Stream sediment samples

were taken from slack water deposits from areas within the main thalweg of the channel. Thirty-five floodplain surface sediment samples (0–2 cm), seven shallow pits (0–2, 2–10, 10–20 cm) and three deeper pits were collected (0–2, 2–10, 10–20, 20–30, 30–40, 40–50 cm), giving a total of 101 samples. Floodplain samples were taken perpendicular to the channel at distances of approximately 50 m, 100 m and 150 m extending out from the top of the channel bank at every second sampling interval (LA1, LA3, etc.). Sampling was extended beyond 150 m if field evidence suggested wider overbank flooding. One (1) floodplain sample was taken approximately 50 m from the top of the channel bank on every alternate interval (LA2, LA4, etc., Fig. 2). Only one side of the floodplain was sampled due to time and access constraints. Z-VAD-FMK nmr Four control/background samples were collected from the Dingo and Bustard creeks that drain from Selleck Pictilisib land

unaffected by the LACM or any related activities (Fig. 2). One channel and one floodplain sample (taken 50 m from the channel) were taken at each tributary at a depth of 0–2 cm. A total of 19 deeper pit samples (10–20; 20–30; 30–40 and 40–50 cm) were also collected from below the floodplain surface throughout the principle study area to provide additional (proxy) information on background sediment-metal composition (cf. the approach used in Taylor et al., 2010). Sediment was collected using a plastic trowel that was washed and cleaned with moistened wipes and deionised water between each sample. The shallow pits were dug using a mattock and shovel and the face of the pit was cleaned off with the trowel prior to sampling to minimise residual effects from the digging tools. Samples were taken from the deepest interval moving upwards to minimise accidental contamination from higher sediments during sampling. Samples were collected from each interval (i.e. Thymidine kinase 10–20 cm), labelled, double bagged and stored in a cool, dry place prior to analysis. Samples were initially oven dried at

40 ± 3 °C for 48 h to remove moisture and then passed through a 2 mm stainless steel sieve to remove stones, debris or large organics, in accordance with NEPC (NEPC, 1999a and NEPC, 1999b) and Australia Standards AS 4479.1-1997 and AS 4874-2000. Sieves were cleaned with compressed air, submerged in an ultrasonic bath of Type II deionised water for 5 min, rinsed several times with Type II deionised water and oven dried for 15 min at 80 °C before reuse. A representative sample was obtained from the <2 mm sieved sample using the Linear Japan Cake Method (Buhrke et al., 1998), which was then milled to <150 μm. Following standard Australian practice, samples were sieved to <2 mm for measurement of total extractable metal and metalloid concentrations.

To establish the conventional BP age of the sedimentary features, 11 organogenic samples were taken for 14C analysis

using fragments of shells of lagoonal mollusks, vegetal and peat remains (Table 1). The CEDAD laboratories at the University of Lecce, Italy, measured radiocarbon ages. The samples were analyzed using the accelerator mass spectrometry (AMS) technique to determine the 14C content. The conventional 14C ages BP include the 13C/12C corrections and were calibrated using the Calib 7.0 program (Stuiver and Reimer, 1993), and the calibration data sets Intcal13 and Marine13 for terrestrial and marine samples, respectively (Reimer selleck products et al., 2013). The regional correction (delta R) for marine reservoir effect was 316 ± 35 (Siani et al., 2000). This study used the following archive documents and historical cartography:

(a) the map of the central lagoon by Domenico Margutti of 1691, (b) the hydrographical map of the lagoon by Augusto Dénaix of ca 1810 and (c) the map of the Genio Civile di Venezia of 1901. The original historical maps are the property of the Archivio di Stato di Venezia where they can be found, but a recent collection of historical map reproductions is available in Baso et al. (2003) and D’Alpaos (2010). The map of Margutti was digitized within the Image Map Archive Gis Oriented (IMAGO) Project ( Furlanetto et al., 2009), covering an area in the central lagoon of about 160 km2. this website The map of Augusto Dénaix of ca 1810 is a military topographical hydrographical map of the Venice Lagoon and its littoral between the Adige and Piave rivers. It comprises 36 tables, out of which only the ones covering the study area were used. The scale is 1:15,000. The map of the Genio Civile di Venezia M.A.V. of 1901 is a topographic and hydrographic map of the Venice Lagoon and its littoral between the Adige and Sile

