To address this question, we evaluated the ability of worms to control bacterial accumulation as a functional selleck marker of intestinal immunity. We considered the effect on longevity of the bacterial species used as nutrient source, as well as host age and host genotype. We studied genes directly related to intestinal immunity and those that are not known to be related. We found a strong inverse relationship between intestinal

bacterial accumulation and C. elegans longevity, operating across a range of host genotypes. These results suggest that intestinal (commensal) bacterial load is an age and host genotype-related phenotype that can be used to predict C. elegans lifespan. By analysis of mutants, Ku-0059436 solubility dmso we begin to establish a hierarchy of the host immune genes that have greatest effect on the intestinal milieu, and thus on longevity. Figure 1 Signaling pathways

important for C. elegans intestinal defenses against bacterial proliferation. A. DAF-2 insulin/IGF-I like signaling pathway. Activation of the DAF-2 receptor results in the phosphorylation of the phosphatidyl inositol 3 kinase (AGE-1) which catalyses the conversion of phosphatidylinositol biphosphate (PiP2) into phosphatidylinositol triphosphate (PiP3). The kinases PDK-1 and AKT-1/AKT-2 are activated by PiP3, which inhibits the transcription factor DAF-16. Relief of this inhibition leads to the expression of a set of stress response and antimicrobial genes. B. p38 MAPK pathway. PMK-1 is homologous to the mammalian p38 MAPK and acts downstream of NSY-1/MAKK kinase kinase and SEK-1/MAPK kinase. No interaction between TOL-1 and TIR-1 has been demonstrated. C. TGF-β pathway. The TGF-β homologue DBL-1 binds to the heterodimeric receptor SMA-6/DAF-4 and signals through the Smad proteins SMA-2, SMA-3 and SMA-4, which activate the transcription of genes involved

in regulation of body size and innate immunity. The expression of lysozyme gene lys-1 is under the control of the p38 MAPK pathway and the DBL-1/TGF-β pathway. D. Mitochondrial enzymes. CLK-1 Avelestat (AZD9668) is an enzyme required for the biosynthesis of ubiquinoe CoQ9, an acceptor of electrons from both complexes I and II in C. elegans cells. Decreased complex I-dependent respiration of clk-1 mutants leads to decreased ROS production with lengthening lifespan and slowing development. TRX-1 is a mitochondrial oxidoreductase with important roles in lifespan regulation and oxidative stress response. Results Role of DAF-2 insulin-signaling pathway on C. elegans lifespan Under typical laboratory conditions at 25°C on NGM agar plates with a lawn of E. coli strain OP50, a culture of wild type (N2) C. elegans has a lifespan of ~ 2 weeks [20]. Lifespans are shorter when lawns are composed of bacteria that are more pathogenic for humans [21]; conversely, host mutations that increase resistance to bacterial infection prolong C. elegans lifespan [22].

The laser sources used in the early-stage research were excimer lasers

with pulse duration of tens of nanosecond (ns). Recently, Tsai et al. deposited CIGS thin films utilizing the femtosecond (fs) mode-locked CB-839 Ti:sapphire laser rather than the excimer laser [10]. The annealing effects on the crystallization, microstructure, surface composition, and photoelectrical property of CIGS films were reported. Comparisons of the growth mechanisms of PLD processes with different laser sources are crucial to understand the characteristics of high-quality CIGS thin films. However, the effect of laser sources on characteristics and growth mechanism of PLD CIGS thin films has not been investigated yet. In this study, the PLD CIGS thin films prepared by ns excimer laser and fs Ti:sapphire laser are compared to delineate the intimate correlations between the film growth mechanism and the associated plasma dynamics. Surface morphologies and grain structures were examined by scanning electron microscope (SEM). The crystalline structures and elemental distributions were

