At the same time, it is clear that coral growth, biogenic sediment production, and wave action can serve to maintain stability and even contribute to island growth, this being the way in which reef islands were formed in the first place. Thus it is clear that development and adaptation strategies (e.g., ecosystem-based adaptation) designed to complement natural

resilience in the coastal system should have a higher probability Akt inhibitor of success. This approach presupposes an understanding of the relevant coastal sedimentary and ecological processes of interest, which highlights the importance of biophysical science as one component of the information package needed for effective coastal management, climate-change adaptation, and disaster risk reduction. In a broader governance context, it is recognized that understanding of key processes forms an essential foundation for sustainable development (Glaser et al. 2012). Effective disaster risk reduction also requires knowledge of

potential threats. In some cases, for rare and exceptional events such as major tsunami or extreme storms, there may be some residual community memory, but often there is not. Effective stakeholder collaboration and attention to local and traditional knowledge are important and may identify issues that would otherwise be overlooked. There is a large and growing literature on the value of indigenous knowledge and protocols MI-503 manufacturer for integrating locally sourced information with other forms of knowledge including western scientific approaches (e.g., Crump and Kelman 2009; Kelman and West 2009; McAdoo et al. 2009; Mercer et al. 2009). The explosive growth of social media, even in remote communities, opens up new possibilities for information exchange and participatory dialogue. New tools are being developed to invite and enable contributions of information from the wider public (e.g., Tienaah 2011;

Nichols et al. 2011). This study has highlighted the variability of island environments and the diversity of dominant processes, hazards, and exposure on various island types. As shown schematically in Fig. 12, differences in the modes of exposure and dominant hazard issues between island types can be correlated to variations in Histamine H2 receptor the relative importance and utility of adaptation actions. Thus, an ecosystem-based adaptation tool such as mangrove conservation or restoration is applicable to continental and volcanic high islands and locally on atolls, but irrelevant on raised carbonate atolls. Coastal setback is a globally recognized proactive adaptation option applicable to all island types, but perhaps most compelling on high carbonate islands such as Bermuda or Niue, where major tropical cyclone waves can demolish cliff-top facilities. Fig. 12 Schematic template showing variable severity of major coastal hazards as a function of island type and a selection of adaptation strategies with varying applicability across types.

E-mail: boss@dtm.​ciw.​edu Gas-Phase Prebiotic Chemistry in the Solar System: How and Where Nadia Balucani Dipartimento di Chimica, Università degli Studi di Perugia, Selleckchem ABT263 Perugia, Italy In the sequence of steps which are believed to have led from elementary particles to the emergence of life, an important one is certainly the formation of simple prebiotic molecules from parent species abundant in the Universe. The aggregation of H, O, N, C (and other element) atoms into molecules and the subsequent chemical evolution are occurring also

now in the Universe, as witnessed by the identification of more than one hundred molecules in the interstellar medium (encompassing also prebiotic

molecules such as glycolaldehyde, formamide and, tentatively, glycine) and by the gas-phase chemical evolution of the atmospheres of several solar objects like Titan. Simple as they might seem compared LCL161 cell line to other processes of relevance in astrobiology, the formation mechanisms of many of the observed gaseous prebiotic molecules and radicals are far from being understood. In this contribution, the focus will be on the gas-phase chemical evolution of planetary atmospheres and cometary comae, the

gaseous environments of our Solar System where gaseous organic molecules have been observed. Similarly to the atmosphere of Earth, the atmospheres of the other planets Dipeptidyl peptidase (or satellites, like Titan) can be described as giant photo-reactors, where the energy deposited mainly by solar photons, but also by cosmic rays and other energetic particles, drives a complex gas-phase chemistry. In this specific context, gas-phase neutral–neutral reactions are expected to play a dominant role. A thorough characterization of the chemical evolution of planetary atmospheres relies on a multi-disciplinary approach: (1) observations allow us to identify the molecules and their number densities as they are nowadays; (2) the chemistry which lies behind their formation starting from atoms and simple molecules is accounted for by complex reaction networks; (3) for a realistic modeling of such networks, a number of experimental parameters are needed and, therefore, the relevant molecular processes should be fully characterized in laboratory experiments.

