Search

The article offers information on a study which presents a rapid and specific identification method for the simultaneous detection of mushrooms Omphalotus guepiniformis and Lentinula edodes. It makes use of multiplex real-time polymerase chain reaction (PCR) assay and mentions that the new assay proved specific to the target species. It informs that the assay is highly sensitive and is applicable to processed food samples and gastric juice contents.

Objective: There is now growing evidence that magnesium (Mg) deficiency is implicated in type 2 diabetes and its complications. However, it has not been fully elucidated whether hypomagnesemia is a predictor of end-stage renal disease (ESRD) in type 2 diabetic nephropathy.Research Design and Methods: This retrospective cohort study included 455 chronic kidney disease (CKD) patients (144 with type 2 diabetic nephropathy and 311 with nondiabetic CKD) who were hospitalized at Osaka General Medical Center for a CKD educational program between April 2001 and December 2007. The primary outcome was progression to renal replacement therapy. Participants were categorized based on serum Mg level into Low-Mg (serum Mg level ≤1.8 mg/dL) and High-Mg (serum Mg level >1.8 mg/dL) groups with the previously published normal lower limit chosen as the cutoff point.Results: Of the subjects with type 2 diabetic nephropathy, 102 progressed to ESRD during follow-up (median, 23 months). A multivariate Cox proportional hazards model showed that after adjustment for various demographic factors and laboratory data, the Low-Mg group had a 2.12-fold higher risk of ESRD than the High-Mg group (95% CI 1.28-3.51; P = 0.004). In contrast, 135 of the nondiabetic CKD subjects progressed to ESRD during follow-up (median, 44 months). No significant difference in outcome was found between the Low- and High-Mg groups of this population (adjusted hazard ratio, 1.15; 95% CI 0.70-1.90; P = 0.57).Conclusions: Hypomagnesemia is a novel predictor of ESRD in patients with type 2 diabetic nephropathy. [ABSTRACT FROM AUTHOR]

OBJECTIVE--There is now growing evidence that magnesium (Mg) deficiency is implicated in type 2 diabetes and its complications. However, it has not been fully elucidated whether hypomagnesemia is a predictor of end-stage renal disease (ESRD) in type 2 diabetic nephropathy. RESEARCH DESIGN AND METHODS--This retrospective cohort study included 455 chronic kidney disease (CKD) patients (144 with type 2 diabetic nephropathy and 311 with nondiabetic CKD) who were hospitalized at Osaka General Medical Center for a CKD educational program between April 2001 and December 2007. The primary outcome was progression to renal replacement therapy. Participants were categorized based on serum Mg level into Low-Mg (serum Mg level ≤1.8 mg/dL) and High-Mg (serum Mg level >1.8 mg/dL) groups with the previously published normal lower limit chosen as the cutoff point. RESULTS--Of the subjects with type 2 diabetic nephropathy, 102 progressed to ESRD during follow-up (median, 23 months). A multivariate Cox proportional hazards model showed that after adjustment for various demographic factors and laboratory data, the Low-Mg group had a 2.12-fold higher risk of ESRD than the High-Mg group (95% CI 1.28--3.51; P = 0.004). In contrast, 135 of the nondiabetic CKD subjects progressed to ESRD during follow-up (median, 44 months). No significant difference in outcome was found between the Low- and High-Mg groups of this population (adjusted hazard ratio, 1.15; 95% CI 0.70--1.90; P = 0.57). CONCLUSIONS--Hypomagnesemia is a novel predictor of ESRD in patients with type 2 diabetic nephropathy. [ABSTRACT FROM AUTHOR]

Background. Hepcidin is a central regulator of iron homeostasis. Increased hepcidin concentrations could cause iron-restricted erythropoiesis in chronic kidney disease (CKD)-associated anemia. This cross-sectional observational study was conducted to evaluate the association between hepcidin and CKD-associated anemia in non-dialysis CKD patients. Methods. A total of 505 non-dialysis CKD patients not treated with parenteral iron were recruited, and serum hepcidin-25 levels were measured by liquid chromatography tandem mass spectrometry. Multiple linear regression analysis was used to examine the relationship between hepcidin and glomerular filtration rate (GFR) and the relationship between hemoglobin concentration and predictors including the hepcidin level. Results. The median hepcidin level among the 505 CKD patients was 15.4 ng/mL (interquartile range, 5.5–33.6 ng/mL). Although hepcidin level significantly increased according to the CKD stage, multivariate analysis did not reveal an association of GFR with the hepcidin level. Hepcidin level was a significant predictor of hemoglobin concentration after the adjustment for confounders, and a significant interaction between hepcidin and ferritin was found. After stratifying at the median ferritin level, 91 ng/mL, we found a negative association between hepcidin level and hemoglobin in the high-ferritin group. A trend toward a negative association between hepcidin level and mean corpuscular volume was observed in the high-ferritin group. Conclusions. Serum hepcidin-25 levels were negatively associated with hemoglobin concentrations in non-dialysis CKD patients with sufficient iron stores. We found that ferritin modified the association between hepcidin level and hemoglobin concentration. In addition, our results confirmed that the serum hepcidin level is not associated with GFR. [ABSTRACT FROM PUBLISHER]

Background: Knowledge of how influenza viruses spread in a community is important for planning and implementation of effective interventions, including social distancing measures. Households and schools are implicated as the major sites for influenza virus transmission. However, the overall picture of community transmission is not well defined during actual outbreaks. We conducted a community-based prospective cohort study to describe the transmission characteristics of influenza in Mongolia. Methods and Findings: A total of 5,655 residents in 1,343 households were included in this cohort study. An active search for cases of influenza-like illness (ILI) was performed between October 2010 and April 2011. Data collected during a community outbreak of influenza A(H3N2) were analyzed. Total 282 ILI cases occurred during this period, and 73% of the subjects were aged <15 years. The highest attack rate (20.4%) was in those aged 1-4 years, whereas the attack rate in those aged 5-9 years was 10.8%. Fifty-one secondary cases occurred among 900 household contacts from 43 households (43 index cases), giving an overall crude household secondary attack rate (SAR) of 5.7%. SAR was significantly higher in younger household contacts (relative risk for those aged <1 year: 9.90, 1-4 years: 5.59, and 5-9 years: 6.43). We analyzed the transmission patterns among households and a community and repeated transmissions were detected between households, preschools, and schools. Children aged 1-4 years played an important role in influenza transmission in households and in the community at large. Working-age adults were also a source of influenza in households, whereas elderly cases (aged ≥65 years) had no link with household transmission. Conclusions: Repeated transmissions between households, preschools, and schools were observed during an influenza A(H3N2) outbreak period in Mongolia, where subjects aged 1-4 years played an important role in influenza transmission. [ABSTRACT FROM AUTHOR]

