Ideally, we would employ a psychosocial mediator such as stress, defined as “the interaction between people and their social Akt inhibitor environment involving psychological processes” (Egan et al.,

2008), but unfortunately such variables were not available in the study. We therefore used the General Health Questionnaire (GHQ-12) to derive a psychological factor for this study. The GHQ-12 comprises 12 self-complete questions describing mood states used to assess psychiatric morbidity, with six of the questions being positively phrased and six negatively phrased (Goldberg and Williams, 1988). Each item of the GHQ-12 has four possible response options and these were scored dichotomously using the GHQ method (all Z-VAD-FMK research buy items coded 0-0-1-1). Missing items were scored zero. The 12 scores were then summed and a cut-off for mental ill health derived from the mean score. For both waves 1 and 5, mean GHQ scores were approximately 2, setting a cut-off of 3 or more as

a case (‘1’) compared to not being considered a case (‘0’). Data on smoking, alcohol consumption, diet and physical activity were based on self-report. Behavioral variables created for these analyses were based, where possible, on contemporary guidelines, as well as making variables homogeneous between waves. Smoking status at both waves 1 and 5 was defined as current (1) versus ex- or non-smoker (0). Weekly alcohol consumption was used to define respondents as below (‘0’) versus above (‘1’) gender-specific recommended weekly limits (⩽21 versus 22+ units for males; ⩽14 versus 15+ units for females) (Changing Scotland’s Relationship Histidine ammonia-lyase with Alcohol, 2009) Alcohol strength changed for some drinks during follow-up (Bromley et al., 2003) and we recalculated this variable in wave 5, although this change had no impact

on our results. Physical activity was based on the number of occasions per week that respondents took part in an activity “lasting more than 20 min” that made them “sweat or (be) out of breath”, reflecting guidelines at the time. Respondents were dichotomized into high physical activity (at least 20 min once a week; ‘0’) versus low physical activity (less than once a week; ‘1’). Diet, from food-frequency questionnaires, was based on the number of days per week on which participants reported eating fruit and vegetables. Respondents were classified as having a poor diet (‘1’) if they had at least one day per week with no fruit or vegetables consumed versus not having a poor diet if they consumed fruit and vegetables every day of the week (‘0’) (See Table 1). For each individual measure (e.g. smoking, income, etc.), and for the combined factors, a cumulative measure was generated using data from both waves of survey data such that each mediator could take a value of 0, 1 or 2, with higher scores representing more negative material, psychological or behavioral exposures.

, 2011). Although the pectin yield obtained in the previous study was significant (11.5 g/100 g dry weight), in this study, we wanted to test an organic acid in an attempt to improve the extraction yield using Selleck Obeticholic Acid an environmentally friendly extraction procedure. Apart to environmental benefits, citric acid was chosen based on reports that demonstrated

that citric acid was more effective for pectin extraction than mineral acids in terms of yield and physicochemical properties (Klieman et al., 2009; Virk & Sogi, 2004; Yapo, 2009a). Initially, a fractional factorial 33−1 design was performed to investigate the influence of the extraction pH, extraction temperature and extraction duration on the pectin yield and the uronic acid content. The experimental design, factors, levels (coded and decoded) and responses are shown in Table 1. The pectin yield ranged from 3.7 to 10.6 g/100 g CPHF. The highest yield was obtained when the CPHF extraction conditions were pH 1.0/60 min/100 °C. The uronic acid content ranged from 54.4 to 68.9 g/100 g of pectin, with the highest percent of uronic acid obtained when the cacao pod husks were treated at pH 3.0/90 min/100 °C. Table 2 shows the estimated effects for the factorial design. The results indicate that the linear effect of temperature

and the quadratic effect of time are significant with respect to pectin yield, while only the linear effect of temperature is significant with respect to uronic acid content. The yield increased significantly (p < 0.05) check details with increasing time and temperature of the extraction, and the uronic acid content increased significantly with increasing temperature. The pH of the extraction did not have a significant effect on either pectin yield or uronic acid content. In contrast, when nitric acid was used in the extraction of pectins from cacao pod husks (Vriesmann, Teófilo, et al., 2011) at the same levels of as those used in the current work, the extraction time did not influence Sirolimus molecular weight pectin yield or the uronic acid content. The extraction yield increased with increasing pH and temperature, whereas the uronic acid

