(1980). The rate of spreading is given as (Mackay et al. 1980): equation(5) dAdt=KSA1/3VA4/3, where KS is a parameter of value 150 s− 1, A is the oil slick area [m2] and V is the volume of the oil slick [m3]. This formula is based on the following assumptions: oil is regarded as a homogeneous mass, the slick spreads out as a thin, continuous layer in a circular pattern and there is no loss of mass from TSA HDAC concentration the slick. The initial area of the spilled oil A0 is determined according

to Fay (1969): equation(6) A0=πk24k12ΔgV05υw1/6, where g is the acceleration due to gravity [m s− 2], ∆ = (ρw − ρ0)/ρw with ρw being the seawater density [kg m− 3], ρ0 is the density of fresh oil [kg m− 3], V0 is the initial volume of the slick, vw is the kinematic viscosity of water [m2 s− 1]

and k1, k2 are constants with respective values of 0.57 and 0.725 ( Flores et al. 1998). Evaporation processes are modelled according to the methodology proposed by Mackay et this website al. (1980), taking into account the influence of oil composition, air and sea temperatures, spill area, wind speed, solar radiation and slick thickness. In addition, the following assumptions are made: no diffusion limitation exists within the oil film; oil forms an ideal mixture; the partial pressures of the components in the air, compared to the vapour pressure, are negligible. The rate of evaporation is then calculated using the following equation: equation(7) Ei=KeiPiSATRTMiρiXi, Methane monooxygenase where Ei is the rate of evaporation of the oil fraction i, Kei is the mass-transfer coefficient of the oil fraction i [m s− 1], PiSAT is the vapour pressure

of the oil fraction i, R is the gas constant [8.314 J K− 1 mol− 1], T is temperature [K], Mi is the molecular weight of the oil fraction i [kg mol− 1], ρi is the density of the oil fraction i [kg m− 3], Xi is the mole ratio of fraction i to the oil mixture [1], i is the subscript referring to the properties of component i. The estimate of Kei is also based on Mackay et al. (1980): equation(8) Kei=0.0292A0.045Sci−2/3Uw0.78, where Sci is the Schmidt number for fraction i [1], and Uw is the wind speed 10 m above the surface [m s− 1]. The process of emulsification is treated according to the empirical expressions defined in IKU (1984). The change in water content YW with time is expressed by: equation(9) dYWdt=F11+Uw2μYWmax−YW−F21CACWμYW, where YWmaxYWmax is the maximum water content in the emulsion [-], YW   is the actual water content, μ   is the oil viscosity [Pas], CW   is the content of wax in the oil [wt%], CA   is the content of asphaltenes in the oil [wt%], F  1 [kg m− 3] and F  2 [kg(wt%) s− 1] are emulsification constants. In model simulations the values of 0.85, 5.7, 0.05, 5E-7 and 1.2E-5 are adopted for YWmaxYWmax, CW, CA, F1 and F2 respectively.

C. Schloot J.L. Sullivan R. Sultana C. Sylvén L.S. Szczepaniak P.J. Talmud T. Tamayo N. Tapola P.S. Tappia L. Tarassenko G. Targher A. Tavani E. Teijeira-fernandez Grzegorz W Telega C.A. Thomson P.J. Thornalley E. Tikkanen F.J Tinahones V. Torri J. Tovar H. Toyoshima E.A. Trautwein M. Trenell V. Trischitta M. Trombetta T. Tsutamoto A. Tufano J. Tuomilehto M.E. Tushuizen R. Uauy P. Uber T. Unger P. Valensi S. Valtuena R.M. Van dam

F.J.M. Van der meer A. .PJ. Van dijk L.F. Van gaal R.E. Van pelt W. A. Van staveren F. Van’t hooft T. Vasankari J. Vassy M. Velten M. Venables J. Vendrell MK0683 price C. Ventura R. Ventura-Clapier P. Verdecchia R. Vettor G. Vicente-Rodríguez R. Vigneri R. Villegas K.R. Vincent F. Violi F. Virgili F. Visioli M.N. Bioactive Compound Library Vissers J-L. Volatier

