First, that the concept of repeated cycles of forcing–responses driven by long-term climate changes and separated by periods of quasi-equilibrium is now known to be false (Phillips, 2009 and Phillips, 2011). Second, that the present dynamics of Earth surface systems cannot be used uncritically to deduce processes, patterns and products of past system

dynamics; in other words that ‘the present is [not] the key to the past’. In more detail, the monitoring of different contemporary Earth surface systems IWR-1 chemical structure in different physical and climatic settings shows that generalisations of the behaviour of such systems and assumptions of forcing–response relationships cannot be made. These systems’ properties, which are incompatible with the ‘strong’ Principle of Uniformitarianism, include: • Earth surface systems do not exist at steady state or in equilibrium with respect to the combination of external forcings that drive system behaviour. Studies have shown that the workings of Earth systems under ongoing climate change (global warming) and direct human activity in combination are increasingly exhibiting Venetoclax datasheet these systems attributes, listed above (Rockström et al., 2009). Earth systems are now operating in ways that are substantially different to how they are believed to have operated in

previous geologic time periods, irrespective of how such systems are or have been measured (e.g., Edwards et al., 2007). Earth systems modelling (e.g., Phillips, 2003, Phillips, HAS1 2009, Phillips, 2010 and Von Elverfeldt and Glade, 2011) has shown that single equilibrium states are rarely achieved and that many systems appear to have multiple or non-equilibrium states (Renwick, 1992). Moreover, nonlinear feedbacks result in both complex system behaviour and unpredictable outcomes as a result of forcing (Murray et al., 2009 and Keiler, 2011). As a result of this greater knowledge of systems behaviour, Earth systems as viewed today have greater

dissimilarity to those that were initially considered by Lyell and others. The Principle of Uniformitarianism derived from those early studies has thus lost its relevance to Earth system processes viewed today and in light of the Anthropocene. Predictability in the context of Earth systems refers to the degree to which the dynamics (or workings) of a system can be forecast into the future based on our understanding of its previous behaviour. This process is dependent on defining both the present state of the system and the outcome of a measurement, which refers to how systems are monitored in order to identify changes in system state. The Principle of Uniformitarianism implies that, by analogy and comparison with the processes that represent the behaviour of present systems, the behaviour of past systems can be evaluated and – by inference – predicted.

For the immunological assays (ELISA and Western Blotting assays), Falcon flexible micro titration plates were used (Becton Dickinson France S.A). The plates were coated overnight at 5 °C with 100 μl of a 5 μg/ml solution of the crude venoms (B. andianus, B. atrox, B. barnetti, B. brazili, B.

pictus and B. hyoprora) in 0.02 M sodium bicarbonate buffer, pH 9.6. The assays were performed as described previously by Chávez-Olórtegui et al. (1991). Absorbance values were determined at 492 nm with a Biorad 680 Microplate Reader. All measurements were made in triplicate and the results expressed as the median of two assays. For Western Blotting the venoms were subjected to electrophoresis SDS-PAGE (15%) according to Laemmli (1970) in reducing

conditions. The proteins were transferred onto nitrocellulose Alpelisib solubility dmso membranes ( Towbin et al., 1979) and blocked with PBS-Tween 0.3% containing 2% casein. The membranes were incubated with PABA (1:10,000) for 1 h at room temperature. Immunoreactive proteins were detected using anti-horse Sigma IgG conjugated with peroxidase (1:3000). After washing three times for 5 min selleck inhibitor with PBS-Tween 0.05%, blots were developed using DAB/chloronaphthol according to the manufacturer’s instructions. The LD50 of B. andianus venom determined in this paper (57.96 μg, Table 1) is similar to the LD50 doses of B. atrox, 49.9 μg/mouse; B. pictus, 58.91 μg/mouse and B. Barnetti, 53.2 μg/mouse ( Laing et al., 2004; Rojas et al., 2005). However, B. brazili venom was three times more potent in the LD50 assay than the other four Peruvian venoms ( Laing et al., 2004). PABA was effective in neutralizing lethality induced by B. andianus venom and showed high neutralizing potency ( Table 1, ED50 of 200 μl anti-venom/mg venom). Furthermore, local hemorrhagic activity of B. andianus venom was evaluated in a mouse model. B. andianus venom directly induced extra vascular bleeding on the underside of the skin 2 h after injection. The estimated MHD is 4.68 μg ± 0.20 ( Table 1). The results obtained concerning the capacity of PABA to neutralize the hemorrhagic effect of B. andianus are shown in Table 1. This Casein kinase 1 anti-venom

