At the end of the experiment, the organs were dissected out and w

29 ± 1.0 versus 12.12 ± 1.1 g, P < 0.001; Fig. 1B). At the end of the experiment, the organs were dissected out and weighed. The META060 supplementation decreased gonadal (1.17 ± 0.2 versus 2.40 ± 0.09 g, P < 0.001) and subcutaneous (0.47 ± 0.09 versus 1.53 ± 0.2 g, P < 0.001) white adipose tissue masses in the HFD-fed mice compared with no-supplement controls ( Fig. 1C). At 15 wk, half the mice in the HFD group were shifted to the HFD/META060 group,

and half the mice in the HFD/META060 group were shifted to the HFD-only group. Body weight was monitored weekly for 5 wk in these four treatment groups. Although the animals maintained on the HFD for the entirety of the experiment continued to gain weight, those shifted to the HFD/META060 group lost a

significant amount of weight during weeks 16 and 17, after which they began to gain weight again (Fig. 1D). A concomitant decrease in food intake was observed learn more in the first 2 wk after switching diets, followed by a rebound to even higher levels than the food intake in mice in the HFD/META060 group that did not switch diets (data not shown), perhaps a reflection of an adjustment to the palatability differences between the distinct diets. To investigate how META060 protects against HFD-induced obesity, an independent 5-wk study was initiated with three treatment groups: HFD, HFD supplemented with META060 (100 mg ∙ kg−1 ∙ d−1), or HFD supplemented with rosiglitazone (1 mg ∙ SCH 900776 in vivo kg−1 ∙ d−1). In the first 5 wk of the 14-wk intervention study, the average weight gained in the HFD group was 5.61 ± 0.7 g, whereas the FER mice supplemented with META060 gained 0.68 ± 0.3 g. In the 5-wk study, the average weight gained in the HFD group was 2.58 ± 0.4 g, and mice supplemented with META060 gained 0.54 ± 0.9 g (Fig. 2). Despite differences in the absolute weight gained, which was likely due to the difference in age of the mice at the start of each study, the META060 supplementation reproducibly decreased

the relative HFD-induced body weight gain in the two experiments. Whole-body substrate use was examined for approximately 36 h during week 4 of the dietary intervention. Four weeks of dietary intervention was chosen because, at this time point in the 14-wk study, body weight was still increasing and a new set point had not yet been reached. Although we did not directly compare the LFD group during the 5-wk study, we knew from published and experimental data that 5 wk of HFD feeding in mice results in an unaltered total energy expenditure (kilocalories per hour) but in changes RER, fat (FA), and CHO oxidation. Daytime RER was 0.84 ± 0.04 versus 0.94 ± 0.04, and night-time RER was 0.84 ± 0.03 versus 0.93 ± 0.04 for the HFD versus LFD group, respectively (P < 0.05). The daytime FA oxidation was 0.17 ± 0.05 versus 0.07 ± 0.04, and the night-time FA oxidation was 0.19 ± 0.05 versus 0.08 ± 0.06 for the HFD versus LFD group, respectively (P < 0.05).

Age, gender, and ambulatory status, defined as 1=GMFCS levels I t

Age, gender, and ambulatory status, defined as 1=GMFCS levels I to III and 0=GMFCS levels IV to V, were adjusted for in each analysis. The following model was used for all analyses: block 1: age, gender, ambulatory status; block 2: anthropometric measure. Each anthropometric measure was entered in a separate analysis to avoid multicollinearity. When systolic blood Epigenetics inhibitor pressure or diastolic blood pressure was the dependent variable of interest, the

analysis was additionally adjusted for self-reported taking of antihypertensive medication (coded as 1 if yes or 0 if no). When TC, HDL-C, LDL-C, or TC/HDL-C ratio was the dependent variable, additional adjustment was made for self-reported taking of cholesterol medication (coded as 1 if yes or 0 if no). To examine whether WC, WHR, or WHtR were associated with cardiometabolic risk factors independent of BMI, follow-up analyses were conducted between each cardiometabolic risk factor and WC, WHtR, and WHR, additionally adjusting for BMI in block

