This correlation data indicate that when CD45RA down-regulates at the end find more of the naïve stage, CCR7 is indeed down-regulated, while CD28 is minimally up-regulated (see

Fig. 4B, blue hatched arrows). Our data are not consistent with the supposition that there is an extra stage as determined by CD45RA−CCR7+CD28+ ( Appay et al., 2002). Events with this phenotype captured by a gating strategy are most likely a mixture of naïve and CM events as defined by this analysis. The CD8+ average model also supports the hypothesis that when CD28 is down-regulated, CD45RA begins to be up-regulated (red arrows, r = 0.56, p < 0.01 with a difference of 1.9 (NS)). The last EF stage, is defined as the point at which the up-regulation of CD45RA has ended. During the developmental progression of memory and effector T cells, a subset of cells may begin to preferentially express markers that might not be expressed in the remaining cells. In PSM, the heterogeneous expression of markers can be visualized with branching expression profiles (see Fig. 5). Fig. 5A shows a progression schematic similar to Fig. 1 but includes a simple branch involving feature C. In this example, when cells reach the checkpoint where feature B is up-regulated, 70% of the cells also up-regulate feature C, while 30%

do not. Fig. 5B delineates the three probability state model EPs that model this simple branch (top = feature A, middle = feature B, and bottom = feature C). Fig. 5C summarizes this progression in the probability state model progression plot, which includes the branching of feature C (see the CB label). Fig. 5D

shows the associated probability Quisqualic acid state model surface dot plots for Venetoclax cell line feature A vs. B (top), feature A vs. C (middle), and feature B vs. C (bottom). Note that branches are not always visible in dot plots, which is why they have been traditionally difficult to detect. Branches are relatively easy to determine with PSM since non-branched EPs are incompatible with branched data, resulting in a dramatic loss of classified events and poor fitting. In this simple example, the branch point is at the end of Stage 2. However, when modeling T-cell branches, the location might be elsewhere along the progression axis. An averaged model featuring 22 samples from healthy donors was used to identify branched markers. Each sample was stained with antibodies against CD3, CD4, CD8, CD45RA, CD28, CCR7 (CD197), CD27, CD62L, CD57, and CD127. Fig. 6 shows the stratification expression profiles of CD45RA, CCR7, and CD28 as well as four branched EPs for CD62L, CD27, CD127, and CD57. Here, CD62L (l-selectin) has a 77% (9%) chance of down-regulating slightly before the end of the naïve stage and correlates best with the down-regulation of CCR7 (blue hatched arrows, r = 0.81, p < 0.00001, diff = − 4.23, NS). CD27 slightly down-regulates with CD45RA and CCR7 at the end of the naïve stage and then has a 75% (17%) chance of fully down-regulating in the middle of the CM stage.

Clonality of P. falciparum infection was assessed as described previously. 32 Bacteraemia with metabolically active

Streptococcus pneumoniae and non-Typhoid Salmonella (NTS) was determined using quantitative PCR on cDNA. 33 Statistical analyses were performed using PASW statistics 18 (SPSS Inc.), GraphPad Prism (GraphPad Software Inc.) and the R-statistical software (R Foundation). Data was log10 transformed for parametric analyses Selumetinib molecular weight to achieve normality, except sequestered biomass (comprising positive and negative values) which was analyzed with non-parametric methods. Unpaired t-tests and likelihood-ratio tests were used to compare means and medians, respectively, of groups. Confounding by age, prior

antimalarial treatment and clonality of infection was assessed by quantile regression (“quantreg” package, R-statistical software): a model including only intercept was compared by means of likelihood-ratio tests to models with any combination of the above covariates or interaction terms. Correlation was assessed using Spearman’s rank correlation coefficient. click here To allow for the multiplicity of tests resulting from multiple responses and multiple comparisons within a response, a false discovery rate (FDR) of 5% was assumed, using the Benjamini and Hochberg approach. 34 Power of likelihood-ratio tests for detecting an X-fold difference in medians was determined by bootstrapping (10,000 replicates):