was efficient in neutralizing the hemorrhagic activity. MPD using an indirect hemolytic assay and inhibition of PLA2 activity by PABA were measured. PLA2 activity was dose dependent (data not shown) and the MPD determined in this study was 5.0 μg (S.D. ± 2.83 μg) ( Table 1). PABA was also able to neutralize B. andianus PLA2 activity with a potency of 350 ± 40.0 (μl anti-venom/mg venom). The proteolytic activity of B. andianus venom was expressed as DMC units (Δ340 nm) hydrolyzed per mg of venom per minute and was found to be 68.5 U/mg min ± 1.75 ( Table 1). PABA was able to neutralize B. andianus proteolytic activity with a potency of 200 ± 11.4 (μl anti-venom/mg venom). Immunological cross-reactivity of PABA against Bothrops venoms was assessed by both ELISA and western blotting.

0, corresponding a concentration of 1 × 108 UFC mL−1 (5 × 108 UFC at final volume). These cells were centrifuged for 6 min at 1200 rpm and the sediment was resuspended in 5 mL of phosphate buffered saline (PBS) and equalized to a concentration of 1 × 106 UFC

at final volume for virulence and immunomodulatory assays [63]. In vivo experiments were performed with 6–10 weeks old female BALB/c mice from University Volasertib supplier of Campinas (Campinas/SP). Mice were housed and used in accordance with guidelines established by the Ethical Committee of Animal Use of University of Brasília (Brasilia/DF), registered under protocol number UnBDOC:83931/2011, and all efforts were made to minimize animal suffering. Mice were divided into 5 groups of 5 animals each ( Table 1). As described above, groups were infected via intraperitoneal (IP) injection with E. coli suspension equalized and diluted in cold PBS to a sub lethal concentration of 1 × 105 UFC (50 μL

in each animal) [54]. Treatments of infected mice were performed with Pa-MAP at 1 and 5 mg kg−1, both dissolved in 100 μL of PBS, respectively. PBS was utilized as the negative control, and ampicillin at 2 mg kg−1 dissolved in 100 μL of PBS was utilized as the positive control. Moreover, an uninfected control was also performed. All mice were housed with constant water and food in an air-filtered environment maintained at 20 ± 2 °C during 72 h and further treated as described above ( Table 1). Treatments occurred 24 h and 48 h after infection. Moreover, all mice were weighed at the beginning selleck compound and at the end of the experiment. Mice were anesthetized by xilazine and ketamine

at 10 mg kg−1 and 50 mg kg−1, respectively, after 72 h. Blood collection was performed by decapitation and serum obtained by centrifugation during and stored at −20 °C. The cytokines interleukin-10 (IL-10), IL-12, interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), and nitric oxide (NO) were measured in serum by enzyme-linked immunosorbent assays (ELISA) using ELISA kit (Peprotech) according to the manufacturer’s instructions. The statistical significance of the experimental results was determined by one-way Student’s t-test or one-way analysis of variance (ANOVA) followed by Dunnett’s test. Values of P < 0.05 were considered statistically significant. Graphpad Prism version 6.0 was used for all statistical analyses. MALDI-ToF evaluation showed an ion with an m/z of 2212.86, corresponding to the calculated value for the peptide sequence, above 95% in purity. All further bioassays were performed using purified Pa-MAP ( Fig. 1A). In order to confirm the in vitro protective effects of Pa-MAP against E. coli, in vivo antibacterial activity was evaluated by a sub-lethal E. coli mice IP infection. Two concentrations of Pa-MAP (1 mg kg−1 and 5 mg kg−1) treatment were tested. Ampicillin at 2 mg kg−1 was used as a positive control.