rivers. It comprises 18 tables, out of which only the ones covering the Glutamate dehydrogenase study area were used. The scale is 1:15,000. The description of the georeferencing procedure can be found in Furlanetto and Primon (2004). For the study area we extracted information about the hydrography by digitizing the spatial distribution of palaeochannels. The interpretation of the acoustic profiles is based on a classical seismic stratigraphic method (in terms of reflector termination and configuration) (Mitchum and Vail, 1977). Detailed analysis of acoustic profiles produced a 2D map of the sedimentary features. The initial and final coordinates of each acoustic reflector, with its description, were saved in a Geographical Information System (GIS) through the software GeoMedia®, for further mapping and interpretation (Madricardo et al., 2007, Madricardo et al., 2012 and de Souza et al., 2013). In the GIS it was possible to correlate the acoustic reflectors and to draw the areal extent of each sedimentary feature.

In this case the sediment, mostly silt and sand, would represent transient sediment that the river is actively moving downstream. The small grain size (and its ability to be transported by saltation and suspended load during high flows), location within the river channel, and the short cores (10–15 cm), all support this explanation of well-mixed sediment. This explanation is explored first for Site 2,

but an alternative hypothesis that the sediment cores represent sequential deposition and that, consequently, trends in radionuclide activities represent individual events is also explored. The sediments from Site 2 (Fig. 1) displayed the highest levels of excess 210Pb activity with some detectable 137Cs at depths greater than 7 cm DAPT in vivo (Fig. 2). In the upper 7 cm of sediments, excess 210Pb was found while 137Cs

was absent (Fig. 2). We consider these sediments as recent (<30 years) if we consider the 137Cs signal at depth to be from the nuclear accidents 20s Proteasome activity in Chernobyl, Ukraine in 1986. The increasing excess 210Pb activity with increasing depth suggests that the sediments were reworked, as this trend is the opposite of what one would expect in undisturbed, accumulating sediments. Surficial soils from the watershed possibly were eroded and transported to the river first, followed by further erosion of deeper soils or legacy sediment in the watershed which had relatively low excess 210Pb activity. The pattern of increasing excess 210Pb with depth repeated itself from 7 to 13 cm depth, however this interval also contained detectable 137Cs (Fig. 2). The 137Cs signal suggests that the sediments have been

buried in the river for at least 25 years. The similar patterns of excess 210Pb activity increasing with depth from the surface to 5 cm and then again from 7 click here to 13 cm suggest that the soil erosion from the watershed is an episodic event occurring on decadal timescales. The data also suggests the sediment originates from surficial sources, as there are not significant changes in grain size that would influence the activity levels. In contrast to Site 2, sediments at Sites 1 and 3 showed essentially no levels of excess 210Pb and 137Cs activities (Fig. 2). The results suggest that the sediments at these sites must be either (1) deposited prior to the nuclear bomb testing in early 1960s, or (2) that the sediments originated from deeper sources, or (3) that the sediments were eroded from legacy sediments stored within the watershed. The combined lack of excess 210Pb and 137Cs information implies that there is no sediment accumulation at these sites from recently exposed surficial sources. The non-detectable level of excess radionuclide activity would fit the characteristics of channel and/or hillslope erosion, as these deeper sediment sources contain little to no excess radionuclides. Sediment storage may have contributed to the low activity levels, and that the signal represents legacy sediment contributions.

The DGRP consists of 205 inbred lines derived from isofemale lines from a wild North Carolina population with fully sequenced genomes. The most recent release of the DGRP documents 4 853 802 single nucleotide polymorphisms (SNPs) and 1 296 080 non-SNP variants (insertions, deletions,

and copy number variants) as well as 16 polymorphic inversions [ 36•]. Sequence variation in this population can be correlated with phenotypic variation. The Drosophila genome is highly polymorphic and an extensive history of recombination has led to little local linkage disequilibrium, except within chromosomal inversions [ 36•]. Linkage disequilibrium decays within a few hundred base pairs [ 34••]. The absence of local linkage disequilibrium, as is found in the human genome [ 37], prevents the Selleck Saracatinib use of tagging SNPs for association studies and instead requires comprehensive Alpelisib analyses of whole genome DNA sequences. The advantage is that causality can be more readily assigned to a gene or even a polymorphism within a gene. Thus, naturally occurring variants that survived the sieve of natural selection are a treasure trove for the analysis

