The definition of the main sedimentary facies in the cores (indicated with different colors in Fig. 2) is useful for interpreting the acoustic profile, identifying the sedimentary features, as well as allowing a comparison with similar environments. Most of the alluvial facies

A are located below the caranto paleosol and belong to the Pleicestocene continental succession. The sediments of the facies Ac in cores SG28 e SG27 are more recent and correspond to the unit H2a (delta plain and adjacent alluvial and lagoonal deposits) of the Holocene succession defined by Zecchin et al. (2009). In the southern Venice Lagoon they define also the unit H1 (transgressive back-barrier and shallow marine deposits) and the unit H2b (prograding delta front/prodelta, shoreface and beach MK-8776 nmr ridge deposits). In the study area, however, the units H1 and H2b are not present: the lagoonal facies L (i.e. the unit H3 of tidal channels and modern lagoon deposit in Zecchin et al.

(2009)) overlies the H2a. A similar succession of seismic units is also found in the Languedocian lagoonal environment in the Gulf of Lions (unit U1 – Ante-Holocene Afatinib nmr deposits and units U3F and U3L, filling channel deposits and lagoonal deposits, respectively) in Raynal et al. (2010), showing similar lagoon environmental behavior related to the sea-level rise during the Flandrian marine transgression ( Storms et al., 2008 and Antonioli et al., 2009). The micropalaeontological analyses

( Albani et al., 2007) further characterize the facies L in different environments: salt-marsh facies Lsm, mudflat facies Lm, Rapamycin solubility dmso tidal channel laminated facies Lcl and tidal channel sandy facies Lcs. As described by Madricardo et al. (2012), the correlation of the sedimentary and acoustic facies identifies the main sedimentary features of the area (shown in vertical section in Fig. 2 and in 2D map in Fig. 3). With this correlation and the 14C ages we could: (a) indicate when the lagoon formed in the area and map the marine-lagoon transition (caranto); (b) reconstruct the evolution of an ancient salt marsh and (c) reconstruct the evolution of three palaeochannels (CL1, CL2 and CL3). The core SG26 (black vertical line in Fig. 2a) intersects two almost horizontal high amplitude reflectors (1) and (2), interpreted as palaeosurfaces (Fig. 2a). A clear transition from the weathered alluvial facies Aa to the lagoonal salt marsh facies Lsm (in blue and violet respectively) in SG26 suggests that the palaeosurface (1) represents the upper limit of the Pleistocene alluvial plain (caranto). The 14C dating of plant remains at 2.44 m below mean sea level (m.s.l.

8 years, and the mean body mass index (BMI) values were 25.6 ± 3.2. The demographic and laboratory data were analyzed at the beginning of the study according to the randomization group ( Table 1); the group of patients randomized for the FO group presented significantly higher CRP values (P = .014) and significantly lower total cholesterol values (P = .007). The laboratory data were collected at baseline for 145 patients due to intention to treat. In the initial analysis, inflammation was present in 89 (61%) of the 145 patients. A statistically significant correlation was found between the BMI and baseline

CRP (Rs = 0.22; P = .022), whereas a negative correlation with similar strength was found between the HDL cholesterol (HDL-c) and baseline CRP levels (Rs = −0.23; P = .032). In GSK2126458 the FO group, the comparison between the first and the last analyses displayed a statistically ABT-888 cost significant decrease in the CRP (P < .001), total cholesterol (P = .004), and low-density lipoprotein (LDL) cholesterol

(P = .001) values and an increase in the HDL-c (P = .004) values; yet, similar findings were not observed in the MO group ( Table 2). Throughout the study, we observed that the CRP variation in the FO group was higher than that observed for the MO group (P < .001). In this interaction assessment, the decrease in the CRP values for the FO group reached a statistical significance (time 1 × time Montelukast Sodium 2 and 3), whereas the values for the MO group remained stable ( Fig. 2). In the mixed-model analysis, the FO group achieved a significant reduction in the CRP values when compared with the MO group (P = .018). In another approach, by comparing the initially inflamed with the noninflamed