content increased with decreasing pH and increasing temperature (Vriesmann, Teófilo, et al., 2011). Marcon, Vriesmann, Wosiacki, Beleski-Carneiro, and Petkowicz (2005) extracted pectins from apple pomace with 5% (w/v) citric acid using a 22 factorial design with different times and temperatures. The obtained yield ranged from 5.7 to 16.8 g/100 g, and the increase in the yield was directly correlated with the increases in time and temperature of extraction, as observed for pectins extracted from CPHF with citric acid. The galacturonic acid content of their fractions (33.4–42.5 g/100 g) was not related to the extraction yield. Canteri-Schemin et al. (2005) extracted pectins from apple pomace with citric, phosphoric, malic, tartaric, hydrochloric, sulfuric and nitric acids. Citric and nitric acids showed the highest yields among the organic and mineral acids tested.

Surface salinity was calculated as monthly means using data obtained from the National Oceanographic Data Center. Surface temperature was calculated using the European Centre for Medium-Range Weather Forecasts database with a 6-h temporal resolution. The Neratinib manufacturer monthly average southern Tyrrhenian surface temperature and salinity were 13.4–28.5 ° C and 37.15–38.07 PSU respectively over the study period. Equation (5) was applied in calculating daily Qin values from May 2006 to June 2009 using the AVISO satellite database. These values were then used

for the whole period studied; although this represents an approximation, it is supported as tides are mainly short-term and periodic and the differences between the monthly average values of surface temperature CX-5461 in vivo and salinity for the eastern and western sides of the Sicily Channel are small. In future work, the Mediterranean climate system will be modelled using a large number of coupled sub-basin models, with the Sicily Channel flow being treated as a baroclinic exchange flow. The sensitivity

of the assumption will be further analysed by running several sensitivity experiments (see section 3.2). Bathymetric information and the area-depth distribution of the studied basin are depicted in Figure 1 and Figure 2. The surface area is 1.67 × 1012 m2, the water volume 2.4 × 1015 m3, the average depth 1430 m and the maximum depth 5097 m. The annual average freshwater runoff was 12 943 m3 s− 1, and the average precipitation and evaporation were 1.58 and 3.76 mm day− 1 respectively. Moreover, the average monthly surface salinity and water temperature over the entire basin ranged from 38.3 to 38.8 PSU and 14.8 to 27 ° C respectively. The cross-sectional area of the Sicily Channel

was calculated from bathymetric data (Figure 2b). Figure 2b shows that the Channel width from the southern to the northern parts is approximately 149 km and that the southern part is deeper than the northern part. The maximum depth across the Channel is 830 m. Satellite data on the sea level across the Sicily Channel were used to calculate the surface current flow from the western to eastern basins using equation (5). Figure 3 depicts some examples from these calculations of how the surface currents can take various routes. These routes must be considered when measuring PtdIns(3,4)P2 or calculating the Channel exchange. To resolve the mesoscale currents passing through the channel, the area was divided into 17 grid cells from which the Qin values were calculated. The temporal variations in the surface- and deep-layer flows are shown in Figure 4. The calculated surface flows over the period (early June 2006-late June 2009) ranged from 0.25 to 2.56 × 106 m3 s− 1, averaging 1.16 ± 0.34 × 106 m3 s− 1, while the deep flows were in the same range but with a slightly lower averaged value of 1.13 ± 0.36 × 106 m3 s− 1, indicating a loss of water in the EMB due to evaporation.

The RAS is composed of an enzymatic cascade in which angiotensinogen (AGT) is converted to Angiotensin (Ang) I by renin and subsequently to Ang II by angiotensin-converting-enzyme (ACE). Another important component of RAS, the Ang-(1-7), is primarily formed from Ang II by angiotensin converting enzyme 2 (ACE2). It is well documented that Ang II, acting via its AT1 receptor, is a potent proinflammatory, pro-oxidant, and prothrombotic agent that interferes with several steps of intracellular insulin

signaling. The ACE2/Ang-(1-7)/Mas axis has been suggested as an important counterregulatory arm in the RAS with opposite effects to those of ACE/Ang II/AT1. The Ang-(1-7) can DAPT in vitro produce NO-dependent vasodilation as well as antiarrhythmic, antiproliferative, and antithrombotic effects [5], [16], [21], [22] and [23]. Recently it was demonstrated that Mas-deficiency in FVB/N mice induces dyslipidemia, lower glucose tolerance and insulin sensitivity, hyperinsulinemia, hyperleptinemia, decreased glucose uptake in white adipose cells, in addition to an increase in adipose tissue mass. On the other hand, transgenic rats with increased circulating Ang-(1-7)

