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F Matsuzaki

Publications and source records attributed to F Matsuzaki.

At least 19 recordsLinked to original sources
PubMed2001

A questionnaire for neurological symptoms in patients with diabetes--cross-sectional multicenter study in Saitama Prefecture, Japan.

This study was designed to investigate the prevalence of neurological symptoms in diabetic patients living in Saitama Prefecture, Japan using 13-item questionnaire. A total of 6472 outpatients with diabetes (3417 men and 3055 women) were recruited from 100 centers. Mean age and mean disease duration were 60.9-year old and 10.4 years, respectively. The questionnaire for monitoring of neurological symptoms was completed at the clinic or hospital visited, and Achilles' tendon reflex, ophthalmologic, blood and urinary examinations were also performed. Of the 6472 patients, 84.8% suffered from a mean of 3.3+/-2.2 neurological symptoms. However, half of these symptoms were not considered to be those of diabetic neuropathy by attending physicians. "Feeling as if a piece of paper is attached to the sole of the foot," "stinging and prickling sensations in feet," and "pain in feet" were the most common symptoms of diabetic neuropathy. The prevalence of diabetic neuropathy as determined by attending physician increased with disease duration and worse control of diabetes. This study found that the majority of diabetics were suffered from neurological symptoms, although half of such symptoms were not considered to be those of diabetic neuropathy by physicians. Furthermore, it is important for diabetics to be diagnosed and treated earlier to prevent progression to severe neuropathic complications by means of optimal glycemic control and use of some chemicals such as aldose reductase inhibitor, and to develop this study to evaluate the efficacy of treatments.

Aged↗
PubMed2000

Role of cortical tumour-suppressor proteins in asymmetric division of Drosophila neuroblast.

Cellular diversity during development arises in part from asymmetric divisions, which generate two distinct cells by transmitting localized determinants from a progenitor cell into one daughter cell. In Drosophila, neuroblasts undergo typical asymmetric divisions to produce another neuroblast and a ganglion mother cell. At mitosis, neural fate determinants, including Prospero and Numb, localize to the basal cortex, from which the ganglion mother cell buds off; Inscuteable and Bazooka, which regulate spindle orientation, localize apically. Here we show that a tumour-suppressor protein, Lethal giant larvae (Lgl), is essential for asymmetric cortical localization of all basal determinants in mitotic neuroblasts, and is therefore indispensable for neural fate decisions. Lgl, which itself is uniformly cortical, interacts with several types of Myosin to localize the determinants. Another tumour-suppressor protein, Lethal discs large (Dlg), participates in this process by regulating the localization of Lgl. The localization of the apical components is unaffected in lgl or dlg mutants. Thus, Lgl and Dlg act in a common process that differentially mediates cortical protein targeting in mitotic neuroblasts, and that creates intrinsic differences between daughter cells.

Amino Acid Sequence↗
PubMed2000

Asymmetric division of Drosophila neural stem cells: a basis for neural diversity.

Recent studies of Drosophila neural precursor cells have unveiled the essential roles played by asymmetric cell divisions in the determination of cell fates during neural development. Our understanding now extends to the molecular nature of the cell polarity that underlies asymmetric divisions. This polarity is conserved among neural stem cells, epithelial cells and fertilized eggs.

Animals↗
PubMed2000

Effect of prostaglandin E1 on vascular endothelial growth factor production by human macrophages and colon cancer cells.

We previously demonstrated that cyclooxygenase-2 (COX-2) was predominantly expressed in macrophages of sporadic human colonic adenomas; however, the role of COX-2-expressing cells during colon carcinogenesis has not yet been elucidated. In the present study, we showed the effect of PGE, on vascular endothelial growth factor (VEGF) production by PMA-differentiated U937 cells, a human macrophage model (H-Mac), and by human colon cancer cells T84. PGE1 dramatically induced VEGF production by H-Mac, but not that by T84. PGE1 significantly increased intracellular cAMP formation by H-Mac, but only modestly increased that by T84. 8-bromo-cAMP and cholera toxin also increased VEGF production by H-Mac. In contrast, neither of these agents modulated VEGF production by T84. EP2 and EP4 (PGE specific receptors) mRNA was expressed in both cells. PG dramatically increased VEGF production by activated macrophages, but not by cancer cells, through a specific PGE receptor-mediated process. These findings suggest that PGs produced by COX-2-expressing macrophages induce VEGF production by macrophages, but not by cancer cells, in an autocrine fashion.

Adjuvants, Immunologic↗
PubMed1999

High expression of cyclooxygenase-2 in macrophages of human colonic adenoma.