groups, we observed lower urea reduction ration (URR) and Kt/V (“dialysis dose”) values for the inflamed group (P < .01). These individuals also presented a higher BMI mean (P = .03), but the comparisons of the other study variables did not present statistically significant differences ( Table 3). Moreover, in the FO group, a decrease in the percentage of inflamed patients was observed throughout the study, falling from 36.3% to 23.9% to 21.2%, respectively, at times 1, 2, and 3 (P = .004). In contrast, no statistically significant differences were observed in the respective times of assessment for the MO group (P = .487). A further analysis was performed by separating the effects of intervention in the inflamed and noninflamed groups. Among the noninflamed patients, neither intervention produced a significant decrease in the CRP levels (FO 1.26 ± 1.25 to 0.68 ± 1.49 and MO 2.14 ± 1.15 to 2.33 ± 1.28; P, nonsignificant). Conversely, as shown in Fig. 3, a statistically significant decrease in the CRP levels was observed in the group of inflamed patients who received FO (P < .001); however, the reduction in the CRP levels for the MO group was minimal and statistically not significant.

Libraries are often where research starts and ends, where expert advice is offered about how and where to find reliable information, where productive discussions occur between researchers, sometimes serendipitously, and where quiet time occurs, critical to writing original

research proposals, papers and reports. Moving or abandoning collections of archival materials, important both regionally and nationally, may lead to irreparable loss of documents and information of scientific and historical importance. This action Staurosporine research buy is being actively opposed by concerned citizens, such as at St Andrews, NB, and site of Canada’s first marine biological station. The cuts and impacts described above are dealing a major blow to Canada’s once proud reputation and capacity in the aquatic and marine sciences. But the wider situation is even more dire. The government’s approach to environmental policy has been to radically alter current resource and environmental legislation through the use of omnibus budgetary bills, i.e., proposed new legislation. Two of these (more are promised!) are Bill C-38 and Bill C-45, the latter the

target of current First Nations protests. Both bills were moved, some say pushed, through Parliament in 2012. Bill C-38, according to the Toronto Star (Jan. 2nd, 2013), “included more than $160 M in cuts to environmental spending, significantly impairing our ability to measure or mitigate MG-132 ic50 our impact on Canada’s wilderness and wildlife”. With the two bills, major changes have been made or are being considered to sections of the Fisheries Act, the Canadian Environmental Assessment Act, the Navigable Waters Protection

Act, the Coasting Trade Act, and the Hazardous Materials Information Review Act. The result will be weakened or non-existent aquatic habitat and waterway protection across the country. Most rivers and lakes will not be protected from disturbance by resource development and other industrial activity. The bills essentially undo decades of progressive environmental and living resource legislation, quite unacceptable behavior by a developed country. In a related federal agency, Parks Canada, personnel have been fired or retired early, eliminating whole research units responsible for HAS1 ecosystem and wildlife research in Canada’s famed National Parks; for instance, 29 of 30 scientific researchers in Calgary responsible for work in the mountain parks have lost their jobs. Others have been told that as public employees, their duty is to support the elected government. As well, some National Parks are now closed seasonally, an unprecedented and amazingly unwise action given the conservation mandate of the National Parks Act. This could affect the UNESCO World Heritage status of several parks and National Historic Sites.

) throughout the coast was also obtained [15], and the proportion of their revenue that comes from selling canned fish was estimated. These estimates were pooled to obtain the total number of people employed per ton of seafood in the local markets. Peruvians, and foreign markets were considered end consumers in the study, and these did therefore not include employment or cost of operation. Similarly, rural farmers, other sectors,

and the national food security program, El Programa Nacional de Asistencia Alimentaria (Pronaa), were also considered end consumers, and there is therefore no account of the derived benefits from the use of Doxorubicin solubility dmso fish products from these groups, including of the employment they provide. Cost structures were reconstructed

from structured interviews of key stakeholders involved with each step of the value chain. Some cost structures for the industrial anchoveta fleet were updated and developed based on estimates in De la Puente et al. [18] and calculations for the artisanal fleet were updated based on estimates in Estrella et al. [10], Alfaro-Shigueto et al. [11]; Estrella and Swartzman [19]. The majority of the cost estimates, however, came from interviews and fieldwork that were undertaken as part of the present study. Included import taxes for materials (e.g., tin cans) were not considered, nor were value added taxes in the costs. This is to some extent countered by not considering the export subsidies that enterprises may get to compensate for the import taxes they have paid. The contribution of the fisheries sector to the Gross Domestic Product (GDP) of Peru was estimated based Selleck Pexidartinib on the income approach [20] by evaluating the following sum for each enterprise type in the fisheries sector as well as for each seafood commodity, equation(1) GDP=Ce+Ip+Ct+Co–IsGDP=Ce+Ip+Ct+Co–Iswhere Ce is the total cost of compensations, Ip is the gross operating profit, Ct is total taxes, Co cost for management, royalties, certification, and monitoring, and Is