of complex traits, including behaviors. All traits that have been measured on the DGRP to date show extensive phenotypic variation, including behavioral traits, such as sleep parameters [38•], startle behavior [17••] and olfactory response to the odorant benzaldehyde [18]. Genome wide association (GWA) studies employ a relatively small number of lines compared to the Resveratrol numbers of polymorphic markers that are tested and, thus, polymorphic markers that are associated with variation in behavior rarely reach genome-wide statistical significance based on Bonferroni correction for multiple testing or permutation thresholds. This issue is, however, mitigated by several

factors. First, since there is minimal genetic variation among individuals within a line, phenotypic values can be determined with great precision, since essentially the same genotype can be measured repeatedly. Second, since all polymorphisms in the population are known, those with the highest P-values for association can be selected as candidate genes for downstream analyses ( Figure 3). Third, mutational analyses using the vast public resources available for the Drosophila community can verify that mutations in candidate genes identified in the GWA study indeed affect the behavioral phenotype. The fraction of such validation tests that confirm association of the gene with the behavior provides an estimate for an empirical false discovery rate. Finally, lines from each extreme of the phenotypic distribution can be intercrossed to form an advanced intercross population.

Stąd obserwuje się wzrost spożycia pokarmów w barach szybkiej obsługi, wzrost spożycia słodyczy, napojów słodzonych. Z tego względu asortyment sprzedawanych w sklepikach szkolnych pokarmów w głównej mierze stanowią produkty typu fast food, słodycze i słodkie napoje. Wyniki dalszych badań własnych przedstawiające korelacje między oferowanymi a kupowanymi produktami w sklepikach szkolnych w Rzeszowie

wskazują, że uczniowie, mimo że mieli wybór potencjalnie zdrowych produktów w sklepikach szkolnych, nie kupowali ich zbyt chętnie [24]. Hindin i wsp. [25] wykazali, że podatność dzieci na reklamę zależy od wykształcenia rodziców. Lepiej wykształceni rodzice częściej robili komentarze do reklam, ucząc dzieci, czym są reklamy, co w konsekwencji zaowocowało większą na nie odpornością. W Ixazomib price 1992 roku Amerykańska Akademia Pediatrii zasugerowała, że nadawanie w telewizji reklam produktów spożywczych skierowanych

do dzieci powinno być zabronione, ponieważ dzieci są nieprzygotowane do właściwego wyboru reklamowanych produktów i nie rozumieją relacji między wyborem spożywanego pokarmu a utrzymaniem stanu zdrowia lub zapobieganiu chorobom [26]. Potrzeba wprowadzenia międzynarodowych regulacji dotyczących SB431542 ic50 reklam żywności wysokokalorycznej i o niskiej wartości odżywczej została zasygnalizowana w 2004 roku przez WHO w dokumencie (Global Strategy on Diet Physical Activity and Health). W krajach, takich jak: Dania, Norwegia, Szwecja i Finlandia, ustawowo RANTES zabroniono koncernom spożywczym sponsorowania

programów dla dzieci, a w Szwecji i Norwegii zakazano reklam skierowanych bezpośrednio do dzieci poniżej 12. roku życia. Zabroniono również przerywania reklamami programów skierowanych do dzieci [27]. Unia Europejska także wprowadziła minimalne przepisy dotyczące regulacji prawnej kierowania reklam do dzieci dla 27 państw członkowskich. Art. 9 pkt 2 dyrektywy 2010/13/UE Parlamentu Europejskiego i Rady Europy z dnia 10 marca 2010 r. w sprawie koordynacji niektórych przepisów ustawowych, wykonawczych i administracyjnych państw członkowskich dotyczących świadczenia audiowizualnych usług medialnych (Audiovisual Media Services Directive) stanowi próbę ochrony dzieci przed reklamami niezdrowej żywności i napojów w programach dla dzieci. Zgodnie z nim, państwa członkowskie i Komisja zachęcają dostawców usług medialnych do opracowania sposobów postępowania wobec niestosownych praktyk handlowych przekazów audiowizualnych, towarzyszących programom dla dzieci lub zawartych w nich, a dotyczących żywności oraz napojów zawierających składniki odżywcze i substancje o działaniu odżywczym lub fizjologicznym, zwłaszcza takie jak tłuszcze, kwasy tłuszczowe trans, sól/sód i cukry, których nadmierne spożycie w ramach ogólnej diety nie jest wskazane [28].