Abstract: Continuous flow synthesis of gold nanoparticles was demonstrated using a microchannel reactor with glucose reduction in aqueous alkaline medium. Particle size, morphology, and visual/optical properties of the dispersion liquid were controlled dynamically by tuning of the rate of NaOH addition. Characteristic star-like nanoparticles formed spontaneously as a quasi-stable state, but they changed the morphology to round shape and showed spectral change over time. [Copyright &y& Elsevier]

Enterovirus 68 (EV68) is a rare enterovirus associated with respiratory illness that, unlike other enteroviruses, has been identified only from respiratory specimens. We identified EV68 from respiratory specimens of children hospitalized with a diagnosis of severe pneumonia in Leyte, Republic of the Philippines. Twenty-one samples showed high similarity with EV68 by sequencing of 5' nontranslated region; 17 of these samples were confirmed as EV68 by sequencing of viral protein 1 capsid coding region. Most previously reported EV68 cases had been identified as sporadic cases. All 21 patients we identified had severe illness, and 2 died, possibly the first reported fatal cases associated with EV68 infection. Our study suggests that EV68 may be a possible causative agent of severe respiratory illnesses. [ABSTRACT FROM AUTHOR]

Abstract: A new reaction setup equipped with micro tubular reactor with thin catalytic metal inner surface (Pd or Pd–Cu alloy) was developed for the reactions in high-pressure and high-temperature water (HPHT-H2O) flow. To evaluate the catalytic performance of this micro tubular reactor, Sonogashira C–C coupling of iodobenzene and ethynylbenzene was investigated by using this system under alkaline aqueous medium. Under the optimized reaction conditions of 250°C and 16MPa of pressure, diphenylethyne was obtained with good yield and 100% selectivity within a very short residence time of ∼1.6s. The reaction proceeds without any additional promoters, additives or organic solvents. Leaching of catalytic metal from the reactor tube was not found under the studied reaction conditions. Alloying of Pd with Cu remarkably improved the efficiency of the reaction due to co-catalytic effect that is related to the easy electron transfer between two metals. [Copyright &y& Elsevier]

Objective: Type 2 diabetes is characterized by diminished pancreatic β-cell mass and function. Insulin signaling within the β-cells has been shown to play a critical role in maintaining the essential function of the β-cells. Under basal conditions, enhanced insulin-PI3K signaling via deletion of phosphatase with tensin homology (PTEN), a negative regulator of this pathway, leads to increased β-cell mass and function. In this study, we investigated the effects of prolonged β-cell-specific PTEN deletion in models of type 2 diabetes.Research Design and Methods: Two models of type 2 diabetes were employed: a high-fat diet (HFD) model and a db/db model that harbors a global leptin-signaling defect. A Cre-loxP system driven by the rat insulin promoter (RIP) was employed to obtain mice with β-cell-specific PTEN deletion (RIPcre(+) Pten(fl/fl)).Results: PTEN expression in islets was upregulated in both models of type 2 diabetes. RIPcre(+) Pten(fl/fl) mice were completely protected against diabetes in both models of type 2 diabetes. The islets of RIPcre(+) Pten(fl/fl) mice already exhibited increased β-cell mass under basal conditions, and there was no further increase under diabetic conditions. Their β-cell function and islet PI3K signaling remained intact, in contrast to HFD-fed wild-type and db/db islets that exhibited diminished β-cell function and attenuated PI3K signaling. These protective effects in β-cells occurred in the absence of compromised response to DNA-damaging stimuli.Conclusions: PTEN exerts a critical negative effect on both β-cell mass and function. Thus PTEN inhibition in β-cells can be a novel therapeutic intervention to prevent the decline of β-cell mass and function in type 2 diabetes. [ABSTRACT FROM AUTHOR]

OBJECTIVE--Type 2 diabetes is characterized by diminished pancreatic β-cell mass and function. Insulin signaling within the β-cells has been shown to play a critical role in maintaining the essential function of the β-cells. Under basal conditions, enhanced insulin-PI3K signaling via deletion of phosphatase with tensin homology (PTEN), a negative regulator of this pathway, leads to increased β-cell mass and function. In this study, we investigated the effects of prolonged β-cell-specific PTEN deletion in models of type 2 diabetes. RESEARCH DESIGN AND METHODS--Two models of type 2 diabetes were employed: a high-fat diet (HFD) model and a db/db model that harbors a global leptin-signaling defect. A Cre-loxP system driven by the rat insulin promoter (RIP) was employed to obtain mice with β-cell-specific PTEN deletion (RIPcre+ Ptenfl/fl). RESULTS--PTEN expression in islets was upregulated in both models of type 2 diabetes. RIPcre+ Ptenfl/fl mice were completely protected against diabetes in both models of type 2 diabetes. The islets of RIPcre+ Ptenfl/fl mice already exhibited increased β-cell mass under basal conditions, and there was no further increase under diabetic conditions. Their β-cell function and islet PI3K signaling remained intact, in contrast to HFD-fed wild-type and db/db islets that exhibited diminished β-cell function and attenuated PI3K signaling. These protective effects in β-cells occurred in the absence of compromised response to DNA-damaging stimuli. CONCLUSIONS--PTEN exerts a critical negative effect on both β-cell mass and function. Thus PTEN inhibition in β-cells can be a novel therapeutic intervention to prevent the decline of β-cell mass and function in type 2 diabetes. Diabetes 59: 3117-3126, 2010 [ABSTRACT FROM AUTHOR]

Background: Perilipin A (PeriA) exclusively locates on adipocyte lipid droplets and is essential for lipid storage and lipolysis. Previously, we reported that adipocyte specific overexpression of PeriA caused resistance to diet-induced obesity and resulted in improved insulin sensitivity. In order to better understand the biological basis for this observed phenotype, we performed additional studies in this transgenic mouse model. Methodology and Principal Findings: When compared to control animals, whole body energy expenditure was increased in the transgenic mice. Subsequently, we performed DNA microarray analysis and real-time PCR on white adipose tissue. Consistent with the metabolic chamber data, we observed increased expression of genes associated with fatty acid β-oxidation and heat production, and a decrease in the genes associated with lipid synthesis. Gene expression of Pgc1a, a regulator of fatty acid oxidation and Ucp1, a brown adipocyte specific protein, was increased in the white adipose tissue of the transgenic mice. This observation was subsequently verified by both Western blotting and histological examination. Expression of RIP140, a regulator of white adipocyte differentiation, and the lipid droplet protein FSP27 was decreased in the transgenic mice. Importantly, FSP27 has been shown to control gene expression of these crucial metabolic regulators. Overexpression of PeriA in 3T3-L1 adipocytes also reduced FSP27 expression and diminished lipid droplet size. Conclusions: These findings demonstrate that overexpression of PeriA in white adipocytes reduces lipid droplet size by decreasing FSP27 expression and thereby inducing a brown adipose tissue-like phenotype. Our data suggest that modulation of lipid droplet proteins in white adipocytes is a potential therapeutic strategy for the treatment of obesity and its related disorders. [ABSTRACT FROM AUTHOR]