1. Variance inflation factors <5 revealed no issue with collinearity. A receiver operating characteristic (ROC) curve analysis was conducted to compare the anthropometric measures at predicting the presence of individual cardiometabolic risk factors (hypertensive blood pressure, hypercholesterolemia, low HDL-C, high LDL-C, hypertriglyceridemia, hyperglycemia, high HOMA-IR index, high-risk CRP) and the presence of ≥2 risk factors. An area under the ROC curve of >.90 is considered Angiogenesis inhibitor excellent; .80 to .90 is considered good; and .70 to .80 is considered fair. All analyses were performed using Analyse-it for Microsoft Excel (version 2.20)c and IBM SPSS Statistics (version 19).d Statistical significance was set at P<.05. The demographic and diagnostic distribution of participants is presented in table 1. A value for CRP and insulin was missing for 1 nonambulatory person and a value for plasma glucose was missing for 1 ambulatory

person, as a result of processing errors. One ambulatory person reported a prediagnosis of type 1 diabetes mellitus. This person was removed from all analyses of blood biomarkers of glucose metabolism (ie, plasma glucose, insulin, HOMA-IR index) and the MetS. Hip circumference was not obtained from 2 nonambulatory adults because of significant contractures. Participants’ anthropometric measures Rucaparib nmr and cardiometabolic outcomes are presented in table 1. Within the study cohort, BMI ranged from 12.3 to 36.8kg/m2, WC ranged from 64 to 126.5cm, WHR ranged from 0.68 to 1.11, and WHtR ranged from .36 to .81. Four participants (7.3%) were obese according to BMI cutoffs. The prevalence of central obesity was 36.4% (table 2). A significant difference between ambulatory and nonambulatory adults was observed for WHR (P<.05), HDL-C (P<.01), and TC/HDL-C ratio (P<.05). There were no other between-group differences. Pearson’s partial correlations revealed that the GMFCS was associated with hip circumference (r=−.356; P<.

Exposure to cylindrospermopsin also induced damage to pulmonary p

Exposure to cylindrospermopsin also induced damage to pulmonary parenchyma as indicated by the increased amount of alveolar collapse, PMN influx, and oxidative stress. In the lungs the toxin concentration decreased and in the liver it increased as a function of time. In the present study we used a sub-lethal dose (0.07 mg/kg) of cylindrospermopsin once human and animal exposures to non-lethal concentrations are more common than acute intoxications. Indeed, no death occurred during the experiments. The literature shows that LD50 of this toxin presents a toxicity that varies in the time of death according to the intraperitoneal dose in mice: 2.0 mg/kg BW causes death in 24 h and 0.2 mg/kg BW along 5–6 days (Norris et al.,

2002). http://www.selleckchem.com/products/Lapatinib-Ditosylate.html Hence, this may suggest its slow and progressive process of poisoning

in the face of sub-lethal doses. In fact, animal and human exposures to these doses occur more frequently than lethal events, damaging many organs, such as liver, kidneys, thymus, heart and lung (Falconer et al., 1999; Humpage and Falconer, 2003; Pegram et al., 2007). We could detect a higher concentration of cylindrospermopsin in the lung along the first 24 h after intratracheal instillation (Fig. 4), possibly due to the direct pathway of the toxin. Furthermore, we observed that the concentration in the liver increased significantly at 96 h after instillation. Since cylindrospermopsin was administered by the intratracheal route, it rapidly reached the lung, then going to the target organs, Selleckchem CHIR-99021 such as liver and kidneys. Considering Tyrosine-protein kinase BLK that the kinetics of cylindrospermopsin and its metabolites in the liver, and mainly in other organs and bloodstream, is poorly understood, the present work does not provide a proven explanation for the increase

in the toxin concentration in the liver at 96 h after intoxication. The kidneys seem to be the most sensitive organs in mice exposed sub-chronically to cylindrospermopsin (Humpage and Falconer, 2003), while the liver plays a key role in the metabolism of that toxin, with the involvement of cytochrome P450 (CYP450) enzymatic system. Froscio et al. (2003) observed protection from cylindrospermopsin toxicity by CYP450 inhibitors; thus it is possible that the early and higher toxicity is related to CYP450-dependent activation, once more toxic cylindrospermopsin metabolites can spread by the bloodstream (Norris et al., 2001). Indeed, these authors reported the presence of the toxin’s metabolites in the liver and kidney tissues of mice exposed intraperitoneally to radiolabelled cylindrospermopsin. According to Bryant and Knights (2010), the parent cylindrospermopsin can also enter the bloodstream and reach other organs. Unfortunately, there is no information in the literature concerning the bloodstream transport of cylindrospermopsin metabolites. The later toxicity would be a consequence of protein synthesis inhibition (Runnegar et al., 2002).

Catalog #P6181) was added at 1:20 ratio of enzyme to substrate an

Catalog #P6181) was added at 1:20 ratio of enzyme to substrate and incubated at 37 °C for ∼24 h Rat.

