial cells. BH4 level was determined by oxidation under acidic conditions as biopterin. Addition of lipopolysaccharide (LPS) to endothelial cells increased mRNA levels of inducible NOS (iNOS) and GTP-cyclohydrolase I (GTPCH), which is a rate-limiting enzyme for BH4 synthesis, and the biopterin level. NOS inhibitors, NO-donors and L-arginine, a substrate of NOS, did not affect the increase in the biopterin level induced by LPS, suggesting that BH4 synthesis is unlikely to be modulated by NO produced by iNOS during LPS treatment. However, carboxy-PTIO increased the biopterin level in the absence and the presence of LPS. Carboxy-PTIO did not affect the expression of GTPCH mRNA level. Moreover, 2,4-diamino-6-hydroxypyrimidine, an inhibitor of GTPCH, inhibited only about 30% of the carboxy-PTIO-induced increase in the biopterin level. Whereas, N-acetylserotonin, an inhibitor of sepiapterin reductase, strongly inhibited the increase in biopterin level. Carboxy-PTIO inhibited the accumulation of pterin, a decomposition product of BH4 in endothelial cells. These findings suggest that carboxy-PTIO accumulates BH4 under basal and LPS-treated conditions in vascular endothelial cells due to both inhibition of the decomposition of BH4 to pterin and activation of the salvage pathway of BH4 synthesis via sepiapterin reductase.

Alcohol Oxidoreductases↗

Primary racemose hemangioma of the bronchial artery.

A 44-year-old woman was admitted to our hospital for repeated hemoptysis. Selective angiography of the bilateral bronchial arteries showed them to be enlarged and convoluted, and revealed shunts between the bronchial and pulmonary arteries. The patient was diagnosed as having racemose hemangioma of the bronchial artery. Although embolization of the bronchial artery with gelatin sponges was performed, hemoptysis emerged again about one year later. Finally, segmentectomy of the right lower lung was performed and primary racemose hemangioma of the bronchial artery was histopathologically confirmed.

Adult↗

Distribution of genes for bone morphogenetic protein-4, -6, growth differentiation factor-5, and bone morphogenetic protein receptors in the process of experimental spondylosis in mice.

OBJECT: Because little is known about the molecular mechanisms underlying the process of spondylosis, the authors examined the extent of genetic localization of several members of bone morphogenetic protein (BMP) and BMP receptors in chondrogenesis during the process of inducing spondylosis in their previously established experimental mice model. METHODS: Experimental spondylosis was induced in 5-week-old ICR mice. The cervical spine was harvested chronologically, and histological sections were prepared. Messenger RNA for BMP-4, growth and differentiation (GDF)-5, BMP-6, and BMP receptors (ALK-3, -6, and BMP-RII) was localized in the tissue sections by in situ hybridization. In the early stage, BMP-4-derived mRNA was localized mainly in cells in the anterior margin of the cervical discs, together with ALK-6 and BMP-RII mRNA. No GDF-5 and BMP-6 mRNA was detected at this stage. In the late stage, cells positive for BMP-4 decreased, whereas GDF-5 and BMP-6 mRNA were localized in cells undergoing chondrogenesis. The ALK-3 mRNA began to appear in this stage, as did ALK-6 and BMP-RII. CONCLUSIONS: The localization of transcripts for BMP-4, -6, and GDF-5 as well as BMP receptors shown during the present experimental model indicate the possible involvement of molecular signaling by these BMPs in the chondrogenic progress in spondylosis.

Animals↗

Curative resection of both primary and second primary lung cancer.

Curative resection of a second primary lung cancer in a patient who survived small-cell lung cancer is reported. Small-cell cancer had been treated with chemotherapy followed by surgical resection 12 years before. The patient developed squamous cell cancer as the second primary tumor and underwent lobectomy with mediastinal node dissection. Patients who undergo two curative pulmonary resections of both primary and second primary lung cancer are extremely rare. The patient is alive 176 months after the initial diagnosis of small-cell lung cancer and 28 months after resection for his second primary lung cancer. Careful follow-up at an interval of 3-6 months beyond 10 years is very important because adequate treatments could lead to longer survival of patients with primary small-cell lung cancer.