Abstract: The 2009 human pandemic influenza (H1N1) virus possesses the HA gene of the H1 subtype. The evolutionary process of the 2009 H1N1 virus remains to be defined. We performed genetic analyses of the HA gene by comparing the 2009 H1N1 virus with seasonal human and swine viruses. We analyzed sequences of 116 2009 H1N1 viruses, and obtained 1457 seasonal H1N1, 365 swine H1, and 1332 2009 H1N1 viruses from the database. Selection pressure for the 2009 H1N1 virus was higher than that for the swine virus and equivalent to that for the seasonal virus. Positions 206 and 264 were found to be positively selected sites. We also identified sites under different selection pressures from the seasonal or swine virus that may be involved in imparting significant biological characteristics. The evolutionary characteristics of the H1 gene of the 2009 H1N1 virus differed from those of seasonal and swine viruses. [ABSTRACT FROM AUTHOR]

Abstract: Novel micro tubular reactors composed of Inconel 625 support, TiO2/Ti intermediate layer and thin catalytic metal film (Pd, Pd−Cu alloy, Pt, Rh, and Au) were fabricated by continuous electroless plating technique. The reactors withstood high temperature (400°C) and high pressure (30MPa) water flow without loss of catalytic metals. The high catalytic efficiency of the reactors was demonstrated by the rapid and complete decomposition of organic dye in the flow system. [ABSTRACT FROM AUTHOR]

Background: Productive agriculture needs a large amount of expensive nitrogenous fertilizers. Improving nitrogen use efficiency (NUE) of crop plants is thus of key importance. NUE definitions differ depending on whether plants are cultivated to produce biomass or grain yields. However, for most plant species, NUE mainly depends on how plants extract inorganic nitrogen from the soil, assimilate nitrate and ammonium, and recycle organic nitrogen. Efforts have been made to study the genetic basis as well as the biochemical and enzymatic mechanisms involved in nitrogen uptake, assimilation, and remobilization in crops and model plants. The detection of the limiting factors that could be manipulated to increase NUE is the major goal of such research. [ABSTRACT FROM PUBLISHER]

Phosphorylated derivatives of phosphatidylinositol, collectively referred to as phosphoinositides, occur in the cytoplasmic leaflet of cellular membranes and regulate activities such as vesicle transport, cytoskeletal reorganization and signal transduction. Recent studies have indicated an important role for phosphoinositide metabolism in the aetiology of diseases such as cancer, diabetes, myopathy and inflammation. Although the biological functions of the phosphatases that regulate phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3) have been well characterized, little is known about the functions of the phosphatases regulating the closely related molecule phosphatidylinositol-3,4-bisphosphate (PtdIns(3,4)P2). Here we show that inositol polyphosphate phosphatase 4A (INPP4A), a PtdIns(3,4)P2 phosphatase, is a suppressor of glutamate excitotoxicity in the central nervous system. Targeted disruption of the Inpp4a gene in mice leads to neurodegeneration in the striatum, the input nucleus of the basal ganglia that has a central role in motor and cognitive behaviours. Notably, Inpp4a-/- mice show severe involuntary movement disorders. In vitro, Inpp4a gene silencing via short hairpin RNA renders cultured primary striatal neurons vulnerable to cell death mediated by N-methyl-d-aspartate-type glutamate receptors (NMDARs). Mechanistically, INPP4A is found at the postsynaptic density and regulates synaptic NMDAR localization and NMDAR-mediated excitatory postsynaptic current. Thus, INPP4A protects neurons from excitotoxic cell death and thereby maintains the functional integrity of the brain. Our study demonstrates that PtdIns(3,4)P2, PtdIns(3,4,5)P3 and the phosphatases acting on them can have distinct regulatory roles, and provides insight into the unique aspects and physiological significance of PtdIns(3,4)P2 metabolism. INPP4A represents, to our knowledge, the first signalling protein with a function in neurons to suppress excitotoxic cell death. The discovery of a direct link between PtdIns(3,4)P2 metabolism and the regulation of neurodegeneration and involuntary movements may aid the development of new approaches for the treatment of neurodegenerative disorders. [ABSTRACT FROM AUTHOR]

Lung cancer is the leading cause of cancer-related mortality in the world, resulting in over a million deaths each year. Non-small cell lung cancers (NSCLCs) are characterized by a poor immunogenic response, which may be the result of immunosuppressive factors such as prostaglandin E2 (PGE2) present in the tumor environment. The effect of PGE2 in the suppression of anti-tumor immunity and its promotion of tumor survival has been established for over three decades, but with limited mechanistic understanding. We have previously reported that PGE2 activates hematopoietic progenitor kinase 1 (HPK1), a hematopoietic-specific kinase known to negatively regulate T-cell receptor signaling. Here, we report that mice genetically lacking HPK1 resist the growth of PGE2-producing Lewis lung carcinoma (LLC). The presence of tumor-infiltrating lymphocytes (TILs) and T-cell transfer into T cell-deficient mice revealed that tumor rejection is T cell mediated. Further analysis demonstrated that this may be significantly due to the ability of HPK1−/− T cells to withstand PGE2-mediated suppression of T-cell proliferation, IL-2 production, and apoptosis. We conclude that PGE2 utilizes HPK1 to suppress T cell-mediated anti-tumor responses. [ABSTRACT FROM AUTHOR]

The cause of atypical respiratory illness in several Mexican states in mid-March 2009 was determined to be a novel pandemic (H1N1) 2009 virus. It has since then spread to six continents, causing illness and death. We review this virus against an epidemiological triangle model for understanding and visualizing communicable diseases that describes the interaction of an agent, host, and environment. We review the agent, i.e., pandemic (H1N1) 2009 virus, hosts focusing on human beings, and the environment, suggesting from this agent-host-environment interaction measures for controlling and preventing infection spread due to pandemic (H1N1) 2009 virus and the related issues. [ABSTRACT FROM AUTHOR]