analyzed by CAL-101 order X-ray diffraction (XRD) spectrum and energy dispersive spectrum (EDS). The reflectance of the PLD CIGS films was measured by UV-visible-near infrared (NIR) spectrophotometer. In addition, defects and their effect on carrier dynamics were measured and investigated by photoluminescence (PL) and fs pump-probe spectroscopy. Methods Growth of PLD CIGS thin films The laser sources used in this experiment were KrF excimer laser (wavelength = 248 nm, pulse width = 20 ns, fluence approximately 10 J/cm2, pulse repetition rate = 10 Hz) and Ti:sapphire mode-locked laser (wavelength = 800 nm, pulse width = 100 fs, fluence approximately Urocanase 1 J/cm2, pulse repetition rate = 5,000 Hz), which were for ns-PLD and fs-PLD growth, respectively. The CIGS thin

films were deposited on soda-lime glass (SLG) substrates in a vacuum chamber. The background pressure was kept at 4 × 10-6 Torr. The distance between the target and substrate was 4 cm. The substrate temperature was monitored by a thermocouple attached to the substrate holder and was kept at optimal temperature of 500°C during the deposition processes. Characterization Powder XRD was conducted by a Bruker D2 PHASER X-ray spectrometer (Ettlingen, Germany) under irradiation of mono-chrome Cu-Kα (λ approximately 1.54 Å). The morphology, nanostructure, and elemental compositions of chalcopyrite films were obtained by field emission SEM (JSE-7001, JEOL, Tokyo, Japan) with attached accessory of EDS (INCA analysis system, Oxford Instruments, Oxfordshire, UK). Reflectance spectroscopy was acquired by the spectrophotometer (U-4100 UV-visible-NIR spectrophotometer, Hitachi, Tokyo, Japan). PL measurements were carried out using a 635-nm CW diode laser excitation source. The signal was dispersed by a monochromator and detected by an InGaAs photodiode (working range = 900 to 2,100 nm).

5 and 2. ABS = acute bacterial sinusitis; ADR = adverse drug reaction;

AE = adverse event; AECB = acute exacerbation of chronic bronchitis; CAP = community-acquired pneumonia; cIAI = complicated intra-abdominal RG-7388 manufacturer infection; cSSSI = complicated skin and skin structure infection; IV = intravenous; PO = oral; SADR = serious ADR; SAE = serious AE; uPID = uncomplicated pelvic inflammatory disease. Patients with Co-Morbidities Because the safety of drugs can be adversely influenced by the patient status and may also worsen it, data were also stratified according to the main pertinent co-morbidities and elimination pathway disorders observed in the population – namely age, diabetes mellitus, renal impairment, hepatic impairment, cardiac disorders, and abnormally low BMI. First, patients were stratified by study design (double blind and open label) and administration route (oral, intravenous/oral, intravenous), and the results are presented in table VIII. To better apprehend potentially meaningful differences, relative risk estimates (moxifloxacin versus comparator) were then calculated for each patient group stratified according to the administration route. The results are presented graphically in figures 2 and 3. On the basis of a threshold of a 2–fold increase

in risk estimates, the GSK1120212 molecular weight only difference seen in patients receiving oral treatment Carnitine palmitoyltransferase II was in those with underlying cardiac disorders (more AEs with fatal outcome for comparator) [figure 3b]; and the only differences seen in those receiving intravenous treatment were in those with (i) age ≥65 years (more ADRs with fatal outcome for comparator [figure 2a]); (ii) diabetes mellitus (more discontinuations due to ADRs for comparator [figure 2b]); (iii) hepatic impairment (more SADRs, discontinuation due to ADRs, and AEs with fatal outcome for moxifloxacin

[figure 3a]); (iv) cardiac disorders (more discontinuations due to AEs for moxifloxacin and more ADRs with fatal outcome for comparator [figure 3b]); and (v) BMI <18 kg/m2 (more discontinuations due to AEs or ADRs, and more AEs with fatal outcome for moxifloxacin [figure 3c]). However, numbers in the intravenous-only studies were small in all cases (1–7 patients). Lastly, the relative risk estimates (moxifloxacin versus comparator) were calculated after substratifying each group according to the comparator used, concentrating for each comparator on patients treated by the most frequent route of administration (if versus a β-lactam: oral, intravenous/oral and intravenous; if versus a macrolide alone: oral; if versus a β-lactam alone or a beta-lactam combined with a macrolide: intravenous/oral; if versus fluoroquinolone: intravenous only). The results are shown graphically in figures 4–6.