Carcinoma, Small Cell↗

IL-12 plays a pivotal role in LFA-1-mediated T cell adhesiveness by up-regulation of CCR5 expression.

The chemokine receptor CCR5 has been implicated in the recruitment of T cells to inflammatory sites. However, the regulation of CCR5 induction on T cells and its contribution to T cell adhesiveness are poorly understood. Using a Th1 clone, 2D6, that can be maintained with interleukin (IL)-12 or IL-2 alone (designated 2D6(IL-12) or 2D6(IL-2), respectively), we investigated how CCR5 is induced on T cells and whether CCR5 is responsible for up-regulating the function of adhesion molecules. 2D6(IL-12) grew, forming cell aggregates, in culture containing IL-12. This was due to lymphocyte function-associated antigen (LFA)-1-intercellular adhesion molecule (ICAM)-1 interaction, because 2D6(IL-12) expressed both LFA-1 and ICAM-1 and cell aggregation was inhibited by anti-ICAM-1 monoclonal antibody. Despite comparable levels of LFA-1 and ICAM-1 expression, 2D6(IL-2) cells did not aggregate in culture with IL-2. It is important that there was a critical difference in CCR5 expression between 2D6(IL-12) and 2D6(IL-2); the former expressed high levels of CCR5, and the latter expressed only marginal levels. Both types of cells expressed detectable albeit low levels of RANTES (regulated on activation, normal T expressed and secreted) mRNA. Unlike IL-12 or IL-2, IL-18 induced high levels of RANTES mRNA expression without modulating CCR5 expression. Therefore, combined stimulation with IL-12 and IL-18 strikingly up-regulated 2D6 cell aggregation. Notably, LFA-1-mediated aggregation of 2D6(IL-12) cells was suppressed by anti-CCR5 antibody. These results indicate that IL-12 plays a critical role in CCR5 expression on Th1 cells and consequently contributes to CCR5-mediated activation of LFA-1 molecules.

Animals↗

[Current condition of early peripheral lung cancer and related problems].

Early peripheral lung cancer is defined as a tumor whose diameter is within 20 mm and that has not metastasized to lymph nodes. We developed thoracoscopic surgery (two windows method) in 1993. We have been conducting this thoracoscopic surgery in early peripheral lung cancers to identify possible indications as well as to clarify problems related to early peripheral lung cancer. The subjects of this study were 176 tumors, with diameters within 30 mm, including 97 lung cancers with diameters within 20 mm. Of the 97 tumors 20 mm or less in diameter, 18 were N 1 or more severe (N 1, 8 cases: N 2, 10 cases). One patient (N 2) died of bone metastasis and two patients died due to diseases other than lung cancer. Nearly 20% of the patients with tumors 20 mm or less were in the advanced stage, suggesting that mediastinal lymph node resection is necessary. Based on these results, it is advisable to define tumors with a diameter of no more than 10 mm as early peripheral lung cancer.

Adenocarcinoma↗

[Surgical techniques for vascular reconstruction of the portal vein and hepatic artery in living-donor liver transplantation].

To decide how to reconstruct the portal vein and hepatic artery for liver transplantation, anatomical variation, diameter, length, and injury to vessels during surgery, and the quality of recipient vessels should be considered. Hence, it is of key importance for donor and recipient surgeries to prepare adequate vessels for reconstruction. For reconstruction of the portal vein, anastomosis with as large a diameter as possible is required to obtain good portal flow. In cases with sclerosing stenosis and old thrombus, technical innovations such as branch-patch, a conduit using a vein graft, and venoplasty using a venous patch are necessary. For reconstruction of the hepatic artery, selecting a satisfactory recipient artery, overcoming size mismatch, and gentle handling of a recipient artery with pathological changes are important. Arteries smaller than 3 mm are anastomosed with a surgical microscope using the united suture technique. The fishmouth technique or funnelization technique can be used for anastomoses with a significant size mismatch, and an autoarterial graft is used when arteries do not reach each other.