re-sampled data from the distribution of sequestered-parasite N-acetylglucosamine-1-phosphate transferase biomass estimates was compared with a similar sample to which (X − 1) times the median sequestered biomass was added. Sensitivity analyses assessed the range within which each model parameter could be varied without rejection of the null hypothesis of equal median sequestered biomass among groups. In addition, the effect of joint variation in the parameters was assessed by sampling 10,000 candidate values from uniform distributions within the limits defined for each individual parameter, determining the frequency with which the likelihood-ratio test did not reject the null hypothesis. The effect of parameter variation on the Spearman’s rank correlation between lactate and sequestered biomass was assessed identically. Complete clinical and laboratory data (Fig. 1) were available from 296 children (Tables 1 and 2), 127 (42.9%) with SM, of whom 5 died (Fig. 2). Children with SM were younger, more anaemic and thrombocytopaenic, and had higher blood lactate, parasitaemia, parasite density, plasma PfHRP2 concentrations, circulating parasite biomass, and total parasite biomass (calculated from PfHRP2 concentration) than children with UM (Table 2 and Fig. 3A).

In fact, the second-best BLASTX hit, after BgP, is to a Eubacterium acidaminophilum FdhC (CAC39240.1) that has been characterized experimentally ( Graentzdoerffer et al., 2003). Formate could serve as an electron donor, carbon substrate, or both. A possible formate dehydrogenase gamma subunit gene (01341_2381) is found in a cluster with other ORFs

variously annotated as formate, thiosulfate, INNO-406 and tetrathionite reductase component genes; it is doubtful whether their in vivo roles can be deduced from the sequences alone. Phosphotransferase systems for carbohydrate uptake typically consist of one or two membrane (EIIC/EIID) and one or two cytosolic (EIIA/EIIB) components specific for a given carbohydrate, and two more general cytoplasmic components (EI and HPr), which may be in various combinations of fused and separate proteins (reviewed in Deutscher et al. (2006)). EI is a phosphoenolpyruvate:protein phosphotransferase, and HPr is a phosphocarrier transferring phosphate groups from EI to EIIA. In Gram-negative bacteria, phosphate groups are transferred in a cascade from phosphoenolpyruvate (PEP) to the membrane PTS components, and thence to a periplasmic carbohydrate

molecule, concomitant with its uptake. The phosphorylated carbohydrates are typically fed into the glycolysis pathway. PTS genes are also involved in transcriptional regulation of carbohydrate metabolism. Pregnenolone Only two sets

selleck screening library of putative PTS-related genes have been annotated in the BOGUAY genome. One is related to ascorbate uptake systems, and includes possible EIIA (ulaC, 00136_0633), EI (ptsI, 00136_0635) and HPr (hprK, 00136_0634) genes; the other is related to regulatory systems that are thought to coordinate nitrogen and carbon uptake, and includes putative EIIA (ptsN, 00726_1444) and HPr (hprK, 00726_1445) genes. No membrane-protein genes have been identified for either of these potential PTS systems, however; they may have strictly regulatory (or other) functions, or novel membrane components. The BOGUAY genome encodes a complete glycolytic pathway, and apparently two types of energy-generating electron transport pathways. In addition to the common oxidative phosphorylation pathway, in several possible variants, it possesses two different genes for most components of a putative Rnf complex, a potentially energy-generating ion pump whose detailed function is not yet well understood. This suggests that the BOGUAY strain may be able to access a range of electron donors and acceptors. Details are discussed immediately below. All glycolysis genes seem to be present in the BOGUAY genome (Table S6), with energy-conserving pyrophosphate-consuming enzymes apparently preferred to those hydrolyzing ATP. There are two possible pyrophosphate-dependent 6-phosphofructokinases (PFKs; Fig.

, 2010). In the present study, we apply inter-species transcriptomics to two, closely related marine flowering plants that occupy different ecological niches ( Den Hartog, 1970 and Phillips and Menez, 1988). The seagrasses, Zostera marina (eelgrass) and