The patch clamp method (Hamill et al., 1981) was used to trace and record, ionic currents from heterologous expression systems over-expressing a recombinant channel. BGB324 ic50 NaV1.3 channels were expressed in HEK-293 cells as described (Cummins et al., 2001). There is some degree of endogenous expression of NaV channels in HEK cells, but their contribution in comparison to exogenously expressed channels is usually minute (Moran et al., 2000). Rat NaV1.8 channels were expressed in ND7-23 cells by using conventional transient or stable transfections as described (Zhou et al., 2003, John et al., 2004, Jarvis et al., 2007 and Zimmermann et al., 2007). HEK cells stably expressing human NaV1.3, human NaV1.8 and human NaV1.7 channels were purchased from Scottish Biomedical (Glasgow, UK). Human NaV1.5 channels were expressed in HEK-293 cells as described

(Van Bemmelen et al., 2004). The patch clamp set up included amplifier and digitizer (Axopatch 200B and DIGDATA 1322A, CP 868596 Axon instruments, USA), microscope (Nikon ECLIPSE 100) and micromanipulator (MP-225-Sutter Instrument Co., USA). Recording pipettes were pulled from Borosilicate glass tubes (Sutter Instrument co., USA). Cells were always perused with control extracellular solutions and changing to reagents containing solutions was performed using ValveLink 16 (Automate Scientific Inc. Berkeley, USA) and a peristaltic pump (Ismatec, Wertheim, Germany) perfusion system. Intracellular (pipette) solution (in mM): 120 CsF, 10 NaCl, 10 TEA-OH, 1 MgCl2, 1 CaCl2, 11 EGTA, Phosphatidylinositol diacylglycerol-lyase 10 HEPES (pH = 7.2 titrated with KOH). The extracellular (bath) solution contained (in mM) 115 NaCl, 20 TEA-OH, 1 MgCl2, 2 CaCl2, 5 glucose, 10 HEPES (pH = 7.4 titrated with NaOH), supplemented with 600 nM TTX when recording rat or human NaV1.8 channel currents. All channels were activated

using the following stimulation protocol: Holding level −100 mV, ramp from −100 to +60 mV (50 ms), delivered every 10 s and recorded at a sampling rate of 10–50 kHz. The ramp protocol is increasingly in use as a quick measure of I–V relationship (see for example Dib-Hajj et al., 2007). Indeed, it is possible that measuring inhibition upon square pulse stimulation, may have yield somewhat different results (maybe shifting the dose response curves). However, the ramp stimulation method has enabled the use of exactly the same stimulation protocol with all channels tested. All chemicals were from Sigma–Aldrich (Rehovot, Israel) apart from TTX from Alomone Labs (Jerusalem, Israel). All results are presented as mean ± standard deviation.

19) Type 2 differs from Type 1 in that aquifers supplying the hi

19). Type 2 differs from Type 1 in that aquifers supplying the high elevation springs are perched or impounded within a vadose zone that is several hundreds of metres thick. Under this regime the units beneath the perching aquitard would be unsaturated. An unpublished commercial report (Maxim Engineering, 1995) selleck inhibitor states that a 1967/1968 water test well located in a ghaut on the northern slopes of CH at ∼200 m amsl was drilled to a depth of 75 m amsl and did not encounter saturated material. Up-valley of this drill site

at the elevations of 315 and 345 m amsl the ghaut is fed by Blackwood Allan and Mongo Springs. In the Type 2 model the spring aquifers are hydraulically connected to the deeper hydrological system and to low elevation coastal aquifers. Under these conditions spring behaviour, temperature and composition is hydraulically coupled with groundwater

conditions and pressure at depth, and therefore to volcanic perturbation. By defining hydraulic connectivity between low and high elevation aquifers, this model can better explain the anomalously warm springs at high elevation on the south side of CH. Certain observations from Montserrat are consistent with either of the major volcanic island conceptual hydrology models. Without deep boreholes within the central portions of Montserrat’s volcanic complexes it is difficult to definitively propose which model best represents the hydrology of this volcanic arc island. Both should be maintained as working hypotheses, with a view to gathering data to better constrain the system. High yielding springs on the flanks of the extinct GDC-973 Centre Hills volcanic complex and low lying aquifers in more distal locations provide an essential water