Anastomosis, Surgical↗

UvrA and UvrB suppress illegitimate recombination: synergistic action with RecQ helicase.

Illegitimate recombination is a major cause of genetic instability in prokaryotes as well as in eukaryotes. This recombination usually occurs at a low frequency, but it is greatly enhanced by UV irradiation or other environmental stresses. DNA damages produced by these environmental stresses are thought to induce DNA double-strand breaks, leading to illegitimate recombination. In this paper we show that UV-induced illegitimate recombination is enhanced by mutations of nucleotide excision repair genes, uvrA or uvrB, and partially by uvrC mutation, but not by uvrD mutation. Unexpectedly, the recombination was enhanced by the uvrA uvrB double mutation even without UV irradiation, but the uvrB uvrC double mutation has not shown this effect, suggesting that illegitimate recombination is mostly suppressed by UvrA and UvrB. Moreover, illegitimate recombination was synergistically enhanced by the recQ uvrA double mutation. In addition, overproduction of the UvrA protein suppressed the hyperrecombination phenotype of the recQ or uvrB mutant, but it did not affect the UV-sensitive phenotype of the uvrB mutant. We concluded that the UvrAB complex suppresses illegitimate recombination in a pathway shared with RecQ helicase. In addition, UvrA protein alone can suppress illegitimate recombination in the pathway, in which RecQ helicase and UvrAB complex work. Possible functions of the proteins involved in these pathways are also discussed.

Adenosine Triphosphatases↗

Cobalt Ion-Doped TiO(2) Photocatalyst Response to Visible Light.

Photocatalytic activity under visible light irradiation was generated by doping a small amount of Co(2+) ions into TiO(2) particles. Nanometer-sized particles with the composition xCoO-(100-x) TiO(2) (xCo/TiO(2); 0</=x</=6.0) were prepared from TiOSO(4).4.5H(2)O and Co(CH(3)COO)(2).4H(2)O in an ethanol-water solution containing NaOH under reflux. The photoreactivity of xCo/TiO(2) was evaluated by the rate of CH(3)CHO degradation. The Co(2+) ion doping (0.01</=x</=0.27) not only enhanced the photocatalytic activity under ultraviolet-visible (lambda>300 nm) light irradiation but also induced the visible light (lambda>400 nm) response. The highest photocatalytic activities were obtained at x=0.03 for both irradiations. Copyright 2000 Academic Press.

Journal Article↗

Assessment of hypermethylated DNA in two promoter regions of the estrogen receptor alpha gene in human endometrial diseases.

OBJECTIVE: DNA methylation in the promoter regions of many genes is associated with the regulation of gene expression. We examined the frequency of DNA hypermethylation at two nucleotide positions, the proximal promoter region (PPR) in exon 1 and the distal promoter region (DPR) in exon 1', of the estrogen receptor alpha (ERalpha) gene in 111 cases of various human endometrial diseases. METHODS: The degree of hypermethylation of PPR and DPR was examined by semi-quantitative competitive polymerase chain reaction assay using restriction enzymes (HpaII, NotI, and SacII). RESULTS: Endometrial tissues in the proliferative phase obtained from patients with leiomyomas and/or adenomyosis and no significant hormonal abnormalities did not show hypermethylation at the HpaII cleavage position of DPR. In 6 of 16 (37.5%) cases of simple endometrial hyperplasia, the PPR was hypermethylated, whereas in cases of atypical endometrial hyperplasia and endometrioid adenocarcinoma the frequencies were extremely low. Hypermethylation of these promoter regions did not correlate with lack of ERalpha protein in the 46 cases that were analyzed by enzyme immunoassay. CONCLUSIONS: ERalpha gene transcription from the distal promoter, rather than from the proximal promoter, is predominant in the proliferative phase of the normal menstrual cycle, because the PPR, but not the DPR, is frequently hypermethylated under those conditions. Conversely, ERalpha gene transcription from the proximal promoter is predominant in precancerous lesions such as atypical hyperplasia and endometrial cancer. However, hypermethylation at the promoter sites we examined was not related to the loss of ERalpha protein in endometrial disease.

