Later, such large unstable chromosomal

find more regions were designated pathogenicity islands (PAIs) [2–4]. A constantly increasing number of similar genetic elements detected in many pathogenic and non-pathogenic microorganisms led to the definition of a family of related genetic elements, termed genomic islands (GEIs), whose members share characteristic features [5–7]. Although PAIs, a subgroup of GEIs, are in several cases superficially similar, they structurally differ with respect to the encoded virulence factors, the size and the presence of different mobile and ARN-509 accessory elements. Due to the presence of mobility genes (integrases, transposases, IS elements) or the occurrence of recombination processes or point mutations, PAIs constantly undergo structural changes [4, 8–12]. Upon acquisition and chromosomal insertion, islands together with additional large regions of flanking chromosomal sequence context can be transferred by conjugation and homologous recombination and thus contribute to genome plasticity and the simultaneous transfer of multiple traits [13]. Nevertheless, PAIs are in many cases not stably integrated into the E. coli host chromosome and may be lost upon deletion. This process can be studied by island probing [10, 14–16]. The influence of different environmental conditions on the stability www.selleckchem.com/products/lgk-974.html of five PAIs of UPEC strain 536 has already been investigated before

[17] indicating that PAI I536, PAI II536, PAI III536, and PAI V536 delete with frequencies between 10-5 and 10-6, while loss of PAI IV536 could not be detected. In UPEC strain 536, PAI deletion is catalyzed by a P4-like

bacteriophage integrase which is encoded on the respective island [18]. Similar deletion frequencies (10-5 – 10-6) were also reported for PAIs of REPEC strain 84/110-1 and S. flexneri 2a [12, 19]. Higher deletion frequencies (10-3 – 10-4) have, Adenosine however, been observed for O-islands 43 and 48 in enterohemorrhagic E. coli (EHEC) O157:H7 isolates [14]. Circular intermediate (CI) formation in the cytoplasm of UPEC strain 536 was demonstrated for PAI II536 and PAI III536. Since none of these two islands apparently contain an origin of replication, it has been hypothesized that CIs are lost upon cell division unless they reintegrate into the chromosome. Furthermore, horizontal gene transfer (HGT) of such circularized PAIs may occur with the help of bacteriophages or conjugative plasmids [17]. A close functional association between PAIs and bacteriophages was reported for several bacterial pathogens. In V. cholerae, the entire 39.5-kb Vibrio Pathogenicity Island (VPI) can be transfered by the general transducing phage CP-T1 [20]. The “”high pathogenicity island (HPI)”" of Yersinia pseudotuberculosis has been shown to be transfered by a bacteriophage [21]. The so-called Staphylococcus aureus pathogenicity islands (SaPIs) can excise and replicate upon induction by other resident S.

Six of the Htrs were predicted to contain no transmembrane domain and are assumed to recognize intracellular signals. The other Htrs contain two or more transmembrane helices and recognize signals at the membrane or extracellularly. The function of only eight Htrs has been assigned to-date (Table 2). Table 2 The halobacterial transducers as preys Htr Gene Name Signal TM A Y W1 W2 R 1 OE3347F HtrI Orange light (A), Batimastat UV light (R) [35–37] 2 ∙ ∙ ∙ ∙   2 OE3481R HtrII Blue light (R), Ser (A) [38, 39] 2 ∙ ∙ ∙ ∙   3 OE3611R BasT Leu, Ile, Val, Met, Cys (A) [33] 2 ∙ ∙ ∙ ∙   4 OE2189R Htr4   2 ∙ ∙ ∙ ∙   5 OE3474R CosT Compatible

osmolytes (A) [34] 2 ∙ ∙ ∙ ∙   6 OE2168R Htr6   2 ∙ ∙ ∙ ∙   8 OE3167F HtrVIII O 2 (A) [40] 6 ∙ ∙ ∙ ∙   14 OE1536R MpcT ΔΨ (A) [41] 2 ∙ ∙ ∙     17 OE3436R Htr17   3 ∙ ∙       18 OE2195F Htr18   2 (∙) ∙       16 OE1929R Htr16   2 ∙         15 OE2392R Htr15   0   ∙ ∙ ∙   11 OE5243F Car Arg (A) [42] 0       ∙   13 OE2474R Htr13   0     ∙ ∙   12 OE3070R Htr12   0         ∙ 7 OE3473F Htr7   3           9 OE2996R Htr9   0           10 OE3150R HemAT O 2 (R) [43] 0           Transducers were grouped according to their interaction patterns.