is the income from subsidies. The value chain module used here is coupled with the Ecopath and Ecosim (EwE) modeling framework, but does not rely on the EwE Resminostat models for parameterization [9] apart from obtaining the landings and fleet structure from the underlying Ecopath model (and these could in principle be entered independently of the Ecopath model). All other information that was needed to develop the value chain analysis as presented in this contribution was thus derived independently of the underlying ecosystem model. The coupling with the EwE models, however, enables evaluation of the full value chain analysis as part of mass-balance modeling [21], time-dynamic simulations [22], policy optimizations [7], spatial optimizations [23], management strategy evaluations, and other analysis where social and economic factors are considered.

Parece-nos que, desde que a crítica seja feita de forma construtiva, irá dar maior vivacidade ao nosso Jornal. Um novo formato de artigo que gostaríamos de passar a ter regularmente consiste na Discussão de um Caso Clínico, um pouco semelhante aos casos do NEJM: «Clinical problem-solving», ao qual iremos dar o nome de Desafios Clínicos. Pedíamos que, sempre que tenham casos que possam constituir um desafio de diagnóstico, PLX3397 in vitro os enviem para esta secção do Jornal, com este tipo de formato. Neste tipo de artigo, deve considerar-se o processo de decisão clínica passo a passo.

Perante cada grupo de dados clínicos apresentados, discute-se quais são as hipóteses de diagnóstico, apresentando-se os argumentos em que se baseiam. Idealmente, deve ter material de suporte,

como radiografias ou exames histológicos ilustrativos. Peço também que, sempre que possível, enviem os artigos em inglês, dado que isso irá facilitar a possibilidade de indexação. O GE é a revista dos Gastrenterologistas e a sua qualidade Ku-0059436 mouse irá sempre depender do empenho e do interesse que os Gastrenterologistas ou os Médicos interessados na Gastrenterologia tenham no Jornal. “
“A doença de Crohn (DC) apareceu como entidade clínica própria no primeiro terço do século xx1. Ao longo do século a doença passou a ser reconhecida também em Pediatria tendo a sua incidência aumentado consideravelmente nos últimos 40 anos. Um estudo europeu referente a 739 crianças com doença inflamatória intestinal calculou uma incidência de DC e de colite ulcerosa em 3,0 e 1,5 casos novos por 100.000 habitantes2. Uma meta-análise recente efetuada com base em 139 estudos efetuados entre 1950 e 2009, provenientes de 32 países, confirma esta tendência3 and 4. Estima-se em 20% o número de casos de DC que se apresentam na infância e adolescência5. A mediana da idade no diagnóstico é de 12 anos2 and 6, coincidindo muitas vezes com a fase de crescimento e desenvolvimento rápidos e a oportunidade única para crescer. Esta questão não se coloca quando o diagnóstico é efetuado no adulto, pois

o crescimento linear já ocorreu. Uma das queixas frequentes antes ou após o diagnóstico, isolada ou associada a outros oxyclozanide sintomas, é o atraso de crescimento. Estima-se que, pelo menos, 40% dos doentes de Crohn diagnosticados antes dos 18 anos sofram de atraso de crescimento em algum período da sua doença5 and 7. O atraso da maturação pubertal também é por si só uma queixa que merece investigação de DC pois pode ser um sinal que precede cronologicamente as queixas gastrointestinais8. Os fatores clínicos que potencialmente afetam a estatura final incluem o intervalo entre o início dos sintomas (que pode ser o atraso estatural isolado) e a data do diagnóstico, a presença de doença jejunal no diagnóstico, o início pré-pubertário de sintomas, o género e, naturalmente, a gravidade da doença8 and 9.

