Alkali Elution Behavior of Steelmaking Slag Packed in an Open Channel Vessel in Seawater

The alkali elution behavior of steelmaking slag in seawater was kinetically investigated and simulated under continuous flow in an open channel vessel with packed bed of steelmaking slag. Two types of steelmaking slags, viz. decarburization slag and dephosphorization slag, were used in this study. The alkali elution rate of decarburization slag was larger than that of dephosphorization slag due to larger free CaO content. The pH value for dephosphorization slag was almost the same as the seawater pH value in 3–4 days, whereas that for decarburization slag was stabilized in 3 days although the pH value was slightly larger than that of seawater. The capacity coefficients of alkali elution for dephosphorization and decarburization slags decreased together in an exponential manner with time. Based on a regression equation on the mass transfer capacity coefficient change with time, the alkali elution behavior was simulated and the calculated results agreed well with the experimental ones. The temporal pH change was predicted by changing slag surface area and seawater flow rate as a parameter. According to the simulation results for dephosphorization slag, the seawater pH value did not reach a high level in the ocean area

Inhibition of Blood Glucose Level Elevation by Low-Carbohydrate Ohagi in Healthy Adults

糖質は血糖値をもっとも上昇させるため，糖質を多く含む菓子類は糖尿病患者において制限されることが多い．和菓子は小豆に砂糖を加えた餡ともち米から成り，菓子類の中でも高糖質食品である．そこで餡ともち米からなるおはぎで糖質の低減が実現できれば他の和菓子への汎用性が高いと考え，エリスリトールを主とした甘味料と大麦を配合した低糖質おはぎを作成し，食後の血糖上昇とセカンドミール効果について検討した．対象は健常成人12名とし，方法は低糖質おはぎ，通常おはぎのいずれかの試験食を単盲検，クロスオーバーにより摂取し，試験食の摂取開始150分後に食事を摂取し，血糖値を測定した．その結果，低糖質おはぎは通常おはぎの摂取と比較し，食後15～30分の急峻な血糖上昇を有意に抑制し，セカンドミール後の血糖上昇曲線下面積（IAUC）では有意に低値を示した．健常成人における低糖質おはぎの摂取は，食後の血糖上昇を抑制する可能性が示唆された．[Aim] The aim of this study was to investigate the postprandial blood glucose response and second meal effect of low carbohydrate Ohagi prepared with barley and erythritol. [Method] The subjects were 12 healthy adults. The method was a single-blind, crossover design in which subjects consumed either low carbohydrate or regular Ohagi as the test meal. After 150 minutes, subjects consumed the meal and their blood glucose levels were measured. [Results] Low carbohydrate Ohagi showed a significantly lower rise in blood glucose levels 15 to 30 minutes after ingestion and a significantly lower glucose incremental areas under the curve (IAUC) after the second meal. [Conclusion] Consumption of low-carbohydrate Ohagi in healthy adults was suggested to improve postprandial glycemic response.departmental bulletin pape

High dose of histone deacetylase inhibitors affects insulin secretory mechanism of pancreatic beta cell line

Objective. Histone deacytylase inhibitors (HDACis) inhibit the deacetylation of the lysine residue of proteins, including histones, and regulate the transcription of a variety of genes. Recently, HDACis have been used clinically as anti-cancer drugs and possible anti-diabetic drugs. Even though HDACis have been proven to protect the cytokine-induced damage of pancreatic beta cells, evidence also shows that high doses of HDACis are cytotoxic. In the present study, we, therefore, investigated the eff ect of HDACis on insulin secretion in a pancreatic beta cell line. Methods. Pancreatic beta cells MIN6 were treated with selected HDACis (trichostatin A, TSA; valproic acid, VPA; and sodium butyrate, NaB) in medium supplemented with 25 mM glucose and 13% heat-inactivated fetal bovine serum (FBS) for indicated time intervals. Protein expression of Pdx1 and Mafa in MIN6 cells was demonstrated by immunohistochemistry and immunocytochemistry, expression of Pdx1 and Mafa genes was measured by quantitative RT-PCR method. Insulin release from MIN6 cells and insulin cell content were estimated by ELISA kit. Superoxide production in MIN6 cells was measured using a Total ROS/Superoxide Detection System. Results. TSA, VPA, and NaB inhibited the expression of Pdx1 and Mafa genes and their products. TSA treatment led to beta cell malfunction, characterized by enhanced insulin secretion at 3 and 9 mM glucose, but impaired insulin secretion at 15 and 25 mM glucose. Th us, TSA induced dysregulation of the insulin secretion mechanism. TSA also enhanced reactive oxygen species production in pancreatic beta cells. Conclusions. Our results showed that HDACis caused failure to suppress insulin secretion at low glucose concentrations and enhance insulin secretion at high glucose concentrations. In other words, when these HDACis are used clinically, high doses of HDACis may cause hypoglycemia in the fasting state and hyperglycemia in the fed state. When using HDACis, physicians should, therefore, be aware of the capacity of these drugs to modulate the insulin secretory capacity of pancreatic beta cells