Signal indicates attractant (A) or EPZ015666 order repellent (R) signal for the respective transducer where known. TM is the number of predicted transmembrane helices. The columns A, Y, W1, W2 and R indicate whether SBI-0206965 cell line the transducer was identified as interaction partner CheA, CheY, CheW1, CheW2 or CheR, respectively. () Htr18 was not identified with the bait CheA but its putatively associated protein OE2196F. While the confirmed processes in Hbt.salinarum taxis signaling have already led to modeling of motor switching and signal processing [44–47], the understanding on a molecular level is still far from complete. For example, it is still unknown why Hbt.salinarum possesses more than one homologue of CheW, CheC and CheF. The function of CheD and the CheC proteins, which build one of the three adaptation systems in B.subtilis[48], is unclear in Hbt.salinarum. The mechanism of action of the switch factor fumarate, which was discovered in Hbt.salinarum 20 years before ago [49, 50], is also unresolved. Because classical

approaches to define function, for example deletion mutant analysis, are not always conclusive, we set out to investigate the taxis signal transduction system of Hbt.salinarum by protein interaction analysis. In the course of this study, we identified and characterized the archaeal chemotaxis protein family CheF that connects the bacterial-like taxis signaling system to the archaeal flagellar apparatus [10]. Here we report the interaction network of the Hbt.salinarum taxis signaling proteins which presents new knowledge about established Che proteins and identifies connections to proteins that were not known to be linked to taxis signal transduction. Results and Discussion Protein-protein interaction analysis in Hbt.salinarum Like all halophilic archaea, Hbt.

Figure 2 Comparison of phylogenetic trees constructed from core and panCB genes. Maximum-likelihood phylogenetic trees of 16 Rhizobiales constructed using the concatenated nucleic acid sequences of 10 housekeeping genes (a) or panC and panB concatenated genes (b). Bootstrap values are

shown over each branch (based on 100 pseudo-replicates). The panCB genes do not fully complement the growth deficiency of a R. etli CFN42 p42f cured derivative in MM It was reported previously that R. etli CFNX186, a Pexidartinib nmr p42f-cured derivative of R. etli CFN42, is unable to grow in MM [18]. To assess if the growth deficiency of strain CFNX186 in MM was due to the absence of the panC and panB genes, plasmid pTV4 (panCB) was introduced into strain CFNX186. The growth of the transconjugant (CFNX186-4) after 15 hours of culture in MM was only 50% that of the WT strain FK228 datasheet grown under the same conditions (Figure 3a). The growth of selleck chemical CFNX186-4 did not improve even after 72 h in culture (data not shown). Interestingly, strain CFNX186-4 had the same growth rate as strain CFNX186 cultured in MM supplemented with 1 μM calcium pantothenate (Figure 3b). This shows that the growth deficiency of CFNX186 is only partly due to the absence of the panCB genes and indicates that other functions encoded in plasmid

p42f are required for growth in MM. Figure 3 panCB genes do not fully restore the growth deficiency of CFNX186. Growth of R. etli CFN42 wild-type strain, its p42f-cured derivative CFNX186, CFNX186 complemented with the panCB genes (CFNX186-4) and CFNX186 complemented with a 20 kb EcoRI fragment of plasmid p42f containing the panC, panB, oxyR and katG genes (CFNX186-24) in: (a) minimal medium, (b) minimal medium supplemented with 1 μM pantothenate. Growth curves are the mean of at least three independent experiments; error bars represent standard deviations. Previous studies have demonstrated that the katG gene, which encodes else the sole catalase-peroxidase

expressed in free-living growth conditions, is located on plasmid p42f of R. etli CFN42. These studies also revealed that the growth rate of a katG mutant in MM was significantly reduced in comparison with that of the wild-type parental strain [19]. On plasmid p42f katG, as well as its putative transcriptional regulator protein encoded by oxyR, are located 80 bp downstream of the panCB genes. We speculated that introduction of the panCB genes together with the katG and oxyR genes might improve the growth of CFNX186 in MM. To test this hypothesis, we used pCos24, which contains a 20 kb fragment of p42f carrying panCB, katG and oxyR (see Material and Methods). pCos24 was introduced into CFNX186 and the resulting transconjugant (CFNX186-24) grown in MM. Figure 3 shows that after 15 hours of culture there was no significant difference between the growth rate of CFNX186 complemented only with panCB (CFNX183-4), and CFNX186 complemented with cosmid pCos24 (CFNX186-24).

