8-10 Our studies have shown that CD4 T cells can function by way of CD154 without de novo antigen-specific activation, and innate immunity-induced CD40 may trigger CD154–CD40 engagement to facilitate tissue inflammation and injury.11 Our recent study has focused on the distinctive features of newly identified TIM-1–TIM-4 signaling in liver IRI.12 Collectively, these studies have documented a previously unrecognized mechanism through which a CD4 T cell–generated positive costimulation signal can amplify Kupffer Ibrutinib cell activity/function

and cross-talk to facilitate IR-triggered immune cascade. Programmed death-1 (PD-1; CD279) is the CD28 homologue expressed selectively by activated T, B, and myeloid cells.13 When cross-linked with PD-L1 (B7-H1; CD274) on hemopoetic and many nonhemopoetic tissues, the PD-1/B7-H1 interaction delivers a potent negative signal that inhibits check details T and B cell activation and may promote immune tolerance. This study is the first to examine the putative role of PD-1/B7-H1 in the pathophysiology of liver IRI. Our results demonstrate that stimulating PD-1 negative signals ameliorates local inflammation and liver damage and suggest that engaging PD-1/B7-H1 costimulation is required for maintaining liver homeostasis during IR-induced insult. AU, absorbance units; B7-H1Ig, B7-H1 immunoglobulin; BMM,bone marrow–derived macrophage; H&E, hematoxylin-eosin;

IFN-γ, interferon-γ; IL, interleukin; IRI, ischemia and reperfusion injury; mAb, monoclonal antibody; PD-1, programmed death-1; sALT, serum alanine aminotransferase; TLR, Toll-like receptor; TNF-α, tumor necrosis factor α; TUNEL, terminal deoxynucleotidyl transferase –mediated dUTP nick-end labeling; WT, wild-type. Male C57BL/6 wild-type (WT) mice (8-12 weeks old) (Jackson Laboratory, Bar Harbor, ME) were housed in the University of California Los Angeles animal facility under specific pathogen-free conditions and received humane care according to the criteria outlined in the Guide for the Care and Use of Laboratory Animals (prepared by the National Academy of Sciences; National Institutes of Health

publication 86-23, revised 1985). We Protirelin used a mouse model of warm partial hepatic IRI.3-5, 7-12 Mice were anesthetized, injected with heparin (100 U/kg intraperitoneally), and the arterial and portal venous blood supply to the cephalad lobes was interrupted by an atraumatic clip. After 90 minutes of local ischemia, the clip was removed. Animals were sacrificed after 6 or 24 hours of reperfusion. Sham-operated mice underwent the same procedure, but without vascular occlusion. Rat anti–B7-H1 monoclonal antibody (mAb) (10F.9G2; Bio X Cell, West Lebanon, NH), recombinant B7-H1 immunoglobulin (B7-H1Ig), a dimeric B7-H1 immunoglobulin fusion protein14 (courtesy of Dr. Xian C. Li, Harvard Medical School, Boston, MA), or control Ig (Bio X Cell) was administered intravenously prior to the onset of ischemia (0.25 mg at day −1 and 0.5 mg at day 0).

8-10 Our studies have shown that CD4 T cells can function by way of CD154 without de novo antigen-specific activation, and innate immunity-induced CD40 may trigger CD154–CD40 engagement to facilitate tissue inflammation and injury.11 Our recent study has focused on the distinctive features of newly identified TIM-1–TIM-4 signaling in liver IRI.12 Collectively, these studies have documented a previously unrecognized mechanism through which a CD4 T cell–generated positive costimulation signal can amplify Kupffer selleck inhibitor cell activity/function

and cross-talk to facilitate IR-triggered immune cascade. Programmed death-1 (PD-1; CD279) is the CD28 homologue expressed selectively by activated T, B, and myeloid cells.13 When cross-linked with PD-L1 (B7-H1; CD274) on hemopoetic and many nonhemopoetic tissues, the PD-1/B7-H1 interaction delivers a potent negative signal that inhibits ICG-001 molecular weight T and B cell activation and may promote immune tolerance. This study is the first to examine the putative role of PD-1/B7-H1 in the pathophysiology of liver IRI. Our results demonstrate that stimulating PD-1 negative signals ameliorates local inflammation and liver damage and suggest that engaging PD-1/B7-H1 costimulation is required for maintaining liver homeostasis during IR-induced insult. AU, absorbance units; B7-H1Ig, B7-H1 immunoglobulin; BMM,bone marrow–derived macrophage; H&E, hematoxylin-eosin;