Endozoochorous seed dispersal by sympatric mustelids, Martes melampus and Mustela itatsi, in western Tokyo, central Japan

We investigated seed dispersal by two sympatric mustelid species, the Japanese marten (Martes melampus) and Japanese weasel (Mustela itatsi), along an intercity forest path in western Tokyo, central Japan, from Jul 2007 to Jul 2008. We aimed to investigate the effect of food/habitat preference of these mustelids (martens are semi-arboreal frugivores while weasels are terrestrial carnivores) on their seed dispersal characteristics, which determine their efficacy as seed dispersers. In total, we analyzed 478 fecal samples collected from the two mustelids (Nmarten = 381, Nweasel = 97). The proportions of feces containing seeds for martens and weasels were 81.4% and 55.7%, respectively. The number of plant species whose seeds were found within the feces were 28 and 17, respectively. Almost all seeds within feces of both mustelids were intact. The number of plant species whose seeds were found within a single fecal sample ranged from one to four, but no significant difference was detected between the two mustelids. However, marten feces contained a significantly greater number of seeds of most plant species as well as total number of seeds than did weasel feces. The numbers of plant species and seeds represented in marten feces varied seasonally, but those represented in weasel feces did not. Our findings suggest the possibility that both mustelids act in some ways as seed dispersers, although martens seem to disperse a greater diversity and total amount of seeds

Microarray Analysis of Novel Candidate Genes Responsible for Glucose-Stimulated Insulin Secretion in Mouse Pancreatic β Cell Line MIN6

<div><p>Elucidating the regulation of glucose-stimulated insulin secretion (GSIS) in pancreatic islet β cells is important for understanding and treating diabetes. MIN6 cells, a transformed β-cell line derived from a mouse insulinoma, retain GSIS and are a popular <i>in vitro</i> model for insulin secretion. However, in long-term culture, MIN6 cells' GSIS capacity is lost. We previously isolated a subclone, MIN6 clone 4, from the parental MIN6 cells, that shows well-regulated insulin secretion in response to glucose, glybenclamide, and KCl, even after prolonged culture. To investigate the molecular mechanisms responsible for preserving GSIS in this subclone, we compared four groups of MIN6 cells: Pr-LP (parental MIN6, low passage number), Pr-HP (parental MIN6, high passage number), C4-LP (MIN6 clone 4, low passage number), and C4-HP (MIN6 clone 4, high passage number). Based on their capacity for GSIS, we designated the Pr-LP, C4-LP, and C4-HP cells as “responder cells.” In a DNA microarray analysis, we identified a group of genes with high expression in responder cells (“responder genes”), but extremely low expression in the Pr-HP cells. Another group of genes (“non-responder genes”) was expressed at high levels in the Pr-HP cells, but at extremely low levels in the responder cells. Some of the responder genes were involved in secretory machinery or glucose metabolism, including <i>Chrebp</i>, <i>Scgn</i>, and <i>Syt7</i>. Among the non-responder genes were <i>Car2</i>, <i>Maf</i>, and <i>Gcg</i>, which are not normally expressed in islet β cells. Interestingly, we found a disproportionate number of known imprinted genes among the responder genes. Our findings suggest that the global expression profiling of GSIS-competent and GSIS-incompetent MIN6 cells will help delineate the gene regulatory networks for insulin secretion.</p> </div

Acinar-to-ductal metaplasia induced by adenovirus-mediated pancreatic expression of Isl1.