Adult↗

Expression of various matrix proteases and Ets family transcriptional factors in ovarian cancer cell lines: correlation to invasive potential.

OBJECTIVES: The aim of our study was to determine the important molecules responsible for the invasive activity of ovarian cancer cells. METHODS: We compared the biological characteristics, that is, growth rate, motility, and invasive activity, of five ovarian cancer cell lines with the gene expression of various matrix proteases (matrix metalloproteinase-1 [MMP-1], MMP-2, MMP-9, membrane-type MMP type 1 [MT1-MMP], MT2-MMP, MT3-MMP, urokinase plasminogen activator [uPA]), their inhibitors (tissue inhibitor of metalloproteinase type 1 [TIMP-1], TIMP-2, plasminogen activator inhibitor type 1, [PAI-1], and PAI-2), and the potential transcriptional regulators E1AF and Ets-1. RESULTS: There was no clear correlation in the growth rate, motility, and invasion, suggesting that there are independent properties for malignant potential in ovarian cancer cells. However, HTBOA, a poorly differentiated cancer cell line, exhibited highly invasive activity, rapid growth, and increased motility. This cell line also expressed both Ets transcriptional factors, E1AF and Ets-1, and many matrix-degrading enzymes. Three cell lines that expressed E1AF showed rapid cell growth. The highly invasive cell lines, HTBOA and HTOA (well-differentiated serous cystadenocarcinoma), produced either MMP-2 or MMP-1, and both cell lines expressed MT1-MMP and uPA. Furthermore, the active forms of pro-MMP-2 and pro-MMP-1 were detected in HTBOA and HTOA by zymography. CONCLUSION: We conclude that activated MMP-2 and MMP-1 are important in the invasive activity of these ovarian cancer cells.

Adenocarcinoma↗

Terminal restriction pattern analysis of 16S rRNA genes for the characterization of bacterial communities of activated sludge.

A culture-independent molecular technique using terminal restriction fragment length polymorphism (T-RFLP) of 16S rRNA genes was applied to the characterization of bacterial communities of activated sludge taken from different municipal sewage treatment plants. 16S rDNA fragments from the bulk DNA of sludge were amplified by PCR with a Cy5-labeled forward primer corresponding to nucleotide positions 8 to 27 and a reverse primer complementary to positions 907 to 926 in the Escherichia coli numbering system. The 16S rDNAs thus obtained were digested with tetrameric restriction enzymes and analyzed using a Pharmacia automated DNA sequencer. A preliminary study on a model DNA mixture prepared from different bacterial species showed that the fluorescence intensity of terminal fragments (T-RFs) of 16S rDNAs amplified and detected was directly proportional to the 16S rRNA gene copy number rather than the amount of genomic DNA of each species present. 16S rDNA fragments amplified from the sludges and digested with HhaI usually generated at least 60 T-RFs, among which T-RFs of around 208 bp were the most abundant regardless of the time or area sampled. Southern blot hybridization with oligonucleotide probes specific to the 5' terminal regions of the 16S rDNA of different phylogenetic groups indicated that the T-RFs of around 208 bp were derived from members of the beta subclass of the class Proteobacteria. Hybridization with a probe specific to the class Actinobacteria failed to detect any appreciable signal. These results did not agree fully with those obtained by quinone profiling. The usefulness and limitations of the T-RFLP method for monitoring bacterial population dynamics in activated sludge were discussed.

Journal Article↗

Polymorphism of the ABO blood group genes in Han, Kazak and Uygur populations in the Silk Route of northwestern China.