Nanozostera noltii (dwarf eelgrass; formerly Zostera noltii) ( Coyer et al., 2013) diverged ~ 14 Mya ( Kato et al., 2003 and Coyer et al., 2013). They provide the foundational habitat for the seagrass community of many, soft-sediment, coastal systems along European coasts. Z. marina ranges from southern Portugal to northern Norway and Iceland, as well as into warm temperate areas of the Mediterranean, LEE011 where it becomes more sparse ( Borum et al., 2004). In contrast, N. noltii ranges from southern Norway to Mauritania, also including the Mediterranean, Black, Aral, and Caspian Seas ( Phillips and Menez, 1988 and Borum et al., 2004). The two species overlap in their distributional range roughly between the northern Mediterranean and southern Norway. Z. marina is predominantly

subtidal, particularly in warmer southern European locations ( Laugier et al., 1999, Billingham et al., 2003 and Massa et al., 2008), where it experiences relatively constant physical conditions and fewer extreme temperatures due to the balancing effect of the surrounding water column. In more northerly latitudes it occurs both subtidally (northern Denmark) and, to a lesser extent, intertidally, (Wadden Sea) ( Oetjen and Reusch, 2007). At the Thau Lagoon location (Mediterranean coast of France) it is sheltered, permanently supplied with nutrients PF-01367338 and less exposed to environmental extremes ( Laugier et al., 1999). In contrast, N. noltii is predominantly an intertidal species, where it experiences more variable environmental conditions of sea and air exposure, as well as physical stressors such as wind and waves ( Laugier et al., 1999 and Massa

et al., 2008). In the Ria Formosa Lagoon in southern Portugal, N. noltii experiences summer temperatures of 36 °C during tidal exposure, which check details is mainly a function of air temperatures and irradiance due to the thin water columns characteristic of intertidal pools ( Massa et al., 2008 and Massa et al., 2011). In this environment local extinction of Z. marina has been correlated with the warmest summers in the Ria Formosa from 2003 to 2008 ( Massa et al., 2008). Extreme weather events are increasing under global warming scenarios and are predicted to have strong influences on ecosystems and associated species (Easterling et al., 2000 and Walther et al., 2002). Water temperatures of ~ 25 °C are the critical threshold for Z. marina in northern Europe ( Reusch et al., 2005, Nejrup and Pedersen, 2008 and Bergmann et al., 2010), but not for N. noltii. Thus, the northerly range expansion of N.

1 Research reports must contain sufficient information to allow readers to understand how a study was designed and conducted, including variable definitions, instruments and other measures, and analytical techniques (Moher et al., 2008). For review articles, systematic or narrative, readers should be informed of the rationale and details behind the literature search strategy. Too often articles fail to include their standard

for inclusion selleck kinase inhibitor and their criteria for evaluating quality of the studies (Simera et al., 2008). As noted by Doug Altman, co-originator of the Consolidated Standards of Reporting Trials (CONSORT) statement and head of the Centre for Statistics in Medicine at Oxford University: “Good reporting is not an optional extra: it is an essential component of good research we all share this obligation and responsibility.” (Altman, June 2008). Reporting guidelines are documents that assist authors in reporting research methods and findings. They are typically presented as checklists or flow diagrams that lay out the core reporting selleck chemicals criteria required to give a clear account of a study’s methods and results. The intent is not just that authors complete a specific reporting checklist but that they ensure that their articles contain key elements. Reporting guidelines should not be seen as an

administrative burden; rather, they are a template by which an author can construct their articles more completely. Reporting guidelines have been developed for almost every study

design. More information on the design, use, and array of reporting Arachidonate 15-lipoxygenase guidelines can be found on the website for the Enhancing the Quality and Transparency of Health Research (EQUATOR) network, (EQUATOR network) an important organization that promotes improvements in the accuracy and comprehensiveness of reporting. Examples include the following: (1) CONSORT for randomized controlled trials (www.consort-statement.org); There is accumulating evidence that the use of reporting guide- lines improves the quality of research. (Turner et al., 2012) established that the use of the CONSORT statement improved the completeness of reporting in randomized controlled trials. Diagnostic accuracy studies appeared to show improvement in reporting standards when the STARD guidelines were applied (Smidt et al., 2006). Early evidence also suggests that inclusion of reporting standards during peer review raises manuscript quality (Cobo et al., 2011). The International Committee of Medical Journal Editors now encourages all journals to monitor reporting standards and collect associated reporting guideline checklists in the process (International Committee of Medical Journal Editors). Furthermore, the National Library of Medicine also now actively promotes the use of reporting guidelines (U.S. National Library of Medicine).