Cyclooxygenase (COX)-2 is a possible molecular target for suppression of colon carcinogenesis by non-steroidal anti-inflammatory drugs (NSAIDs). However, the expression of COX-2 in human colonic tumors during the adenoma-carcinoma sequence has not been elucidated. In the present study, we examined immuno-histochemically the expression and localization of the COX-2 protein in human colonic adenomas and cancers. Twelve human colonic adenomas and 9 advanced cancers were studied. Immunoreactive COX-2 was predominantly and strongly expressed in sub-epithelial interstitial cells broadly present in the surface area of adenomas. The staining pattern of macrophages was similar to that observed for COX-2 in adenomas. Adjacent normal colonic mucosa was negative for COX-2 expression. In contrast, COX-2 was relatively weakly expressed in both tumor cells and interstitial cells in advanced colon cancers. In conclusion, the target of NSAIDs in preventing colon carcinogenesis may be the COX-2 expressed in interstitial cells, possibly macrophages, of colonic adenomas.

Adenoma↗
PubMed1999

Nonsteroidal anti-inflammatory drugs may prevent colon cancer through suppression of hepatocyte growth factor expression.

Nonsteroidal anti-inflammatory drugs which inhibit cyclooxygenase have been reported to suppress colon carcinogenesis. However the mechanism has not yet been elucidated. Growth factors such as hepatocyte growth factor, which are produced by fibroblasts, have been shown to be important in carcinogenesis and the progression of various human cancers. In the present study, we tested the hypothesis that nonsteroidal anti-inflammatory drugs inhibit hepatocyte growth factor expression through an endogenous prostaglandin-mediated pathway in cultured human colonic fibroblasts. Human colonic fibroblasts were obtained from a resected colon and cultured. Hepatocyte growth factor and prostaglandin E2 were measured by enzyme-linked immunosorbent assay. Induction of cyclooxygenase-1 and cyclooxygenase-2 protein was estimated by immunoblotting. Prostaglandins increased hepatocyte growth factor production significantly in a dose- and time-dependent manner. Cholera toxin and 8-bromo cAMP also stimulated hepatocyte growth factor production. Further, prostaglandin E1 significantly increased cellular cAMP. The prostaglandin EP2 and EP4 receptors were detected by reverse transcription-polymerase chain reaction. Interleukin-1beta dramatically increased prostaglandin E2 production and significantly stimulated hepatocyte growth factor synthesis. Interleukin-1beta induced cyclooxygenase-2 but not cyclooxygenase-1 protein. Indomethacin significantly reduced interleukin-1beta-induced prostaglandin E2 release and hepatocyte growth factor production. These results suggest that prostaglandin is a factor for the production of hepatocyte growth factor by human colonic fibroblasts. Nonsteroidal anti-inflammatory drugs may suppress colon carcinogenesis, in part, through the suppression of hepatocyte growth factor expression by inhibiting endogenous prostaglandin production.

Alprostadil↗
PubMed1999

Transcription factors Mash-1 and Prox-1 delineate early steps in differentiation of neural stem cells in the developing central nervous system.

Like other tissues and organs in vertebrates, multipotential stem cells serve as the origin of diverse cell types during genesis of the mammalian central nervous system (CNS). During early development, stem cells self-renew and increase their total cell numbers without overt differentiation. At later stages, the cells withdraw from this self-renewal mode, and are fated to differentiate into neurons and glia in a spatially and temporally regulated manner. However, the molecular mechanisms underlying this important step in cell differentiation remain poorly understood. In this study, we present evidence that the expression and function of the neural-specific transcription factors Mash-1 and Prox-1 are involved in this process. In vivo, Mash-1- and Prox-1-expressing cells were defined as a transient proliferating population that was molecularly distinct from self-renewing stem cells. By taking advantage of in vitro culture systems, we showed that induction of Mash-1 and Prox-1 coincided with an initial step of differentiation of stem cells. Furthermore, forced expression of Mash-1 led to the down-regulation of nestin, a marker for undifferentiated neuroepithelial cells, and up-regulation of Prox-1, suggesting that Mash-1 positively regulates cell differentiation. In support of these observations in vitro, we found specific defects in cellular differentiation and loss of expression of Prox-1 in the developing brain of Mash-1 mutant mice in vivo. Thus, we propose that induction of Mash-1 and Prox-1 is one of the critical molecular events that control early development of the CNS.

Animals↗
PubMed1998

A novel homeobox gene mediates the Dpp signal to establish functional specificity within target cells.