In higher plants the glutamate dehydrogenase (GDH) enzyme catalyzes the reversible amination of 2-oxoglutarate to form glutamate, using ammonium as a substrate. For a better understanding of the physiological function of GDH either in ammonium assimilation or in the supply of 2-oxoglutarate, we used transgenic tobacco (Nicotiana tabacum L.) plants overexpressing the two genes encoding the enzyme. An in vivo real time 15N-nuclear magnetic resonance (NMR) spectroscopy approach allowed the demonstration that, when the two GDH genes were overexpressed individually or simultaneously, the transgenic plant leaves did not synthesize glutamate in the presence of ammonium when glutamine synthetase (GS) was inhibited. In contrast we confirmed that the primary function of GDH is to deaminate Glu. When the two GDH unlabeled substrates ammonium and Glu were provided simultaneously with either [15N]Glu or 15NH4+ respectively, we found that the ammonium released from the deamination of Glu was reassimilated by the enzyme GS, suggesting the occurrence of a futile cycle recycling both ammonium and Glu. Taken together, these results strongly suggest that the GDH enzyme, in conjunction with NADH-GOGAT, contributes to the control of leaf Glu homeostasis, an amino acid that plays a central signaling and metabolic role at the interface of the carbon and nitrogen assimilatory pathways. Thus, in vivo NMR spectroscopy appears to be an attractive technique to follow the flux of metabolites in both normal and genetically modified plants. [ABSTRACT FROM PUBLISHER]

This study was aimed at investigating the physiological role of ferredoxin-glutamate synthases (EC 1.4.1.7), NADH-glutamate synthase (EC 1.4.1.14) and carbamoylphosphate synthetase (EC 6.3.5.5) in Arabidopsis. Phenotypic analysis revealed a high level of photorespiratory ammonium, glutamine/glutamate and asparagine/aspartate in the GLU1 mutant lacking the major ferredoxin-glutamate synthase, indicating that excess photorespiratory ammonium was detoxified into amino acids for transport out of the veins. Consistent with these results, promoter analysis and in situ hybridization demonstrated that GLU1 and GLU2 were expressed in the mesophyll and phloem companion cell–sieve element complex. However, these phenotypic changes were not detected in the GLU2 mutant defective in the second ferredoxin-glutamate synthase gene. The impairment in primary ammonium assimilation in the GLT mutant under nonphotorespiratory high-CO2 conditions underlined the importance of NADH-glutamate synthase for amino acid trafficking, given that this gene only accounted for 3% of total glutamate synthase activity. The excess ammonium from either endogenous photorespiration or the exogenous medium was shifted to arginine. The promoter analysis and slight effects on overall arginine synthesis in the T-DNA insertion mutant in the single carbamoylphosphate synthetase large subunit gene indicated that carbamoylphosphate synthetase located in the chloroplasts was not limiting for ammonium assimilation into arginine. The data provided evidence that ferredoxin-glutamate synthases, NADH-glutamate synthase and carbamoylphosphate synthetase play specific physiological roles in ammonium assimilation in the mesophyll and phloem for the synthesis and transport of glutamine, glutamate, arginine, and derived amino acids. [ABSTRACT FROM AUTHOR]

Abstract: To clarify adsorption–equilibrium relationship at liquid–atmosphere interface, adsorption behavior of bisphenol-A (BPA) and diethyl phthalate (DEP) onto bubble surface was studied by using nonfoaming adsorptive bubble separation (NFBS) technique. The adsorption isotherms of BPA and DEP were obtained experimentally. The experimental results showed that adsorption equilibrium of BPA and DEP on bubble surface followed Langmuir''s adsorption isotherm. Two adsorption parameters, the adsorption equilibrium constant and the saturated adsorption density on bubble surface could be determined and were 2.04×105 cm3/g and 1.35×10−8 g/cm2 for BPA and 9.41×104 cm3/g and 1.79×10−8 g/cm2 for DEP, respectively. [Copyright &y& Elsevier]

We investigated the role of glutamine synthetases (cytosolic GS1 and chloroplast GS2) and glutamate synthases (ferredoxin-GOGAT and NADH-GOGAT) in the inorganic nitrogen assimilation and reassimilation into amino acids between bundle sheath cells and mesophyll cells for the remobilization of amino acids during the early phase of grain filling in Zea mays L. The plants responded to a light/dark cycle at the level of nitrate, ammonium and amino acids in the second leaf, upward from the primary ear, which acted as the source organ. The assimilation of ammonium issued from distinct pathways and amino acid synthesis were evaluated from the diurnal rhythms of the transcripts and the encoded enzyme activities of nitrate reductase, nitrite reductase, GS1, GS2, ferredoxin-GOGAT, NADH-GOGAT, NADH-glutamate dehydrogenase and asparagine synthetase. We discerned the specific role of the isoproteins of ferredoxin and ferredoxin:NADP+ oxidoreductase in providing ferredoxin-GOGAT with photoreduced or enzymatically reduced ferredoxin as the electron donor. The spatial distribution of ferredoxin-GOGAT supported its role in the nitrogen (re)assimilation and reallocation in bundle sheath cells and mesophyll cells of the source leaf. The diurnal nitrogen recycling within the plants took place via the specific amino acids in the phloem and xylem exudates. Taken together, we conclude that the GS1/ferredoxin-GOGAT cycle is the main pathway of inorganic nitrogen assimilation and recycling into glutamine and glutamate, and preconditions amino acid interconversion and remobilization. [ABSTRACT FROM AUTHOR]

Better preparedness for an influenza pandemic mitigates its impact. Many countries have started developing and implementing national influenza pandemic preparedness plans. However, the level of preparedness varies among countries. Developing countries encounter unique and difficult issues and challenges in preparing for a pandemic. Deaths attributable to an influenza pandemic could be substantially higher in developing countries than in industrialized countries. Pharmaceutical interventions such as vaccines and antiviral agents are less likely to be available in developing countries. The public health and clinical infrastructure of developing countries are often inadequate to deal with a widespread health crisis such as an influenza pandemic. Such an event will inevitably have a global effect. Therefore, improving pandemic preparedness in every country, particularly developing ones, is urgently needed. [ABSTRACT FROM AUTHOR]

PTEN is a tumor suppressor gene mutated in many human cancers. We generated a bronchioalveolar epithelium-specific null mutation of Pten in mice [SP-C-rtTA/(tetO)(7)-Cre/Pten(flox/flox) (SOPten(flox/flox)) mice] that was under the control of doxycycline. Ninety percent of SOPten(flox/flox) mice that received doxycycline in utero [SOPten(flox/flox)(E10-16) mice] died of hypoxia soon after birth. Surviving SOPten(flox/flox)(E10-16) mice and mice that received doxycycline postnatally [SOPten(flox/flox)(P21-27) mice] developed spontaneous lung adenocarcinomas. Urethane treatment accelerated number and size of lung tumors developing in SOPten(flox/flox) mice of both ages. Histological and biochemical examinations of the lungs of SOPten(flox/flox)(E10-16) mice revealed hyperplasia of bronchioalveolar epithelial cells and myofibroblast precursors, enlarged alveolar epithelial cells, and impaired production of surfactant proteins. Numbers of bronchioalveolar stem cells (BASCs), putative initiators of lung adenocarcinomas, were increased. Lungs of SOPten(flox/flox)(E10-16) mice showed increased expression of Spry2, which inhibits the maturation of alveolar epithelial cells. Levels of Akt, c-Myc, Bcl-2, and Shh were also elevated in SOPten(flox/flox)(E10-16) and SOPten(flox/flox)(P21-27) lungs. Furthermore, K-ras was frequently mutated in adenocarcinomas observed in SOPten(flox/flox)(P21-27) lungs. These results indicate that Pten is essential for both normal lung morphogenesis and the prevention of lung carcinogenesis, possibly because this tumor suppressor is required for BASC homeostasis. [ABSTRACT FROM AUTHOR]