TTM has been known inhibit copper-binding proteins that regulate copper see more physiology through formation of a sulfur-bridged copper–molybdenum cluster, rather than by direct chelation of copper ions [10]. In the current study, TTM caused profound cessation of the growth of P. falciparum; this arrest resulted from inhibition of schizogony of the parasite. In contrast, treatment of uninfected RBCs with higher concentrations of

TTM caused only slight growth arrest. Thus, the target molecule(s) of TTM may be present predominantly in the parasite, although the molecule(s) involved in the growth arrest of the parasite remain to be determined. Also, the possibility that the excess TTM affects, directly or indirectly, various proteins that do not bind to copper, and thus causes developmental arrest of the parasite, remains to be elucidated. Chelation with Neocuproine, which selectively removes Cu1+ [11], inhibited the successive ring–trophozoite–schizont progression of P. falciparum effectively at extremely low concentration; blockage of trophozoite progression from the ring stage was shown at higher concentrations. In contrast, the growth of P. falciparum pretreated with Neocuproine was arrested only to a very small

extent, even when treated with much higher concentrations. This is quite different from the profound developmental arrest of P. falciparum maintained in the presence of Neocuproine throughout the culture period. We surmise that either the binding of Neocuproine may be reversible CP690550 or copper Methane monooxygenase ions may be replenished by host cells. RBCs contain copper at levels as high as a mean value of 18 μM, although most of the copper present in RBCs is bound to the enzyme superoxide dismutase [17, 18]. Developmental arrest of P. falciparum, similar to that in CDRPMI and GFSRPMI in the presence of Neocuproine and TTM, was detected in the parasite cultured in CDM-C16alone. We have demonstrated previously, using genome-wide transcriptome profiling and various CDMs, profound down-regulation of the putative copper channel

in parasites cultured in CDM-C16alone. This was associated with the blockage of trophozoite progression from the ring stage of the parasite. In the current study, the expression of genes encoding copper-binding proteins of P. falciparum was investigated, in detail, with cultures in CDM-C16alone, CDRPMI, and GFSRPMI. Transcript levels of not only a putative copper channel, which has previously been detected by genome-wide transcriptome profiling [7], but also a copper transporter were profoundly decreased during the arrested development of the parasite at the ring stage in CDM-C16alone. The severe down-regulation of copper-binding proteins of the parasite cultured in CDM-C16alone is considered to affect copper pathways and trafficking; this maybe involved in the perturbation of copper homeostasis and developmental arrest of the parasite, similar to the growth arrest seen with TTM and Neocuproine.

GadX has been shown to suppress the expression of perA encoded by a plasmid of enteropathogenic E. coli [14], but activate gadX, gadA, gadB, and gadC in response to acid stress [15–19]. GadA and GadB are isozymes of glutamate decarboxylases that convert glutamate to γ-aminobutyric acid (GABA) which is then exported by the antiporter protein GadC [20, 21]. An intracellular proton is consumed during GABA production [22], but the released GABA, which is less acidic than glutamate, provides local buffering of the extracellular environment. The expression of gadX is activated by the alternative sigma factor RpoS during the stationary phase

of growth [15, 19, 21], but is repressed during the exponential Paclitaxel chemical structure phase by the