Serum amylase and lipase levels were unchanged during the present study, though serum trypsin levels increased after the ASNase injection. Serum PSTI levels increased after the ASNase injection as well. Acute pancreatitis develops with unregulated trypsin activity after breakdown

of critical protective mechanisms and copious secretion of pancreatic enzymes such as amylase and lipase.[21,22] The present results indicate that inhibitors of trypsin could potentially prevent development of pancreatitis, and suggest the presence of subclinical pancreatitis in cases who do not develop pancreatitis during administration of ASNase. Not only ASNase but also prednisolone has been implicated as an agent capable of inducing pancreatitis.[23] Previous reports suggest that ASNase is the more likely source of pancreatitis on the basis of histologic examination of the pancreas, the relative infrequency of prednisolone-induced check details pancreatitis, and a negative result after rechallenge with prednisolone.[14,18,24] In the present study, one of 29 patients (3%) developed ASNase-induced pancreatitis, similar to the morbidity rates in previous reports.[4,6,9,16,25] Since the patient developed severe pancreatitis, ASNase was contraindicated during the rest of her treatment for ALL. The results of her blood tests were similar to the results from those patients

who did not develop EGFR inhibitor acute pancreatitis, so there was no parameter that could be used to predict acute pancreatitis. When ASNase-induced pancreatitis

occurs, treatment with Erwinia chrysanthemi asparaginase is an option. As it can also lead to pancreatitis, Erwinia asparaginase is a second-line therapy for ALL after hypersensitivity to Escherichia coli asparaginase.[26] Furthermore, there are no widely accepted guidelines for use of Erwinia asparaginase, and such treatment is not covered by health insurance providers in Japan. Previous reports have shown that there is a mean of almost 10 days from the last administration of ASNase to diagnosis of pancreatitis.[5,9,16] Similarly, Japanese case reports of ASNase-induced pancreatitis have shown that 50 of 56 patients (89%) who developed Selleckchem Gemcitabine ASNase-induced pancreatitis did so within 10 days (median 2 days, range 0–23 days) after administration of ASNase.[27] This period is similar to the time period in the present study when the levels of plasma amino acids, serum trypsin, and serum PSTI changed. In the rat model, it has been proposed that ASNase-induced pancreatic injury can involve disruption of the plasma amino acid balance that is caused by ASNase. Disruption of protein synthesis in acinar cells then causes inhibition of exocytosis following the histologic morphologic changes.[28] The present results imply that the plasma amino acid level imbalance could also be a factor in ASNase-induced pancreatitis in humans.

However, at the time of protein harvest in this study (16 hours post inoculation), its overall abundance in unadapted cultures was extremely low (when compared to that within adapted cultures) and, in all probability, under the detection limit for silver staining. PA exposure has been correlated with de novo protein synthesis [5]; therefore, the observed

increase in abundance of ribosomal proteins in this study is not surprising. Specifically, this study establishes a direct link between PA exposure and the overexpression of ribosomal proteins. The 50 S ribosomal proteins RplE and RplF (both components of the spc operon) have not been studied in abundance in Salmonella. However, it is known that the synthesis of ribosomal proteins fluctuates in accordance to the cell’s environment [35]. RplE was discovered to be crucial for cell viability 3-deazaneplanocin A in E. coli [20]. Knockout mutants lacking this gene were unable to compensate

for the loss in vitro and its absence ultimately proved to be lethal. It is quite possible that RplE may play a similar role in S. Enteritidis; however, this hypothesis Selleckchem Bafilomycin A1 has yet to be tested in Salmonella. It is certain the abundance of these ribosomal proteins in PA adapted cultures serves a purpose; however, this and other hypotheses must be tested to gain insight into their role in PA adapted cultures before further speculation can be made. Of the five proteins overexpressed in PA adapted

cultures, Dps and CpxR are those normally associated with virulence and pathogenesis in Salmonella and other enteropathogenic bacteria [28, 36]. Interestingly, these are also the only two proteins over-expressed at the mRNA level as well. The fact that RplE, RplF, and SodA were either suppressed (sodA and rplF) or unaffected (rplE) at the transcriptional level, yet overexpressed at the translational level is not highly unusual. In fact, studies comparing mRNA and protein abundances has demonstrated that, in general, the amount of mRNA levels in a cell at a given instance shows no correlation with the amount of protein that is produced by the cell [37, 38]. A potential mechanism for regulation of Dps in response to prolonged PA exposure may stem Phosphoprotein phosphatase from the fact that this protein is translationally regulated by the RNA-binding protein Hfq during stationary phase [38] and that expression of Dps is reduced in an Hfq deletion mutant during this time. (Expression of RplF is also reduced in an Hfq mutant; however, this expression pattern is specific to growth in acidified minimal medium.) PA exposure may increase the expression of Hfq during stationary phase and ultimately result in increased translation of Dps. Additionally, an interesting aspect with regards to RplE expression during stationary phase and Hfq-dependent regulation can be pointed out.