The present study analyses changes in nitrogen compounds, amino acid composition, and glutamate metabolism in the resurrection plant Sporobolus stapfianus during dehydration stress. Results showed that older leaves (OL) were desiccation-sensitive whereas younger leaves (YL) were desiccation-tolerant. OL lost their soluble protein more rapidly, and to a larger extent than YL. Enzymes of primary nitrogen assimilation were affected by desiccation and the decrease in the glutamine synthetase (GS, EC 6.3.1.2) and ferredoxin-dependent GOGAT (Fd-GOGAT, EC 1.4.7.1) activities was higher in OL than in YL, thus suggesting higher sensibility to dehydration. Moreover, YL showed higher total GS enzyme activity at the end of the dehydration stress and was shown to maintain high chloroplastic GS protein content during the entire stress period. Free amino acid content increased in both YL and OL between 88% and 6% relative water content. Interestingly, OL and YL did not accumulate the same amino acids. OL accumulated large amounts of proline and γ-aminobutyrate whereas YL preferentially accumulated asparagine and arginine. It is concluded (i) that modifications in the nitrogen and amino acid metabolism during dehydration stress were different depending on leaf development and (ii) that proline and γ-aminobutyrate accumulation in S. stapfianus leaves were not essential for the acquisition of desiccation tolerance. On the contrary, the accumulation of large amounts of asparagine and arginine in the YL during dehydration could be important and serve as essential nitrogen and carbon reservoirs useful during rehydration. In this context, the role of GS for asparagine accumulation in YL is discussed. [ABSTRACT FROM PUBLISHER]

Abstract: Protein phosphatase 2Cβ (PP2Cβ) is a member of a family of protein Ser/Thr phosphatases (PP2C) that is composed of at least twelve different gene products. Recent studies have revealed that PP2Cβ mRNA accumulates in mature sperm, unfertilized metaphase II-arrested oocytes and zygotes, but that the mRNA level then decreases sharply between the early two-cell and eight-cell stages, remaining at low levels during the 16-cell to blastocyst stages of mice. These observations raised the possibility that PP2Cβ plays a crucial role during gametogenesis, fertilization, and/or early stages of embryonic development. In this study, we employed a gene knockout technique in mice to test this possibility. We found that PP2CβΔ/wt mice generate normal mature gametes. However, PP2CβΔ/Δ embryos die between the two-cell and eight-cell stages. To our interest, PP2CβΔ/Δ ES cells which had been generated by transfecting PP2Cβ3lox/3lox ES cells with Cre-expressing plasmid were viable. In addition, knockdown of PP2Cβ using siRNA did not affect the proliferation of wild-type ES cells. These observations suggest that relatively high PP2Cβ expression is specifically required during the early stages of pre-implantation development. The possible mechanisms for the early pre-implantation lethality of PP2CβΔ/Δ mice are discussed. [Copyright &y& Elsevier]

Leptin and insulin have been identified as fuel sensors acting in part through their hypothalamic receptors to inhibit food intake and stimulate energy expenditure. As their intracellular signaling converges at the PI3K pathway, we directly addressed the role of phosphatidylinositol3,4,5-trisphosphate-mediated (PIP3-mediated) signals in hypothalamic proopiomelanocortin (POMC) neurons by inactivating the gene for the PIP3 phosphatase Pten specifically in this cell type. Here we show that POMC-specific disruption of Pten resulted in hyperphagia and sexually dimorphic diet-sensitive obesity. Although leptin potently stimulated Stat3 phosphorylation in POMC neurons of POMC cell-restricted Pten knockout (PPKO) mice, it failed to significantly inhibit food intake in vivo. POMC neurons of PPKO mice showed a marked hyperpolarization and a reduction in basal firing rate due to increased ATP-sensitive potassium (KATP) channel activity. Leptin was not able to elicit electrical activity in PPKO POMC neurons, but application of the PI3K inhibitor LY294002 and the KATP blocker tolbutamide restored electrical activity and leptin-evoked firing of POMC neurons in these mice. Moreover, icv administration of tolbutamide abolished hyperphagia in PPKO mice. These data indicate that PIP3-mediated signals are critical regulators of the melanocortin system via modulation of KATP channels. [ABSTRACT FROM AUTHOR]

Glutamate (Glu) metabolism and amino acid translocation were investigated in the young and old leaves of tobacco (Nicotiana tabacum L. cv Xanthi) using [15N]ammonium and [2-15N]Glu tracers. Regardless of leaf age, [15N]ammonium assimilation occurred via glutamine synthetase (GS; EC 6.1.1.3) and Glu synthase (ferredoxin [Fd]-GOGAT; EC 1.4.7.1; NADH-GOGAT; EC 1.4.1.14), both in the light and darkness, and it did not depend on Glu dehydrogenase (GDH; EC 1.4.1.2). The [15N]ammonium and ammonium accumulation patterns support the role of GDH in the deamination of [2-15N]Glu to provide 2-oxoglutarate and [15N]ammonium. In the dark, excess [15N]ammonium was incorporated into asparagine that served as an additional detoxification molecule. The constant Glu levels in the phloem sap suggested that Glu was continuously synthesized and supplied into the phloem regardless of leaf age. Further study using transgenic tobacco lines, harboring the promoter of the GLU1 gene (encoding Arabidopsis [Arabidopsis thaliana] Fd-GOGAT) fused to a GUS reporter gene, revealed that the expression of Fd-GOGAT remained higher in young leaves compared to old leaves, and higher in the veins compared to the mesophyll. Confocal laser-scanning microscopy localized the Fd-GOGAT protein to the phloem companion cells-sieve element complex in the leaf veins. The results are consistent with a role of Fd-GOGAT in supplying Glu for the synthesis and transport of amino acids. Taken together, the data provide evidence that the GS-GOGAT pathway and GDH play distinct roles in the source-sink nitrogen cycle of tobacco leaves. [ABSTRACT FROM AUTHOR]