(TGR) have improved lipid and glucose metabolism [22] and [23]. A recent study confirmed the increased Ang-(1-7) plasma levels in TGR (51.82 ± 6.3 in TGR vs. 29.17 ± 8.7 pg/mL in Sprague–Dawley rats); and also showed a lower body weight (278.3 ± 13.3 g in TGR vs. 375.7 ± 10.2 g in Sprague–Dawley rats), improved insulin sensitivity and diminished triglycerides plasma levels (14.82 ± 3.77 mg/dL in TGR vs. 35.22 ± 3.39 mg/dL in Sprague–Dawley rats) in this model click here [23] However, the role of Ang-(1-7) in hepatic gluconeogenesis and glycogenolysis pathways is still poorly understood. Thus, the present study evaluated both pathways in the liver of transgenic rats which express Ang-(1-7) releasing fusion protein

(TGR) showing approximately twofold increase in Ang-(1-7) plasma levels compared to Sprague–Dawley (SD) rats. Ten TGR and control Sprague–Dawley (SD) rats were obtained from the transgenic animal facilities at Laboratory of Hypertension (Federal University Clostridium perfringens alpha toxin of Minas Gerais, Belo Horizonte, Brazil). The animals were kept under controlled light and temperature conditions, with free access to water and chow diet, in accordance to the ethical guidelines of our institution. Rats were sacrificed by decapitation and samples of blood and hepatic tissue were collected, weighed and immediately frozen in dry ice and stored at −80 °C for further analysis. Serum was obtained after centrifugation (3200 rpm for 10 min at 4 °C). ELISA kits were used to measure serum glucagon (ALPCO; Boston, USA) [10]. Hepatic glycogen was extracted and determined as glucose following acid hydrolysis. Briefly, liver samples were placed in tubes with 30% KOH (Sigma; St. Louis, MO, USA) saturated with Na2SO4 (Sigma; St. Louis, MO, USA).

The value of −0.0534 was inadvertently repeated from a3. The correct value of a2 is 0.885. The error does not affect any of the results in the paper because the correct polynomial coefficients

were used. However, use of the erroneous coefficient of a2 = −0.0534 for FAST* results in an under-estimation of human cardiac forward creatine kinase reaction rates by about 8%. The corrected Table 4 is shown below. The publisher would like to find more apologise for any inconvenience caused. “
” One of the brightest, most original and most lucid members of our community has left us. Sir Paul Terence Callaghan, GNZM, FRS, FRSNZ, passed away last March at the age of 64 after a long battle with cancer. Paul was a guiding beacon to all of us who had the privilege of knowing

him – both to those of us that had the luck to meet him through Science, but also to those that encountered him through Paul’s untiring educational and social actions. In terms of scientific contributions in general, and of his contributions to magnetic resonance in particular, anything I could write appears particularly superfluous: Paul was SUCH a towering figure in all matters concerning imaging, diffusion, anisotropic interactions, low-field NMR, polymer NMR, dynamics, MR hardware, physical concepts in general – that it seems somewhat naïve to try and summarize in a few sentences Paul’s 230 + record of most original publications. In fact I believe few ON1910 of us, particularly those of us who have been plowing in this field for a few decades, ever stepped into an area where Paul had not been (and had left his mark) before. Also Paul’s teaching activities are

probably familiar Inositol oxygenase to most of us; my own upbringing – and in fact I believe much of the seduction that NMR imaging concepts have to contemporary practitioners in this area – owe a big debt to the clarity and intellectual appeal with which Callaghan’s “Principles of Nuclear Magnetic Resonance Microscopy” explains even its most involved concepts. No wonder he was such a sought-after speaker by all magnetic resonance communities! Arguably, however, most of Paul’s educational efforts spilled outside the world of hard-core academia, as he sought to instill the same love and enthusiasm that he felt for Science, on his surrounding fellow-men at large. Those efforts, which included public lectures, articles in the mass-media, books, radio-programs, and YouTube postings, were particularly successful within his beloved “Kiwi” community – which among numerous prizes and accolades, voted him in 2011 “New Zealander of the Year”. Here at the Journal Magnetic Resonance, we were extraordinarily privileged to have Paul working with us, and being part of our scientific family. His advice, experience and scope were simply invaluable.