resource to the island’s population, as it recovers from over 15 years of volcanic activity. Recharge models predict annual recharge of 10–20% of annual rainfall with a strong seasonality; models predict that over 70% of the islands recharge occurs between July and December. Land use is a critical control on recharge; during extended periods of quiescence changes next in vegetation type, including colonisation and eventual afforestation of young deposits in the south, and deforestation for agriculture around Centre Hills, are expected to modify the current recharge conditions. Recharge will also be affected by any fluctuations in rainfall patterns associated with climate change; this will, no doubt, have implications for spring yield. The development of springs at elevations of 200–400 m amsl, on an island with only ephemeral rivers and no other surface water, requires the presence of low permeability units. Assuming a recharge rate of 0.27 m/yr the surface recharge area required to supply the highest yielding spring on Montserrat is over 40 times the topographically defined catchment.

This relationship was also observed through the Pearson correlati

This relationship was also observed through the Pearson correlation coefficient between the expansion ratio and density (r = −0.952, p < 0.001), thus indicating a strong negative correlation between these two dependent variables. Density is a parameter that can also be used to assess the degree of expansion of the extrudates. While the expansion ratio considers only the cross-section of the material, density EGFR assay considers expansion in all directions. Low density is desirable for extruded products ( Meng, Threinem, Hansen, & Driedger, 2010). The same temperature effect on extrudate density was observed by Yuliani et al. (2009) in relation to extrusion of corn starch with d-limonene and by Saeleaw

et al. (2012) in relation to extrusion of rye flour. The cutting force of the extrudates ranged from 20.98 to 51.60 N, which was close to the range of values found by Conti-Silva et al. (2012) for the cutting force of flavored corn grit extrudates, which was 23.7–34.2. The best fit for the cutting force of extrudates was also observed for the linear model, and only the extrusion temperature was significant (Table 2). It was observed that increasing the extrusion temperature not only decreased the density but also decreased

the cutting force of the extrudates, also verified by the negative sign of the coefficient of the linear find more term of temperature (Table 2). Since temperature increases reduce the viscosity of the dough and promote growth of air bubbles, the thickness of cell walls in the extrudates decrease (Yuliani et al. 2006a), thus reducing the cutting force. The cutting force of the extrudates was negatively correlated with the expansion ratio (r = −0.628, p = 0.007) and positively Bay 11-7085 correlated with the density (r = 0.726, p = 0.001), given that extrudates presenting greater expansion or lower density may be structurally more fragile or have lower mechanical strength ( Yuliani et al., 2009). Volatile compounds retention ranged from not-detected (ND) to 0.49 mg/g of extrudate for isovaleraldehyde, from 0.05 to 0.62 mg/g of extrudate for ethyl butyrate

and from ND to 36.10 mg/g of extrudate for butyric acid. The bigger retention was found to the butyric acid, followed by ethyl butyrate and isovaleraldehyde, as found by Conti-Silva et al. (2012). This behavior is due to vapor pressure and boiling temperature of the volatile compounds. Isovaleraldehyde, the compound less retained in all extrusion conditions, has the biggest vapor pressure (4009 Pa) and lowest boiling temperature (92.5 °C), as opposed to butyric acid that was more retained because of the lowest vapor pressure (57 Pa) and biggest boiling temperature (163.7 °C) (Lide, 1997). The low volatility promotes a higher diffusivity of the compound through the matrix of the extrudate, resulting in a bigger encapsulation and, consequently, higher retention.

It should be noted that a permanent operational oceanographic sys

It should be noted that a permanent operational oceanographic system with both monitoring components (observation/modelling) in place has not yet been established

in Croatia. In the last decade there have been some periodic and intensive monitoring programmes with the participation of Croatian institutions, covering the entire area of the Adriatic (ADRICOSM Project (Acta Adriatica 2006); Adriatic Sea Monitoring Programme (Andročec et al. 2009)), or only parts of the Adriatic basin (MAT Project (Science of the Total Environment 2005); the Croatian National Monitoring Programme CDK inhibitor (www.cim.irb.hr/projekti/projekt-jadran/)).