Enseignant et élèves construisent,

à chaque instant du cours, le temps didactique par le fait qu’un nouvel objet de savoir est introduit dans le milieu. Ils s’appuient également sur la mémoire didactique du système pour faire évoluer l’apprentissage. La topogenèse (gestion des territoires) est relative aux espaces occupés par l’enseignant et les élèves tout au long du processus d’enseignement/apprentissage, ainsi qu’aux partages des responsabilités Epacadostat nmr dans l’avancée du savoir. Ainsi, à chaque instant du cours, les acteurs de la situation didactique construisent leurs places (topos) respectives par rapport aux tâches didactiques réalisées. Des travaux en didactique des www.selleckchem.com/products/SRT1720.html sciences et techniques se sont ancrés sur la TACD dépassant largement la didactique des mathématiques (par exemple, Pautal et al., 2013 and Venturini and Amade-Escot, 2009). Les approches didactiques comparatistes étudient la comparaison de systèmes didactiques pour envisager leurs spécificités et généricités. Les cadres d’analyse des pratiques d’intervention au sein de ce courant relèvent de la TACD et/ou de la TAD. La didactique

comparée s’intéresse au didactique dans ses dimensions, institutionnelles, contextuelles, cognitives et identitaires (Schubauer-Leoni, 2000) dans le but de comprendre et d’expliquer les phénomènes d’enseignement et d’apprentissage. Dans la TAD, les phénomènes transpositifs renvoient à des mécanismes dépendant de l’institution scolaire. Dans le champ de la didactique comparée, l’option retenue est celle d’une « transposition enough didactique ascendante », dans laquelle « la vérité n’est ni du côté des savoirs, ni du côté des sujets » ( Schubauer-Leoni, 2008, p.69). La « transposition didactique ascendante » relève d’une co-construction des savoirs, dépendant des actions conjointes des différents acteurs impliqués dans la logique de la TACD.Comme le précise Brière-Guenoun

(2012), contrairement à la transposition didactique descendante (des savoirs savants vers les savoirs appris), l’analyse ascendante prend appui sur les savoirs effectivement mis à l’étude dans la classe tout en envisageant leurs relations avec les références externes (savantes, expertes, personnelles), qui représentent des « moyens de contrôle épistémologique de ce qui se passe en classe » ( Schubauer-Leoni, 2008, p.70). Des travaux de didactique des mathématiques ont été conduits parallèlement dans le sillage de Vergnaud avec le concept de schème ( Vergnaud, l994), concept qui sera mobilisé par la didactique professionnelle. L’importance accordée aux situations conduit à mettre l’accent sur les connaissances-en-acte, c’est-à-dire des concepts qui sont mobilisés dans l’action, qui la structurent, la rendent efficace et ne sont pas nécessairement explicites ni connus du sujet.

Real-time polymerase chain reaction (qPCR) was performed using a StepOne thermocycler (Applied Biosystems). The reaction included 1 μL of the RT reaction product in a 20 μL total volume PCR reaction mix that included: 8 μL of nuclease-free water,

10 μL of TaqMan qPCR master mix and 1 μL of TaqMan gene expression assays, including forward, reverse primers and fluorophore-conjugated probe (Applied AP24534 datasheet Biosystems) for rat genes (see Table 1). The cycling conditions used for all primers were pre-optimised: 50 °C for 2 min and 40 cycles of: 95 °C for 15 s and 60 °C for 1 min. The determination of the relative levels of gene expression was performed using the cycle threshold method and normalised to the housekeeping gene GAPDH. Results are represented as the mean mRNA expression from duplicate measurements normalised by internal control GAPDH and expressed as fold change over the levels determined in cDNA samples prepared from healthy (non-ligated) control gingival tissues. Activation of STAT1 and STAT3 as well

as the global expression of SOCS1 and SOCS3 was assessed using samples of total protein extracted from gingival Etoposide tissues collected from rats sacrificed in the different experimental periods (7, 15 and 30 days after ligature placement). A detergent-based extraction buffer (T-PER, Tissue Protein Extraction Reagent – Pierce) containing a protease inhibitor cocktail (Protein Stabilizing Cocktail – Santa Cruz Biotechnology) was used for protein extraction. The tissue samples were macerated in 30 μL of ice-cold buffer, centrifuged for 5 min at 13,000 RPM at 4 °C and the supernatant was collected. Concentration of