nucleoid protein H-NS due to its binding to the gadX promoter or its destabilizing effect on RpoS [23–25]. However, the acid stress increases the RpoS level and thus induces gadX expression even during the exponential phase of growth [26]. GadW, like GadX, belongs to the family of AraC-like regulators. It represses the expression of gadX and inhibits the activation of gadA and gadBC by GadX [15, 18, 27]. In addition to these trans-acting proteins, the production of GadX is also controlled by gadY that is located between gadX and gadW in an opposite orientation Selleck PLX4032 to gadX [28, 29]. The gadY gene has no known protein products. It produces three RNA species of 105, 90, and 59 nucleotides with a common 3′ end [28]. The 3′ ends of gadX and gadY RNAs overlap by at least 30 nucleotides and are complementary to each other. Annealing of gadY RNA to the 3′ end of gadX mRNA stabilizes gadX mRNA, resulting in an increased production of the GadX protein [28]. BtuB is also involved in the import of colicins such as colicin E7 (ColE7) [30–34]. ColE7 is composed of three domains responsible for the translocation

of ColE7 through the OmpF porin, binding of ColE7 to BtuB, and cleavage of DNA [35, 36], respectively. The import Idoxuridine of ColE7 is dependent on the Tol (tolerance to colicin) system that is composed of TolQ, TolR, TolA, and TolB proteins [35, 36]. Deletion or mutation of BtuB, OmpF, or any of the Tol proteins renders E. coli resistant to ColE7 [33, 37, 38]. Based on this information, we used a ColE7 resistance assay in this study to search for transcriptional regulators of btuB from a genomic library of E. coli strain DH5α and found that gadX and gadY genes down regulate the expression of btuB. Results Screening of genes conferring E. coli resistance to ColE7 To search for genes that can confer E. coli resistance to ColE7, plasmids in the genomic library were transformed into the ColE7-sensitive E. coli strain DH5α, and the transformants were plated on LB agar plates containing 50 μg/ml of ampicillin and 5.0 ng/ml of His6-tagged ColE7/ImE7. Two colonies were seen after incubation at 37°C overnight.

This method of counter-selection has been found to be useful for several other environmental bacteria [11, 12, 18]. Plasmids pSSK10,

Selumetinib in vitro pEX100T, and pJQ200 have been successfully used to obtain A. baumannii mutants by this method [11–13]. However, most bacteria subjected to homologous recombination, even under negative selection for the sacB gene, are wild-type and it is not possible to isolate the desired mutant directly [19–21]. Another disadvantage of this method is that integration of the DNA may not always provide the desired replacement, since foreign DNA with low or no sequence homology would rely on illegitimate recombination events, as previously reported for Acinetobacter and other species [14, 16]. In addition, all of these gene replacement methodologies are time-consuming, and require several steps involving subcloning into a suicide delivery

vector followed by electroporation into E. coli and subsequent transfer into A. baumannii by electroporation or conjugation. To avoid such situations, we propose a method based on the electroporation of A. baumannii electrocompetent cells with linear DNA, a PCR product including an antibiotic resistance cassette flanked by regions homologous to the target locus. However, as expected, we noted an important disadvantage of the replacement method (which requires two recombination events), with respect to the gene disruption method (which only requires see more one recombination event), i.e. the low efficiency with regard to obtaining mutants (10-7 vs. Akt inhibitor 10-5). In addition, we observed more illegitimate recombination events with the new method than with the gene disruption technique, since several colonies acquired the resistance antibiotic cassette (confirmed by PCR), although the wild-type target gene was not replaced (Figures 1, 2, and 4). Nevertheless, the new method is a useful genetic tool for systematic generation of knockouts. Moreover, to our knowledge, there are no previous reports of double knockout mutant strains of A. baumannii. However, we demonstrate that the combination

of both gene disruption and gene replacement techniques is an easy and useful procedure for obtaining double gene-knockout mutants in A. baumannii. Taking into account the results presented here, it intuitively appears that the gene replacement method would be successful with any strain of A. baumannii, including clinical strains, with the only limitation being the use of an appropriate antibiotic resistance marker. Although the kanamycin resistance cassette cannot be used in clinical strains (all the clinical strains of A. baumannii taken from our collection were kanamycin resistant: data not shown), use of another antibiotic resistance marker such as rifampicin (for which a low level of resistance has been demonstrated in approximately 50% of multidrug-resistant A.