The influence of a given cytokine is not singular, and at different times, might

be pro- or anti-inflammatory, and thus have neuro-protective or neuro-destructive effects. Free radicals are increased by up-regulation of iNOS; and astrocytes simultaneously induce HO-1 which promotes reduction of damaging ROS (Min et al., 2006). During activation, microglia proliferate, and proliferation is stimulated by IL1-β and TNF-α (Mander et al., 2006). If microglial activation becomes chronic, microglia synthesize neurotoxic levels of quinolinic Regorafenib acid (Espey et al., 1997) and promote extracellular glutamate concentrations sufficient to cause neuritic beading and cell death (Takeuchi et al., 2005). Pro-inflammatory cytokines inhibit glutamate transporters, which sustain abnormally high levels of extra-cellular glutamate and thus, cyclic re-activation (Minami et al., 1991). Findings from in vivo and in vitro studies show that Pb exposure alters cellular functions in ways that might be expected to promote chronic microglial activation. Pb accumulation in erythrocytes results in increased brain δ-ALA which enhances and prolongs microglial activation (Kaushal et al., 2007). Moreover, microglia interact functionally with astrocytes, via cytokines (Verderio and

Matteoli, 2001), prostaglandins (Mohri et al., 2006) and nitric oxide synthase (Sola et al., 2002). Excess δ-ALA irreversibly inhibits glutamate uptake by astrocytes, via alteration of the glutamate transporter GLT-1 (Emanuelli Z-VAD-FMK et al., 2003). Glutamate potentiates astrocytic increases in Ca2+ via activation of metabotropic glutamate receptors (Zonta et al., 2003). δ-ALA triggers astrocytic Ca2+ Acyl CoA dehydrogenase waves which in turn activate microglia over large distances (Schipke et al., 2001). Thus, by way of multiple mechanisms, free-floating Pb in brain tissue and increased brain δ-ALA might be expected to promote neuroimmune system disruption, chronic microglial activation and microglia proliferation, as evidenced by altered levels of pro- and anti-inflammatory markers including

TNF-α, IFN-γ, IL6, IL10, iNOS and HO-1, increased microglial mean cell body number, and mean cell body volume. The aim of this study was to examine evidence of neuroimmune and brain structure differences in young C57BL/6J mice, with and without chronic Pb exposure. In child studies, Pb exposure has been associated with reduced short-term and working memory (see Section 1), which are subserved by dentate gyrus (DG) (Niewoehner et al., 2007), a sub-component of the hippocampal formation. In rodent models, low-level Pb exposure resulted in diminished recognition memory (see Section 1) which is also subserved by dentate gyrus (Jessberger et al., 2009); moreover, DG microglia have been shown to play a critical role in the maintenance of neural genesis and spatial learning and memory (Ziv et al., 2006).

Toxic cyanobacterial blooms in South American water bodies, with occurrence of MCs, reveal the extent of this problem as an emerging concern to public health authorities (Dörr et al., 2010). However not only water, but also food contaminated Akt inhibitors in clinical trials with cyanotoxins and other pollutants can pose a serious treat for humans, Mohamed and Hussein (2006) found MCs in liver, kidney, gut and muscle of O. niloticus in an Egyptian fish farm. Cazenave et al. (2005) detected MC in liver, gills, muscle and brain of Odontesthes bonariensis collected from a reservoir

in Argentina on two sampling dates. Xie et al. (2005) measured MC in gut, liver, kidney, muscle, blood and bile of eight species of fish in Lake Chaohu of China. Jang et al. (2003) measured MC content in body tissue of two native fishes in Hoedong Reservoir. Lake Paranoá is a Brazilian tropical reservoir that is typically eutrophic due to inadequate sewage treatment associated with high population growth (Altafin et al., 1995). T. rendalli and O. niloticus

are the fish species from Lake Paranoá that are most sold in local markets. Our previous study showed that both species are sensitive to different clastogens such as cyclophosphamide, mitomycin C, 5-fluorouracil and bleomycin ( Grisolia and Cordeiro, 2000). The aim in the present study Apitolisib was to evaluate the genotoxicity to tilapia fish O. niloticus, as induced by an extract of cyanobacteria containing MCs, using two administration routes and different endpoints, such as micronucleus, comet and apoptosis-necrosis testing. O. niloticus used in this study were obtained from a local fish farm, where breeding Clomifene and sanitary conditions were controlled and monitored constantly. The criterion for fish selection was body length of 7–10 cm. Fish of both sex were acclimatized in the Genetics Laboratory of the University of Brasilia for a week in tanks of 250 L volume, with continuously aerated filtered and dechlorinated

tap water. Fish were maintained at a constant temperature of 25 ± 2 °C, conductivity (550 ± 50 μS), pH = 7.0 ± 0.5, photoperiod (14:10 light:dark) and fed twice a day with granular fish chow. The ammonium level in the water was constantly monitored and the water was periodically renewed. The extract was obtained from a bloom taken from Lake Paranoá (Brazil) on June 25, 2006. The lyophilizated sample was resuspended in distilled water and ultrasonicated. Soon afterwards, a small sample aliquot was filtrated in a Microcon unit (Ultracel Ym-10, Millipore) and submitted to HPLC-PDA analyses. The chromatography was carried out under isocratic conditions using a reverse phase C18 column (Synergi 4ì Fusion-RP 80 (250 × 4, 60 mm; Phenomenex)), mobile phase of 20 mM ammonium formate, pH 5.0 and acetonitrile (7:3, v:v) for 30 min.