Such theories have already proven successful in other health promotion interventions such as in educational materials for smoking cessation [11]. A critical component of constructivist learning theory is elicitation of cognitive dissonance [12]. Cognitive dissonance occurs when a person’s preconceived notions about the self and the world clash with new knowledge

Dabrafenib research buy acquisition; the discrepancy that is evoked results in a state of tension known as cognitive dissonance [12]. Our educational intervention for reducing benzodiazepine use was developed to create cognitive dissonance by soliciting an aversive motivational state in recipients by confronting two inconsistent cognitions on benzodiazepine use. The theory holds that as the experience of dissonance is unpleasant, the individual will be motivated to remove the pressure caused by this conflict by altering one of these perceptions to achieve consonance [12]. Erlotinib supplier For instance, if an individual previously believed that benzodiazepines were safe, the threatening

content of the tool challenges this belief by providing information that benzodiazepines incur several harmful risks, thus putting into question whether consumption should be continued [13] and [14] We also incorporated social comparison theory into the content of the intervention to reassure participants about their newfound uncertainty regarding benzodiazepine use. Social comparison states that: “people evaluate their opinions and abilities by comparison respectively with the opinions and abilities of others”[15]. It thus consists of comparing oneself with others in order to evaluate or to enhance some aspects of the self [16]. Here, the evaluation of the ability or inability to

do a specific action relies on the success of a proxy performer. The efficacy of this theory depends on whether the comparer assimilates or contrasts him/herself to others [17]. Comparability with a peer champion’s narrative and previous agreement with the peer’s views Histidine ammonia-lyase are important factors for the comparison to work [16]. A self-assessment component was also introduced, which aimed to promote insight about potential misinformation or beliefs held about benzodiazepine use by providing feedback on incorrect assumptions [18] and [19]. Textual content of the intervention was based on a systematic review of the evidence as well as guidelines concerning the use of benzodiazepines in the elderly. A geriatrician and graduate student drafted the initial content of the tool, which was then validated by a panel of colleagues with expertise in geriatric pharmacy and reviewed by a health librarian to ensure that the wording met standards for patient literacy at the Grade 6 level. The tool was developed in English, and backward and forward translated into French.

While our data on linking MAG, SPNA2 and NEFL expression to grip strength are preliminary, epidemiological data suggest significant correlations of TBI to the development of CNS pathologies with long-term motor dysfunction, including; amyotrophic lateral sclerosis (ALS), Parkinson’s disease, Alzheimer’s disease and chronic traumatic encephalopathy

[[10], [11], [12] and [13]]. For example, TBI has been linked to a ˜3-fold increased risk of ALS [13,59], and the genes and environmental exposures in veterans with ALS (GENEVA) case-control study revealed Osimertinib significantly increased risk of ALS in veterans with a TBI [12]. Lastly, we briefly discuss two of the proteins shown in Table 1 that did not exhibit statistically significant correlations to post-injury time and/or grip strength: GSTM5 and GPI. GSTM5 is a member of the glutathione s-transferase superfamily: a major group of detoxification enzymes that alleviates the damage from lipid peroxidation by-products (e.g., 4-HNE and acrolein) by catalyzing their conjugation with glutathione [60,61]. Our results indicate increased lipid peroxidation during mTBI, which could be exacerbated by decreased levels of GSTM5 [62]. GPI is a dimeric enzyme that catalyzes the reversible isomerization of glucose-6-phosphate and fructose-6-phosphate. In the cytoplasm, Selleckchem RG7420 GPI

is involved in glycolysis and gluconeogenesis, while outside the cell it functions as a neurotrophic factor for spinal and sensory neurons. Interestingly, we also observed that GPI levels were decreased in mTBI vs. sham. In contrast, we observed increased levels of GPI in our previous work on a mouse model of multiple sclerosis [22]. M2 proteomics was developed

to provide the following advantages: to improve sample throughput by decreasing lengthy sample preparation times, to improve sensitivity by decreasing adsorptive losses, and to improve statistical power by enabling quantitative MS/MS-based proteomic studies with relatively large numbers of specimens. One disadvantage is the greater computational burden that comes with larger numbers of specimens and MS/MS spectra. A rigorous comparison of the analytical figures Janus kinase (JAK) of merit for M2 proteomics vs. other proteomics methods is beyond the scope of this work, including: M2 proteomics vs. conventional approaches for quantitative MS/MS-based proteomics, bead-based immunoassays, and gel-based proteomic methods such as two-dimensional electrophoresis. However, since our initial publications on M2 proteomics [22,23], we have successfully applied M2 proteomics to a variety of preclinical and clinical studies. Moreover, there is a growing number of reports of high-throughput sample preparation by microwave-assisted digestion [63,64] or by magnetic beads [65], high-sensitivity on-bead digestions [66], and isobaric labeling reagents for multiplexed protein quantification by MS/MS-based proteomics [67,68].

elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Author, Dr Rao M. Adibhatla, and the Editor-in-Chief following finding of research misconduct [data falsification] against the Author by the US Office of Research Integrity. See Fed. Regist., 78 (17) (January 25th 2013). “
“This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy).

This article has been retracted at the request of the corresponding Author owing to the inadvertent duplication BIBW2992 supplier of some data [p-Drp-1 blots presented in fig. 2] between this article and “Dynamic changes of mitochondrial fusion and fission proteins after transient cerebral ischemia in mice”, Liu, W, Tian, F, Kurata, T, Morimoto, N, Abe, K. J. Neurosci. Res., 90 (6) (2012) 1183–1189, http://dx.doi.org/10.1002/jnr.23016. “
“Stroke is currently a critical public health problem and a major cause of death and disability in adults worldwide (Lloyd-Jones et al., 2009 and Lotufo, 2005). Several pathophysiological events are triggered in brain tissue after an ischemic injury, including the inflammatory response and oxidative stress damage (Brouns and De Deyn, 2009 and Deb et al., 2010). Thus, drugs with anti-inflammatory and antioxidative actions have been expected to have BMS-354825 research buy a protective effect in brain ischemia. Polyphenols are natural substances found in plant products, as leaves and

fruits, oils, wine and tea. They are divided into phenolic acids, flavonoids and non-flavonoid polyphenols (Ramassamy, 2006). Like beta-carotene and ascorbic acid, polyphenolic compounds are related to protective effects against cancer and cardiovascular disease (Heim et al., 2002). Flavonoids are part of this large group of polyphenolic compounds, and more Avelestat (AZD9668) than 2000 flavonoids have been identified (Ramassamy, 2006). The most important pharmacological properties of flavonoids are its anti-inflammatory and antioxidative actions (Benavente-García and Castillo, 2008, Formica and Regelson, 1995, Juurlink and Paterson, 1998 and Procházková et al., 2011). The use of flavonoids has been proposed for pathologies of central nervous system, such

as Parkinson’s disease, Alzheimer’s disease and stroke, due to such properties and to data from epidemiological studies (Ramassamy, 2006 and Sun et al., 2008). Rutin, also called as quercetin-3-O-rutinoside, is a flavonoid glycoside composed of the flavonoid quercetin and the disaccharide rutinose that have antioxidative, anti-inflammatory, antiallergic, anti-viral and anti-carcinogenic actions (Araújo et al., 2011). Few studies have evaluated the treatment with rutin in models of global and focal brain ischemia, showing positive effects (Gupta et al., 2003 and Khan et al., 2009). Rutin administration has been evaluated in a model of focal brain ischemia, revealing protective action (Khan et al., 2009). However, only pre-ischemic administration was assessed (Khan et al., 2009).

7–97.7%) with a ratio effect of comparable effect size (1.7%) with larger SD (2.97%). However, considering the similar size of the overall accuracy and distance effects in relation to Price et al. (2007), in our study the .1% between group

ratio effect difference we found can be considered practically zero. This is confirmed by the fact that the bootstrap 95% confidence interval of the non-symbolic comparison ratio effect was clearly focused on zero (see Fig. 3.), the very small confidence intervals were approximately symmetric around zero and SEs were very small, about .4%. All the above suggests that there was not much variability or directional bias in our data and that there was not even an indication of a difference in the ratio effect between the groups. Fourth, regarding the symbolic magnitude

comparison task the mean of the between group difference was 2% and the SD of the data was about 5.71%. The DD group showed a smaller LDK378 in vitro absolute value distance effect than the control group (3.26% vs 5.24%). Crucially, DD actually showed slightly better performance on the task than the controls while RTs were practically identical. This makes it unlikely that DD had impaired access to MRs in this task. Nevertheless, in the data from the Arabic number comparison task of Mussolin et al., 2010a and Mussolin et al., 2010b the overall mean distance effect (calculated for all four ratios used; see ibid. Table 2) was actually exactly the same in the Lapatinib ic50 control and DD groups (2.76%) and the difference between the most extreme distance levels was also the same in both groups (8.3%). The DD and the control