The MIRU-VNTR technique provides numerous advantages: it provides a rapid, adaptable technique to comment on selleck products the presence of clonal complexes within isolates linked using an epidemiological method [16]. Coding the results as a series of numbers allows an easy exchange of results between different labs. On the practical side, this

technique also enables evaluation of the possibility of laboratory contamination in cultures from different isolates. Using MIRU-VNTR markers, we also confirmed the identity of isolates collected from the same patients when they had a relapse of their illness. This stability was observed invitro with subcultures of the same isolate, and invivo for the same infected patient. This result contrasted with results obtained by the MIRU-VNTR technique on strains of M. tuberculosis, which provided an example of frequent exogenous infections [17]. We did not find any difference in the genetic profile of serial strains found in our patients, which permitted us to exclude the possibility of re-infection with a new strain of M. intracellulare. For the clustering analysis of MIRU-VNTR profiles, a graphing algorithm termed minimum spanning tree was used. This method has been introduced by some authors to improve Torin 2 supplier analysis of VNTR

profiles [14]. Similar to maximum-parsimony phylogenetic tree reconstruction methods, minimum spanning tree constructs a tree that connects all the genetic profiles Methane monooxygenase in such a way that the summed genetic distance of all branches is minimized. The differences in mathematical approach between minimum spanning tree and UPGMA methods explain changes in strains clustering. Thus, minimum spanning tree allowed us to group strains which were unclustered with UPGMA (isolates 54 in complex II and 34 in complex I). Our study permitted us to

characterize the statistical power of the MIRU-VNTR technique as applied to M. intracellulare. The global discriminatory index of 0.98 presented in this work confirmed the possible use of this technique, in agreement with results obtained with other species of the avium complex [7]. Interestingly, Ichikawa et al. [10] also described an HGDI of 0.98 for the MLVA of M. intracellulare. Forty-four MIRU-VNTR types were obtained in our study for the 61 M. intracellulare clinical isolates, a number similar to that described by Ichikawa [10]. Our results confirmed the data very recently described for M. intracellulare [10] showing that this method seemed to harbor a great discriminatory power for identification of genetically similar isolates. Mycobacterium avium-intracellulare complex agents, in addition to a broad host range, are environmental mycobacteria found in numerous biotopes including the soil, water, aerosols, and vegetation. Nevertheless, little is known about genetic variations among patient and environmental isolates of M. intracellulare.

All genes had the stop codon inserted in the reverse oligonucleotide, with exception of centrin that uses the stop codon of vector. The PCR products were then inserted into pDONR 221 (Invitrogen) by BP recombination and then transferred to pTcGW vectors by LR recombination. The TcRab7 gene was inserted into pTcGFPN (for localization experiments) and pTcCFPN (for co-localization experiments). The PAR 2 gene was inserted into pTcGFPN (for localization experiments) and pTcGFPH (for co-localization), while Tcpr29A and TcrL27 were inserted into pTcTAPN. The putative centrin was inserted into pTcMYCN (for localization experiments),

and into pTc6HN. For construction of GFPneo-CTRL and TAPneo-CTRL, first, a hypothetical T. cruzi gene (Tc00.1047053510877.30) was inserted in these vectors. Then, this genetic element was removed by restriction endonuclease digestion (SmaI), preserving the attB selleck chemicals recombination sites. Transfection of the parasites Epimastigote forms of T. cruzi Dm28c were grown at 28°C in liver infusion tryptose (LIT) medium, supplemented with 10% fetal calf serum (FCS), to a density of approximately 3 × 107 cells ml-1. Parasites were then harvested by centrifugation at 4,000 × g for 5 min at room temperature, washed once in phosphate-buffered-saline (PBS) and resuspended in 0.4 ml of electroporation