Tubular complexes (TCs) are aggregates of duct-like monolayered cells in the developing and regenerating pancreas. Recent studies showed that TCs have regenerative potential, including islet neogenesis. We previously delivered adenovirus vector (AdV) into exocrine cells of the pancreas by intra-common bile ductal (ICBD) injection, and found that AdV expressing Pdx1, a pancreas-specific transcription factor, causes TC formation and islet neogenesis. We also established RTF-Pdx1-EGFP mice, which ubiquitously express Pdx1 when tetracycline is removed from the drinking water. However, exogenous Pdx1 expression in adult RTF-Pdx1-EGFP mice did not cause any pathological changes in the pancreas during three weeks of observation after tetracycline withdrawal. To examine whether the host immune response induced by AdV was involved in TC formation, we delivered AdVs expressing pancreas-related transcription factors or an irrelevant protein into the pancreas of RTF-Pdx1-EGFP mice. Histological analyses showed that both AdV injection and Pdx1 expression are required for TC formation. We also analyzed the effects of these ICBD-injected AdVs. AdV expressing Isl1, a proendocrine transcription factor, effectively induced TC formation through acinar-to-ductal metaplasia, and exogenous Pdx1 expression facilitated this process. Considering the regenerative potential of TCs, a strategy that efficiently induces TC formation may lead to novel therapies for diabetes

Insulin content and secretion of MIN6 cells.

<p>Insulin content of Pr-LP, Pr-HP, C4-LP, and C4-HP MIN6 cells (A). The insulin content of Pr-HP cells was lower than that of Pr-LP, C4-LP, or C4-HP cells. Values are means ± SD and n = 5–6. *<i>P</i><0.05. Insulin secretion/insulin content from Pr-LP, Pr-HP, C4-LP, and C4-HP MIN6 cells stimulated with 3 mM (3G), 25 mM (25G) glucose, 100 nM glybenclamide (SU), or 30 mM KCl (B, C). Values are means ± SD and n = 5–6. *<i>P</i><0.05 v.s. insulin secretion at 3 mM glucose.+<i>P</i><0.05 v.s. insulin secretion of Pr-LP, C4-LP, and C4-HP cells at 3 mM glucose by Student's <i>t</i>-test.</p

Quantitative RT-PCR analysis of imprinted genes.

<p>Expression of imprinted genes, <i>Rian</i> (A), <i>Plagl1</i> (B), <i>Dlk1</i> (C), and <i>Kcnq1</i> (D) in Pr-LP, Pr-HP, C4-LP, and C4-HP MIN6 cells. <i>Plagl1</i>, <i>Dlk1</i>, and <i>Rian</i> were confirmed to be responder genes, whereas <i>Kcnq1</i> was a non-responder gene. Values are means ± SD and n = 4–5. *<i>P</i><0.05.</p

Insulin secretion from MIN6 cells.

<p>Insulin secretion from Pr-LP, Pr-HP, C4-LP, and C4-HP MIN6 cells stimulated with 3 mM (3G), 8 mM (8G), 15 mM (15G), or 25 mM (25G) glucose (A, B), 100 nM glybenclamide (SU), or 30 mM KCl (C, D). Pr-HP cells showed higher basal insulin secretion at 3 mM glucose compared with Pr-LP cells, but their insulin secretion did not increase further at higher glucose concentrations or with the addition of glybenclamide or KCl, whereas both C4-LP and C4-HP MIN6 cells showed a better insulin secretory response to glucose and glybenclamide than Pr-LP cells. Values are means ± SD and n = 5–6. *<i>P</i><0.05 v.s. insulin secretion at 3 mM glucose.+<i>P</i><0.05 v.s. insulin secretion of Pr-LP, C4-LP, and C4-HP cells at 3 mM glucose by Student's <i>t</i>-test.</p