Genetic polymorphism in the ABO blood group gene of Han, Kazak and Uygur populations inhabiting the most northwestern part of China was investigated using polymerase chain reaction-based techniques. The present study enrolled 43 healthy unrelated Han, 37 Kazak and 59 Uygur volunteers. The allele in A1 blood group is distinguished A0101 and A0102 in difference of nucleotide position 467. The A0101 allele is more frequent in Caucasian and the A0102 allele is characteristic in Mongoloid. It must be notable that A0201 in the A2 group (with a single base deletion at nucleotides 1059 to 1061) which was characteristic of Caucasian was observed in Kazak and Uygur populations but not in Han. Further, 00201 (with no nucleotide deletion at 261 and three nucleotide differences), which is frequent in different races including Caucasian except for Mongoloid, was detected also in Kazak and Uygur populations. The frequencies of B0101 in Kazak, Uygur and Han were comparable to those of other Asian populations but higher than those of Caucasian populations. Collectively, these results reveal that the allele frequencies of Kazak and Uygur at the ABO blood group locus are an intermediate between those of Mongoloid and Caucasian, suggesting the admixed feature of Kazak and Uygur with Mongoloid and Caucasian.

ABO Blood-Group System↗

Differential IL-12 responsiveness of T cells but not of NK cells from tumor-bearing mice in IL-12-responsive versus -unresponsive tumor models.

While IL-12 administration induces tumor regression through stimulating T cells in tumor-bearing mice, this IL-12 effect is observed in some but not all tumor models. The present study aimed to compare IL-12 responsiveness of T cells from tumor-bearing mice in IL-12-responsive (CSA1M and OV-HM) and -unresponsive (Meth A) tumor models. Tumor regression in IL-12-responsive tumor models required the participation of T cells, but not of NK1.1(+) cells. Because a NK1.1(+) cell population was the major producer of IFN-gamma, comparable levels of IFN-gamma production were induced in IL-12-responsive and -unresponsive tumor-bearing mice. This indicates that the amount of IFN-gamma produced in tumor-bearing individuals does not correlate with the anti-tumor efficacy of IL-12. In contrast, IL-12 responsiveness of T cells differed between the responsive and unresponsive models: purified T cells from CSA1M/OV-HM-bearing or Meth A-bearing mice exhibited high or low IL-12 responsiveness respectively, when evaluated by the amounts of IFN-gamma produced in response to IL-12. T cells from CSA1M- or OV-HM-bearing but not from Meth A-bearing mice exhibited enhanced levels of mRNA for the IL-12 receptor (IL-12R). These results indicate that a fundamental difference exists in IL-12 responsiveness of T cells between IL-12-responsive and -unresponsive tumor models, and that such a difference is associated with the expression of IL-12R on T cells.

Animals↗

Docosahexaenoic acid and vitamin E can reduce human monocytic U937 cell apoptosis induced by tumor necrosis factor.

The effects of polyunsaturated fatty acids and vitamin E on tumor necrosis factor (TNF)-induced apoptosis of human monocytic U937 cells was explored to assess to what extent these nutrients could attenuate apoptosis. Preincubation of U937 cells with arachidonic acid for 24 h did not affect TNF-induced apoptosis. Eicosapentaenoic acid slightly but significantly reduced the proportion of apoptotic cells only when apoptosis was induced by TNF without cycloheximide (CHI). In contrast, preincubation with docosahexaenoic acid (DHA) greatly (40 approximately 70%) attenuated apoptosis induced by stimulation with either TNF or TNF + CHI for 3 h. The inhibition of apoptosis was accompanied by enrichment of DHA in membrane phospholipids, indicating that DHA probably exerted its inhibitory activity after being incorporated into the phospholipids. Vitamin E also played a role as a partial inhibitor of apoptosis 3 h after TNF addition. This vitamin could further reduce the apoptosis of DHA-treated cells, and such an additive effect was obvious when apoptosis was induced at a low frequency. Longer-range stimulation of U937 cells with TNF showed that inhibition of apoptosis by preincubating cells with either DHA or vitamin E was not significant 9 h after TNF addition, but that preincubation with both DHA and vitamin E could reduce the proportion of apoptotic cells even at this time point. Our findings suggested that ingestion of nutrients such as DHA and vitamin E might exert beneficial effects on organ dysfunction associated with various TNF-related diseases.

Apoptosis↗