buffer pH 7.5 (140 mM NaCl, 25 mM HEPES, 0.74 mM Na2HPO4) to a density of 1 × 108 cells ml-1. Cells were then transferred to a 0.2 cm gap cuvette and 15 to Alvocidib solubility dmso 100 μg of DNA was added. For co-localization assays, 15 μg of each plasmid was used in the same cuvette. The mixture was placed on ice for 10 min and then subjected to 2 pulses of 450 V and 500 μF using the Gene Pulser II (Bio-Rad, Hercules, USA). After electroporation, cells were maintained on ice until being transferred into 4-10

ml of LIT medium containing 10% FCS, where they were incubated at 28°C. After 24 h of incubation, the antibiotic (hygromycin or G418) was added to an initial concentration of 125 μg ml-1. Then, 72 to 96 h after electroporation, cultures were diluted 1:10 and antibiotic concentrations were doubled. Stable resistant cells were obtained approximately 18 days after transfection. Southern blot analysis DNA extraction was performed according Angiogenesis inhibitor to Medina-Acosta & Cross [49], with some modifications. Briefly, 1 × 108 cells were pelleted, washed once with PBS and lysed with 1.5 ml of TELT buffer (50 mM Tris-HCl, pH 8.0, 62.5 mM EDTA, pH 8.0, 2.5 M LiCl and 4% Triton X-100). DNA was purified three times using phenol/chloroform/isoamilic alcohol (v/v). After that, DNA was precipitated by adding 100% ethanol (1:1, v/v), then washed three times with 1 ml of 70% ethanol, dried at 25°C and resuspended in 100 μl of TE containing 10 μg ml-1 RNase A. T. cruzi DNA (10 μg) was restriction digested with HindIII (Amersham Biosciences, Piscataway, USA) and was resolved on a 0.8% agarose gel in TBE buffer.

Considerable effort has been made to determine the prevalence of E. coli

O157 in cattle worldwide (Brazil: [17], Canada: [18], Denmark: [19], England: [20], Iran: [21], Netherlands: [22]; Norway: [23], Spain: [24], Sweden: [25], United States: [26]). Estimates of prevalence range from 0 to 71% of animals and 0 to 100% of herds [27]. Two of the world’s largest surveys of animal E. coli O157 prevalence were conducted in the past decade in Scotland. The first [28] estimated herd-level and animal-level prevalence for 952 farms throughout Scotland in a study funded by the Scottish Executive Environment and Rural Affairs Department (SEERAD) conducted from March 1998 to May 2000. Since then a second survey, funded by the Wellcome EPZ5676 price Foundation International Partnership Research Award in Veterinary Epidemiology (IPRAVE) was selleck chemicals conducted on a subsample of the 952 SEERAD farms, from February

2002 to February 2004. Data from the SEERAD and IPRAVE studies are presented in this paper. In Scotland, the first reported cases of human E. coli O157 infection were identified in 1984. Currently, Health Protection Scotland (HPS) conducts active, population based enhanced surveillance in close collaboration with the Scottish E. coli O157/VTEC Reference laboratory (SERL) [29]. Over the 10 year period 1998-2007, an annual average of 221 culture positive cases has been reported to HPS, which is an average annual rate of 4.28 cases per 100,000 population [30]. Rates in Scotland are generally higher than in most other Glutathione peroxidase United Kingdom, European and North

American countries [30–33]. A recent publication proposed a specific mechanism for the link between human infection and livestock carriage of E. coli O157 [34] which involved a subset of shedding animals known as super-shedders. Super-shedders are individuals who for a period yield more infectious organisms (here E. coli O157) than typical individuals of the same host species [34]. Shedding high concentrations of E. coli O157 has been proposed as a major contributor to cattle-to-cattle transmission [34–36] and possibly cattle-to-human transmission. Although little is known about super-shedders it has been shown that they have been associated with the presence of phage type (PT) 21/28 whereas non super-shedders are more likely to be associated with PT32 [37]. Recent evidence has shown PT21/28 to be associated with higher transmission in livestock when compared to PT32 [38]. PT21/28 is the most predominant phage type in both cattle [37] and human cases [39] whereas PT32 is a common phage type in cattle only [37]. In humans, PT21/28 is of particular concern because of its association with more severe morbidity. In the UK and Ireland (1997-2001), the mean risk of developing diarrhoea-associated HUS was significantly higher in children in Scotland infected with PT21/28 compared with other phage types [40].