C. Voulgari K. Wachtell T.A. Wadden K. Walker V. Wallenius YX. Wang M. Ward J. Warnberg P.J.M. Weijs A. Weimann S. Wein J.C K. Wells F.K. Welty A. Wende I. Wilcox S.S. Wing T.M.S. Wolever A. Wolk J. Yang T. Yates W.Y. Yau H-C. Yeh M. Yoshinaga C-M. Yu A. Zambon M. Zamboni P. Zammit A. Zampelas I. Zavaroni M. Zeyda Y. Zhang W. Zhang H. Zhang F. Zheng K. Zhou E. Zimmermann G. Zoppini “
“Drugs of the fibrate class, such as fenofibrate, are potent activators of Peroxisome Proliferator Activated Receptor α (PPARα) [1]. These lipid-lowering drugs effectively reduce triglyceride, moderately reduce low density lipoprotein (LDL) cholesterol, and elevate high density lipoprotein (HDL) cholesterol [2]. Furthermore, fibrates may exert anti-inflammatory effects and improve vascular function [3]. Therefore, targeting PPARα can be an effective way to improve features belonging to the metabolic syndrome and to reduce cardiovascular risk. As PPARs can be seen as lipid

sensors, dietary n-3 fatty acids deserve attention in this respect. Especially the marine n-3 long chain polyunsaturated fatty acids (n-3 LCPUFA) eicosapentaenoic 3-mercaptopyruvate sulfurtransferase acid (EPA) and docosahexaenoic acid (DHA) preferentially bind to and activate PPARα [1]. However, these n-3 LCPUFA can also activate PPARγ and PPARδ, two other PPAR isoforms [1]. As fibrates, dietary n-3 LCPUFA have potent hypotriglyceridemic effects and can increase HDL cholesterol [4]. Furthermore, the suggested beneficial effects on inflammation and endothelial function may further contribute to a reduction in cardiovascular risk. Stalenhoef et al. have compared in hypertriglyceridemic subjects gemfibrozil with n-3 LCPUFA and showed that both treatments had favorable effects on serum lipid concentrations and lipoprotein particle heterogeneity [5]. However, in that study markers reflecting low-grade systemic inflammation and endothelial function were not examined.

, 2004). Furthermore, adjustments in the mitochondrial aerobic properties of cod (Gadus morhua) at the gene level were shown to be crucial

in seasonal acclimatization as well as in evolutionary adaptation to Arctic cold ( Lucassen et al., 2006). Exploring the underlying genetics of temperature adaptation in fish species has helped identify a multitude of mechanisms by which various fish species cope with different environments. It has also helped to explain the depth and biogeographical distribution of fish populations and has enabled researchers to predict the potential impacts of climate Rapamycin order change on many marine ectotherms. Despite this, a holistic understanding of the gene expression differences underlying fish populations adapted to different environments is lacking. In addition to this there have been no studies looking at the underlying genetic mechanisms of temperature adaptation in a tropical estuarine species such as barramundi. Next-generation RNA sequencing (e.g., Illumina mRNA-seq) allows for PI3K Inhibitor Library purchase the profiling of large quantities of

expression data from many samples simultaneously, where individual genes or entire ontology’s can be identified and examined in response to an experimental hypothesis (Wolf, 2013). This methodology is ideal for examining temperature adaptation in fish populations as numerous genes and pathways are likely to be involved and RNA sequencing allows for examination of the entire transcriptome. In the current study the transcriptomic differences underlying growth differences due to temperature adaptation were examined in two populations of barramundi from different thermal environments (warm-adapted Darwin and cool-adapted Gladstone) using next generation

sequencing data (Illumina GAIIx) and GO analysis, in conjunction with growth experiments. Two genetically distinct stocks of barramundi (L. calcarifer) ( Keenan, 1994 and Keenan, 2000, Fst = 0.146, p < 0.001 Smith-Keune et al. unpublished data) representing a northern, warm-adapted (Darwin, Northern Territory, 12° 27′ S, 126° 50′ E) and southern, cool-adapted (Gladstone, Queensland 23° 50′ S, 151° 15′ E) populations were obtained filipin from commercial fish hatcheries. Fish were kept indoors in a temperature controlled room (~ 25 °C) with a 12 h light:dark photoperiod and fed a commercial diet twice a day to satiation throughout the experiment (Ridley Aquafeed, http://www.agriproducts.com.au). Prior to the experiment, fish from each population were graded to a standard length (125 ± 2 mm) and weight (48 ± 1.5 g) and were divided evenly into replicates of three treatments and introduced to either a cool 22 °C, a control 28 °C or a hot 36 °C water temperature at the rate of 1 °C/h and kept stable for 1 month.