OVK, PDM, RCD, and DS aided in sample processing for proteomic analysis. PE and OVK performed MS runs. VS performed statistical analysis on MS data. All authors read and approved the final manuscript.”
“Background WZB117 ic50 Pseudomonas aeruginosa is a versatile Gram-negative bacterium, able to metabolise multiple carbon sources and exploit diverse ecological niches, e.g. soil, water, plants and animal hosts [1, 2]. This opportunistic pathogen causes a range of human infections, including acute infections

of severe wounds [3] and burns [4, 5] and chronic lung infections in cystic fibrosis (CF) patients [6]. P. aeruginosa forms biofilms in the CF lung that are highly resistant to antibiotics and clearance by the immune system [7]. Once established, such biofilms cannot be eradicated and are associated with greatly increased morbidity and mortality [8]. Several CF-associated transmissible selleck chemicals strains of P. aeruginosa, capable of between patient transmission, have been identified in the UK, Europe, Australia and North America [9]. The Liverpool Epidemic Strain (LES), a UK transmissible strain, was first isolated in 1996 at Alder Hey Children’s Hospital (AHCH), Liverpool [10]. This strain is capable of super-infection, supplanting pre-existing P. aeruginosa populations in the CF lung [11]. Chronic infection with LES is associated with increased morbidity and

mortality compared to other P. aeruginosa strains [12]. The LES is highly prevalent within individual hospital CF units [13] and is the most abundant selleck products P. aeruginosa strain amongst CF patients in the UK [14]. It was also recently isolated from the sputa of CF patients in North America [15]. Sequencing of the earliest LES isolate, LESB58, demonstrated that the genome shares 95% similarity

with the lab strain PAO1. However, its core genome is punctuated by multiple norfloxacin-inducible prophages [16]. Specifically, there are five inducible prophage genomes (LESφ2; LESφ3 LESφ4 LESφ5 and LESφ6) that are mosaic in nature. The gene organisation of LESφ2 and LESφ3 resembles that of lambdoid phages. These two phage genomes share 82.2% PD184352 (CI-1040) identity across a 13.6-kb region at their 3’ ends that makes up 32% of the phage genomes. The closest known relative to both these phages is the Pseudomonas phage F10 [17]. LESφ3 also contains a 7.5 kb region that shares 99.8% homology with LESφ5, which exhibits a considerable sequence similarity to the O-antigen converting phage D3 [18]. LESφ4 is a transposable Mu-like phage that closely resembles phage D3112 [19]. The LESφ6 sequence resembles a pf1-like filamentous phage [16]. Temperate phages have been shown to confer selective, beneficial traits to a range of P. aeruginosa hosts [20]. For example, phage D3 orchestrates O antigen conversion from O5 to O16 in PAO1, which may aid evasion of the immune system and resistance to phage superinfection [18, 21].

Other ‘international’ health-economic studies in the field of osteoporosis followed a similar approach: in these studies, the effect of fractures on quality of life was not based on country-specific sources; whereas for the costs, country-specific data were available [56–59]. Conclusions Our study shows that, especially for France and Sweden, the societal burden of hip fractures associated with low calcium

Fedratinib research buy intake is quite substantial. Improving the dairy consumption is likely to be effective in decreasing this public health burden and the associated health care expenditures. Our findings support the use of a food-based approach to help maintain bone health or prevent age-related bone loss. This is in line with the position of the French Agency for the Safety MAPK Inhibitor Library concentration of Health Products (AFSSAPS) which recommends to correct calcium and/or vitamin D deficiencies before prescribing anti-osteoporotic drugs [60]. It would be worth performing a cost-effectiveness analysis of a community-based educational health campaign. Behavioral changes, especially related to diet and exercise, form the backbone of public health recommendations for the prevention and treatment of osteoporosis [61], are supported by several RCTs [62, 63] and meta-analyses [50, 64, 65]. Yet, the cost-effectiveness of such recommendations remains largely unexplored. Our model had to rely on the existing figures that do not take into

account the long-term advantages of prevention, mainly focusing on the senior population C1GALT1 where bone density is already affected and where dietary interventions will complete the clinical management of diagnosed osteoporosis [66]. Yet, it is no less important to focus on younger people as well, because eating practices established in childhood are likely to be

maintained throughout life, and an adequate calcium intake during childhood and adolescence, necessary for the development of peak bone mass, may contribute to bone strength and reduce the risk of osteoporosis and fractures later in life [67, 68]. Although the methods may be further refined, this model appears to be a solid and straightforward, easy-to-use method to assess the health, well-being and cost outcomes of food products from a health economics perspective. Acknowledgements We thank Dr. Nelly Ziadé (APEMA, Paris, France) for providing us more specific data on the mortality rates for France and Dr. Marga Ocké (RIVM, The Netherlands) who provided us detailed data on calcium intake in the general Dutch population. Furthermore, we would like to thank Dr. Östen Ljunggren (Sweden) for his see more constructive remarks on an earlier version of the manuscript. Funding This research was supported by an unrestricted grant from Danone Research. No information used in preparation of this manuscript was owned by the sponsor. First and second authors contributed equally to the manuscript. Conflicts of interest None.