RNA was collected by centrifugation at 18630 × g (4°C), washed with 70% ethanol and resuspended in water. Any contaminating DNA was removed by DNase digestion (Turbo-DNase, Ambion) according to the manufacturer’s instructions. Quality and quantification of CCI-779 total bacterial mRNA extracted was assessed using the Experion system (Experion RNA Standard Sense Kit, Bio-Rad). Complementary DNA was synthesised from 1 μg total RNA using the Transcriptor First Strand cDNA Synthesis Kit (Roche) and random

hexamer primers (supplied) according to manufacturer’s instructions. Real-time and reverse-transcriptase PCR Real-Time PCR reactions were performed in the LightCycler version 1.5 (Roche Diagnostics) using either the LightCycler MasterPlus SYBR Green (Roche) or the Master SYBR Green kit (Roche). PCR master mixes (SYBR Green dye and FastStart Taq DNA polymerase were supplied) were prepared according to the manufacturer’s instructions. A four step experimental protocol was used: (i) activation (95°C for 15 min) (ii) amplification step

repeated for 45 cycles (95°C for 10 sec; primer-specific Tm for 10 sec, 72°C for 10 sec with a single fluorescence measurement) (iii) melting curve analysis (65°C-95°C with a heating rate of 0.1°C per second and a continuous fluorescence measurement) (iv) cooling step down to 40°C (see Table 1 for annealing temperatures). Refer to Table 5 for a complete list of Tariquidar clinical trial primer sequences used to analyse the genes of interest. RNA template and no-template controls were included to determine DNA contamination of RNA samples or PCR reactions. All PCR reactions as well as all biological experiments were done in triplicate. Relative quantification of gene expression was done using the REST-384 Version 1 software with PCR efficiency correction for individual real-time PCR transcripts [48]. SigA was used as the internal standard to normalise target gene expression levels in each RNA sample [59] as it has been shown that sigA expression selleck screening library remains constant

under various growth and stress conditions [60]. Table 5 Primer sequences used for the relative quantification of glutamine synthetase and glutamate dehydrogenase genes.* Gene Sense Primer (5′-3′) Antisense Primer (5′-3′) Product size (bp) Annealing Temperature (°C) glnA1 ATGTGCTGCTGTTCAAGT TGAAGGTGACGGTCTTGC 66 55 sigA GACTCGGTTCGCGCCTA CCTCTTCTTCGGCGTTG 64 55 msmeg_6272 TGATCCGCCACATCCTG GATGTAGGTGCCGATGC 65 56.5 msmeg_5442 AGATCATGCGGTTCTGTC GTGTATTCACCGATGTGCC 61 55 msmeg_4699 GTGAGGACTTCCGCACC CCGCTTGACGACGAATC 104 55 *The product size and annealing temperatures are also given. sigA was used as an internal control or housekeeping gene. Reverse transcriptase PCR reactions were carried out in the GeneAmp PCR System 9700 Reverse transcriptase PCR reactions were carried out in the GeneAmp PCR System 9700 (Applied Biosystems) using HotStar Taq DNA Polymerase (Qiagen) according to manufacturer’s instructions.

Table 4 Significant predictors of mortality by logistic regression   OR P value Confidence interval Area under ROC curve* Thoracotomy 20 selleck chemicals llc 0.027 1.4-282.4 0.81 IVC ligation 45 0.012 2.28-885.6 0.86 Significant inverse predictors of mortality by logistic regression   OR P value Confidence interval Area under ROC curve* GCS 0.6 0.026 0.46-0.95 0.85 *Area under ROC curve as a measure of model fit. Table 5 GCS as a determinant of mortality by linear regression   Beta coefficient

P value* R2 + GCS -0.07 0.005 0.44 Intercept 1.27     *Inverse relation between GCS and mortality by linear regression. + R-squared as a measure of model fit. Table 6 Mortality by mechanism of injury Mechanism Number Mortality rate* Blunt 1 (6.25%) 0% GSW 9 (56.25%) 44.4% SW 6 (37.5%) 33.3% Total 16 37.5% *P = 0.6 (NS), Kruskal–Wallis analysis of variance rank test. Table 7 Mortality by number of injuries and IVC level of injury Level of injury Number of injuries Number of deaths Mortality rate Infrarenal 4 (25%) 1 25% Pararenal 4 (25%) 1 25% Suprarenal 5 (31.2%) 3 60% Retrohepatic 1 (6.25%) 1 100% Intrapericardial Torin 2 datasheet 2 (12.5%) 0 0%   P value = 0.8

