These results suggest that differences in flipper shape have an evolutionary component and are likely largely in response to ecological requirements. “
“The population status of harbor porpoises has been of concern for several years, and the establishment of Marine Protected Areas (MPAs) has been suggested as a method to protect the harbor porpoise (Phocoena phocoena, Linneaus 1758) and other small cetaceans. In order to designate MPAs, high-density areas for the species must be identified. Spatial distribution of small cetaceans is usually assessed from ship or aerial surveys. As a potentially more accurate alternative, this study examined the movements and area preferences of 64 harbor porpoises, satellite tagged

between 1997 and 2007, in order to determine the distribution in the North Sea, the western Baltic, and the waters in between. Results show that harbor porpoises are not evenly distributed, but congregate RG-7388 in nine high-density areas within the study area. Several of these areas are subject to significant seasonal variation. The study found no differences in the home range size of males and females, but immature harbor porpoises have larger home ranges than mature

porpoises. The use of satellite telemetry for identifying areas of high harbor porpoise density can be of key importance when designating MPAs. “
“Cetaceans evolved flippers that are unique in both size and shape Selleckchem GSK126 probably due to selection pressures associated with foraging and body size. Flippers function as control surfaces for maneuverability and stability. Flippers of cetaceans and engineered

hydrofoils are similar with streamlined cross-sections and wing-like from planforms, which affect lift, drag and hydrodynamic efficiency. Scale models of the flippers from large-bodied (body length > 6 m) cetaceans (fin whale, killer whale, sperm whale) were constructed from computed tomography (CT) scans of flippers. Flipper planforms were highly tapered for the fin whale, a rounded, paddle-like design for the killer whale, and a square geometry for the sperm whale. Hydrodynamic properties of the models at varying angles of attack (−40º to 40o) were determined in a water tunnel with a multi-axis load cell. The flippers were found to have hydrodynamic characteristics similar to engineered wings. Differences in flipper morphology of large-bodied cetaceans and their hydrodynamic performance are associated with the requirements of aquatic locomotion involved with ecology of the whales. The flippers of the killer whale provided the greatest maneuverability, whereas the flippers of the fin whale had low drag for lunging and the flippers of the sperm whale provided lift for diving. “
“Bottlenose dolphins (Tursiops truncatus) have individually distinctive signature whistles. Each individual dolphin develops its own unique frequency modulation pattern and uses it to broadcast its identity.

Several of these studies showed improvement

in biochemical markers of liver function selleck or nutritional parameters, but were unable to demonstrate an improvement in short-term survival.195 At least in some trials, however, subgroups of patients who achieved nutritional goals and positive nitrogen balance had improved survival compared to those who did not.196 As an example, in one study the mortality rate was 3.3% in the 30 patients in whom positive nitrogen balance was achieved, but 58% in patients who remained in negative nitrogen balance.196 A recent study of nutritional therapy compared the outcomes of 35 patients randomized to 1 month of enteral tube feeding of 2000 kcal/day versus 40 mg of prednisone/day.197 GSI-IX in vitro No difference in mortality was noted, but the time course of

deaths was different, with the patients randomized to enteral feeding dying at a median of 7 days, versus 23 days in the steroid treated group. Patients treated with nutritional support who survived past the first month seemed to have a decreased mortality compared to the steroid-treated patients (8% versus 37%).197 Although technically a negative study, the similar overall mortality rate in the treatment groups suggests a role for nutritional intervention,198 particularly in light of the relatively benign risk:benefit ratio. Based on these data, other societies have recommended oral or parenteral supplements for patients with AH at risk of undernutrition.199 The most extensively studied intervention in alcoholic hepatitis is the use of steroids, based on 13 clinical trials that date back

pheromone almost 40 years (Table 7). Most of these trials were small, and therefore had only limited statistical power to detect even moderate treatment effects; five suggested an improvement in outcome, with decreased short term mortality in steroid-treated patients compared to placebo-treated patients, whereas eight showed no effect. It is important to note, however, that these trials used varying inclusion and exclusion criteria, dosing, and were done in a variety of patient populations. Three meta-analyses have analyzed data from these trials and showed an improvement in survival in treated patients200–202; one meta-regression, however, using different statistical weighting of the varying trials, was unable to show any difference.203 The most recent meta-analysis of these data did not show a statistically significant effect of steroids on mortality among all patients treated, although it did demonstrate an effect of steroids in the subgroup of patients with hepatic encephalopathy and/or a MDF score ≥ 32.204 The presence of substantial statistical heterogeneity in this subgroup of studies prevented the authors from reporting an overall beneficial effect.