Abstract: Luminescent properties of GaN and AlN based semiconductors containing rare earth metals of Gd and Dy are studied. Cathodoluminescent spectra from AlGdN show a clear and sharp peak at 318nm following LO phonon satellites. Photoluminescence spectra from GaDyN by the above-gap excitation also show several peaks in addition to the broad luminescence band emission. For GaGdN, the sharp PL peaks are also observed at 650 and 670nm, and they are assigned to the intra-f orbital transitions by their time decay measurements. The broad band at around 365nm for AlGdN, 505nm for GaGdN and GaDyN are commonly observed. The origin of these broad bands is discussed. [Copyright &y& Elsevier]

Serine hydroxymethyltransferase (SHMT) is part of the mitochondrial enzyme complex catalysing the photorespiratory production of serine, ammonium and CO2 from glycine. Potato plants ( Solanum tuberosum cv. Solara) with antisensed SHMT were generated to investigate whether photorespiratory intermediates accumulated during light lead to nocturnal activation of the nitrogen-assimilating enzymes glutamine synthetase (GS) and glutamate synthase (GOGAT). The transformant lines contained 70–90% less SHMT protein, and exhibited a corresponding decrease in mitochondrial SHMT activity. SHMT antisense plants displayed lower photosynthetic capacity and accumulated glycine in light. Glycine was converted to serine in the second half of the light period, while serine, ammonium and glutamine showed an inverse diurnal rhythm and reached highest values in darkness. GS/GOGAT protein levels and activities in the transgenics also reached maximum levels in darkness. The diurnal displacement of NH4+ assimilation was accompanied by a change in the subunit composition of GS2, but not GS1. It is concluded that internal accumulation of post-photorespiratory ammonium is leading to nocturnal activation of GS/GOGAT, and that the time shift in ammonia assimilation can constitute part of a strategy to survive photorespiratory impairment. [ABSTRACT FROM AUTHOR]

In higher plants, ferredoxin (Fd):NADPH oxidoreductase (FNR) catalyzes reduction of NADP+ in the final step of linear photosynthetic electron transport and is also implicated in cyclic electron flow. We have identified three leaf FNR isoenzymes (LFNR1, LFNR2, and LFNR3) in maize (Zea mays) chloroplasts at approximately equivalent concentrations. Fractionation of chloroplasts showed that, while LFNR3 is an exclusively soluble enzyme, LFNR1 is only found at the thylakoid membrane and LFNR2 has a dual location. LFNR1 and LFNR2 were found to associate with the cytochrome b6ƒ complex following its partial purification. We cloned LFNR3 and produced all three isoenzymes as stable, soluble proteins. Measurement of Fd reduction ability showed no significant differences between these recombinant enzymes. Column chromatography revealed variation between the interaction mechanisms of LFNR1 and LFNR2 with Fd, as detected by differential dependence on specific intermolecular salt bridges and variable sensitivity of interactions to changes in pH. A comparison of LFNR transcripts in leaves of plants grown on variable nitrogen regimes revealed that LFNR1 and LFNR2 transcripts are relatively more abundant under conditions of high demand for NADPH. These results are discussed in terms of the functional differentiation of maize LFNR isoenzymes. [ABSTRACT FROM AUTHOR]

PTEN is an important tumor suppressor gene. Hereditary mutation of PTEN causes tumor-susceptibility diseases such as Cowden disease. We used the Cre-loxP system to generate an endothelial cell-specific mutation of Pten (Tie2CrePten) in mice. Tie2CrePtenflox/+ mice displayed enhanced tumorigenesis due to an increase in angiogenesis driven by vascular growth factors. This effect was partially dependent on the PI3K subunits p85α and p110γ. In vitro, Tie2CrePtenflox/+ endothelial cells showed enhanced proliferation/ migration. Tie2CrePtenflox/flox mice died before embryonic day 11.5 (E11.5) due to bleeding and cardiac failure caused by impaired recruitment of pericytes and vascular smooth muscle cells to blood vessels, and of cardiomyocytes to the endocardium. These phenotypes depend strongly on p110γ rather than on p85α and were associated with decreased expression of Ang-1, VCAM-1, connexin 40, and ephrinB2 but increased expression of Ang-2, VEGF-A, VEGFR1, and VEGFR2. Pten is thus indispensable for normal cardiovascular morphogenesis and post-natal angiogenesis, including tumor angiogenesis. [ABSTRACT FROM AUTHOR]

Pten (phosphatase with tensin homology), a dual-specificity phosphatase, is a negative regulator of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. Pten regulates a vast array of biological functions including growth, metabolism, and longevity. Although the PI3K/Akt pathway is a key determinant of the insulin-dependent increase in glucose uptake into muscle and adipose cells, the contribution of this pathway in muscle to whole-body glucose homeostasis is unclear. Here we show that muscle-specific deletion of Pten protected mice from insulin resistance and diabetes caused by high-fat feeding. Deletion of muscle Pten resulted in enhanced insulin-stimulated 2-deoxyglucose uptake and Akt phosphorylation in soleus but, sur- prisingly, not in extensor digitorum longus muscle compared to littermate controls upon high-fat feeding, and these mice were spared from developing hyperinsulinemia and islet hyperplasia. Muscle Pten may be a potential target for treatment or prevention of insulin resistance and diabetes. [ABSTRACT FROM AUTHOR]

Pten is an important phosphatase, suppressing the phosphatidylinositol-3 kinase/Akt pathway. Here, we generated adipose-specific Pten-deficient (AdipoPten-KO) mice, using newly generated Acdc promoter-driven Cre transgenic mice. AdipoPten-KO mice showed lower body and adipose tissue weights despite hyperphagia and enhanced insulin sensitivity with induced phosphorylation of Akt in adipose tissue. AdipoPten-KO mice also showed marked hyperthermia and increased energy expenditure with induced mitochondriagenesis in adipose tissue, associated with marked reduction of p53, inactivation of Rb, phosphorylation of cyclic AMP response element binding protein (CREB) and increased expression of Ppargc1a, the gene that encodes peroxisome proliferative activated receptor gamma coactivator 1 alpha. Physiologically, adipose Pten mRNA decreased with exposure to cold and increased with obesity, which were linked to the mRNA alterations of mitochondriagenesis. Our results suggest that altered expression of adipose Pten could regulate insulin sensitivity and energy expenditure. Suppression of adipose Pten may become a beneficial strategy to treat type 2 diabetes and obesity. [ABSTRACT FROM AUTHOR]