For the purpose of detecting the spread this website of oil spills within the Adriatic area, the SAR/GIS monitoring system (Morović & Ivanov 2011) is already in place but has not been followed up with numerical model implementation at operational level for forecasting and strategic decision-making. In the early morning hours of 6 February 2008, a Turkish freighter caught fire in the Adriatic Sea 13 nautical miles west of the town of Rovinj (Figure 1). An SOS was sent at 04:04 hrs local time. The 193 m long ship was sailing from Istanbul in Turkey to Trieste in Italy and was carrying 200 trucks and nine tons of hazardous material, in addition to a few hundred tons of ship fuel, causing fears of environmental damage. 3-mercaptopyruvate sulfurtransferase As the fire had started inside the ship (Figure 1), there was no way of extinguishing it from the outside. Motivated by this incident, we conducted a numerical analysis with hypothetical scenarios of oil spreading resulting from a 12-hour continuous crude oil spill from a stationary ship at 18.5 kg s− 1, reaching a total amount of 800 tons. Therefore, the present study includes several steps: a) running a numerical

model that defines a three-dimensional unsteady and non-uniform sea current, temperature and salinity fields for the continuous period 1 January–15 November 2008; b) running an oil pollution transport model based on reactive and dispersive processes, also accounting for the intense surface horizontal spreading in the first stage after the oil spill. Analysis of wind data for the position of the ‘Und Adriyatik’ when it failed (Figure 1) during the sea circulation simulation period (1 January–15 November 2008) shows seven situations in which the wind, regardless of its direction, had a speed higher than 7 m s− 1 continuously for 24 hours.

In total,

9 studies had the backdrop of African countries

In total,

9 studies had the backdrop of African countries, in different regions of the continent, with emphasis on the studies carried out in Nigeria (5 studies). The studies conducted in Nigeria revealed a variation of prevalence of violence in pregnancy of 17%16 to 58,6%,13 however, the samples were variables, as well as the data collection instruments, representing a research bias, which makes the establishment find more of a uniform parameter difficult to measure. With regard to the profile of victims and aggressors, the results of the Nigerian research were uniforms. The victims were monogamous women, with low level of education and financial dependence of their respective partners.12, 13 and 16 The aggressors, most of them were intimate partners,12, 13, 16 and 17 the low level education is repeated. In the remaining countries of the African continent, other factors emerge as aggravating to the risk factors for violence as the infidelity of a partner, the fact of the woman being single in current pregnancy and have children from different fathers, besides, the refusal

of the woman to use contraceptive methods.18 This last event will result in significant repercussions on women’s health and the future child, since it will increase the number of unwanted pregnancies, such fact, will Veliparib purchase focus on women’s mental health, shaping up as a risk factor for depression and the abortion practice.19 When categorized the types of violence, there is a prevalence of violence defined as verbal and emocional.17, 20 and 21 However, the physical and sexual violence, and the economic abuse practiced by intimate partners were recorded at high rates, the physical abuse, for example, reaches 17%.20 and 22 In the countries of the Asian continent, studies that underscore the religiosity and culture as predictors in the phenomenon

of violence against women Etomidate were found. A study conducted in Iran showed that the abuse during any previous period was a strong risk factor for subsequent abuse. Other risk factors associated to abuse were: woman testifying previously domestic violence, the use of opium by her husband, the woman education < or = 12 years, the age of marriage of the woman < 18 years, the husband’s education < or = 12 years, the economic dependence of the woman.23 It is noteworthy in this context the emergence of a psychoactive substance popular in that country (opium), and the early age of marriages, common in the culture of Islamic countries. Other relevant data with regard to risk factors is related to the fact that women who witnessed domestic violence are more likely to be victims of this abuse, for a cultural issue.

Effects on algae and fish were only observed at extremely high SA

Effects on algae and fish were only observed at extremely high SAS concentrations that exceed current cut-off values for classification as hazardous. No effects on growth and reproduction parameters were found in daphniae or aquatic midge. Even after direct injection into the yolk of zebrafish embryos, no adverse effects were seen with spherical silica particles, while nanowires caused malformations. Toxicity to bacteria and damage to the cell membrane in yeast were observed only at very

high silica concentrations PF-01367338 solubility dmso of ≥1000 ppm. In humans, SAS did not induce silicosis, lung cancer or any other form of cancer. There is no evidence that SAS induces mutations either in vitro or in vivo. Though genotoxicity was observed in a few in vitro test systems, this was generally at dose levels and concentrations that also induced cytotoxicity. No genotoxicity was found after in vivo exposure of experimental animals. In rats, SAS produced transient lung inflammation, and reversible increases of pro-inflammatory cytokines and chemokines at exposure levels of 5 mg/m3 (respirable dust) or higher with