IFN-γ, interferon-γ; IL, interleukin; IRI, ischemia and reperfusion injury; mAb, monoclonal antibody; PD-1, programmed death-1; sALT, serum alanine aminotransferase; TLR, Toll-like receptor; TNF-α, tumor necrosis factor α; TUNEL, terminal deoxynucleotidyl transferase –mediated dUTP nick-end labeling; WT, wild-type. Male C57BL/6 wild-type (WT) mice (8-12 weeks old) (Jackson Laboratory, Bar Harbor, ME) were housed in the University of California Los Angeles animal facility under specific pathogen-free conditions and received humane care according to the criteria outlined in the Guide for the Care and Use of Laboratory Animals (prepared by the National Academy of Sciences; National Institutes of Health

publication 86-23, revised 1985). We Methocarbamol used a mouse model of warm partial hepatic IRI.3-5, 7-12 Mice were anesthetized, injected with heparin (100 U/kg intraperitoneally), and the arterial and portal venous blood supply to the cephalad lobes was interrupted by an atraumatic clip. After 90 minutes of local ischemia, the clip was removed. Animals were sacrificed after 6 or 24 hours of reperfusion. Sham-operated mice underwent the same procedure, but without vascular occlusion. Rat anti–B7-H1 monoclonal antibody (mAb) (10F.9G2; Bio X Cell, West Lebanon, NH), recombinant B7-H1 immunoglobulin (B7-H1Ig), a dimeric B7-H1 immunoglobulin fusion protein14 (courtesy of Dr. Xian C. Li, Harvard Medical School, Boston, MA), or control Ig (Bio X Cell) was administered intravenously prior to the onset of ischemia (0.25 mg at day −1 and 0.5 mg at day 0).

The prevalence of NAFLD and

NASH is likely higher than previously estimated and is associated GDC-0449 order with the growing epidemics of obesity and diabetes. Increasing evidence supports the fact that NASH can progress to HCC. The overall prevalence of HCC in patients with NAFLD remains low, although the incidence of HCC in developed countries is rising. Idiopathic, or CC, which accounts for 6.9%-50% of these cases of HCC, is clearly associated with diabetes, insulin resistance, and obesity. A large proportion of CC likely represents end stage NASH. Obesity, diabetes, iron deposition, advanced fibrosis, and age significantly increase the risk of NASH patients progressing to cirrhosis and subsequent HCC. HCC secondary to NASH typically develops in the setting of cirrhosis, although rare cases of HCC arising in NASH without cirrhosis raises the possibility that carcinogenesis secondary to NAFLD can occur in the absence of advanced liver disease. Obesity, diabetes, and hepatic steatosis are also risk factors for the development of HCC in other liver diseases such as chronic HCV. Efforts to maximize the

management of these conditions should be should be considered in patients with any form of chronic liver disease. Because of the long, indolent clinical course of NASH, patients this website with significant disease may be overlooked, and often present with advanced age, multiple comorbidities, and larger tumor size, portending a poor prognosis. The connection between NAFLD and progression to HCC is becoming clearer, and the increasing burden of NASH, DM, and obesity is becoming heavier. Community awareness of the potential for this disease to progress to HCC is critical. Complications of NASH are expected to increase with the continuing epidemics of obesity and diabetes. Once the diagnosis of cirrhosis is made, screening for HCC should be pursued. Given recent epidemiologic data in diabetes, thought should be given to the use of statins in

NASH patients, particularly those with diabetes and hyperlipidemia. Further research is urgently needed to better elucidate the signaling pathways for HCC development in the Bumetanide setting of insulin resistance. Studies evaluating potential targets for treatment of NASH and HCC, including targeting JNK activation, should be actively pursued. “
“Malato Y, Naqvi S, Schurmann N, Ng R, Wang B, Zape J, et al. Fate tracing of mature hepatocytes in mouse liver homeostasis and regeneration. J Clin Invest 2011;121:4851-4860. (Reprinted with permission.) Recent evidence has contradicted the prevailing view that homeostasis and regeneration of the adult liver are mediated by self duplication of lineage-restricted hepatocytes and biliary epithelial cells.