The northern eddy is characterized by a cyclonic circulation, while selleck kinase inhibitor the southern one has an anticyclonic circulation (Supić et al., 2000 and Beg et al., 2005). Thus, in the first few days, the oil slick moves westwards, after which it begins to spread intensively in the opposite E direction towards the coast of Istria, more specifically along the dividing line between the northern and southern eddies (see Figure 12e). The oil slick reaches the coast on 22 February 2008, 16 days after the oil spill. The coastal area around Rovinj is most exposed to the oil pollution, an oil slick of thickness > 10 μm

being in contact with the coastline for 3% of the total simulation period (see Figure 12f). At the beginning of the oil spill simulation of 4 March 2008, NE and NNE winds are blowing, with a predominantly NNW circulation along the eastern coast. With such a circulation, the oil slick moves towards the north-western part of the area under investigation (see Figure 13e). The bora gains in strength

until 7 March, when it reaches its maximum, again inducing the formation of two eddies. The cyclonic circulation of the northern eddy facilitates the retention of the oil slick in the central and north-western parts of the spatial domain (see Figure 13a). After the cessation of the bora, a steadier outgoing flow is established along the western coast, and consequently, removal

of oil from the modelled area is intensified. The oil slick reaches the coastline 48 days after the spill Protein Tyrosine Kinase inhibitor (on 21 April 2008), on the stretch between Poreč and Rovinj. Retention of oil along the coastline from with > 10 μm thick layer is recorded in the following two days, that is ≈ 3% of the total simulation period (see Figure 13f). The fourth oil spill situation, of 13 July 2008, is characterized by the impact of winds from quadrants II, III and IV. A cyclonic and coastal circulation is predominant, with the pair of eddies being absent and the occurrence of the ICCC (Istrian Coastal Counter-Current). Such a circulation speeds up the removal of the oil slick from the modelled area (see Figure 14e), so that during the simulation period of 60 days no part of the coastline is exposed (see Figure 14f). In the final oil spill situation to be analysed, dated 13 September 2008, an outgoing circulation along the western coast of Istria is predominant. The bora, blowing between 26 and 28 September 2008, does not bring about the occurrence of the cyclonic and anticyclonic pair of eddies, but merely amplifies the outgoing circulation and of the removal of the oil spill along the western coast (see Figure 15e). From 2 to 4 October 2008 the impact of a libeccio (SW wind) moves the surface layer of the sea, shifting the remaining oil slick towards the central part of the model domain (see Figure 15b).

g., minocycline), excitatory amino acid antagonists (e.g., topiramate, memantine), free radical scavengers (e.g., N-acetylcysteine, vitamins E/K), and antiapoptotic agents (e.g., erythropoietin, insulin-like growth factor-1). To translate these interventions to the clinical

arena, it is critical to determine their direct relevance to the human premature brain. Recent advanced neuropathologic studies of premature brain suggest that many cellular and molecular events demonstrable in experimental models appear to occur also in human PVL and that several of the agents just AZD2014 purchase observed, at least theoretically, could be useful. Yet, are they safe? Safety relates EPZ 6438 in considerable part to the likely duration of therapy required. How long should a preterm infant be treated to prevent PVL? The answer to this key question is not entirely known. Treatment with several of these agents for a day or two is quite different, in terms of safety, than when the duration must be many weeks. Indeed, considerable clinical evidence suggests that the insults responsible for PVL (hypoxic-ischemic or inflammatory or both) are chronic and cumulative, perhaps occurring over many weeks. Safety concerns concomitantly are greatly enhanced. Formulation of human clinical trials must be preceded by careful animal

studies that involve long durations of therapy. In spite of personal involvement over many years in basic and clinical research delineating pathogenetic mechanisms in PVL and discovering potential preventative interventions, too rapid a leap to the clinical arena cannot be justified. We must use direct neuropathologic studies of the premature brain to ensure relevance of experimental models to

the human lesion, and we must ensure that we will not harm the infant by translational therapies, especially when administered over relatively long periods. The most notable example of this lesson is illustrated best by the brain abnormalities occurring in the preterm infant. Beginning about 40 years ago, conventional neuroimaging has revealed a subsequent disturbance in myelination in preterm selleck chemicals infants with PVL. The cellular basis for this disturbance was not clearly revealed until the late 1990s and early 2000s when advanced neuropathologic studies by us (led by Dr. Hannah Kinney and Dr. Stephen Back) and others demonstrated that the predominant oligodendroglial cell in the human premature white matter is an early differentiating, premyelinating oligodendrocyte (pre-OL) and that this cell differentiates to myelin-producing mature OLs largely after term. This rapidly developing cell was demonstrated in experimental models to be vulnerable to injury by hypoxia ischemia and inflammation, the two key insults leading to human PVL.

