Soil-nutrient availability and the nutrient-use efficiencies of forests along an altitudinal gradient on Yakushima Island,Japan

The vegetation on Yakushima Island, Japan, grows on soils derived from Akahoya volcanic ash, released from the Kikai Caldera about 7300 years ago. The eruption was devastating and it is believed that primary succession and soil formation reinitiated across all altitudes at this point. We hypothesize that the concentrations of soil total phosphorus (P) and labile P fractions increase with increasing altitude because the soil formation has progressed less in upslope areas as a result of the cooler temperature and because of the ample P source of the volcanic ash. Conversely, we hypothesize that the concentration of soil inorganic nitrogen (N) decreases with increasing altitude. Available soil P and N would result in increasing P limitation downslope and increasing N limitation upslope, respectively. We studied soil P fractions and soil inorganic N, and P- and N-use efficiencies of the seven forests on Yakushima along an elevation gradient (170–1550 m a.s.l.). Contrary to our hypotheses, soil total P, labile soil P fractions, and inorganic N decreased with increasing altitude. The P- and N-use efficiencies of the forests were negatively correlated with the concentration of soil total active P (total P minus occluded P) and inorganic N, respectively. We suggest that progressive soil acidity and slower decomposition under cooler and wetter environments upslope must have dissolved the P contained in volcanic ash and accelerated P leaching. Forest ecosystems on Yakushima that show a distinct altitudinal zonation are, therefore, characterized by increasing P and N shortage with increasing altitude.     

Gene expression pattern of glucose transporters in the skeletal muscles of newly hatched chicks

The gene expression pattern of the glucose transporters (GLUT1, GLUT3, GLUT8, and GLUT12) among pectoralis major and minor, biceps femoris, and sartorius muscles from newly hatched chicks was examined. GLUT1 mRNA level was higher in pectoralis major muscle than in the other muscles. Phosphorylated AKT level was also high in the same muscle, suggesting a relationship between AKT and GLUT1 expression.     

CCR5-Delta32 Allele is Associated with the Risk of Developing Multiple Sclerosis in the Iranian Population

The 32-base pair deletion on the C–C chemokine receptor 5 gene (CCR5-delta32) is known as a protective allele against immune system disorders. We have studied this variation in Iranian multiple sclerosis (MS) patients and healthy controls. DNA samples were prepared from the whole blood of 254 patients with MS and 380 healthy controls. We amplified the fragment including the CCR5-delta32 polymorphism and visualized the products in a documentation system after agarose gel electrophoresis. Data were analysed using one-way ANOVA and Fisher’s exact tests with SPSS-v13 and STATA-v8 software. The delta32 allele was more frequent in MS patients when compared with controls (OR = 2.3, P < 0.0001). Also, we found a significant difference in the frequency of the delta32/delta32 genotype among patients and controls (OR = 7.4, P < 0.001). The mean age at onset and progression index was not significantly different between patients with various genotypes. According to our study, the delta32 allele of the CCR5 gene might be a predisposing factor for MS development in the Iranian population. However, there were no associations between this polymorphism and the clinical course of the disease in this study.     

In vitro hydroxylation of a norlignan: From agatharesinol to sequirin C and metasequirin C with a microsomal preparation from Cryptomeria japonica

In vitro hydroxylation of the norlignan agatharesinol to sequirin C and metasequirin C was demonstrated for the first time. After incubating agatharesinol with a microsomal preparation from the heartwood side of the intermediate wood of Cryptomeria japonica in the presence of cofactors, the aromatic ring-monohydroxylated derivatives of agatharesinol, sequirin C and metasequirin C, were formed. Although hydroxylation hardly occurred in the absence of cofactors, it could be initiated by adding NADPH or NADH, and was enhanced by further adding FAD or FMN. When microsomal preparations from the sapwood or from the sapwood side of the intermediate wood were used, hydroxylation did not occur. This in vitro conversion of the norlignans indicates that the hydroxylation of agatharesinol to sequirin C and metasequirin C is part of the in vivo biosynthetic pathway of norlignans. Another C. japonica norlignan, sugiresinol, which is a side chain-cyclized isomer of agatharesinol, does not seem to be accepted as a substrate, because hardly any hydroxysugireinol was formed after similar incubation with the enzyme.     

Galantamine-induced amyloid-{beta} clearance mediated via stimulation of microglial nicotinic acetylcholine receptors