The prevalence of NAFLD and

NASH is likely higher than previously estimated and is associated MEK inhibitor with the growing epidemics of obesity and diabetes. Increasing evidence supports the fact that NASH can progress to HCC. The overall prevalence of HCC in patients with NAFLD remains low, although the incidence of HCC in developed countries is rising. Idiopathic, or CC, which accounts for 6.9%-50% of these cases of HCC, is clearly associated with diabetes, insulin resistance, and obesity. A large proportion of CC likely represents end stage NASH. Obesity, diabetes, iron deposition, advanced fibrosis, and age significantly increase the risk of NASH patients progressing to cirrhosis and subsequent HCC. HCC secondary to NASH typically develops in the setting of cirrhosis, although rare cases of HCC arising in NASH without cirrhosis raises the possibility that carcinogenesis secondary to NAFLD can occur in the absence of advanced liver disease. Obesity, diabetes, and hepatic steatosis are also risk factors for the development of HCC in other liver diseases such as chronic HCV. Efforts to maximize the

management of these conditions should be should be considered in patients with any form of chronic liver disease. Because of the long, indolent clinical course of NASH, patients MK-2206 nmr with significant disease may be overlooked, and often present with advanced age, multiple comorbidities, and larger tumor size, portending a poor prognosis. The connection between NAFLD and progression to HCC is becoming clearer, and the increasing burden of NASH, DM, and obesity is becoming heavier. Community awareness of the potential for this disease to progress to HCC is critical. Complications of NASH are expected to increase with the continuing epidemics of obesity and diabetes. Once the diagnosis of cirrhosis is made, screening for HCC should be pursued. Given recent epidemiologic data in diabetes, thought should be given to the use of statins in

NASH patients, particularly those with diabetes and hyperlipidemia. Further research is urgently needed to better elucidate the signaling pathways for HCC development in the ID-8 setting of insulin resistance. Studies evaluating potential targets for treatment of NASH and HCC, including targeting JNK activation, should be actively pursued. “
“Malato Y, Naqvi S, Schurmann N, Ng R, Wang B, Zape J, et al. Fate tracing of mature hepatocytes in mouse liver homeostasis and regeneration. J Clin Invest 2011;121:4851-4860. (Reprinted with permission.) Recent evidence has contradicted the prevailing view that homeostasis and regeneration of the adult liver are mediated by self duplication of lineage-restricted hepatocytes and biliary epithelial cells.

“
“In Japan, genotypes B and C are the predominant genotypes isolated from patients with chronic hepatitis B, while genotype A predominates in patients with acute hepatitis B. Globalization, however, appears to have changed the distribution of the hepatitis B virus (HBV) genotypes. Thus, the viral characteristics of HBV genotypes other

than genotypes A, B and C were examined. Screening of genotypes was performed by enzyme immunoassay and/or polymerase chain reaction INVADER http://www.selleckchem.com/products/Belinostat.html method in 222 patients with HBV. The full-length nucleotide sequences of unusual strains were compared to those in the database, followed by construction of a phylogenetic tree. Unusual HBV strains were isolated from two patients: a 27-year-old Japanese bisexual man with acute

hepatitis B with HIV co-infection and a 52-year-old Japanese man with chronic hepatitis B. The former strain was classified as genotype H, showing an overall identity Selleck Alectinib of 99.8% to the Thailand strain (EU498228), while the nucleotide sequence of the latter strain showed similarity to the genotype B strains isolated in Malaysia (JQ027316) and Indonesia (JQ429079) between DR2 and DR1 in the X region, with identities of 96.9%. However, this strain was classified as genotype H by full-length sequence analysis, and the sequence between nt2023 and nt2262 showed no similarity to that in any previously reported strains. HBV strains showing recombination between genotype B and H strains were found even in chronic hepatitis patients in Japan. Globalization dipyridamole may yield HBV strains of possible novel genotypes containing novel nucleotide sequences in the precore/core region. “
“The need for standardized language is increasingly obvious, also within gastrointestinal endoscopy. A systematic

approach to the description of endoscopic findings is vital for the development of a universal language, but systematic also means structured, and structure is inherently a challenge when presented as an alternative to the normal spoken word. The efforts leading to the “Minimal Standard Terminology” (MST) of gastrointestinal endoscopy offer a standardized model for description of endoscopic findings. With a combination of lesion descriptors and descriptor attributes, this system gives guidance to appropriate descriptions of lesions and also has a normative effect on endoscopists in training. The endoscopic report includes a number of items not related to findings per se, but to other aspects of the procedure, formal, technical, and medical. While the MST sought to formulate minimal lists for some of these aspects (e.g. indications), they are not all well suited for the inherent structure of the MST, and many are missing.