microplus in China [58]. Detection of the

Screening Library in vitro R. microplus -associated Cytoskeletal Signaling inhibitor Borrelia in the gut and ovary reported here parallels the systemic infection with B. theileri where no adverse effects were observed in tick viability [33, 59]. Like the Borrelia DNA sequences detected in this study, specific identification awaits for other Borrelia microbes isolated from R. microplus in diverse geographic locations [60–62]. However, R. microplus may be acting as a bridging vector facilitating the transmission of microbes across vertebrate hosts and possibly influencing ecological and evolutionary aspects of their natural history. The degree of similarity at the nucleotide level between a Mexican isolate of B. theileri and Borrelia spp. infecting A. americanum from the Northeast region of the USA suggests recent divergence [63]. Because white-tailed deer and cattle used to be sympatric throughout the southern USA prior to 1943, which is when cattle ticks were officially eradicated, it has been hypothesized that spirochetes infecting A. americanum may represent a host shift of B. theileri as R. microplus could have transmitted the spirochete to both ungulate hosts [64]. A Borrelia spp. detected in R. microplus from

Brazil was shown to be closely related to B. theileri and Borrelia lonestari and the cattle tick-deer relationship was suggested as a natural process for the spread and/or maintenance of Borrelia spp. [65]. Although bacteria in the genus Wolbachia are generally found in reproductive tissues, the R. microplus -associated Wolbachia Epigenetics inhibitor was not detected in ovarian tissue, but in the two adult female ticks assayed individually. Since ticks from a laboratory colony established in 1999 were the source of the ovarian tissue samples, it is plausible that Ribose-5-phosphate isomerase Wolbachia infection was lost during the colonization process. It is also possible that laboratory rearing conditions allowed the Coxiella strain in the R. microplus ovaries sampled to out-compete pre-existing Wolbachia microbes with the eventual loss of infection in La Minita strain. Detection of the Wolbachia- type microbe in adult female ticks does not necessarily

mean that the ovary was the only tissue infected. Disseminated Wolbachia infection has been documented in other arthropod vector species and similar events were reported for a Coxiella endosymbiont infecting A. americanum where the salivary glands were also infected [50, 66]. The possibility for horizontal transmission would exist if Wolbachia infection of the R. microplus salivary glands were to occur. The horizontal transmission of Wolbachia microbes has been documented to occur more often than previously thought [67–69]. However, it has been shown in mosquitoes that the size of Wolbachia symbionts would prevent its free passage through the salivary ducts [70]. The functional relevance of our findings and observations needs to be tested.

Participants initially this website performed a 1RM for squat, dead lift, and barbell lunge exercises. On the second visit, subjects

performed four sets of at least 10 repetitions at 80% of their 1RM for the exercises with 90 seconds between sets. On visits three (24 hours from visit two) and four (48 hours from visit two), participants performed four sets of squats with the previous weight and performed as many repetitions per set as possible [32]. Hoffman et al. [32] found that the group receiving the proprietary protein blend performed significantly more repetitions at visits three and four than did subjects receiving the placebo. These findings provide evidence that protein supplementation pre- and post-workout is useful in maximizing weight-training performance, as well as in hastening exercise recovery 24 and 48 hours post-exercise. Timing of supplementation in relation to the resistance workout also has been studied [33]. Cribb et al. assigned 23 male bodybuilders to one of two groups: those who received a supplement a) before and after a workout, or b) in the morning and evening. The supplement contained 40 g protein (from whey isolate), 43 g carbohydrate