group showed a difference because the closest levels of distance differed more in the DD than in the control group. However, this means that the DD group was .6% less accurate at the closest level of distance while it was actually 1.1% more accurate than the controls at the second closest level of distance. The difference between the groups was 1.7% (controls: 2.7%; DD: 4.4%) and the SD of the data was about 1.75% (this is not very clear as the table reports exactly the same standard deviation values for both groups which is probably a mistake). Hence, the group difference was .97SD. For our 12 subjects such an effect size would give Power > .99. (It is to note that crucial Galeterone analysis results in Mussolin et al. (2010) relied on trials collected from 5 different stimulus formats (5 × 24 = 120 trials for each level of distance) rather than from an individual stimulus format.) However, we only measured a 2% (.33SD) between group difference in the distance effect. In addition, as noted above, the somewhat higher accuracy in the DD than in the control group also makes it unlikely that our DD group had problems with accessing the magnitude of single Arabic digits. Fifth, it is important to emphasize the difference between the robustness (large effect size) of WM and inhibition results in contrast to MR-related results.

We validated our hits with quantitative realtime RT-PCR assays for Hepcidin expression and characterized them

by their effects on genes regulated by BMP’s or Stat3, as well as Western blots to detect phosphorylation of Smad1,5,8 or Stat3. We confirmed 16 small molecule Hepcidin stimulating agents in a broad range of functional classes. All of the chemicals identified increased expression of bone morphogenic protein-dependent and/or Stat3-dependent genes, however none of them strongly increased phosphorylation of Smad1,5,8 selleck inhibitor or Stat3. Several of the Hepcidin stimulatory chemicals inhibit growth factor receptor dependent signaling (AG1296, GTP 14564, AS252424, 10058-F, SU6668, and pterostilbene), decrease inflammation (leflunomide, amlexanox), or impair DNA repair and promote apoptosis (daunorubicin, 9-aminocridine, ethacridine), while the small molecules, vorinostat and SB 204741, inhibit histone deacetylase and serotonin receptor 2B, respectively. Two of the molecules, ipriflavone and vorinostat, were active at concentrations that were 10-fold below those required for genistein’s effect and thus appear to be intriguing candidates for further development. The human hepatocarcinoma cell line, HepG2, (American Type Culture Collection, Manassas, VA) was maintained in α-Minimum Essential Medium

(α-MEM)/10% certified endotoxin-free fetal bovine serum (FBS)/1% penicillin–streptomycin (Life Technologies, Grand Island, NY) at 37 °C, 5% CO2. To generate a Hepcidin reporter cell line, HepG2 cells, were transfected using SuperFect Selleckchem Nutlin3a (Qiagen, Valencia, CA) transfection Amylase reagent and a reporter construct including a 2.7 kb fragment of the

human Hepcidin promoter upstream of a firefly luciferase promoter (gift of Drs. Ganz and Nemeth). Transfected clones were selected for resistance to G418 (Life Technologies) and subsequently maintained in the conditions described above with the addition of G418 1 mg/ml. Bone morphogenic protein 6 (BMP6) (R&D Systems, Minneapolis, MN), interleukin-6 (R&D Systems), and genistein (Sigma-Aldrich, St. Louis, MO) were used as positive controls for Hepcidin-luciferase activity, while dorsomorphin (#171260, Calbiochem, Billerica, MA) was used as a negative control. WP1066 (#573097, Calbiochem) was used as an inhibitor of Stat3 signaling. Interleukin-6, EGF, FGF, PDGF, and VEGFA were obtained from R&D Systems. The Institute of Chemistry and Cell Biology (ICCB) Screening Facility at Harvard Medical School provided drug libraries. The complete list of chemicals screened and the screening data are provided in Supplementary Table 1. The day before the addition of compounds, HepG2-Hepcidin luciferase cells were plated at 5000 cells in 30 μl per well of a 384-well microtiter plate (Nunc 142762) in α-MEM/1% penicillin/streptomycin using a WellMate MicroPlate Dispenser (Thermo Scientific, Rockford, IL).