The only prescription NSAID approved the FDA for the treatment of migraine is Cambia (Depomed, Inc, Newark, CA, USA), a powder form of diclofenac that can be dissolved in water for better

absorption. For those with severe nausea or vomiting, a nasal spray of ketorolac (brand name Sprix [Regency Therapeutics, Shirley, NY, USA]) or injectable ketorolac can be useful options. The formerly known brand name Toradol made by Roche Bioscience (Nutley, NJ, USA) is no longer available in the US, but the generic injectable version remains available. Sometimes an individual’s medical conditions prohibit the use of triptans, DHE, and NSAIDs, or these medicines are ineffective. Medications MI-503 research buy such as metoclopramide and prochlorperazine have a very different mechanism of action by blocking a chemical called dopamine. Prochlorperazine comes as a tablet and as a rectal suppository, so it can be used in migraineurs who vomit. Both medications are helpful in treating the nausea associated with migraines. Either of them can be used with any other acute migraine treatment including triptans, DHE, and NSAIDs. Unfortunately, with long-term continuing use, they can cause a movement disorder, and must be stopped completely in the Selleck Pifithrin�� event this occurs. Metoclopramide is rated

pregnancy category B, that is, there is no evidence of fetal harm with its use. This is the only acute migraine intervention discussed that is generally considered safe in pregnancy other than acetaminophen. Acetaminophen is used for migraine pain as a safe alternative treatment. Unfortunately, it is often ineffective, perhaps because of its lesser anti-inflammatory action. It has no specific anti-migraine action. Triptans, NSAIDs, and probably DHE, when taken too frequently, can result in migraineurs getting more frequent headaches, or headaches that are resistant to treatment. This is called medication overuse headache or rebound headache. A good rule of thumb is to use acute medications no

more than 2 days per week. Sometimes, patients believe that if they use one type of medication for 2 days per week, and Dimethyl sulfoxide another type on other days, that rebound can be avoided. Unfortunately, this is not the case. It is safest to remember sticking to 2 days per week of acute medication, and if there is a consistent need to treat more often than that, improved preventive strategies need to be added. Multiple noninvasive devices are undergoing evaluation for the treatment of acute migraine. At this time, only one device has been approved by the FDA for acute treatment, and it is not yet available at the time of this writing. A transcranial magnetic stimulator called Spring TMS, manufactured by eNeura, Baltimore, MD, was approved for acute treatment of migraine with aura.

4 Overall, SVR rates were similar (45% versus 49%,

P = 0.37). In patients who attained a rapid virological response (RVR), the rate of SVR was not significantly different for patients who were treated for 48 or 24 weeks (87% versus 77%; P = 0.12), although the relapse rate was higher in the 24-week treatment arm. In slow responders, 72 weeks of therapy was associated with a higher rate of SVR than 48 weeks (63.5% Maraviroc in vitro versus 38.1%). Therefore, the ability to identify individual patients who are likely to respond to 24 weeks of therapy or who will benefit from extended duration therapy appear clinically valuable.4, 8, 9, 11, 12 Host interleukin-28B (IL28B) polymorphism has recently been identified to be the stronger baseline predictor of SVR in HCV-1 patients treated with PEG-IFN and RBV.13-15 Although the underlying mechanism remains unclear, IL28B variation is strongly associated with on-treatment viral kinetics.16, 17 However, the role of IL28B in the context of response-guided treatment protocols involving individualized treatment duration has not yet been evaluated. Our cohort provided a unique opportunity to investigate the relevance of IL28B genotype to treatment outcome in the context of genotype 1 HCV patients