Reduction of brain amyloid-β (Aβ) has been proposed as a therapeutic target for Alzheimer disease (AD), and microglial Aβ phagocytosis is noted as an Aβ clearance system in brains. Galantamine is an acetylcholinesterase inhibitor approved for symptomatic treatment of AD. Galantamine also acts as an allosterically potentiating ligand (APL) for nicotinic acetylcholine receptors (nAChRs). APL-binding site is located close to but distinct from that for acetylcholine on nAChRs, and FK1 antibody specifically binds to the APL-binding site without interfering with the acetylcholine-binding site. We found that in human AD brain, microglia accumulated on Aβ deposits and expressed α7 nAChRs including the APL-binding site recognized with FK1 antibody. Treatment of rat microglia with galantamine significantly enhanced microglial Aβ phagocytosis, and acetylcholine competitive antagonists as well as FK1 antibody inhibited the enhancement. Thus, the galantamine-enhanced microglial Aβ phagocytosis required the combined actions of an acetylcholine competitive agonist and the APL for nAChRs. Indeed, depletion of choline, an acetylcholine-competitive α7 nAChR agonist, from the culture medium impeded the enhancement. Similarly, Ca(2+) depletion or inhibition of the calmodulin-dependent pathways for the actin reorganization abolished the enhancement. These results suggest that galantamine sensitizes microglial α7 nAChRs to choline and induces Ca(2+) influx into microglia. The Ca(2+)-induced intracellular signaling cascades may then stimulate Aβ phagocytosis through the actin reorganization. We further demonstrated that galantamine treatment facilitated Aβ clearance in brains of rodent AD models. In conclusion, we propose a further advantage of galantamine in clinical AD treatment and microglial nAChRs as a new therapeutic target.     

The Influence of a High‐Fat Dietary Environment in the Fetal Period on Postnatal Metabolic and Immune Function

Few reports show whether a high‐fat (HF) dietary environment in the fetal period affects immune function or the development of lifestyle‐related disease at maturity. We examined the influence of an HF dietary environment in the fetal period on postnatal metabolic and immune function. A total of 16 pregnant mice were given control (CON) diet and 16 were given HF diet in the gestational period, from mating to delivery. After delivery lactating mice were given either CON or HF diet, resulting in four groups. After weaning, the offspring mice were given the same diet that their mothers received during lactation. HF dietary intake in the postnatal period increased fat pad weights, serum glucose, and leptin levels. An HF diet in the fetal period resulted in fewer splenic lymphocytes, a thinner thymic cortex, and impaired antigen‐specific immune reactions. Furthermore, tumor necrosis factor (TNF)‐α production and serum triglyceride levels were elevated in the fetal HF group. In addition, the HF‐HF group showed a consistent decrease in ovalbumin (OVA)‐specific IgG and elevation of IgE, associated with advanced fatty changes in the liver. Results from this study suggest that HF environment during the fetal period induces epigenetic propensity toward obesity and immunological burden in part due to increased adipose tissue mass, significant reduction in the number of immune cells and decreased activities of immune cells.     

The proline-rich protein palladin is a binding partner for profilin

Palladin is an actin-associated protein that has been suggested to play critical roles in establishing cell morphology and maintaining cytoskeletal organization in a wide variety of cell types. Palladin has been shown previously to bind directly to three different actin-binding proteins vasodilator-stimulated phosphoprotein (VASP), alpha-actinin and ezrin, suggesting that it functions as an organizing unit that recruits actin-regulatory proteins to specific subcellular sites. Palladin contains sequences resembling a motif known to bind profilin. Here, we demonstrate that palladin is a binding partner for profilin, interacting with profilin via a poly proline-containing sequence in the amino-terminal half of palladin. Double-label immunofluorescence staining shows that palladin and profilin partially colocalize in actin-rich structures in cultured astrocytes. Our results suggest that palladin may play an important role in recruiting profilin to sites of actin dynamics.     

Transient expression of Drosophila melanogaster deoxynucleoside kinase gene enhances cytotoxicity of nucleoside analogs

The Drosophila melanogaster deoxynucleoside kinase gene was introduced into HeLa cells with cationic lipids to allow its transient expression, and cytotoxic effects of several nucleoside analogs in the transfected cells were examined. Of the analogs tested, cytotoxicities of 1-beta-D-arabinofuranosylcytosine (araC), 5-fluorodeoxyuridine (FUdR), and 1-(2-deoxy-2-methylene-beta-D-erythro-pentofuranosyl)cytosine (DMDC) were increased by the deoxynucleoside kinase gene. These results suggest that the combination of the transient expression of the Drosophila deoxynucleoside kinase gene and these nucleoside analogs is a candidate for the suicide gene therapy.     

Single nucleotide polymorphisms associated with aggressive periodontitis and severe chronic periodontitis in Japanese

Periodontitis is a common inflammatory disease causing destruction of periodontal tissues. It is a multifactor disease involving genetic factors and oral environmental factors. To determine genetic risk factors associated with aggressive periodontitis or severe chronic periodontitis, single nucleotide polymorphisms (SNPs) in multiple candidate genes were investigated in Japanese. We studied 134 patients with aggressive periodontitis, 117 patients with severe chronic periodontitis, and 125 healthy volunteers without periodontitis, under case-control setting, and 310 SNPs in 125 candidate genes were genotyped. Association evaluation by Fisher's exact test (p < 0.01) revealed statistically significant SNPs in multiple genes, not only in inflammatory mediators (IL6ST and PTGDS, associated with aggressive periodontitis; and CTSD, associated with severe chronic periodontitis), but also in structural factors of periodontal tissues (COL4A1, COL1A1, and KRT23, associated with aggressive periodontitis; and HSPG2, COL17A1, and EGF, associated with severe chronic periodontitis). These appear to be good candidates as genetic factors for future study.