total proteins was determined with a Bradford-based assay (Bio-Rad Lab.) and clonidine 30 μg of total protein were added to a sample buffer containing 2% SDS, 10 mM of DTT as a reducing agent, glycerol and bromophenol blue dye (Cell Signaling), heated-denaturated at 97 °C for 5 min and chilled on ice of 5 min before loading on 10% SDS–polyacrylamide gels. Electrophoresis on discontinuous acrylamide gels was carried out at constant 100 V for 90 min and subsequently electrotransfered to 0.4 μm nitrocellulose membranes using a 300 mA constant current for 1 h. The membranes were blocked for 1 h in Tris-buffered saline containing 5% non-fat dry milk and 0.1% Tween-20 and subsequently washed for 10 min (three times) with TBS–0.1% Tween-20. The membranes were then incubated with pre-optimised dilutions of the primary antibodies overnight at 4 °C with mild agitation. Membranes were washed in TBS-T buffer three times for 10 min each and incubated with secondary antibodies conjugated to horseradish peroxidase (1:5000 dilution in the blocking buffer) for 1 h at room temperature and washed again three times for 10 min with TBS-T buffer.

The magnitude of arterial steal was calculated using changes in mean flow velocities (MFVs) during TCD-monitoring and net deficit in metabolic perfusion after acetazolamide-challenge

on HMPAO-SPECT (Fig. 3). Interestingly, identification of intracranial steal phenomenon on TCD had satisfactory agreement with detection of inadequate vasodilatory reserve leading to perfusion deficit on acetazolamide-challenged HMPAO-SPECT. Moreover, a strong linear correlation was identified between intracranial steal magnitude (%) on TCD [calculated as [(MFVm − MFVb)/MFVb] × 100, Oligomycin A clinical trial where m = minimum and b = baseline MFVs during the 15- to 30-s period of a total 30 s of breath-holding] [27] and net perfusion deficit on SPECT after Diamox-challenge in patients who exhibited both steal phenomenon on TCD and failed vasodilatory reserve on SPECT (Fig. 4). Alexandrov et al. conducted a pilot study to investigate the prevalence of RRHS in a consecutive series of patients with ACI. They showed that among 153 patients admitted within 48 h from ACI onset, 21 (14%) had steal phenomenon (median steal magnitude, 20%; interquartile range, 11%; range, 6–45%), and 11 (7%) selleck chemicals had RRHS. RRHS was most frequent in

patients with proximal arterial occlusions in the anterior circulation (17% versus 1%; p < 0.001). Male gender, younger age, persisting arterial occlusions, and excessive sleepiness (evaluated by the Epworth Sleepiness Scale and Berlin Questionnaire) were independently associated with RRHS on multivariate logistic regression models [31]. The same group also sought to determine the potential association of RRHS with risk of early

recurrent stroke. Their findings indicated that patients with acute anterior circulation ischemic events and RRHS have a significantly higher Interleukin-3 receptor risk of new ischemic stroke occurrence than acute stroke patients without this condition [32]. This longitudinal association persisted even after adjustment for demographic characteristics, vascular risk factors, and secondary prevention therapies. They also observed that all recurrent strokes in the RRHS subgroup occurred in the anterior circulation vascular territory ipsilateral to the index event [32]. Moreover the risk of recurrent stroke was front-loaded with a four-fold increase being documented during the first 30 days of ictus [30-day stroke risk in RRHS(+) and RRHS(−) patients: 12% and 3%, respectively] [32]. These findings indicate that the hemodynamic compromise caused by the vascular steal phenomenon may be an underlying mechanism linking large vessel atherosclerosis both with neurologic deterioration in the acute stroke setting as well as with recurrent cerebral ischemia during the first month after the index event.

Whether these reach their target at the lateral or medial surface of the occipital horn depends upon whether the cortical area they originate from lies lateral or medial on the sagittal plane through the middle of the occipital horn. This plane separates the lingual gyrus from the medial part of the fusiform gyrus at the basal surface. The fibre system originating from the fusiform gyrus – often a tightly packed layer, which is clearly differentiable from the rest of the fibres (6.) – climbs vertically and breaks through both sagittal

layers by dividing them into three parts. The inner-most part (7.) runs at the basal surface of the Antidiabetic Compound Library ic50 posterior horn almost horizontal to it and bends slightly upwards, to insert in the yet-to-be-described small part of the forceps. A smaller middle part (8.) bends in sagittal direction and strengthens the outer half of the forceps fibres Ivacaftor that run sagittally on the inferior [part] of the posterior horn. The lateral largest part (9.) runs along the outer surface of the posterior horn, adjacent and lateral to the thin layer of the horn. I shall call all callosal fibres at the outside of the occipital horn “outer forceps layer”. During its course along the outer surface of the posterior horn, this layer is continuously strengthened by fibres originating from the convexity underneath the intraparietal sulcus.