Background: Although the regenerative stem cell is expected to exist in many adult tissues, the cell contributing to the regeneration of the kidney remains unknown in its type and origin.Methods: In this study, we isolated cells that show low stain with a DNA-binding dye Hoechst 33342 (Hoechst(low) cells) from adult rat kidney, and investigated their differentiation potentials.Results: Hoechst(low) cells, generally termed side population cells, existed at a frequency of 0.03% to 0.1% in the cell suspension of the digested kidney. Analysis of the kidney-derived Hoechst(low) cells after bone marrow transplantation indicated that some of the cells were derived from bone marrow. When enhanced green fluorescent protein (EGFP)-labeled kidney-derived Hoechst(low) cells were intravenously transplanted into wild-type adult rats, EGFP(+) cells were not detected in the kidney, but EGFP(+) skeletal muscle, EGFP(+) hepatocytes and EGFP(+) bone marrow cells were observed. Even after the induction of the experimental glomerulonephritis and gentamicin-induced nephropathy that promote the differentiation of bone marrow-derived cells into repopulating mesangial cells and tubular component cells, respectively, EGFP(+) mesangial or tubular cells were not observed. Neither with an in vitro system, which we established to produce mesangial-like cells from crude bone marrow culture, did Hoechst(low) cells yield mesangial-like cells.Conclusion: These findings implicate that Hoechst(low) cells in the kidney may have potentials for hematopoietic and nonhematopoietic lineages, but are not stem cells for renal cells, especially mesangial and tubular cells. [ABSTRACT FROM AUTHOR]

Hematopoietic and nonhematopoietic potentials of Hoechstlow/side population cells isolated from adult rat kidney. Background. Although the regenerative stem cell is expected to exist in many adult tissues, the cell contributing to the regeneration of the kidney remains unknown in its type and origin. Methods. In this study, we isolated cells that show low stain with a DNA-binding dye Hoechst 33342 (Hoechstlow cells) from adult rat kidney, and investigated their differentiation potentials. Results. Hoechstlow cells, generally termed side population cells, existed at a frequency of 0.03% to 0.1% in the cell suspension of the digested kidney. Analysis of the kidney-derived Hoechstlow cells after bone marrow transplantation indicated that some of the cells were derived from bone marrow. When enhanced green fluorescent protein (EGFP)-labeled kidney-derived Hoechstlow cells were intravenously transplanted into wild-type adult rats, EGFP+ cells were not detected in the kidney, but EGFP+ skeletal muscle, EGFP+ hepatocytes and EGFP+ bone marrow cells were observed. Even after the induction of the experimental glomerulonephritis and gentamicin-induced nephropathy that promote the differentiation of bone marrow–derived cells into repopulating mesangial cells and tubular component cells, respectively, EGFP+ mesangial or tubular cells were not observed. Neither with an in vitro system, which we established to produce mesangial-like cells from crude bone marrow culture, did Hoechstlow cells yield mesangial-like cells. Conclusion. These findings implicate that Hoechstlow cells in the kidney may have potentials for hematopoietic and nonhematopoietic lineages, but are not stem cells for renal cells, especially mesangial and tubular cells. [ABSTRACT FROM AUTHOR]

Cofilin plays an essential role in actin filament dynamics and membrane protrusion in motile cells. Cofilin is inactivated by phosphorylation at Ser-3 by LIM kinase and reactivated by dephosphorylation by cofilin-phosphatase Slingshot (SSH). Although cofilin is dephosphorylated in response to various extracellular stimuli, signaling pathways regulating SSH activation and cofilin dephosphorylation have remained to be elucidated. Here we show that insulin stimulates the phosphatase activity of Slingshot-IL (SSH1L) and cofilin dephosphorylation in cultured cells, in a manner dependent on phosphoinositide 3-kinase (PI3K) activity. Consistent with this, the level of Ser-3-phosphorylated cofilin is increased in PTEN (phosphatase and tensin homolog deleted in chromosome 10)-overexpressing cells and decreased in PTEN-deficient cells. Insulin induced the accumulation of SSH1L and active Akt (a downstream effector of PI3K), together with a PI3K product phosphatidylinositol 3,4,5-trisphosphate, onto membrane protrusions. Cofilin, but not Ser-3-phosphorylated coillin, accumulated in membrane protrusions in insulinstimulated cells, indicating that cofilin is dephosphorylated in these areas. Finally, suppression of SSHIL expression by RNA interference abolished insulin-induced cofilin dephosphorylation and the membrane protrusion. These findings suggest that SSHIL is activated downstream of PI3K and plays a critical role in insulin-induced membrane protrusion by dephosphorylating and activating cofilin. [ABSTRACT FROM AUTHOR]

The genus Thecotheus is reported in Australia for the first time. A new species, Thecotheus urinamans is described and illustrated and included in a key to all known species of the genus. Critical macro- and micromorphological comparisons are presented to distinguish the new species from several closely related species, particularly the widespread fungus Thecotheus crustaceus. Thecotheus urinamans was growing on rotting, moist, plant litter from an experimental plot treated with urea (ammonia) in the indigenous jarrah (Eucalyptus marginata) forest of Western Australia. [ABSTRACT FROM AUTHOR]

Examines the role of stress-activated protein kinase/c-Jun NH[sub 2]-terminal kinase (SAPK/JNK) in stress signaling. Generation of mkk7 mouse embryonic stem (ES) cells in addition to sek1 cells; Comparison of the two kinases in terms of the activation and phosphorylation of JNK; Generation of MKK7-deficient ES cells.

Geographic variation in some aspects of chimpanzee behavior has been interpreted as evidence for culture. Here we document similar geographic variation in orangutan behaviors. Moreover, as expected under a cultural interpretation, we find a correlation between geographic distance and cultural difference, a correlation between the abundance of opportunities for social learning and the size of the local cultural repertoire, and no effect of habitat on the content of culture. Hence, great-ape cultures exist, and may have done so for at least 14 million years. [ABSTRACT FROM AUTHOR]

There are few reports concerning the sorting mechanisms of mammalian HSP60 into the mitochondria from the cytoplasm. In the present study we investigated the protein import system. Based on immunoblotting and immuno-histochemistry, HSP60 was detected in both the cytoplasm and mitochondria. The purified cytoplasmic HSP60 showed chaperone activity, and the protein was imported into the mitochondria in vitro by a mitochondrial import assay. HSP60 mRNA was increased in the kidney papilla of rats that had been water restricted for three and five days, but no changes in HSP60 mRNA were detected in the cortex or the medulla of the rat kidneys. Upon immunoblotting, HSP60 was detected in both the cytoplasm and the mitochondria of normal rat kidney cortex, medulla, and papilla in almost the same quantity. HSP60 was remarkably decreased in the kidney papilla of rats that were water restricted but the protein was increased in the mitochondria of the rat kidney papilla. We also analysed binding of the protein to the signal sequence of HSP60 using signal sequence-affinity column chromatography. We identified only one protein band with a molecular mass of 70 kDa on SDS/PAGE. The protein was eluted from the affinity column by an excess of signal peptide or by 5 mm ATP. Upon immunoblotting, the 70-kDa protein cross-reacted with an antibody against HSP70. These results suggested that mammalian HSP60 is located both in the cytoplasm as a stable cytoplasmic HSP60 and also in the mitochondria under normal conditions. The cytoplasmic HSP60 is quickly imported into the mitochondria under severe conditions by cytoplasmic HSP70. [ABSTRACT FROM AUTHOR]