Damit im Plasma in physiologischer Kupferspiegel aufrecht erhalten bleibt, wird Kupfer durch die Leber aus LBH589 dem Blutkreislauf entfernt. Es wurde vorgeschlagen, dass

hCTR1 auch in der basolateralen Membran der Hepatozyten vorliegt und so den Uptake von Kupfer in die Hepatozyten ermöglicht [49]. Wenn der intrazelluläre und/oder der systemische Kupferspiegel erhöht ist, wird ATP7B in Vesikel verlagert, die mit Kupfer angefüllt sind und mit der apikalen Membran fusionieren, um das Kupfer in die Galle zu exportieren [50]. Es haben sich zelluläre und molekulare Mechanismen zur Regulation des Uptake, des Efflux, der Speicherung und der Verwendung von Kupfer entwickelt, so dass die Konsequenzen eines Mangels oder

Überschusses vermieden werden. Die Kupferhomöostase und damit der Kupferstatus werden auf der Ebene des gesamten Körpers sowohl durch die Resorption im Duodenum als auch durch die biliäre Exkretion reguliert (Abb. 1). In Situationen niedriger Kupferzufuhr steigt die Retention von resorbiertem Kupfer an und die Exkretion über die Galle geht zurück [19]. Umgekehrt wird bei hoher Kupferzufuhr eine Abnahme der Resorption und eine Zunahme endogener Verluste beobachtet. Die Hepatozyten sind sowohl für die Exkretion von Kupfer als auch für die Kontrolle der systemischen Kupferhomöostase von entscheidender Bedeutung. Bei Überlegungen zur Kupferzufuhr und zum Kupferbedarf sowie zu diesbezüglichen Empfehlungen (siehe folgende Abschnitte) muss berücksichtigt

werden, dass die Menge an Kupfer, www.selleckchem.com/products/pifithrin-alpha.html die vom Körper selbst letztendlich verwendet wird, nicht durch die Kupferzufuhr bestimmt wird. Die Bioverfügbarkeit ergibt sich sich vielmehr aus der Menge an Kupfer, die tatsächlich für die Resorption zur Verfügung steht, relativ zu der in der Nahrung vorhandenen Menge [51]. Der Mensch hat nur beschränkten Zugang zu Kupfer in der Umwelt. Nahrungsmittel, Trinkwasser und kupferhaltige Nahrungsergänzungsmittel Clomifene sind die Hauptquellen für Kupfer. Die Mengen, die durch Inhalation oder über die Haut aufgenommen werden, können vernachlässigt werden. Der Kupfergehalt in der Nahrung variiert beträchtlich, da sich verschiedene Nahrungsmittel in ihrem natürlichen Kupfergehalt stark unterscheiden [52]. Faktoren wie die Jahreszeit (die Kupferkonzentration ist in grünen Pflanzenanteilen höher), die Bodenqualität, die geographische Lage, die Herkunft des Wassers und der Einsatz von Dünger beeinflussen den Kupfergehalt in Nahrungsmitteln [52] and [53]. Bei normaler Versorgung übersteigt die Kupfermenge, die mit der Nahrung aufgenommen wird, deutlich die Menge an Kupfer, die aus anderen Quellen stammt. Trotzdem stellt diese Zufuhr kein Gesundheitsrisiko dar, da leistungsfähige und redundante Mechanismen die Resorption, Speicherung und Exkretion von Kupfer über einen breiten Bereich mit der Nahrung angebotener Kupfermengen wirkungsvoll kontrollieren.