(glucose), and seven g creatine monohydrate per 100 g. Each participant was given the supplement in quantities selleck chemical of 1.0 g.kg-1 body weight. All participants followed a preliminary resistance weight-training program for 8–12 weeks before baseline measurements were taken. Participants then started the 10-week resistance weight-training session which was divided into three distinct stages: preparatory (70–75% 1RM), overload

phase 1 (80–85%1RM), and overload phase 2 (90–95% 1RM) [33]. Results indicated significant differences in body composition in the group consuming the supplement pre- and post-workout [33]. This group experienced increased LBM and decreased body fat. Both groups demonstrated increases in strength, but the pre- and post-workout group demonstrated significantly greater gains [33], indicating that timing of the ingestion of the protein supplement was crucial. This is contradictory Erythromycin to the findings of Hoffman et al. [31] with respect to changes in body composition. This could be because Cribb et al. [33] used a supplement that was a combination of protein, carbohydrate and creatine whereas, Hoffman et al. [31] supplemented with protein only. The major finding of this study was that after 10 weeks of training, supplementation pre/post each workout resulted in greater improvements in 1RM strength and body composition (increased LBM and decreased body fat percentage) compared with a matched group who consumed supplement in the morning and evening, outside of the pre- and post-workout time frames.

], CDC United States, Public Health Service, Office of the Surgeon General (2006) The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Rockville, MD, U.S. Dept. of Health and Human Services, Public Health Service, Office of the Surgeon General Veglia F, Matullo G et al (2003) Bulky DNA adducts and risk of cancer: a meta-analysis. Cancer Epidemiol Biomarkers Prev 12:157–160 Vulimiri SV, Wu X et al (2000) Analysis

Selleck JNK-IN-8 of aromatic DNA adducts and 7, 8-dihydro-8-oxo-2′ deoxyguanosine in lymphocyte DNA from a case-control study of lung cancer involving minority populations. Mol Carcinog 27:330CrossRef Wang S, Chanock S et al (2008) Assessment of interactions between PAH exposure and genetic polymorphisms on PAH-DNA adducts in African American, Dominican, and Caucasian mothers and newborns. Cancer Epidemiol Biomarkers Prev 17:405–413CrossRef Weiserbs KF, Jacobson JS et al (2003) A cross-sectional study of polycyclic aromatic hydrocarbon-DNA adducts and polymorphism of glutathione S-transferases among heavy smokers by race/ethnicity. Biomarkers 8:142–155CrossRef Whyatt RM, Perera FP et al (2000) Association between polycyclic aromatic hydrocarbon-DNA adduct levels in maternal and newborn white blood cells and glutathione S-transferase P1 and CYP1A1 polymorphisms.

Cancer Epidemiol Biomarkers Prev 9:207–212 https://www.selleckchem.com/products/pha-848125.html Whyatt RM, Jedrychowski W et al (2001) Biomarkers of polycyclic aromatic hydrocarbon-DNA damage and cigarette smoke exposures in paired maternal and newborn blood samples as a measure of differential susceptibility. Cancer Epidemiol Biomarkers Prev 10:581–588 Wiencke JK, Thurston SW et al (1999) Early age at smoking initiation and tobacco carcinogen DNA damage in the lung. J Natl Cancer Inst 91:614–619CrossRef Wilson SE, Kahn RS et al (2005) Racial differences in exposure to environmental tobacco smoke among children. Environ Health Perspect 113:362–367CrossRef Wilson SE, Kahn RS et al (2007) The role of air nicotine in explaining racial differences in cotinine among tobacco-exposed

children. Chest 131:856–862CrossRef Yolton K, Khoury J et al (2008) Environmental tobacco smoke exposure and child behaviors. J Dev Behav Pediatr 29:450–457CrossRef”
“Introduction Common mental disorders (i.e., mild to moderate depressive and anxiety disorders, Stansfeld and Candy 2006) at workplaces Liothyronine Sodium have imposed economic and social burdens on the whole society as leading factors of increasing sickness absence and disability cost in Western industrialized countries (Beck and Koenig 1996; Houtman 2005; NIOSH 2004; Schaufeli and Kompier 2001). Adverse psychosocial work characteristics such as low job control, high job demands, and low social support at work have been reported as risk factors for poor mental health in several longitudinal epidemiological studies (Bültmann et al. 2002; Marchand et al. 2005; Niedhammer et al. 1998; Stansfeld et al. 1998, 1999; Wang and Pattern 2004).