2E and Supporting Fig. 5). These findings suggest increased β oxidation in Thrsp-overexpressed livers. Interestingly,

expression levels and activities of glucose-6-phosphatase selleck chemicals (G6pase), a key gluconeogenic enzyme, were significantly increased in Thrsp-overexpressed livers (Fig. 2E and Supporting Fig. 2E), suggesting that Thrsp may increase the release of glucose from the liver and contribute to type 2 diabetes. To further confirm the lipogenic effect of Thrsp in the liver, hepatic Thrsp expression was silenced by a siRNA-based approach. As expected, liver Thrsp expression was decreased approximately 2-fold at the protein level in db/db mice with Thrsp gene knockdown (Supporting Fig. 6A). Hepatic Thrsp gene silencing significantly reduced hepatic TG content (Supporting Fig. 6B). Thrsp gene knockdown also significantly ameliorated liver steatosis of db/db mice, as evidenced by Ivacaftor chemical structure morphological changes and Oil Red O staining (Supporting Fig. 6C). Consistently, expression of FAS was also markedly reduced after Thrsp gene knockdown (Supporting Fig. 6A). In addition, coinciding with the amelioration of fatty liver, serum alanine aminotransferase

activity and hepatic interleukin-1 expression were significantly reduced in db/db mice with hepatic Thrsp gene knockdown (Supporting Fig. 7A,B), Thiamine-diphosphate kinase suggesting a hepatoprotective effect of Thrsp knockdown on the liver. To determine the role of Thrsp in LXR-induced hepatic lipogenesis, we transfected murine primary hepatocytes with si-Thrsp or scrambled siRNA. Six hours after transfection, cells were treated with TO901317 or dimethyl sulfoxide for 36 hours. TO901317 significantly

increased the expression of Thrsp, which was abolished by si-Thrsp transfection (Supporting Fig. 8A). TO901317-induced lipid deposition in hepatocytes was significantly attenuated, but not completely abolished, by the knockdown of Thrsp (Supporting Fig. 8B). TO901317 treatment increased the expression of SREBP-1, FAS, and ACC, and Thrsp gene silencing markedly reduced ACC expression with a declining trend in SREBP-1 and FAS expression (Supporting Fig. 8C). These results imply that Thrsp mediates, at least in part, the lipogenic effects of LXR activation in hepatocytes and further supports our conclusion that Thrsp promotes hepatic lipogenesis. Because activation of the NR, LXR, also leads to enhanced lipogenesis in the liver,[8] and Thrsp expression is regulated by several NRs,[12, 13, 23] we sought to determine whether LXRs might regulate the expression of Thrsp. Mice were treated with TO901317 (5 mg/kg/day) for 3 days, and TG levels were examined. In line with previous reports,[8] TO901317 treatment resulted in significantly enlarged livers (Supporting Fig.

5%, P = 0.22). Roscovitine chemical structure Using a fixed-effects model, the prevalence of homozygous MTHFR C677T mutation was significantly higher in BCS patients than in healthy controls (OR = 2.01, 95% CI = 1.12–3.61, P = 0.02) (Fig. 3a). The subgroup analysis of Asian studies demonstrated a significantly higher prevalence of homozygous MTHFR C677T mutation in BCS patients than in healthy controls (Table 2). However, one European study did not show any significant difference between them. Four studies compared the prevalence of heterozygous MTHFR C677T mutation between BCS patients and healthy controls. The heterogeneity among studies was not

significant (I2 = 0%, P = 0.83). Using a fixed-effects model, the prevalence of heterozygous MTHFR C677T mutation was similar between BCS patients and healthy controls (OR = 0.97, 95% CI = 0.64–1.49, P = 0.90) (Fig. 4a). Regardless

of Asian or European studies, the subgroup analyses did not show any significant difference between them (Table 2). Two studies compared the prevalence of hyperhomocysteinemia between BCS learn more patients and healthy controls. The heterogeneity among studies was not significant (I2 = 0%, P = 0.74). Using a fixed-effects model, the prevalence of hyperhomocysteinemia was significantly higher in BCS patients than in healthy controls (OR = 2.57, 95% CI = 1.19–5.51, P = 0.02) (Fig. 5a). One Asian study showed a significantly higher prevalence of hyperhomocysteinemia in BCS patients than in healthy controls; contrarily, another European study did not show any significant difference between them (Table 2). Four studies compared the plasma homocysteine level between BCS patients and