Int J Hydrogen Energy 2011, 36:11085–11092.CrossRef 27. Deepak FL, John NS, Govindaraj A, Kulkarni GU, Rao CNR: Nature and electronic properties of Y-junctions in CNTs and N-doped CNTs obtained by the pyrolysis of organometallic

precursors. Chem Phys Lett 2005, 41:468–473.CrossRef 28. Charpentier PA, Maguire A, Wan WK: Surface buy Selisistat modification of polyester to produce a bacterial cellulose-based vascular prosthetic device. Appl Surf Sci 2006, 252:6360–6367.CrossRef 29. Namgung S, Baik KY, Park J, Hong S: Controlling the growth and differentiation of human mesenchymal stem cells by the arrangement of individual carbon nanotubes. ACS Nano 2011, 5:7383–7390.CrossRef 30. Yang W, Cui FZ, Qing XL: Behavior of phosphatidylcholine adsorption on CN x coated PTFE films. Curr Appl Phys 2006, 6:827–832.CrossRef 31. Ferrari AC, Rodil SE, Robertson J: Interpretation of infrared and Raman spectra of amorphous carbon nitrides. Phys Rev Biol 2003, 67:155306–155325.CrossRef 32. Horbett TA: The role of adsorbed proteins in animal cell adhesion. Colloids Surf B Biointerfaces 1994, 2:225–240.CrossRef 33. Takemoto S, Kusudo Y, Tsuru K, Hayakawa S, Osaka A, Takashima S: Selective protein AUY-922 supplier adsorption and blood compatibility of hydroxy-carbonate apatites. J

Biomed Mater Res 2004, 69A:544–551.CrossRef 34. Yokota T, Terai T, Kobayashi T, Iwaki M: Cell adhesion to nitrogen-doped DLCS Diflunisal fabricated by plasma-based ion implantation and deposition method. Nucl Instrum Methods Phys Res B 2006, 242:48–50.CrossRef 35. Lacerda SHDP, Semberova J, Holada K, Simakova O, Hudson

SD, Simak J: Carbon nanotubes activate store-operated calcium entry in human blood platelets. ACS Nano 2011, 5:5808–5813.CrossRef 36. Baurschmidt P, Schaldach M: Alloplastic materials for heart-valve prostheses. Med Biol Eng Comput 1980, 18:496–502.CrossRef 37. Owens AP, Mackman N: Tissue factor and thrombosis: the clot starts here. Thromb Haemost 2010, 104:432–439.CrossRef 38. Zhang L, Chen M, Li ZY, Chen DH, Pan SR: Effect of annealing on structure and haemocompatibility of tetrahedral amorphous hydrogenated carbon films. Mater Lett 2008, 62:1040–1043.CrossRef 39. Gao JC, Li LC, Wang Y, Qiao LY: Corrosion resistance of alkali heat treated magnesium in bionics simulated body fluid. Rare Metal Mater Eng 2005, 30:903–907. 40. Alanazil AS, Hirakuri KJ: Blood compatibility of DLC films. Eur Cells Mater 2010, 20:15–20. Competing interests The authors declare that they have no competing interests. Authors’ contributions DL and HG designed this work. MZ, YC, and XL performed the experiments; MZ collected and analyzed the data and wrote the manuscript. JD supported the experiments. All authors read and approved the final manuscript.

Am J Surg 2010,200(4):483–488.PubMedCrossRef 11. Murata A, Matsuda S, Kuwabara K, Fujino Y, Kubo T, Fujimori K, Horiguchi H: Evaluation of compliance with the Tokyo guidelines for the management of acute cholangitis based on the Japanese administrative database associated with the diagnosis