,

2004), respectively. Genes were annotated with transcription start-site (TSS) using REFLINK and REFFLAT tables downloaded from the UCSC genome browser data on August 23, 2010 (Karolchik et al., 2003). Within each AHRE-motif, a PhyloHMM conservation score was calculated across different species. The scores vary from 0 to 1, with a score of 0 meaning NVP-BGJ398 that there is a minimal conservation and 1 meaning that there is a strong conservation. Motifs that are evolutionarily well conserved are particularly likely to be functional (Siepel and Haussler, 2004). Primers and probes were designed using the real-time PCR Assay Design Tool on the Integrated DNA Technologies (IDT, Coralville, IA) website (http://www.idtdna.com/Scitools/Applications/RealTimePCR). To ensure specificity, probes were compared with Rattus norvegicus nr/nt database using nucleotide Basic Local Alignment Search Tool (BLAST). Similarly, primer pairs were compared to the same database using Primer BLAST (http://www.ncbi.nlm.nih.gov/blast) ( Altschul PFI-2 et al., 1990 and Altschul et al., 1997). Total RNA samples were reverse transcribed using the High-Capacity cDNA Reverse Transcription Kit (Applied

Biosystems). In addition, for each reverse-transcribed sample, a similar preparation was made where all the reagents were included except for the reverse transcriptase.

The above reactions were conducted with 1 μg of RNA as outlined in the manufacturer’s instruction. PCR reactions were prepared with 5 ng of cDNA using the TaqMan Gene Expression Master Mix (Applied Biosystems) with gene-specific primers/probes ( Table 1). A total of 84 biological replicates were analyzed for H/W rats and 68 replicates for L-E rats, each performed Methane monooxygenase with two technical replicates in a 10 μL reaction volume. PCR reactions were run on the 7900HT Fast Real-Time PCR System (Applied Biosystems) using default settings for relative quantification calculated from comparative Ct values. qPCR results were then collected using Sequence Detection System Software v2.3 (Applied Biosystems) and the quantitated data were loaded into the R statistical environment (v2.12.2). These data were then processed and normalized as previously described ( Barsyte-Lovejoy et al., 2006) using the previously validated housekeeping genes Gapdh and Pgk1 ( Pohjanvirta et al., 2006). Normalized data were log2-transformed and visualized across the different doses and time points tested for both L-E and H/W rats.

No other dental anomalies beyond agenesis were observed. We also randomly included 15 individuals, without any dental agenesis, as a control group (all Whites). Genomic DNA was extracted from saliva using the QIAamp DNA MiniKit (Qiagen). PAX9 exon 3 (138 bp) and its

5′and 3′ flanking intronic segments (232 bp and 219 bp, respectively) were amplified using primers and conditions described in Pereira et al. 30 Primers were designed to amplify PAX9 exons 2 (640 bp) and 4 (247 bp) ( Table S1, Supplementary Data). With this approach all PAX9 coding regions were covered (since exon 1 presents just the initiation code) MSX1 exon 2 (698 bp, involving both the homeodomain and the untranslated region) was amplified using primers and conditions described in Xuan et al. 33. PCR products were purified using exonuclease I and alkaline phosphatase (Amersham Biosciences). Both DNA strands were sequenced using ABI Prism BigDye and this website an ABI 310 Genetic Analyzer. Information about the 360 patients was collected and organized in a database with complete dental description. The SPSS program

(version 16) was used to analyse the data concerning dental agenesis. Nonparametric tests (distribution free Kruskal–Wallis and Chi-square) were used to compare agenesis by gender, age, skin colour (White or Black), tooth types (third molars, molars, premolars, canine and incisors) and other dental categories (left and right quadrants; upper and lower arches). Sequences were aligned and their trans-isomer molecular weight quality, as well as the precision of the resulting HSP90 data, was ascertained using the PHRED, PHRAP and CONSED program (http://www.genome.washington.edu). All chromatograms were visualized and checked manually to detect possible mutations in the sequence. Deviations from the reference sequence were compared with available genome databases (Ensembl – http://www.ensembl.org/index.html, UCSC Genome Browser – http://genome.ucsc.edu) and SNP banks (dbSNP http://www.ncbi.nlm.nih.gov/snp/, Hapmap – http://hapmap.ncbi.nlm.nih.gov/). Allele frequencies were determined by direct counting. Haplotypes for the PAX9 and MSX1 genes were estimated from phase-unknown

multi-site genotypes using multiple locus haplotype analysis (MLOCUS). 34 and 35 Observed allele and genotype frequencies of patients and controls were compared by Chi-square with a 95% confidence interval using the SPSS program (version 16). Genes related to odontogenesis were compiled in the Gene Ontology website database using the AmiGO browser (http://amigo.geneontology.org/cgi-bin/amigo/browse.cgi). Association between these genes and dental development was tested using the STRING software (known and predicted protein–protein interactions – http://string.embl.de/database), assuming the highest confidence value (0.900). Table 1 shows that a total of 119 (33%) of the 360 patients presented non-syndromic dental agenesis.