healthy controls. The heterogeneity among studies was significant (I2 = 75.6%, P = 0.006). Using a random-effects model, the plasma homocysteine level was significantly higher in BCS patients than in healthy controls (WMD = 3.30, 95% CI = 0.94–5.66, P = 0.006) (Fig. 6a). The subgroup analysis of Asian studies showed a significantly higher plasma homocysteine level in BCS patients than SPTLC1 in healthy controls; contrarily, the subgroup analysis of European studies did not show any significant difference between them (Table 2). Six studies compared the prevalence of total MTHFR C677T mutation between non-cirrhotic PVT patients and healthy controls. The heterogeneity among studies was not significant (I2 = 17.9%, P = 0.30). Using a fixed-effects model, the prevalence of total MTHFR C677T mutation was similar between the two groups (OR = 1.35, 95% CI = 0.80–2.29, P = 0.26) (Fig. 2b). Funnel plot demonstrated that all included studies laid within the 95% CI, implying no proof of publication bias (Fig. S2). Similarly, Egger test did not demonstrate any significant publication bias (bias = 1.853826, 95% CI = −1.182272 to 4.889924, P = 0.1653).

Key Word(s): 1. sedation; 2. iv propofol; 3. adverse events; 4. trained staffs; Presenting Author: SEKINA Selleck GDC-0449 GHUMAN Additional Authors: HAMID KHAN Corresponding Author: SEKINA GHUMAN, HAMID KHAN Affiliations: Wrexham Maelor Hospital Objective: The value of routine ileoscopy during colonoscopy is unclear, but intubation of the terminal ileum (TI) is considered to be the main method of confirming completeness

of colonoscopy. TI intubation rates are variable and intubation is often omitted due to time constraints and the perception of little added diagnostic value. Our aim was to assess the diagnostic yield of TI intubation during colonoscopies at our hospital. Methods: A retrospective study was undertaken at Wrexham Maelor Hospital. Colonoscopy data over a 5 year period (1st October 2007 to 30th September 2012), were retrieved from the Endoscopy Reporting System database (Unisoft, Enfield, UK). Patients GPCR Compound Library with ileo-caecal resection were excluded. Demographic data, TI pathology (endoscopic and histopathologic) and indications for colonoscopy were analysed Results: 8016 colonoscopies were performed with an overall unadjusted caecal intubation rate of 90.3%. The endoscopists were of different grades including gastroenterologists, colorectal surgeons and a nurse endoscopist. 206 with previous ileo-caecal resection were excluded. Further analysis was performed

on 7810 colonoscopies. Mean age was 61 with a female preponderance at 52.6%. The TI was intubated in 1845 (23.5%). Endoscopic TI pathology was identified

in 42 patients (2.3%). Histology was available for 31, of which 23 (1.3%) had confirmed histological abnormalities. Diagnoses on ileoscopy included one adenocarcinoma, one carcinoid tumour, one metastatic malignant melanoma and 20 with terminal ileitis, of which 6 had histological Ribociclib clinical trial features of Crohn’s. The most common indications in those with TI pathology were diarrhoea (15), abdominal pain (8) and rectal bleeding (8). Conclusion: Although overall diagnostic yield was low, TI intubation identified significant pathologies requiring further action, including three malignancies. Routine ileoscopy at colonoscopy is a simple manoeuvre, which, apart from quality assurance can identify important pathology. The most common indication in those with confirmed TI pathology was diarrhoea, therefore ileoscopy may have added diagnostic value in this context. Key Word(s): 1. Terminal ileum; 2. Ileal Intubation; 3. Colonoscopy; 4. Ileoscopy; Presenting Author: FAN ZHANG Additional Authors: KE TAO, HONG XU Corresponding Author: HONG XU Affiliations: No; China Objective: Atrophic gastritis (AG) is a well-characterized premalignant condition with a significantly increased risk for developing gastric neoplasia. A rigorous upper endoscopy surveillance program has been shown to undoubtedly reduce this risk.