Morphogen gradients of secreted molecules play critical roles in the establishment of the spatial pattern of gene expression. During midgut development in Drosophila, secreted molecules of Decapentaplegic (Dpp) and Wingless (Wg) establish unique transcriptional regulation within target cells to specify the resultant cell types. Here we report the identification of a novel homeobox gene, defective proventriculus (dve), which is required for the midgut specification under the control of Dpp and Wg. In dve mutants, two distinct parts of the midgut, the proventriculus and middle midgut, are abnormally organized. The Wg signal regulates dve expression during proventriculus development. On the other hand, dve is a downstream target of Dpp in the middle midgut and defines the functional specificity of copper cells along with another Dpp target gene, labial. Thus, the dve gene acts under the two distinct extracellular signals at distant parts of the midgut primordia.

Amino Acid Sequence↗
PubMed1998

Nonsteroidal anti-inflammatory drugs may delay the repair of gastric mucosa by suppressing prostaglandin-mediated increase of hepatocyte growth factor production.

Prostaglandins (PGs), hepatocyte growth factor (HGF), and induction of cyclooxygenase (PG synthetase, COX) play important roles in the repair process of gastric mucosa. We hypothesized that nonsteroidal anti-inflammatory drugs (NSAIDs), including indomethacin (IND), retard the healing of ulcers by suppressing these factors. In this study, we investigated the effects of cytokines, growth factors, and IND on production of PG and HGF, and induction of COX using cultured human gastric fibroblasts. Exogenous PGs significantly increased HGF production in a dose-dependent manner. Among various potential stimulants tested, interleukin-1 beta (IL-1 beta) dramatically increased PGE2 production and significantly stimulated HGF production. IL-1 beta induced COX-2 but not COX-1 protein. IND significantly reduced both basal and IL-1 beta-induced PGE2 release and HGF production. These results suggest that the IL-1 beta-PG-HGF pathway plays a role in the repair process of gastric mucosa. Further, NSAIDs may delay the healing of gastric mucosal ulcer, in part through suppression of HGF expression via inhibition of endogenous PG production.

Alprostadil↗
PubMed1998

Regulation of cyclin D-dependent kinase activity in rat liver regeneration.

The regulation of cyclin D-dependent kinase activity in tissue regeneration in vivo has not been fully described. In young adult rat liver after 70% partial hepatectomy, the association of cyclin D1 with cdk4 was significantly promoted during G1 phase and was maximal at 18 hr, corresponding mainly to late G1. Cyclin D1-dependent kinase activity also strongly increased during G1 phase. The timing of the induction of cyclin D1 / cdk4 complex assembly correlated well with that of cyclin D1-dependent kinase activity. At 18 hr after partial hepatectomy, the amounts of CDK inhibitors p21(CIP1) and p27(KIP1) were also maximal, while only one-tenth of p21(CIP1) and of p27(KIP1) was associated with cyclin D1. These findings suggest that cyclin D1, cdk4 and their association act as promoting factors, and that both p21(CIP1) and p27(KIP1) may have physiological functions as adaptor proteins in additions to their roles as CDK inhibitors in rat liver regeneration.

Animals↗
PubMed1998

Endoscopic ligation for non-esophageal variceal upper gastrointestinal hemorrhage.

BACKGROUND: Endoscopic ligation can be used for bleeding lesions in non-fibrotic tissue; however, only small numbers of patients with non-esophageal variceal upper gastrointestinal hemorrhage have been treated in this way. To evaluate the utility of the technique, we performed the procedure to treat hemorrhage not from esophageal varices during emergency endoscopy. PATIENTS AND METHODS: Bleeding was identified from gastric Dieulafoy's ulcers (n=4), duodenal ulcers (n=3), gastric angiodysplasia (n=2) and Mallory-Weiss tears (n=3). The bleeding points were aspirated and controlled by endoscopic ligation and complete hemostasis was achieved in all cases. RESULTS: Although these lesions were located in difficult areas where endoscopic injection therapy and clipping sometimes fail, endoscopic ligation was performed easily and effectively without complications. Six of the patients had severe underlying disease, including acute and chronic myelogenous leukemia, liver cirrhosis and chronic renal failure; none suffered deterioration in their general condition after endoscopic ligation. CONCLUSIONS: Our findings suggest that endoscopic ligation is an easy and effective method of treatment for patients with gastrointestinal hemorrhage not from esophageal varices, and is safe even in patients with poor general health.

Adult↗
PubMed1998

miranda localizes staufen and prospero asymmetrically in mitotic neuroblasts and epithelial cells in early Drosophila embryogenesis.