procedure combination system. J Hepatobiliary Pancreat Sci 2011,18(1):53–59.PubMedCrossRef https://www.selleckchem.com/products/DAPT-GSI-IX.html 12. Salvador VB, Lozada MC, Consunji RJ: Microbiology and antibiotic susceptibility of organisms in bile cultures from patients with and without cholangitis at Asian academic medical center. Surg Infect (Larchmt.) 2011,12(2):105–111.CrossRef 13. Yokoe M, Takada T, Mayumi T, Yoshida M, Hasegawa H, Norimizu S, Hayashi K, Umemura S, Orito E: Accuracy of Inhibitor Library price the Tokyo Guidelines for the diagnosis of acute cholangitis and cholecystitis taking in consideration the clinical practice pattern in Japan. J Hepatobiliary Pancreat Sci 2011,18(2):250–257.PubMedCrossRef 14. Laparoscopic approach to acute abdomen. Consensus Development Conference of the Società Italiana Chirurgia Endoscopica e nuove tecnologie (SICE); Associazione Chirurghi Ospedalieri Italiani (ACOI); Società Italiana di Chirurgia (SIC); Società Italiana Chirurgia d’Urgenza e Trauma (SICUT), Società Italiana Chirurghi dell’Ospedalità Privata (SICOP) and the European Association for Endoscopic Surgery

(EAES) [http://​www.​snlg-iss.​it/​cms/​files/​CC_​laparoscopia_​addome.​pdf] 15. Winbladh A, Gullstrand P, Svanvik J, Sandström P: Systematic review of cholecystostomy as a treatment option in acute cholecystitis. HPB (Oxford) 2009,11(3):183–93.CrossRef 16. Borzellino G, Sauerland S, Minicozzi AM, Verlato G, Di Pietrantonj C, de Manzoni G, Cordiano C: Laparoscopic cholecystectomy for severe acute cholecystitis. Mannose-binding protein-associated serine protease A meta-analysis

of results. Surg Endosc 2008,22(1):8–15.PubMedCrossRef 17. Ayurek N, Bulent S, Osman Y, Tugan T, Irkorucu I, Yucel C, Oktar S, Tatlicioglu E: Management of acute calculous cholecystitis in high-risk patients. Surg Laparosc Endosc percutan tech 2005, 15:315–320.CrossRef 18. Weschbilling-Meunier K, Pessaux P, Lebigot J, Lermite E, Aube Ch, Brehant O, Hamy A, Arnaud JP: Percutaneous cholecystostomy for high-risk patients with acute cholecystitis. Surg Endosc 2005, 19:1256–1259.CrossRef 19. Ito K, Fujita N, Noda Y, Kobayashi G, Kimura K, Sugarawa T, Horaguchi J: Percutaneous cholecystostomy versus gallbladder aspiration for acute cholecystitis: a prospective randomized controlled trial. AJR 2004, 183:193–196.PubMed 20. Melloul E, Denys A, Demartines N, Calmes JM, Schafer M: Percutaneous drainage versus emergency cholecystectomy for treatment of acute cholecystitis in critically ill patients: does it matter? World J Surg 2011, 35:826–833.PubMedCrossRef 21. Neugebauer EAM, Sauerland S: Guidelines for emergency laparoscopy. World Journal of Emergency Surgery 2006, 1:31.

The chromatographic separation was achieved

on a ChiralPak AD-H, 4.60 × 150 mm, 5 μm LC–MS column, with a mobile phase. The mass spectrometer was operated in positive mode, and HDAC phosphorylation the resolution setting used was unit for both Q1 and Q3. The MRM transition was m/z 234 → 84 for MPH, and the MRM transition was m/z 243 → 93 for the internal standard, MPH-D9. The assay ranges were from 0.05 to 50 ng/mL for guanfacine analysis, based on a plasma sample volume of 200 μL, and from 0.25 to 100 ng/mL for d-MPH and l-MPH analysis, based on a plasma sample volume of 100 μL. Safety was evaluated by collecting data on reported AEs, physical examination findings, vital signs, and 12-lead ECGs. At the end of each treatment period, biochemical and hematologic assessments were performed and urinalysis was conducted. Staff contacted subjects 7 days after the last dose of the last investigational agent to collect data on new-onset AEs and other treatment-related concerns. 2.4 Statistical Methods The primary