These fibres run diagonally from the ventral convexity towards dorsal medial areas. Among them the most ventral fibres are close to a vertical direction. The more dorsal these fibres reach, the more horizontal they run, until they join fibres that cross to the upper part of the forceps directly above the intraparietal sulcus. They form small tracts, visible to the naked eye, that traverse both sagittal layers in the same direction as before

and thus divide the latter in even smaller tracts. They then bend upwards in a vertical direction and join the ascending fibres. The whole layer thus becomes thicker as it ascends and bends from a vertical to a sagittal direction at the level of the upper part of the forceps. Also these fibres, like all callosal fibres, do not simply join from below or outside the already existing forceps system; they rather follow the same course of the callosal fibres [originating] from the dorsal cortex, i.e. they penetrate the forceps for a ASK1 [certain] distance before bending in a sagittal direction. The fibres of the sagittal veil which are directly adjacent to the lateral surface of the posterior horn (2.) traverse diagonally along an anterior – superior [direction] and merge with the dorsal branch of the forceps. In the same way, the thickened bundle bends at the lateral aspect of the inferior occipital horn (8.) more anterior and close to the opening of the occipital horn where it runs upwards and diagonally towards the front and then directly upwards to reach the same termination.

Unlike other studies reporting atrophy during LBP (Parkkola et al., 1993; Hides et al., 1994; Danneels et al., 2000; Barker et al., 2004), we were not able to reveal differences in total or lean muscle CSA during remission of recurrent LBP. We speculate that muscle size was not reduced, or, had recovered in this specific population. Support for recovery from atrophy is provided by associations showing that 62 and 64% (R2 = 0.623; R2 = 0.640) of the variance in lean and total CSA, respectively, can be explained by the time

DAPT concentration elapsed between testing and previous LBP episode (mean: 64, min: 31, max: 144 days). This finding appears in contrast to Hides et al. (1996), who observed no alteration in localized MF asymmetry after about 42 pain-free days. In addition to the methodological differences discussed above, our association was irrespective of pain side, muscle or http://www.selleckchem.com/products/nutlin-3a.html level and observed in a wider timeframe. Further longitudinal research

of the natural course of lumbar muscle morphometry during resolution of LBP is needed. Below, several hypotheses for decreased lumbar muscle size in relation to LBP are discussed in view of our lack of atrophy during remission of LBP. First, atrophy may result from muscular disuse e.g. general deconditioning and local disuse (altered recruitment) (Hides et al., 1994; Danneels et al., 2000; Hodges et al., 2006). With regard to conditioning status, both groups had similar scores for physical activity, comparable to scores from young adults Adenosine (Baecke et al., 1982). Altered recruitment of muscles cannot be discounted as there is evidence for decreased (Macdonald et al., 2009), unchanged (Macdonald et al., 2010) and increased (Macdonald et al., 2011; D’Hooge et al., in press) MF recruitment during remission of recurrent LBP. Second, experimentally-induced spinal injury

(disc and nerve root lesion) has been shown to cause specific patterns of muscle wasting in the porcine MF within 3 days of the lesion (Hodges et al., 2006). It is not known what muscular replications can particularly be expected from non-specific LBP, 64 days at average after LBP resolution. Third, if peripheral nociception would reduce muscle CSA directly, this could contribute to marked differences observed during LBP compared to less conclusive evidence during LBP remission. Further research that investigates the isolated effect of nociception on lumbar muscle size may be able to confirm this hypothesis. MFIs in lean muscle tissue were increased during remission of LBP, which reflects increased relative amounts of intramuscular lipids (Elliott et al., 2010). The extent of lean fatty infiltration was generalized rather than localized (multiple muscles and levels, both previously painful and non-painful sides). The main causes of fatty infiltration are muscular disuse and spinal injury, similar to the causes of atrophy (Elliott et al., 2006; Hodges et al., 2006).