Data are means ± SD of 3 independent experiments. *P < 0.05; ΔlytSR vs. WT; ΔlytSR(pNS-lytSR) vs. ΔlytSR(pNS-lytSR). We further examined cell viability inside biofilm of 1457ΔlytSR and the wild-type strain by using a fluorescence-based Live/Dead staining method. With an appropriate mixture (1:1, m/m) of the SYTO 9 (green) and PI (red), bacteria with intact cell membranes were stained fluorescent green, whereas bacteria with damaged membranes were stained fluorescent red. Significantly decreased level of red fluorescence was observed inside biofilm of 1457ΔlytSR, comparing with that inside biofilm of the wild-type

strain, as shown in Figure 8. Complementation of 1457ΔlytSR with plasmid pNS-lytSR restored the level of red fluorescence to that observed inside biofilm of the wild-type strain (Figure 8C, D). A quantitative method based on measuring the red/green fluorescence ratio AZD4547 was 4SC-202 price carried out to determine the relative cell viability inside biofilm. The percentage of dead cells inside 24-hour-old biofilms of 1457ΔlytSR

and the wild-type strain were 6% and 15% respectively, as shown in Figure 9. Inside the biofilm of lytSR complementation strain, the percentage of dead cells was restored nearly to the wild-type level. Figure 8 Confocal photomicrographs of 24-hour-old biofilms. Biofilms containing S. epidermidis 1457 strains wild-type (A), ΔlytSR (B), ΔlytSR(pNS-lytSR) (C) and ΔlytSR(pNS) (D) were visualized by using the

live/dead viability stain (SYTO9/PI). Green fluorescent cells are viable, whereas red fluorescent cells have a compromised cell membrane, as indicative of dead cells. Scale bars = 5 μm. The result is a stack of images at approximately 0.3 μm depth increments and represents one of the three experiments. Figure 9 Quantitative analysis of bacteria Baf-A1 order cell death in 24-hour-old biofilms. Live/dead stained biofilm cells were scraped from the dish and dispersed by pipetting. The integrated intensities of the green (535 nm) and red (625 nm) emission of suspensions excited at 485 nm were measured and the green/red fluorescence ratios (RatioR/G) were calculated. The percentage of dead cells inside biofilm was determined by comparison to the standard curve of RatioR/G versus percentage of dead cells. Data are means ± SEM of 3 independent experiments. *P < 0.05; ΔlytSR vs. WT; ΔlytSR(pNS-lytSR) vs. ΔlytSR(pNS-lytSR). Transcriptional profiling of 1457ΔlytSR strain To investigate the regulatory role of LytSR, we used custom-made S. epidermidis GeneChips to perform a transcriptional profile analysis of the wild type and 1457ΔlytSR strains. Two criteria including 2-fold or greater change in expression level and P < 0.05 were employed to select the genes with significantly different expression. It was found that expression of 164 genes was affected by lytSR mutation, in which 123 were upregulated and 41 were downregulated.

Int J Sustain High Educ 7(3):226–251CrossRef Youth Encounter on Sustainability (YES) Home page at: http://​www.​sustainability.​ethz.​ch”
“Sustainable development and academia In April 1989, I became president of the University of Tokyo and served in that capacity for 4 years. During my tenure, I argued that universities must be centers of scholarship that contribute to the sum total of human wisdom on a level that transcends disciplinary distinctions, such as between science and the humanities.

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In 1995, the Japanese government implemented the Basic Law on Science and Technology and followed up in 1996 with the Science and Technology Basic Plan. This plan, which is revised every 5 years, has helped spur check details a dramatic increase in competitive funding and other outlays for science and technology research. Even so, research and education in Japan still face many problems. First of all, funding for the humanities and social sciences is far too meager. If we are to contribute to the advancement of humanity, we must encourage the balanced development of both the hard sciences and the humanities, for which the latter area in particular requires more investment. Second, funding remains woefully insufficient for education on all levels—primary, secondary, and higher. From the standpoint of long-term policy for our nation, substantive improvement in this area should be a major priority for Japan. The University of Tokyo, like other universities, has recently seen criticism

aimed at the ‘reductionist’ fragmentation of academic disciplines, with many voices calling for a merging of the sciences and humanities. While I strongly advocate balanced development in both areas, I personally consider it impossible for any one individual to master the entire spectrum of knowledge. Rebamipide Therefore, I think it is unrealistic to expect all students and researchers to gain a comprehensive knowledge of both the sciences and humanities. What I do hope is that scholars in either area will acquire a certain degree of familiarity with the other. At universities, this can be achieved by requiring a minor as well as a major of students. For this same reason, is it not unrealistic to envision a generation of sustainable development ‘specialists’ whose perspective simultaneously encompasses the entire field? What research for sustainable development demands is, if anything, increasingly specialized work by experts in such fields as energy, food, and water; however, they must also be capable of collaborating in the overall effort to solve global environmental problems.