We Ivacaftor cost used antibodies raised in guinea pigs against residues 264–413 or 264–411 of maize PIN1-like variants PIN1a and PIN1b, respectively, and, as expected on the basis of published work [ 55], found that both antibodies gave strong polar plasma membrane-targeted signal in maize leaf sections used as a positive control ( Figures 3A and S3). We used an antibody against an abundant ER-targeted protein, BIP2, as a control to test for ER colocalization. In our moss experiments, we found that the BIP2 signal (blue) localized broadly across the undifferentiated leaf tissues of P1–P5 ( Figure 3C). In contrast, the PIN signal

(red) was restricted mainly to narrow bands spanning the adaxial-abaxial leaf axis at the junctions between cells and did not colocalize with the BIP2 signal ( Figures 3C and 3D). We also detected signal on the internal faces of cells around the presumptive midvein, but signal at the outermost cell edges was absent. Thus, Physcomitrella PINs are plasma membrane targeted, can polarize, and localize in tissues that are responsive to disruption of auxin levels. Physcomitrella PINs A–C are canonical and share

many sequence motifs with Arabidopsis PIN1 in the central intracellular loop, whereas PIND is highly divergent [ 45], and PINA and PINB, but not PINC, were strongly expressed in gametophores ( Figures S4A and S4B). Therefore, to analyze PIN function in Physcomitrella, we engineered targeted disruptants for HKI-272 molecular weight PINA and PINB by homologous recombination [ 56] ( Figures S4C–S4E). Several lines with the same phenotypes were recovered for each insertion, suggesting that mutant phenotypes were caused by lesions in targeted loci ( Figure S4F). RT-PCR showed that disrupted PINA and PINB transcripts were present at low levels in pinA, pinB, and pinA pinB double mutants ( Figures S4G and S4H), suggesting that the mutants may not be null. pinA and pinB single mutant shoots were not obviously different from wild-type (WT) ( Figures 4A and 4B), but quantitative analysis showed that pinB gametophores

were longer than WT ( Figure S5). Double disruptants had class II shoot defects and defects in oriented leaf growth and cell division ( Figures 4A and S5). pinA pinB double mutants therefore resemble plants treated with auxin ( Figure S1), Epothilone B (EPO906, Patupilone) suggesting that they accumulate auxin as a result of a deficiency in auxin transport. The pinA pinB double mutant phenotype comprises class II defects, but more-severe defects were not observed. We reasoned that this may be due to residual PINC activity or residual activity in other components of the auxin transport pathway, such as PGP or ABC transporters [ 57]. We also reasoned that if we had reduced the auxin transport capacity, mutants would be more sensitive to exogenous auxin treatment than WT plants. To test this hypothesis, we grew mutants on 100 nM NAA for 4 weeks.

Following the mounting, well-publicised evidence of

disturbance of the behaviour of birds, bats and insects, there is now growing concern that light pollution might exert damaging effects on aquatic species in lakes, Cobimetinib nmr rivers and our seas, especially in coastal areas. All organisms equipped with an optic orientation system are potentially susceptible. In the sea, the behaviour, reproduction and survival of marine invertebrates, amphibians, fish and birds have been shown to be influenced by artificial lights (Verheijhen, 1985). These effects arise from changes in orientation, disorientation, or misorientation and attraction or repulsion from altered light environments (Longcore SB431542 in vivo and Rich, 2004 and Salmon et al., 1995). In animals exhibiting compulsive

stimulus behaviour, the strength and number of artificial lights may override any feedback control mechanisms. This is exemplified by sea turtles hatchlings that rely on visual cues to orient themselves seaward, which consequently renders them vulnerable to light pollution. In one anecdotal report, 500 green sea turtle hatchlings crawled to their deaths in an unattended bonfire on a beach of Ascension Island (Mortimer, 1979). On a Turkish beach, light pollution arising from a paper mill, a tourist resort and a coastal village led to less than 40% of loggerhead turtle hatchlings reaching the surf (Peters and Verhoeven, 1994).