HepG2 cells were isolated from a human hepatoblastoma and they retained

the activity of certain enzymes of phase I and phase II, enzymes that are related to the activation and detoxification of genotoxic carcinogens and, thus, have been widely used in genotoxicity studies (Uhl et al., 1999 and Uhl et al., 2000). The cells were obtained from the American Type Culture Collection (ATCC No HB 8065, Rockville, MD) and were grown in culture flasks of 25 cm2 in 5 mL of MEM (Minimum Essential Medium – Cultilab), supplemented with 10% of foetal bovine serum (FBS) and 0.1% of antibiotic-antimycotic learn more solution (penicillin 10.000 U.I./mL/streptomycin 10 mg/mL, Cultilab) in CO2 incubator (5%), until they reached confluence. The MTT test (Thiazolyl Blue Tetrazolium Bromide – CAS n. 298-93-1, Sigma) with HepG2 cells was performed according this website to the protocol of Mosmann (1983), with some modifications. In each well of a 96 well plate, 2.34 × 104 cells were seeded. Subsequently, this plate was incubated for 24 h for stabilization

of the cells. After this period, the medium was removed from the wells and it was added 200 uL of culture medium (without serum) in the negative control (NC), culture medium without serum plus Triton X-100 at 1% in the positive control (PC) and culture medium without serum plus the treatments (different concentrations of GBA3 the wasp venom). After 3 h of incubation, the treatments were removed from the wells and it was added 150 uL of a solution of 5 mg/mL of MTT. The plate was incubated for 4 h, in incubator

at 37 °C. After this period, the MTT solution was discarded and it was added, in each well, 100 μL of dimethyl sulfoxide (DMSO). The plates were then read in spectrophotometer with microplate reader (Apparatus Multiskan FC – Thermo Scientific) in filters of 540 nm. The statistical analysis was performed by the ANOVA parametric statistic test (1 way), followed by the Dunnet’s comparison test (p < 0.05). The comet assay was performed to evaluate the genotoxic and antigenotoxic potential of the wasp venom and it was made according to the protocol described by Singh et al. (1988) and Tice et al. (2000), with some modifications. The assays were conducted in triplicate/treatment. For the genotoxicity and antigenotoxicity assay, 5 × 105 cells were seeded in culture flasks of 25 cm2. The flasks were incubated for 24 h in incubator at 37 °C, 5% CO2 in humid atmosphere, for a stabilization period. After this period, two evaluations were made, one to assess the genotoxicity, where the cells were exposed to different concentrations of the wasp venom for 3 h, and the other to evaluate the antigenotoxicity, where four different types of treatment were performed: – pre-treatment (PT): the cells were exposed to the different concentrations of the wasp venom for 3 h.

Hence, as no other MR-related measure discriminated between groups, counting-range slope findings seem to be related to inhibition ability and not to MR function. It is important to point out that there is substantial variation across studies in defining children with DD due to the fact that there is no agreed definition of DD. The range of cutoffs used to define DD in demographic studies ranges from performance

below the 3rd percentile to performance http://www.selleckchem.com/products/Perifosine.html below the 25th percentile (2SD–.68SD below the mean; for review see Devine et al., 2013). Here we used very stringent criteria to assure that children only had mathematical difficulties. We screened 1004 children and diagnosed DD if performance on two standardized mathematical measures was worse than 1SD while there was no ADHD and dyslexia, verbal IQ/reading was normal on four different tests and non-verbal IQ was normal on two tests. For example, Price et al. (2007) screened 55 children and WISC block-design performance differed by more than 1SD between DD and controls. In Piazza et al. (2010) about half the DD group was diagnosed with dyslexia. Mussolin et al. (2010a) screened 187 children and diagnosed DD if performance was worse than −1SD (15th percentile) on a multiplication test. However, multiplication relies heavily on verbal memory (Ashcraft, 1982). Mazzocco et al. (2011) screened