1 mg/m3 (respirable dust) being the No-observed-effect-level (NOEL). As elimination mechanisms include the clearance of particles by macrophages and since human macrophages have about four times selleck compound the volume of rat macrophages ( Krombach et al., 1997), the rat is assumed to respond with more chronic inflammation and epithelial responses as compared to humans. Important insight into the mechanisms and modes of action of SAS, including Protirelin colloidal silica, has been gained from mechanistic studies (e.g., via intratracheal instillation in experimental animals) and from in vitro models. In this context, it has to be considered that results of studies using a suspension medium to apply silica particles either to animals via intratracheal instillation or in in vitro studies, are strongly influenced not only by the particle characteristics but also by the protein and lipid content of the suspension medium which may influence the degree of

particle aggregation. Furthermore, using intratracheal instillation or pharyngeal aspiration as the delivery route to the respiratory tract of experimental animals involves administration of high doses as a bolus, i.e., within a very short time period whereas it would take much longer (hours, days or even weeks) to deliver the same dose via inhalation exposure. This bolus administration implies that many physiological defence mechanisms may be disrupted and artificial health responses be generated that would not occur under physiological in vivo conditions. Interestingly, milder effects have been shown after intratracheal instillation of “nano” silica as compared to micrometre-sized silica particles, possibly because of a faster translocation and elimination ( Chen et al., 2004). Findings from studies employing the intratracheal route can nevertheless be useful as proof-of-principle studies.

9 °C, with a high standard deviation Even at the highest experim

9 °C, with a high standard deviation. Even at the highest experimental temperature of 42.4 °C the wasps showed “rest” according to our definition at least for some minutes ( Fig. 2D, data point (D) in Fig. 3). Some wasps like the individual in Fig. 2E (Ta = 38.5 °C) showed an unusually cool spot at the head which was caused by wetting of the mouthparts

with regurgitated liquid droplets. This behavior cools the head and to some extent also the thorax at high temperatures. However, those wasps were usually active, cooling individuals at rest were an exception. Negative values Talazoparib of the thoracic temperature excess (i.e. the thorax was cooler than the abdomen) may have been caused by the aforementioned evaporative cooling of head and thorax in some individuals, but may also have occurred due to slight vertical temperature gradients inside the measurement chamber and the orientation of the wasp body in this gradient ( Fig. 3, e.g. individual at Ta = 12 °C). Respiration data from clearly identified V. vulgaris   and V. germanica   ( Bellmann, 1995 and Clapperton et al., 1989) did not differ significantly (ANOVA: P   = 0.4857, F   = 0.49), so results of all individuals were pooled (V. vulgaris  : n   = 26, V.

germanica  : n   = 12). With increasing experimental ambient temperature (T  a), CO2 production rate increased exponentially, from 5.658 μl g−1 min−1 at 8.3 °C to 18.504 μl g−1 min−1 at 20.2 °C, 58.686 μl g−1 min−1 at 35.3 °C, and approaching 102.84 μl g−1 min−1 at 40 °C ( Fig. 4). The following exponential function fitted the data best: VCO2=A1∗expTa/t1+A2∗expTa/t2+A3∗expTa/t3+y0VCO2=A1∗expTa/t1+A2∗expTa/t2+A3∗expTa/t3+y0where

www.selleckchem.com/Androgen-Receptor.html VCO2VCO2 is carbon dioxide production rate [μl g−1 min−1] and Ta   is the ambient temperature [°C] in the measurement chamber (R  2 = 0.96275, n   = 846, 38 individuals; the range of validity is 7.7–42.4 °C). Parameters: A1 = 9.7023*10−5, Tobramycin t  1 = 3.11195, A2 = 4.63097, t  2 = 14.6382, A3 = 56769.01521, t  3 = 3.81259*1084, y0 = −56770.80269. The mean Q10 was 2.27 (SD = 0.30, n   = 23). However, with this function the Q10 was not constant. It decreased from 2.98 at a mean T  a of 13 °C (±5 °C) to 1.97 at a T  a of 23 °C and increased to 2.84 at a T  a of 35 °C. This function fitted the data better than a conventional exponential equation (VCO2=a∗bTaVCO2=a∗bTa; R2 = 0.9404; a = 1.37152, b = 1.11652) particularly in the range of Ta = 20 to 35 °C. At high Ta above 35 °C ( Fig. 4, dashed line) CO2 production increased steeply until the wasp’s upper respiratory critical thermal maximum (resp CTmax). Individual wasps differed in their thermal tolerance. Our experiments were not conducted to determine the lethal temperature, nevertheless some wasps died due to continuous exposure to high experimental temperatures. Below 35 °C all wasps survived at least for 6 h (which was the minimal duration of an experiment). At higher temperatures some wasps died already at a Ta below the mean CTmax.