As the benefits of a top-down approach are countered by the cost and risks of adverse events, more emphasis is placed on identifying predictors of aggressive disease or using a rapid step-up strategy. Patient age under 40, stricturing disease, weight loss, corticosteroid requirement at presentation and perianal disease have all been suggested as indicators of severe disease.47,48 Loss of response.  While the anticipated duration of therapy with biological agents is often Regorafenib mw undefined, loss of response occurs in approximately 13%

of patients per year of treatment.49 Drug trough levels have been proposed as a predictor of continued response, or to explain the cause of loss of response.50 Neutralizing antibodies to anti-TNF agents can result in reduction in trough levels, and subsequent non-response. Anti-drug antibodies may also be associated with injection site and infusion reactions. The rheumatological literature reports a progression from decreasing trough levels to detection of anti-drug antibodies and finally a loss of response.51 Anti-drug

antibodies are seen in 9–28% of those treated with infliximab,5 and 3–17% of those treated with adalimumab.25,50,52 They occur more frequently with intermittent anti-TNF therapy.53 Co-administration with Tamoxifen order a second immunosuppressive agent reduces the risk of antibody development.54 Strategies to prevent their development include scheduled maintenance therapy and co-administration of corticosteroids or other immunomodulators (see below). With decrease in response, dose intensification,

decreased dosing interval, re-induction or drug switching can be performed.20,27,55–57 Only the latter two approaches are government subsidized in Australia.58 Evidence relating to anti-drug antibodies to trough levels and a loss of response is at times unclear.50 It is unknown which (if any) strategies to maintain trough levels will Liothyronine Sodium result in prolonged clinical effect. Anti-TNF agent trough level, and anti-drug antibody measurement is not widely available at present. Treatment failure.  Treatment failure comprises primary non-response, adverse drug reactions and loss of response. It occurs in up to 50% of those on scheduled maintenance therapy.48 Enrollment in trials of new therapeutic agents such as ustekinumab and vedolizumab, and surgery remain options for failure of existing biological agents. Switching.  Changing anti-TNF agents secondary to treatment failure or loss of response is an accepted therapeutic maneuver. The efficacy of adalimumab59–63 and certolizumab pegol64 in those with loss of response or treatment failure prior to biological therapy has been shown in open label studies, while the success of adalimumab in this setting has been demonstrated in a placebo-controlled trial.56 Switching to a third anti-TNF agent following failure of the two other anti-TNF agents is safe and effective.

Response to milk free diet Results: N = 26, M: F – 14:12. Median age: 16.88 months (SD +/− 10.27). Mean duration between presentation and introduction of cow milk: 8.18 months (0.5–29). Presentation: 15 (57.6%) – chronic diarrhea and blood in stool, 10 (38.4%) – chronic diarrhea and failure to thrive. Endoscopic rectal mucosal biopsies were performed in 20 (76.9%) and EGD with duodenal

biopsies in 6 (23%) – all were positive. Mean follow up: 7.23 BMS-354825 chemical structure months (SD +/− 5.49). All patients responded to milk free diet. Peptide based chicken formula prescribed in 9 (34.6%) and extensively hydrolyzed amino acid formula given to 3 (11.5%). Remaining 14 (53%) were managed on home made diet. Re-challenge was undertaken in 7 after parental consent. Re – challenge was done at 2 years of age or one year after stopping milk. Only one patient presented with recurrence following re-challenge. Conclusion: Chronic diarrhea, blood in stool and failure to thrive are common presenting symptoms of CMPA. Mucosal biopsies help in establishing diagnosis. More than 50% patients can be managed with a home-modified diet. Key Word(s): 1. cow milk protein allergy;

2. milk protein allergy; 3. paediatric diarrhoea Presenting Author: ERIC CHEAH Additional Authors: KEVIN GASKIN, MICHAEL STORMON, SHOMA DUTT, ANNABEL MAGOFFIN, EDWARD O’LOUGHLIN Corresponding Author: ERIC CHEAH Affiliations: https://www.selleckchem.com/products/carfilzomib-pr-171.html The Children’s Hospital at Westmead, The Children’s selleck chemicals llc Hospital at Westmead, The Children’s Hospital at Westmead, The Children’s Hospital at Westmead, The Children’s Hospital at Westmead