Prochloroccus ecotypes are therefore designated on the basis of their physiology and are classically designated as high light clades (HL) I–IV and low light (LL) clades I–IV. HL clades predominate in the upper water column to ~ 50 m depth RG7420 in vivo in highly stratified tropical waters ( West et al., 2011 and Johnson et al., 2006) while LL clades will persist down to between 150 and 200 m where they become light limited at ~ 0.1% of surface irradiance. Occasionally the LLI clade has been shown to be relatively abundant in near surface waters, or throughout the photic zone ( Johnson et al., 2006) and may

represent an intermediate ecotype ( Partensky and Garczarek, 2010). Distinct HL clades display temperature related optima in abundance. The HL I clade is adapted to cold temperate waters, while the HL II is dominant in both moderate and warm (sub)tropical waters ( Johnson et al., 2006 and Zinser et al., 2007). Clades HL III and HL IV are generally less abundant, accounting for between 5% and 20% when present, but are confined to warm equatorial waters > 26 °C ( Malmstrom et al., 2013, Rusch et al., 2010 and West et al., 2011). Marine Synechococcus classifications are more complicated than those of the Prochlorococcus, and the ecological strategies this website of the different types are less well characterized. The current status is well documented by recent multi-locus phylogenetic studies by Mazard et al. (2012) and Ahlgren and Rocap (2012). Marine

Synechococcus belong to three “sub clusters” 5.1, 5.2 and 5.3, with 5.1 the dominant sub-cluster in

most systems including coastal and open ocean regions. These sub-clusters are further divided in numerous clades and sub-clades. For example, the dominant marine sub-cluster 5.1 is sub-divided into at least 16 ( Ahlgren and Rocap, 2012) and potentially more than 30 ( Mazard et al., 2012) distinct clades. Synechococcus clades also appear to represent ecotypes specifically adapted to a variety of environmental conditions ( Mazard et al., 2012). For example, clades I and IV predominate in both coastal and open ocean temperate and cold environments ( Zwirglmaier et al., 2008) and may vary seasonally in their relative abundances ( Tai and Palenik, 2009), Clade III is the dominant lineage in tropical C59 clinical trial and subtropical oceanic gyres ( Zwirglmaier et al., 2008) and Clade II is found predominantly in tropical open ocean environments ( Ferris and Palenik, 1998, Toledo and Palenik, 2003 and Ahlgren and Rocap, 2006). While there is gathering evidence for the ecological partitioning of Synechcococcus lineages, the physiological bases for potential ‘ecotypes’ is not as clearly defined as for Prochlorococcus. However, distinct growth temperature optima ( Pittera et al., 2014), substrate utilization profiles ( Moore et al., 2005), and spectral tuning of light harvesting antennae ( Six et al., 2007) are some adaptations that may contribute to niche partitioning of clades and sub-groups.

The reports therefore compare different populations from each time period, and, although a number of weighting procedures are used, the estimates remain susceptible buy LY294002 to selection bias. One smaller study from Wales (n = 24,421) used the same ICD-10 definitions as our study and also found an overall reduction in case fatality but did not report variceal and nonvariceal hemorrhage mortality trends separately or trends in different age and comorbidity strata.10 Other nonvariceal hemorrhage studies from Spain (n = 17,663),1 The Netherlands (n = 1720),2 Greece (n = 1304),21 France (n = 1165),23

and Italy (n = 1126)22 did not identify reductions in nonvariceal inpatient mortality. Although these were large studies, they may have been underpowered to detect a change, and none of them adjusted the trends in case fatality for changes in comorbidity. Furthermore, none of these studies identified deaths that occurred after discharge. The remainder of the studies contained less than 1000 patients and therefore could not provide accurate estimates of mortality trends. For variceal hemorrhage, the largest study on mortality after hospitalization because of varices (n = 12,281; compared with 14,682 for this study) did not differentiate between hemorrhage and nonhemorrhage admissions.26 The next largest

study (n = click here 1475) compared variceal hemorrhage mortality between control groups in randomized trials 1960–2000 and showed a similar reduction in mortality.27 However, these control groups were from different geographical populations with different study exclusion criteria. Comparisons were therefore susceptible to selection bias. Other studies of trends in variceal hemorrhage mortality contained less than 1000 patients. The other finding of note in our study in relation to variceal hemorrhage is the small proportion of overall hemorrhages that they represent. In the context of the increasing burden of liver disease28 and an apparent increase in variceal hemorrhage in the recent BSG audit,8 a higher proportion might have been expected. Our finding, however, was similar