The construction of buildings in close proximity to critically important nesting beaches, as seen in the recent urban development in Gabon’s capital, Libreville, places human populations and their attendant light sources close to critical nesting sites for the endangered leatherback sea turtle (Bourgeois et al., 2009). Disorientation and misorientation due to light pollution often divert hatchlings along their paths to the sea leading to unnecessary energy expenditure and increased risks of dehydration and terrestrial predation (Bourgeois et al., 2009 and Verheijhen, 1985). Urban skylines can present irregular silhouettes and as a result, unreliable cues to female turtles. The confusing horizon field presented to new hatchlings which rely heavily on horizon elevation cues results in increased Etofibrate mortality (Salmon, 2006). Indirect adverse effects of artificial lighting include a higher risk of human interference via greater likelihood of approach towards more visible animals and of abandonment of nesting attempts if turtles become aware of humans prior to oviposition. Other ecological effects of light pollution include disruption of predator–prey relationships. For example, Harbor seals (Phoca vitulina) congregate to feed in illuminated areas on juvenile salmon as they migrated downstream. Predation falls off when the lights are turned off ( Yurk and Trites, 2000).

We compared data taken at 1 and 10 m perpendicular to shoreline using a linear regression analysis to determine coherence with distance. We tested for differences in the concentration of PAHs

in wetland soils categorized in the SCAT surveys using a one-way ANOVA, and tested for differences between oil and un-oiled sites using a Student’s t-test and a Tukey’s HSD post hoc test for significant differences, with an alpha = 0.05. We created box and whisker plots (minimum to maximum; 25th to 75th percentile) of the concentration of alkanes and aromatics for the three estuaries (Breton Sound, Barataria Bay and Terrebonne Bay) Natural Product Library order that were sampled before the oil reached the marsh in May 2010. We divided Barataria Bay into east and west components using Grand Isle as the border and compared the concentrations of alkanes and aromatics in September 2010. We then used a Kruskal–Wallis non-parametric analysis to test for differences in the concentration of total alkanes and total aromatics among estuaries for all data in May 2010 and September 2010, and amongst sampling at the four Bay Batiste sampling trips to the same 30 sites. The total target alkane and PAH concentrations in the 405 samples ranged

from 0.4 to 8,640 mg kg−1, and from below detection limits (0.1 μg kg−1) to 355,744 μg kg−1, respectively. Samples with the lowest concentrations were collected during the pre-impact sampling in selleckchem May 2010, when the concentration of target alkanes and PAHs averaged 0.98 ± 0.005 mg kg−1 and 23.9 ± 1.61 μg kg−1, respectively. Some samples from May 2010 had measurable traces of petroleum in them, but no identifiable MC252 oil. We consider these May 2010 data to

be a baseline against which we compared oiling amounts from after the MC252 spill in 2010 and subsequent re-distributions. MC252 oil was detected in 34 of the 94 samples collected in September 2010 and February 2011. The average concentration of target alkanes and PAHs in these 34 samples was 991 ± 377 mg kg−1 and 29,977 ± 11,410 μg kg−1, respectively (Table 3). The average target alkane and PAH concentrations Meloxicam in the MC252 oiled wetlands was, therefore, over 1,015 and 1,255 times, respectively, the concentration of these alkanes and aromatics in the relatively un-oiled wetland sediments sampled in May 2010. All samples contained numerous alkanes, with some samples having obvious odd carbon preferences and others not. Samples with significant oiling contained normal alkanes with the typical pattern of alkanes, as well as the isoprenoid alkanes pristane and phytane seen in crude oils. Except for samples with highly elevated amounts of oil, many alkane patterns had biogenic and petrogenic source signatures. In general, the samples with low levels of alkanes exhibited a pattern associated with the various biogenic sources, with only some having odd carbon preferences. The average concentration of target alkanes within 1 m of the water’s edge for 91 paired samples was 37.3 ± 26.

Consistent Selleckchem Bleomycin with this idea, behavioral work in humans [55] found more intrusions (see Box 2) from a second learned list (List 2) when recalling the initial list (List 1) if participants had been reminded of List 1 before encoding List 2. This finding was recently replicated

in rodents using ‘lists’ of ordered feeder locations [56], with animals that learned two lists in the same relative to different spatial contexts producing more intrusions. These findings are consistent with the proposal that integration occurs via reactivation of prior memories; here, this work further highlights that integration can be encouraged by reminding the learner of the original encoding context. Other factors selleck inhibitor hypothesized to impact integration include (1) the nature of the underlying memory representations — with more distributed as opposed to localized representations proposed to promote integration [57]; and (2) the degree of competition between new content and prior memories (i.e., whether or not the two memories can coexist), with integration preferentially occurring in cases when competition is minimal [58]. With the related content