Objective: Eosinophilic oesophagitis (EO) is a chronic, immune/antigen-mediated oesophageal disease characterized by oesophageal dysfunction and histologically by eosinophil-predominant inflammation. This study will report on our 5 year experience in children diagnosed with EO at the Children’s Hospital at Westmead, a tertiary paediatric institution in Sydney, Australia. Methods: A retrospective audit was performed between January 1, 2008 and December 31, 2012 to evaluate all patients newly diagnosed with EO. The follow up period was included up to May 31, 2014. Demographic data, clinical symptoms, associated conditions, atopic history and treatment modalities were collated. Results: A total of 108 patients were diagnosed with EO: 71% male, median age 6.8 years (range 0.8–16.8 years); representing an average of 4% of total endoscopies performed per year. 41 patients had dysphagia symptoms, 34 patients had gastro-oesophageal reflux symptoms, 11 patients with abdominal pain and 23 patients with non-EO symptoms. Atopic history was elicited in 54% of patients whilst 36% had food allergy. Concomitant diagnosis included coeliac disease, Helicobacter pylori gastritis and proctitis/ulcerative colitis. Endoscopic appearance was normal in 8.3% of patients. Patients required a median of 2 (range 0–10) follow up endoscopies. Treatments are presented in Table 1.

Serum levels of alanine aminotransferase, and liver myeloperoxidase content were assessed. Serum and liver tumor necrosis factor-α (TNF-α), macrophage inflammatory protein-2 (MIP-2) and keratinocyte chemokine (KC) were also assessed. Hepatic reactive oxygen species (ROS) levels were assessed.

For in vitro experiments, isolated hepatocytes and Kupffer cells were treated with IL-37 and inflammatory stimulants. Cytokine and chemokine production by these cells were assessed. Primary hepatocytes underwent induced cell injury and were treated with IL-37 concurrently. Hepatocyte cytotoxicity and Bcl-2 expression Decitabine solubility dmso were determined. Isolated neutrophils were treated with TNF-α and IL-37 and neutrophil activation and respiratory burst were assessed. Results:  IL-37 reduced hepatocyte injury and neutrophil accumulation in the liver after I/R. These effects were accompanied by reduced serum levels of TNF-α and MIP-2 and hepatic ROS levels. IL-37 significantly reduced MIP-2 and KC productions from lipopolysaccharide-stimulated hepatocytes and Kupffer cells. IL-37 significantly reduced cell death and increased Bcl-2 expression in hepatocytes. IL-37 significantly suppressed TNF-α-induced neutrophil activation. Conclusions:  IL-37 is protective against hepatic I/R injury. These effects are related to the ability of IL-37 to reduce proinflammatory cytokine and chemokine production by hepatocytes and Kupffer cells as well as having a direct protective effect

Opaganib nmr on hepatocytes. In addition, IL-37 contributes to reduce liver injury through suppression of neutrophil activity. “
“Chronic hepatitis C virus infection is associated with an oxidative stress response that contributes to fibrosis and hepatocellular carcinoma but paradoxically also serves to limit viral replication. HCV also induces stress response pathways but these frequently fail in the presence of alcohol and other factors. FOXO3, a longevity-associated transcription factor, is one of several regulators of oxidative stress responses that are modified by HCV. We have previously shown that HCV activates the transcriptional activity of FOXO3 by causing a change in its pattern of phosphorylation,

methylation and ubiquitination. The mechanisms of these changes Tenofovir are largely unknown but a number of upstream enzymes have been shown to modify FOXO3 including the arginine methyltransferase PRMT1 and the ubiq-uitin carboxyl-terminal hydrolase USP7. HCV has previously been reported to decrease the activity of PRMT1. We postulated that this might initiate other FOXO3 modifications associated with HCV. The AIM of this study was thus to determine how HCV-induced changes in PRMT1 effect the ubiquitin carboxylterminal hydrolase USP7 and the consequences of this for the FOXO3-dependent stress response. RESULTS: Immunoprecipitation studies demonstrated that PRMT1 directly complexes with USP7 and arginine methylates USP7. Methylation of USP7 was increased by PRMT1 overexpression and inhibited by PRMT1 knockdown.