When neuroblasts divide, prospero protein and mRNA segregate asymmetrically into the daughter neuroblast and sibling ganglion mother cell. miranda is known to localize prospero protein to the basal cell cortex of neuroblasts while the staufen RNA-binding protein mediates prospero mRNA localization. Here we show that miranda is required for asymmetric staufen localization in neuroblasts. Analyses using miranda mutants reveal that prospero and staufen interact with miranda under the same cell-cycle-dependent control. miranda thus acts to partition both prospero protein and mRNA. Furthermore, miranda localizes prospero and staufen to the basolateral cortex in dividing epithelial cells, which express the three proteins prior to neurogenesis. Our observations suggest that the epithelial cell and neuroblast (both of epithelial origin) share the same molecular machinery for creating cellular asymmetry.

Alleles↗
PubMed1997

Miranda directs Prospero to a daughter cell during Drosophila asymmetric divisions.

Asymmetric cell division is a general process used in many developmental contexts to create two differently fated cells from a single progenitor cell. Intrinsic mechanisms like the asymmetric transmission of cell-fate determinants during cell division, and extrinsic cell-interaction mechanisms, can mediate asymmetric divisions. During embryonic development of the Drosophila central nervous system, neural stem cells called neuroblasts divide asymmetrically to produce another multipotent neuroblast and a ganglion mother cell (GMC) of more restricted developmental potential. Intrinsic mechanisms promote asymmetric division of neuroblasts: for example, the transcription factor Prospero localizes to the basal cell cortex of mitotic neuroblasts and then segregates exclusively into the GMC, which buds off from the basal side of the neuroblast. In the GMC, Prospero translocates to the nucleus, where it establishes differential gene expression between sibling cells. Here we report the identification of a gene, miranda, which encodes a new protein that co-localizes with Prospero in mitotic neuroblasts, tethers Prospero to the basal cortex of mitotic neuroblasts, directing Prospero into the GMC, and releases Prospero from the cell cortex within GMCs. miranda thus creates intrinsic differences between sibling cells by mediating the asymmetric segregation of a transcription factor into only one daughter cell during neural stem-cell division.

Alleles↗
PubMed1997

Minimum inhibitory concentration of various single agents and the effect of their combinations against Helicobacter pylori, as estimated by a fast and simple in vitro assay method.

OBJECTIVES: Fast and simple in vitro methods of accurately assaying anti-Helicobacter pylori (H. pylori) activity are needed to facilitate the selection of optimal drugs for the eradication of H. pylori. With that purpose in mind, we developed a broth microdilution technique that uses a 96-well flat-bottom microplate. METHODS: Clinical isolates of H. pylori were placed in 25-cm2 tissue culture flasks and were grown in an atmosphere of 5% CO2 in air at 37 degrees C and 100% humidity. Then they were inoculated in 96-well flat-bottom microplates. After 24 h, the bacterial growth was assessed by automatic measurement at A450 with a microplate reader. Minimum inhibitory concentrations (MICs) of 11 drugs against H. pylori and the effect of two-drug combinations were respectively evaluated by the broth microdilution technique and by calculating the fractional inhibitory concentration index according to the checkerboard titration method. RESULTS: The MICs of all drugs tested with this system roughly agreed with those of previous reports in which the agar dilution method was used. The MIC of lansoprazole, a proton pump inhibitor, was low (0.88 microg/ml) and surpassed that of metronidazole (3.15 microg/ml). The effect of the combination of macrolide antibiotics with tetracycline was favorable. The proton pump inhibitor demonstrated a strong additive effect with macrolide antibiotics and fostered the activity of ecabet sodium (mucosal protective agent). CONCLUSION: This system could estimate the MIC of individual drugs quickly and simply, and could accurately measure the efficacy of two-drug combinations in vitro.

Anti-Bacterial Agents↗
PubMed1995

Asymmetric segregation of the homeodomain protein Prospero during Drosophila development.

Asymmetric divisions that produce two distinct cells play fundamental roles in generating different cell types during development. In the Drosophila central nervous system, neural stem cells called neuroblasts divide unequally into another neuroblast and a ganglion mother cell which is subsequently cleaved into neurons. Correct gene expression of ganglion mother cells requires the transcription factor Prospero. Here we demonstrate the asymmetric segregation of Prospero on neuroblast division. Prospero synthesized in neuroblasts is retained in the cytoplasm and at mitosis is exclusively partitioned to ganglion mother cells, in which it is translocated to the nucleus. Differential segregation of Prospero was also found in the endoderm. We have identified a region in Prospero that is responsible for this event. The region shares a common motif with Numb, which also shows unequal segregation. We propose that asymmetric segregation of transcription factors is an intrinsic mechanism for establishing asymmetry in gene expression between sibling cells.

Amino Acid Sequence↗
PubMed1995

[IGF I, IGF II].

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Adolescent↗