reinstated in the brain, hippocampal area CA1 (Figure 2) is thought to compare prior memories with incoming information from the environment [14]. CA1 may signal the presence of novelty (i.e., when new experiences violate memory-based predictions) and facilitate new encoding by increasing the plasticity of neighboring CA3 neurons [15]. Recent high-resolution fMRI work has shown that activation in human CA1 during the encoding of events that overlap with prior experiences relates to a behavioral measure of memory integration [14], consistent with the notion that CA1 triggers integration. The resulting integrated memories are highly structured, with shared elements Vitamin B12 coded similarly across experiences 16• and 17. One recent study [16•] has shown that

hippocampal CA field firing patterns for overlapping events reflect a hierarchy of features coded according to their behavioral relevance. This organization scheme could then be exploited to extract commonalities across episodes and support a host of behaviors, as discussed below. Medial PFC may influence memory integration by biasing reactivation toward behaviorally relevant memories 12, 18 and 19. Across a number of domains, mPFC is thought to represent mental models that guide behavior 20 and 21. While its specific role in memory is only starting to be uncovered, some suggest that mPFC forms mental models based on mnemonic content (i.e., memory models) 22• and 23, which may include features such as behavioral relevance and appropriate response [19].

Various genotoxicity endpoints have been used to evaluate the diverse hypotheses on the mechanistic principles of particle-induced tumor development, as reviewed in several recent publications (Gonzalez et al., 2008, Landsiedel et al., 2009, Schins and Knaapen, 2007 and Singh et al., 2009). Nevertheless, knowledge about the in vivo situation is still insufficient. To enlarge the body of knowledge, new experimental approaches are highly needed. In the present study, we therefore investigated whether local DNA damage in particle-exposed lung tissue can be detected and quantified in situ with immunohistochemical methods. One advantage of this approach is the possibility to use paraffin-embedded lung tissue from

previous studies. In the present study, www.selleckchem.com/products/carfilzomib-pr-171.html we used lung tissue from 3-month satellite groups of an existing carcinogenicity study, where animals had been exposed to particles by intratracheal instillation of high doses of crystalline silica (quartz DQ12), carbon black

(Printex® 90), or amorphous silica (Aerosil® 150). A variety of parallel data on histopathology, inflammation, toxicity, and tumor incidences buy Z-VAD-FMK enabled assessment of the feasibility and informative value of the approach. A panel of genotoxicity markers with different degrees of informative value was chosen to enable identification of the genotoxic modes of action in alveolar lining cells predominantly consisting of epithelial cells, as target cells of lung tumor development. The well-established genotoxicity markers poly(ADP-ribose) (PAR), phosphorylated H2AX (γ-H2AX), 8-hydroxy-2′-deoxy-guanosine (8-OH-dG), and 8-oxoguanine DNA glycosylase (OGG1) were selected for immunohistochemical detection and quantification in the available lung tissue samples. PAR is a posttranslational protein modification

that has been used as a general, overall marker of genotoxic stress (Bürkle, 2001). Its synthesis reflects an early cellular reaction to DNA PD184352 (CI-1040) single- (SSB) or double-strand breaks (DSB). Additionally, PAR is involved in the regulation of cell division and cell cycle progression (for review, see Hakmé et al., 2008) and plays a role in inflammatory processes in asthma and other lung diseases (Virág, 2005). Gamma-H2AX is a phosphorylated core histone variant phosphorylated after DSB induction (Rogakou et al., 1998) and γ-H2AX-containing foci seem to correlate directly with the number of DSB (Sedelnikova et al., 2002). In addition, γ-H2AX formation also occurs during apoptosis (Sluss and Davis, 2006), but nevertheless can be used as a sensitive genotoxicity marker (Watters et al., 2009). 8-OH-dG, a well-characterized oxidative DNA base lesion, is an important and well-established marker of oxidative stress (Kasai, 1997). It is probably the most mutagenic oxidative DNA base modification (Shibutani et al., 1991) and is commonly found in lung tumors (Husgafvel-Pusiainen et al., 2000).