6 These comprise proinflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (TNF-α).7 TNF-α plays a key role in bystander killing of infiltrating cytotoxic T lymphocytes, thereby contributing to the immunopathology associated with HCV.8 In 1992, Dahl et al.9 reported the expression of a novel gene in peripheral cells of patients receiving high doses of IL-2

and cloned the complementary DNA (cDNA) from a human natural killer (NK) cell library; the cDNA was designated NK4. However, for the next 12 years the function of NK4 remained unknown. Kim et al.10 expressed the NK4 cDNA and purified the recombinant protein in 2005. Recombinant NK4 exhibited properties of a proinflammatory cytokine inducing IL-1β and TNF-α in human monocytic cells and they renamed NK4 as IL-32. Subsequently, IL-32 GSI-IX cost was reported

to be involved in several chronic inflammatory diseases including Crohn’s disease, ulcerative colitis,11, 12 and rheumatoid arthritis.13 Other studies demonstrated its proinflammatory role in various disease models. IL-32 expression is increased in lung tissue of patients with chronic obstructive pulmonary disease (COPD).14 In that study, IL-32 staining correlated with that of TNF-α and with the degree of airflow obstruction. Two recent studies demonstrated that IL-32 is expressed and functional as a proinflammatory mediator in human vascular endothelial JQ1 ic50 cells.15, 16 IL-32 propagated vascular inflammation, and endothelial expression of IL-32β in transgenic mice

promoted inflammation and worsened sepsis.16 Moreover, IL-32 has been implicated in infectious diseases such as mycobacterium tuberculosis, Dolutegravir influenza A virus, and human immunodeficiency virus (HIV)-1 infections.17-20 Importantly, IL-32 was reported to suppress HIV-1 replication.19, 20 IL-32 is not only induced during infection with Mycobacterium tuberculosis,17 but as recently demonstrated might also play a role in the host defense against this bacterium.21 Thus, the aim of this study was to evaluate the role of IL-32 in chronic HCV infection. Specifically, we examined IL-32 in patients with untreated chronic HCV infection to assess any association with viral load and liver fibrosis, steatosis, or inflammation. In vitro, we determined the impact of proinflammatory cytokines and type I interferon on endogenous IL-32 expression in human hepatocytes. Moreover, using HCV luciferase reporter viruses we investigated (1) whether HCV infection affects expression of IL-32 in vitro and (2) studied the influence of IL-32 on HCV replication.

For example, although genets Genetta genetta are common and widely distributed, Cardillo et al. (2004) identify genets (along with several other viverrids) as likely to become endangered by 2030 due to their overlap in distribution with

areas of high human population density. However, genets have been observed living alongside humans in urban habitats in Africa (PWB pers. obs.) and Europe (Larivière & Calzada, 2001 and references therein). The perseverance of carnivores such as genets in significantly anthropogenically Tyrosine Kinase Inhibitor Library supplier disturbed habitats is likely to rely on physiological and behavioural adaptability of these charismatic animals. Our thanks to Stephen Harris for his comments on red foxes in the UK and three referees for helpful suggestions. Thanks also to Rob Morley for sharing his observations. “
“Alongside the eusocial naked mole-rat, Heterocephalus glaber, Heliophobius argenteocinereus represents the second oldest lineage within the African mole-rat family Bathyergidae, and phylogenetically intermediate between the East African Het. glaber and the South African genera Bathyergus and Georychus. Across its geographic range, Hel.. argenteocinereus is widely distributed on both sides of the East African Rift System (EARS), Alectinib concentration and is a key taxon for understanding

the phylogeographic patterns of divergence of the family as a whole. Phylogenetic analysis of 62 mitochondrial cyt b sequences, representing 48 distinct haplotypes from 26 geographic locations across the range of Heliophobius, consistently

and robustly resolved six dipyridamole genetically divergent clades that we recognize as distinct evolutionary species. Early species descriptions of Heliophobius were synonymized into a monotypic taxonomy that recognized only Hel. argentocinereus. These synonyms constitute available names for these rediscovered cryptic lineages, for which combined morphological and genetic evidence for topotypical populations endorses the recognition of six to eight distinct taxa. Bayesian estimates of divergence times using the fossil Proheliophobius as a calibration for the molecular clock suggest that the adaptive radiation of the genus began in the early Miocene, and that cladogenesis, represented in the extant species, reflects a strident signature of tectonic activity that forged the principal graben in the EARS. “
“Corrigendum to doi: 10.1111/j.1469-7998.2010.00740.x Unfortunately, the data presented in Table 5 of the original manuscript is incorrect for the gross dry matter intakes (DMI) needed by kangaroos and sheep to meet their daily field metabolic rates (FMR) or basal metabolic rates (BMR). Please see the correct values presented in Corrigendum Table 5.