to that from the 1993 BSG audit (4%) and to other studies.9 and 29 It is possible that some of the variceal much hemorrhages in our study may have been incorrectly coded to esophageal hemorrhage, but a sensitivity analysis, assuming the most likely misclassification of all esophageal hemorrhage codes being miscoded variceal bleeds, did not alter the adjusted reduction in mortality. The previous difficulties in detecting a reduction in mortality might imply that we are reaching the point where mortality becomes unavoidable because of age and comorbidity. However, because the mortality in our study continued to improve right up to the end of the study period, improvements in management would appear to be continuing to have an impact on mortality following gastrointestinal hemorrhage. The reasons for the reduction in mortality we have observed are likely to be complex.

Bone healing of fractures and small bone defects is a unique and very effective process involving complex and well-orchestrated interactions between cells, cytokines, osteo-conductive matrix and a mechanically VE 821 stable environment with a good blood supply, according to the “diamond concept” [22] to generate new bone instead of a fibrous scar, as occurs in other connective tissues. This complex dynamic process requires the precise orchestration of various events during overlapping stages [23] with distinctive

histological characteristics, from the initial inflammatory response, the formation of a cartilaginous soft callus, the formation of a bone hard callus, and finally the bone union followed by remodeling. As is widely accepted, this bone repair in adults recapitulates the normal development of the skeleton during embryogenesis [24]. Moreover, the current paradigm of bone tissue engineering also relies on biomimetics to reproduce bone formation from development biology [25] and [26]. Prenatal bone formation starts with mesenchymal cell condensation and subsequent differentiation to chondrocytes

(through endochondral ossification) or, in precise cases, straight forward to osteoblasts (through intramembranous ossification) [27]. Both processes are implicated in the callus formation after fracture [24]. However, callus formation in adult bone is highly influenced by factors such as inflammation, presence of pluripotent and osteoprogenitor cells, gap distance between bone fracture Selleck Cilengitide endings, and mechanical stabilization and loading. The endochondral ossification mechanism predominates in the majority of fracture healing cases, advancing through several phases that involve multiple cellular and molecular events [28] in the so-called “bone healing cascade” [29] from hematoma and inflammation to angiogenesis and chondrogenesis, to finally complete osteogenesis followed by bone remodeling.

The interruption of vascular endothelium integrity is the first step following trauma, accompanied by a disruption of the blood supply and hematoma formation, associating the presence of necrotic material. This facilitates a potent inflammatory response related to the production of pro-inflammatory cytokines from aggregated platelets, as interleukin-1 (IL-1), IL-6 Dimethyl sulfoxide or tumor necrosis factor-α, which have chemotactic activity towards endothelial cells, fibroblasts, lymphocytes and monocytes–macrophages [30]. Specifically, transforming growth factor b1 (TGFb1) is a potent chemotactic stimulator of mesenchymal stem cells that enhances osteoblast precursors and chondrocyte proliferation, and may participate in recruitment of bone cells in the trauma area [31]. In addition, TGFb1 induces the production of extracellular bone matrix proteins such as collagen, osteopontin, and alkaline phosphatase [7] and regulates different cell types implicated in bone turnover and fracture healing [31].

Moreover, data suggest that BIL fails to induce apoptosis in cultured human nontransformed cells. These results suggest that BlL has a promising potential for application in the therapy and/or diagnosis of cancer. Future studies are needed to elucidate the details of BlL induced-apoptosis mechanism in several tumor cell lines. The authors declare that there are no conflicts of interest. The authors express their gratitude to the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) for research grants and fellowship (LCBBC and MTSC) and to the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior

(CAPES) and Fundação de check details Amaparo à Ciência e Tecnologia do Estado de Pernambuco (FACEPE) for research grants. Authors are deeply grateful to Maria Barbosa Reis da Silva, Maria D. Rodrigues and João Antônio Virgínio for their technical assistance. “
“Loxoscelism is a set of signs and symptoms caused by the bite of spiders of the genus Loxosceles ( Da Silva et al., 2004). Loxosceles (Araneae, Sicariidae) can be found in temperate and tropical regions of America, Oceania, Asia, Africa and Europe ( Swanson and Vetter, 2006, Hogan et al., DAPT purchase 2004 and Souza et al., 2008). This genus represents a public health problem in Brazil, mainly in South and Southeast regions, with more than 3000 cases reported annually by

the Ministry of Health ( Hogan et al., 2004). Usually, the clinical manifestations of loxoscelism are characterized by necroulcerative dermatitis Demeclocycline at the site of the bite (83.3% of the cases). However the envenoming can also cause systemic effects (16% of the victims) leading to acute renal failure, which may be lethal ( Málaque et al., 2002, Hogan et al., 2004 and Abdulkader et al., 2008). Locally, lesions caused by Loxosceles venom present edema, hemorrhage, inflammation with predominance of neutrophils, rhabdomyolisis, damage to the vessels wall, thrombosis, and dermonecrosis ( Futrell, 1992, Ospedal et al., 2002 and Pereira et al., 2010). In addition, according to some studies, Loxosceles venom causes cytoplasmic vacuolization, loss of adhesion ( Hogan et al., 2004, Veiga et al., 2000 and Veiga et al.,

2001) and apoptosis of endothelial cells ( Pereira et al., 2010). The family of Loxtox proteins ( Kalapothakis et al., 2007), such as: sphingomyelinase-d, SMA protein, phospholipase-d dermonecrotic protein (DP) and dermonecrotic factors (DNF) were found and characterized in the venom of Loxosceles and were associated with local and systemic loxoscelism ( Barbaro et al., 2005, Felicori et al., 2006 and Da Silveira et al., 2007). The systemic and local effects of the venom are well described in human, rabbit, and guinea pig cutaneous tissue. The use of the murine model in loxoscelism study is restrained to inflammatory events analysis, since the dermonecrotic lesion does not develop in mouse following intradermal injection of the venom ( Sunderkötter et al., 2001 and Barbaro et al., 2010).

crassidens) a relatively high percentage of teeth were worn down to the cingulum level. Teeth worn down to the root level were registered in relatively high frequencies (over 40%) in two species with distinct body and tooth size, the false killer whale P. crassidens and the much smaller Clymene dolphin, S. clymene. Superficial wear (Index 1) was commonly observed in dolphins and, for most of the species, was registered in more than 40% of the teeth (Fig. 6). Only for the false killer whale the superficial wear was less frequent than moderate (Index 2) and severe wear (Index 3). Superficial wear (Index 1) was relatively important for the Guiana dolphin S. guianensis, striped dolphin S. coeruleoalba, Fraser’s

JQ1 clinical trial dolphin L. hosei and killer whale O. orca. In these species 60% or more of the teeth were worn superficially. Moderate (Index 2) and severe wear (Index 3) were registered less frequently for most dolphin species. Only for the Clymene dolphin S. clymene, false killer whale P. crassidens and Atlantic spotted dolphins S. frontalis, moderate and severe wear were relatively conspicuous and registered Roxadustat in more than 20% of the teeth. Differences in dental wear prevalence among males and females were assessed only for the Guiana dolphin S. guianensis and

bottlenose dolphin Tursiops truncatus. Other species had few individuals of known sex. In the Guiana dolphin, frequencies DNA ligase of wear were statistically similar among males and females (t = 0.3597; p = 0.7196). Males presented an average wear prevalence

of 77% of their teeth (SD = ±31), and females of 75% (SD = ±33). On the other hand, wear frequencies were statistically different in males and females of the bottlenose dolphin (t = 3.1659; p = 0.0029). For this species, females had an average of 90% of their teeth worn (SD = ±13), while for males the average was 63% (SD = ±35) ( Fig. 7). The association between indexes of wear intensity (Indexes 1–3) with the total body length (TBL) of the specimens was tested using a correlation matrix. This analysis was performed only for the long-beaked common dolphin D. capensis, Fraser’s dolphin L. hosei, Guiana dolphin S. guianensis, Atlantic spotted dolphin S. frontalis and the bottlenose dolphin T. truncatus, species that had a sufficient number of individuals with known TBL. In cases where the variables showed statistically significant correlation, a linear regression was applied ( Table 3). The linear regression evidenced that only for the bottlenose dolphin T. truncatus all three categories of wear intensity showed a positive relationship of dependence with the TBL. This result in an increase of wear indexes with increasing of body size. For the Atlantic spotted dolphin S. frontalis, only indexes of superficial (Index 1) and moderate wear (Index 2) increased with body size. For the other species evaluated, results were distinct. The Guiana dolphin S.