Sr is likely a non-essential trace element, but in recent years, studies have shown that Sr is able to influence bone turnover [20] and has been applied in the form of strontium ranelate in therapeutic treatment of osteoporosis. Sr is chemically very similar to calcium (Ca), and can replace Ca, but still little is known about the role of Sr in normal bone metabolism as well as in bone disorders. Pb is a non-essential trace element and represents a highly toxic heavy metal. One of the main threats to human health from heavy metals is associated with exposure to Pb. Exposure to Pb is associated with chronic diseases in the nervous, selleck chemical hematopoietic, skeletal, renal and endocrine systems

[21] and [22]. Pb has been stated also as a potential risk factor for osteoporosis [23] and osteoarthritis [24]. Approximately 95% of the total body Pb burden is stored in skeleton [25] indicating that the bone tissue has a high capacity to accumulate and store Pb. In this context the bone tissue seems to have also the function to keep down the serum levels of such highly toxic elements. Human bone is essentially composed of a non-homogeneous and non-isotropic arrangement of mineralized

collagen fibrils. Cortical and trabecular bones are formed by individual osteons and bone packets (so called bone structural units — BSUs). HSP inhibitor They are produced at different moments during the (re)modeling cycle by the coordinated activity of bone cells, whereby the osteoblasts synthesize, secrete and deposit the collagenous matrix, which

then gradually mineralizes. Thus, each BSU has a certain mineral content depending on the time of deposition [26]. In general these BSUs are connected by a thin layer of mineralized non-collagenous proteins, the so called cement line/layer produced during the remodeling cycle [27]. Only very little data are available regarding the detailed spatial distribution of trace elements within such a bone tissue. Thus, the aims of this study were to map the trace elements Zn, Sr and Pb in bone tissue and to elucidate the following questions: i) is there a differential accumulation pattern of Zn, Sr and Pb selleck depending on Ca content of mineralized bone matrix in the bone packets, osteons, and interstitial bone? and ii) is the accumulation of Zn, Sr and Pb in cement lines different from that of mineralized bone matrix? Taking into account that the spot size of the confocal SR μ-XRF setup is about 5 times wider than the width of the cement lines the measured intensities are actually a huge underestimate of the real levels of trace elements in this region. For this purpose we analyzed trabecular and cortical bones from human femoral necks and heads using SR μ-XRF in combination with quantitative backscattered electron imaging (qBEI).

Further, because paraspinal and PS muscles have different nerve supplies (dorsal vs. ventral rami of lumbar nerves, respectively) selleckchem and MFI is increased bilaterally, denervation is not considered a plausible explanation in the current study. Finally, the positive correlation between fatty infiltration and episode frequency (mean: 4.4, min: 2, max: 9 per year; R2 = 0.450), may suggest a role for nociception in fatty infiltration.

This assumption is consistent with previous observations of generalized inhibition of MF, ES and PS recruitment with experimentally-induced pain ( Dickx et al., 2008; D’Hooge et al., submitted for publication). Further research is required to determine if peripheral nociception is involved in fatty infiltration via a reflex-mediated decrease in neural drive. Previously, Hultman

et al. (1993) found no difference in paraspinal muscle density on CT during remission of intermittent LBP. Results of fatty infiltration in the presence of LBP are less consistent than CSA measures. Some authors demonstrate increased fatty infiltration (Parkkola et al., 1993; Hultman et al., 1993; Mengiardi, 2006; Kjaer et al., 2007), whereas others show no difference to healthy controls (McLoughlin et al., 1994; Danneels et al., 2000; Kjaer et al., 2007). The discrepancy in results may be due to methodological JNK animal study differences such as the ROI in which fatty infiltration is determined (total vs. lean muscle, isolated MF vs. paraspinals grouped) or measuring technique (qualitative vs. quantitative, CT vs. MRI). The current study measured fatty infiltration

in two complementary modes yielding divergent results: lean fatty infiltration was increased, without macroscopic alterations. Similarly, Mengiardi (2006) revealed increased metabolic fat content with proton MR spectrocoscopy, which was not detectable with a semi-quantitative visual grading system using conventional MRI. Using a multifaceted approach to investigate lumbar muscle structure, the current study showed that fatty infiltration in lean muscle tissue was increased, without alterations in muscle size or macroscopic fat deposition during MRIP remission of LBP. This emphasizes the importance of differentiating muscle quantity (CSA) and quality (composition). In this respect, Elliott et al. reported enlarged cervical muscle CSAs and fatty infiltration in relation to whiplash-associated disorders, acknowledging that caution must be exercised during interpretation of CSA measurements in the presence of intramuscular fat (Elliott et al., 2008a, 2010). Similarly, lean fatty infiltration may be masking a reduction in muscle size in our results. It is assumed that fatty infiltration may negatively affect muscle contractility when muscle fibers are replaced with non-contractile tissue. Consequently, the deteriorated muscle composition may contribute to LBP recurrence.