On average, someone has a stroke every 40 seconds. The gaps for patients diagnosed with a stroke are the availability

of physicians who specialize in stroke care and access to evidence-based stroke care. Telemedicine has assisted in bridging this gap to provide effective stroke treatment. The purpose of this article is to describe how the implementation AZD6244 manufacturer of a hub and spoke model using telemedicine has assisted in increasing patient access to neurology expertise and receiving evidence-based treatment of recombinant tissue plasminogen activator, thereby improving patient outcomes. Cindy Murray, Elizabeth Ortiz, and Cay Kubin The purpose of this article is to present an option for a model of care that allows small rural hospitals to be able to provide specialty physicians for critical care patient needs in lieu of on-site critical care physician coverage. A real-time, 2-way audio and video remote presence robot is used to bring a specialist to the bedside to interact with patients. This article discusses improvements in quality and finance outcomes as well as care team and patient satisfaction associated with this model. Discussion also includes expansion of the care model to the emergency department for acute stroke care. Kristine K. Powell and Rita J. Fowler This article describes the Baylor Health Care System (BHCS) approach to decreasing sepsis-related mortality within a large complex adaptive health care Selleckchem Venetoclax system. BHCS implemented

sepsis care improvement initiatives based on the Surviving Sepsis Campaign early goal directed therapy guidelines. By adhering to rigorous process improvement and evidence-based practice principles, BHCS has demonstrated improvements in sepsis care processes and a significant reduction in sepsis mortality. Amy Veenstra and Emylene Untalan Surgical patients with known or unknown obstructive sleep apnea are at increased risk for postoperative complications. By implementing evidence-based practices and a validated screening tool, the postoperative surgical patients at the authors’ hospital have Thiamine-diphosphate kinase a decreased risk of postoperative complications, specifically oversedation.

This article discusses the pathophysiology, prevalence, risk factors, care of the postsurgical patient, and use of the validated STOP-Bang questionnaire with obstructive sleep apnea as the focus. Ryan Beseda, Susan Smith, and Amy Veenstra Providing evidence-based care to patients with return of spontaneous circulation after a cardiac arrest is a recent complex innovation. Once resuscitated patients must be assessed for appropriateness for therapeutic hypothermia, be cooled in a timely manner, maintained while hypothermic, rewarmed within a specified time frame, and then assessed for whether hypothermia was successful for the patient through neuroprognostication. Nurses caring for therapeutic hypothermia patients must be knowledgeable and prepared to provide care to the patient and family.

The data also suggest that somatic POLE mutations occur very early during colorectal tumorigenesis, because the frameshift mutations found learn more often at APC in unselected CRCs are not seen in tumors with EDMs. POLE and POLD1 may not to act as classical tumor suppressor genes. Enzyme loss-of-function mutations are thought unlikely to be pathogenic, since for proofreading can fail, successful polymerisation must have occurred first. Another point against a classical tumor suppressor model is the fact that only a minority of tumors with POLE or POLD1 EDMs show LOH or other inactivating mutations that could act as ‘second hits’. On the other hand, data from mice only indicate a mutator phenotype and increased frequency

of tumor formation when Pole mutations are homozygous [ 20••]. Overall, we can certainly envisage a situation in which the pathogenic

EDMs are selectively haploinsufficient, but we also note that somatic MSH2 and MSH6 mutations secondary to the EDM are common ( Figure 2) and may contribute to tumorigenesis. Although mutations in the exonuclease domain of POLD1 and POLE have previously been described in yeast and mouse models, the identification of germline and somatic mutations that drive tumorigenesis in humans is a recent finding. However, the consequences of polymerase EDMs are not yet clear and further analysis will be needed to understand how these mutations contribute to tumorigenesis. We do not know how proofreading fails or why the resulting mismatch is not repaired by either a wildtype copy of POLE or POLD1 or by MMR. There is additionally intriguing speculation that patients

with PD-0332991 purchase POLE-mutant CRCs and ECs have superior survival to those with other patients, perhaps as a result of the general or specific mutation burden conferred by the ultramutator phenotype. That same burden might also make those Fossariinae ultramutator cancers sensitive to mutation-inducing or DNA repair-blocking therapies. Finally, we emphasise that although pathogenic polymerase EDM cancers form a rare subtype of tumor apparently restricted to the colorectum and endometrium, there is no reason to regard them as an unimportant group. On the contrary, fine-scale classification of cancers using molecular and other methods is likely to form the basis of improved patient management in the future. Papers of particular interest, published within the period of review, have been highlighted as: • of special interest Core funding to the Wellcome Trust Centre for Human Genetics was provided by the Wellcome Trust (090532/Z/09/Z). “
“Current Opinion in Genetics & Development 2014, 24:114–119 This review comes from a themed issue on Cancer genomics Edited by David J Adams and Ultan McDermott For a complete overview see the Issue and the Editorial Available online 5th March 2014 0959-437X/$ – see front matter, © 2014 The Authors. Published by Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.gde.2013.12.