(NS)*   P value = 0.3 (NS)* *Kruskal–Wallis analysis of variance rank test. Discussion Traumatic IVC injuries are a relatively rare event, occurring in only up to 5% of penetrating injuries and only up to 1% of blunt abdominal trauma [8]. Nonetheless, IVC trauma continues to

present a formidable challenge to trauma surgeons, carrying an overall high mortality rate in spite of recent improvements in pre-hospital care, resuscitation upon arrival at a trauma center, diagnostic imaging, and timely surgical care. Our overall mortality rate for IVC trauma (37.5%) is consistent with previous reports of IVC trauma mortality ranging from 21% to 56%, with an overall mortality rate of 43% [1, 5, 7–10, 14, 16–18]. Previous reports have described predictors of mortality to be level of injury, shock on admission, timing of diagnosis to definitive management, blood loss, requirements for blood transfusions, associated injuries, ED thoracotomy, preoperative lactate and base deficits, ISS, and GCS [1, 5, 7–10, 16–18]. In our cohort, we found statistically significant associations with the risk of mortality with hypotension upon arrival at Methane monooxygenase the ER, thoracotomy, operative time, injury severity expressed as ISS, and GCS. There was a trend towards ascending mortality as the level of injury approached the heart, however we were unable to find a statistically significant relation between level of injury and mortality. This is likely due to the small size of our cohort, and the fact that the two patients in our series with intra-perdicardial lesions, both survived. Upon regression analysis, significant predictors of mortality were thoracotomy, IVC ligation as operative management, and GCS.

This is because, in the absence of c 2, we can define free energy functions $$ Q^x_r = \left( \fraca_xb_\!x \right)^r-1 , \qquad Q^y_r = \left( \fraca_yb_\!y \right)^r-1 , $$ (A9)which generate the equilibrium distributions $$ c_r^eqx = Q_r^x c_1^r = \fracb_\!xa_x \left(\fraca_x c_1b_\!x \right)^r \;\; > \;\; c_r^eqy = Q_r^y c_1^r = \fracb_\!ya_y \left( \fraca_y c_1b_\!y \right)^r . $$ (A10)If

a x /b x  < a y /b y then the latter (Y) will be the dominant crystal type at equilibrium, whilst X is the less stable morphology at equilibrium. These last two words are vital, since, at early times, the growth rates depend on the relative sizes of the growth rates a x and a y . It is possible for the less stable form to grow first and EVP4593 manufacturer more quickly from solution, and be observed for a significant period of time, since the rate of

convergence to equilibrium also depends on the fragmentation rates and so can be extremely slow (see Wattis 1999 for details). In the presence of grinding, the crystal size distributions also depend upon the strength of dimer interactions, that is, the growth rates α x c 2 + ξ x x 2, α y c 2 + ξ y y 2 and the grinding rates β x , β y . The steady-state size distributions will depend on the relative this website growth ratios due to grinding (α x c 2 + ξ x x 2)/β x and (α y c 2 + ξ y y 2)/β y as well as the more traditional terms due to growth from solution,

namely a x c 1/b x and a y c 1/b y . Such systems with dimer interactions have been analysed previously by Bolton and Wattis (2002). The presence of dimer interactions can alter the size distribution, and in non-symmetric Silibinin systems such as those analysed here, dimer interactions can alter the two distributions differently. Two points are worth noting here: (i) for certain parameter values, the less stable stable form (Y, say, with a y /b y  < a x /b x ) may be promoted to the more stable morphology by grinding (if (α y c 2 + ξ y y 2) / β y is sufficiently greater than (α x c 2 + ξ x x 2) / β x );   (ii) grinding may make a less rapidly nucleating and growing form (Y, say, with a y  < a x ) into a more rapidly growing form if α y c 2 + ξ y y 2 is sufficiently greater than α x c 2 + ξ 2 x 2.   In systems which can crystallise into three or more forms, we may have the case where x is more stable than y and y is more stable than z; thus, at equilibrium x will be observed. Furthermore, if a x  < a y  > a z we may observe type y at early times due to it having faster nucleation and growth rates than x and z.