We have characterized the biochemical properties of the testis and brain-specific 105-kDa protein which is cross-reacted with an anti-bovine HSP90 antibody. The protein was induced in germ cells by heat stress, resulting in a protein which is one of the heat shock proteins [Kumagai, J., Fukuda, J., Kodama, H., Murata, M., Kawamura, K., Itoh, H. & Tanaka, T. (2000) Eur. J. Biochem. 267 , 3073–3078]. In the present study, we characterized the biochemical properties of the protein. The 105-kDa protein inhibited the aggregation of citrate synthase as a molecular chaperone in vitro . ATP/MgCl2 has a slight influence of the suppression of the citrate synthase aggregation by the 105-kDa protein. The protein possessed chaperone activity. The protein was able to bind to ATP–Sepharose like the other molecular chaperone HSP70. A partial amino-acid sequence (24 amino-acid residues) of the protein was determined and coincided with those of the mouse testis- and brain-specific APG-1 and osmotic stress protein 94 (OSP94). The 105-kDa protein was detected only in the medulla of the rat kidney sections similar to OSP94 upon immunoblotting. The purified 105-kDa protein was cross-reacted with an antibody against APG-1. These results suggested that APG-1 and OSP94 are both identical to the 105-kDa protein. There were highly homologous regions between the 105-kDa protein/APG-1/OSP94 and HSP90. The region of HSP90 was also an immunoreactive site. An anti-bovine HSP90 antibody may cross-react with the 105-kDa protein similar to HSP90 in the rat testis and brain. We have investigated the localization and developmental induction of the protein in the rat brain. In the immunohistochemical analysis, the protein was mainly detected in the cytoplasm of the nerve and glial cells of the rat brain. Although the 105-kDa protein was localized in all rat brain segments, the expression pattern was fast in the cerebral cortex and hippocampus and slow in the cerebellum. [ABSTRACT FROM AUTHOR]

Investigates the regulation of myocardial contractility and cell size by signaling pathways. Decline of cardiac contractility following inactivation of tumor suppressor P13K-PTEN; Effects of G protein subunits on heart contraction; Regulator of decreased contractility in dilated cardiomyocytes.

Neural stem and precursor cells reside in the ventricular lining of the fetal forebrain, and may provide a cellular substrate for brain repair. To selectively identify and extract these cells, we infected dissociated fetal human brain cells with adenoviruses bearing the gene for green fluorescence protein (GFP), placed under the control of enhancer/promoters for two genes (nestin and musashi1) that are expressed in uncommitted neuroepithelial cells. The cells were then sorted by fluorescence-activated cell sorting (FACS) on the basis of E/nestin- or P/musashi1-driven GFP expression. Both P/musashi1:hGFP- and E/nestin:EGFP-sorted cells were multipotent: limiting dilution with clonal expansion as neurospheres, in tandem with retroviral lineage analysis and xenograft to E17 and P0-2 rat forebrain, revealed that each phenotype was able to both self-renew and co-generate neurons and glia. Thus, fluorescent genes placed under the control of early neural promoters allow neural stem cells to be specifically targeted, isolated, and substantially enriched from the fetal human brain. [ABSTRACT FROM AUTHOR]

Reports that genetic inactivation of the p110-gamma catalytic subunit of phosphoinositide-3-OH kinase (PI(3)Ks) leads to development of invasive colorectal adenocarcinomas in mice. Role of the subunit in tumorigenesis; Finding that p110-gamma can block the growth of human colon cancer cells.

Presents information on a study which demonstrated how phosphoinositide 3-kinases (P13K) gamma control thymocyte survival and activation of mature T cells but has no role in the development or function of B cells. Cellular responses that P13K regulate; Definition of the physiological roles of P13K gamma; Conclusion.

Investigates the carbonylative cross-coupling reaction of arylboronic acids with aryl electrophiles, in the presence of a palladium catalyst and a base. Identification of arylmetal reagents which have undergone the carbonylative coupling; Previous studies on the palladium-catalyzed cross-coupling reaction of organoboron compounds with organic electrophiles; Examination of the reaction of phenylboronic acid.

Incubation of wild-type ferredoxin (Fd) with Chlamydomonas reinhardii crude extract in the presence of a carboxyl activator resulted in the formation of a unique 1:1 covalent complex with nitrite reductase. However, glutamate synthase was able to form two covalent complexes of Fd: GOGAT with 1:1 and 2:1 stoichiometries. These complexes were functional only when reduced methyl viologen was used as electron donor. Kinetic studies of complex formation suggested the presence of two Fd-binding domains with similar affinity for Fd in the glutamate synthase molecule. Using site-directed mutagenesis with recombinant Fd. we have shown that Fd-Glu91 is directly involved in Fd interaction with glutamate synthase and nitrite reductase. Moreover, a negative core of residues in the α1 helix of Fd was also critical in binding the enzymes. These data highlight the analogy in the Fd-binding sites of nitrite reductase and glutamate synthase, which may compete for the electrons coming from the photosynthetic chain. [ABSTRACT FROM AUTHOR]

Presents a study which examine the bifurcation in 20-GHz gain-switched 1.55-...m multiple-quantum-well (MQW) lasers and its control by injection seeding. Small gain compression factor of MQW laser; Details on the experiments conducted to examine game switching; Information on a rate-equation analysis which was conducted; Results of this study.

The article reports on the results of a study of inter-subspecies hybrid dikaryons of oyster mushroom independently isolated in Vietnam and Japan. A description of the experimental set-up and measurement methods is presented. The study concluded that the asexual reproduction might allow stable maintenance of a particular pair of nuclei.

Business continuity plans (BCPs) can be effective and proactive countermeasures to respond flexibly to crises caused by unexpected natural disasters such as large tsunamis. BCP guidelines for fisheries are being issued by the Fisheries Agency (Japan) and the utilization of such BCPs has been spreading in Japan. Despite the need to promote the social implementation of BCPs in the fisheries industry, there is a lack of quantitative criteria for the tsunami damage threshold of various fishing ports and facilities. In this research, we surveyed the damage to the fishing facilities from the tsunami generated by the 2011 Tohoku-oki earthquake. Data were collected on the tsunami damage for various fishery facilities and used to establish criteria for tsunami damage thresholds. In addition, tsunami damage inferred from 1506 scenarios of tsunami computations was predicted probabilistically for a model region as the Nachi Katsu'ura Fishery Port in Wakayama Prefecture. The method we developed in this research makes it possible to assess the probabilistic tsunami damage by combining a tsunami hazard assessment method with criteria for damage occurrence for fishery port facilities and equipment. [ABSTRACT FROM AUTHOR]