analysis was the pharmacokinetic analysis performed using data from the pharmacokinetic 5-Fluoracil cell line population. This population consisted of all subjects who received at least one dose of study medication, had at least one postdose safety assessment, and had evaluable concentration–time profiles for guanfacine, d-MPH, or l-MPH. Pharmacokinetic parameters were determined from the plasma concentration–time data by noncompartmental analysis and included Cmax, time to Cmax (tmax), AUCt, AUC∞, apparent elimination half-life (t½), apparent oral-dose clearance (CL/F), and apparent volume of distribution during the terminal phase after oral administration (Vλz/F). CL/F and Vλz/F were corrected for bodyweight. Summary statistics, including

Tangeritin the numbers of observations, means, standard deviations (SDs), medians, maximums, minimums, and geometric means, were determined for all pharmacokinetic parameters for all treatment regimens. The means of the log-transformed pharmacokinetic parameters were compared among (between) treatments, using an analysis of variance (ANOVA) with sequence, period, and treatment as fixed effects, and subject nested within sequence as a random effect for a crossover study design. To estimate the magnitude of the treatment differences in Cmax and AUC∞, the geometric mean ratio (GMR, defined as the least squares mean difference in the log-transformed parameters back-transformed to the original scale) and their 90 % confidence intervals (CIs) were also calculated. The hypothesis of a drug interaction of GXR and MPH would be rejected if either of the following were to fall within the interval of 0.80–1.25: (i) the 90 % CIs of the GMR of guanfacine following GXR alone to guanfacine following GXR in combination with MPH; or (ii) the 90 % CIs of the GMR of d-MPH following MPH alone to d-MPH following MPH in combination with GXR.

There are a wide variety of sustainability indicators currently in use, whose LEE011 nmr geographical targets vary from global/international scale to national and local/city level. The representative indicators for the national and global levels include, but are

not limited to, the United Nations Commission on Sustainable Development (UNCSD) indicators, the environmental sustainability index (ESI), and the human development index (HDI). The UNCSD Indicators for sustainable development is a set of 58 indicators with flexible adaptation at the national level. The indicator framework uses four dimensions (society, environment, economy, and institutions) and each dimension is further divided into themes, sub-themes, and indicators. For instance, one theme of the environmental dimension is the atmosphere, which is divided into three sub-themes: climate change, ozone layer depletion, and air quality. Each sub-theme has one or more indicators; in the case of climate change,

for example, the indicator PFT�� in vivo is greenhouse gas emissions (UNCSD 2001). The ESI, developed at Columbia and Yale universities, is designed to utilize the following five components: environmental systems, environmental stresses, human vulnerability, social and institutional capability, and global stewardship. Each component has a group of so-called indicators (21 in total) and each indicator has a set of variables, for a total of 76 variables (Esty et al. 2005). The ESI is the equally weighted average of the 21 indicators and five components. Masitinib (AB1010) For example, air quality is one of the indicators of the ‘environmental systems’ component. This indicator has four variables: NOx concentration, SOx concentration, particulate concentration, and indoor air quality. The ESI published its environmental sustainability rankings at the country level in 2001 and 2005. The HDI considers three basic dimensions for human development: health, measured in terms of life expectancy at birth; education,

measured in terms of adult literacy and primary, secondary, and tertiary enrolment; and, finally, standard of living, measured in terms of GDP per capita (UNDP 2006). As a basic indicator, the HDI ranks countries in terms of human development. Another important feature is that the HDI has been calculated on the yearly basis since 1975. It should be stressed that indicators, such as ESI and HDI, are categorized as indicative assessment methods, aiming to analyze the relative status of sustainability or specific components of sustainability among targeted areas in the form of integrated scores, as opposed to the definitive type of assessment that attempts to argue the absolute status of sustainability, per se. At the local level, it is worth mentioning the Sustainable Seattle initiative (1998). Community members consisting of local citizens selected 40 comprehensive indicators under five large categories of environment, population and resources, economy, youth and education, and health and community.