161 children and diagnosed 10 children below −1.3SD (10th percentile) with DD and children below −.65SD (25th percentile) as low maths achievers without MEK inhibitor using any other criteria. Various tests were used as covariates in analyses. However, the tests were recorded in various years during a 7-year long period and as noted above, ANCOVAs cannot ‘correct for’ major differences along independent variables (Miller and Chapman, 2001 and Porter and Raudenbush, 1987). Obviously, definition and measurement discrepancies can contribute to disagreeing findings across studies. In summary, there is evidence that IPS morphology and perhaps

function differ between DD and control participants Phosphoprotein phosphatase (Isaacs et al., 2001, Rotzer et al., 2008, Price et al., 2007 and Mussolin et al., 2010b). However, there is insufficient evidence for the argument that IPS dysfunction in DD can be linked to MR dysfunction: (1) Only one out of six fMRI studies found supporting behavioral data (Price et al., 2007). (2) The frequently used dot comparison task is seriously compromised by non-numerical confounds (Gebuis and Reynvoet, 2012 and Gebuis and Reynvoet, 2012; Szűcs et al., 2013). (3) Several behavioral and fMRI DD studies focusing on the MR theory of DD do not have non-numerical control conditions. (4) Adding to several negative findings (see above) our study used several measures of the MR but could not detect any clear MR impairment effects in DD.

The preliminary finding suggest that physiologically harmful pH changes in rodent lungs after a few cryogenics-free hp gas deliveries are not likely, even with the high Rb density at 83Kr SEOP conditions and in the absence of gas filters. Although filter usage may still be prudent for ABT-263 purchase further reducing any potentially

remaining Rb contamination, a study detailing the exact quantity of the Rb carried through the gas extraction process and the effects of filtering techniques upon the spin polarization is beyond the scope of this work. Extraction scheme 2 was modified to generate hp gas mixtures with a precisely selected O2 concentration. After transfer of the hp gas into the volume Vextmax of the extraction unit, O2 was added and resulted in a carefully regulated pressure increase signaling pathway until the desired O2 concentration was

reached. The total pressure in the large volume Vextmax = 790 ml was typically between 10–20 kPa and the mixing of the gasses was sufficient within 5 s after addition of O2. The method was tested by measuring the 129Xe longitudinal relaxation rates caused by paramagnetic O2 as a function of O2 density (or corresponding oxygen concentration; shown in Fig. 7). The O2 density dependent relaxation data shown in Fig. 7a (filled triangles) demonstrated the accuracy in the preparation of the gas mixture. The data was obtained using a series of small flip angle pulses at physiologically relevant, (i.e. ambient) pressure. The resulting slope of the oxygen density dependent 129Xe relaxation rate equation(2) 1T1ρO2129Xe290K,9.4T=0.360±0.007s-1amagat-1at 9.4 T field strength and 290 K was in good agreement with that obtained by Jameson et al.

with thermally polarized 129Xe at high xenon and oxygen densities [31]: equation(3) 1T1ρO2129Xe9.4T=0.343s-1amagat1·(T/300K)-0.03where T   is the temperature of the gas mixture in Kelvin. An amagat is defined in this work as the density of an ideal gas at standard pressure and temperature of 101.325 kPa and 273.15 K and therefore 1amagat=2.6868×1025m-3. At the conditions used in this work, N2, O2, Kr, and Xe are considered to follow ideal gas laws. According to Eq. (2), a relaxation time of T1 = 14.2 s was observed for a 21% O2, 79% hp 129Xe–N2 mixture contained also in an NMR test tube at 9.4 T and ambient pressure. However, the experimental setup used in this work was also applied to relaxation measurements in lungs as shown in Fig. 7c after SEOP, hp gas extraction, mixing with a quantified amount of O2, compression, transfer into a storage container, and inhalation by the excised lungs. The average longitudinal relaxation rate for two excised lungs was found to have the following dependence: equation(4) 1T1ρO2129Xe290K,9.4T=0.361±0.020s-1amagat-1 Eq. (4) describes the oxygen dependent term of the 129Xe T  1 relaxation, however the average longitudinal relaxation rate measured in the absence of oxygen (i.e.