treated with variable (shortened/extended) or standard 48-week therapy. BMI, body mass index; CI, confidence interval; EOT, end of treatment; HCV, hepatitis C virus; IL28B, interleukin-28B; OR, odds ratio; PEG-IFN, pegylated CHIR-99021 nmr interferon-alfa; RBV, ribavirin; RVR, rapid virological response; Std, standard; SVR, sustained viral response; Var, variable. A total of 696 HCV-1 patients were enrolled in the primary multicenter randomized controlled trial

that recruited patients in 13 clinical sites in Italy.4 In the original study, 237 were randomized to a standard (Std) treatment duration (48 weeks) and 459 to a variable (Var) treatment Avelestat (AZD9668) duration according to time to first undetectable HCV RNA. Patients achieving undetectable HCV RNA at week 4 were treated for 24 weeks, patients achieving undetectable HCV RNA at week 8 were treated for 48 weeks, and patients firstly negative or with a >2 log10 IU/mL drop at week 12 were treated for 72 weeks. Patients received PEG-IFN alfa-2b (PegIntron; Schering Plough, Kenilworth, NJ) 1.5 μg/kg/week, or PEG-IFN alfa-2a (Pegasys; Roche Laboratories, Nutley, NJ) 180 μg/week combined with RBV (Rebetol; Schering Plough, or Copegus, Roche Laboratories) 1,000 mg/day if body weight was ≤75 kg or 1,200 mg/day if body weight was >75 kg. PEG-IFN and RBV dose modification followed standard criteria and procedures. Inclusion and exclusion criteria and on-treatment response definition were reported in the original study.4 To ensure that patients who did not achieve SVR were true nonresponders, only patients who completed treatment at the full dose with 100% compliance were selected for this genetic substudy.

Therefore, only

prospective studies on VWD with laboratory parameters tested by expert centres should be considered in clinical trials. In 2000, the first large study on VWD1 began [34]. Working on the MCMDM–1VWD project was the turning point in investigating type 1 VWD. The criteria for correct diagnosis were bleeding history, low VWF activity and inheritance. For the first time a score was assigned for each bleeding symptom. Bleeding score was evaluated according to the age of the patient. Scores differed in affected and non-affected family members. Cutaneous bleeding, surgical bleeding and bleeding after minor wounds were predictable of VWD1, but oral bleeding and postpartum haemorrhage were less so (Fig. 4 [34]). The major article summarizing the most important selleck chemicals llc data published in 2007 gave details of the phenotype and genotype [35]. It was found that in the cohort of cases previously diagnosed as type 1 VWD a few patients had abnormal multimers and in these a mutation was found in the majority of cases. Among those cases with normal multimers there were some patients

with a mutation not easily detected. There was an association between the presence of mutations and VWF level in index cases. The study also looked at the quickest way to measure VWF, and this was the focus of an article Selleck STI571 published in 2010, which used the VWF–LIA test to determine VWF:Ag in patients with type 1 VWD [36]. Another paper computed the likelihood of having VWD as a function of the bleeding score, the VWF level and the number of first-degree family members with a reduced VWF level [37]. Castaman for the MCMDM–1VWD investigators looked at the response to DDAVP and how it is influenced by the genotype

and phenotype in type 1 VWD [38]. The aim of the study was to stratify responders, partial responders and non-responders. Response to DDAVP in these VWD patients seemed to be associated with the location of the causative mutation. The presence of subtle multimeric abnormalities did not hamper potential clinically useful responses, as in typical Florfenicol VWD1. With regard to management of patients with VWD1, in mild forms of VWD1 with baseline levels of VWF:RCo >30 U dL−1 and FVIII:C >40 U dL−1 all spontaneous bleeds usually occur rarely in agreement with their relatively low bleeding symptoms. Haematologists must suspect a mild form of VWD1 when unexpected bleeds occur and be ready to provide an appropriate therapy. DDAVP and/or VWF concentrates should be given when trauma or minor/major surgeries increase the risk of bleeding. Patients with VWD1 who are not well diagnosed and/or regularly followed up usually have the worst outcomes. Issues still to be addressed in the years 2012–2016 are determinants of bleeding, influence of VWF modifiers, benefit and limits of DDAVP and indications for VWF concentrates.

Therefore, only

prospective studies on VWD with laboratory parameters tested by expert centres should be considered in clinical trials. In 2000, the first large study on VWD1 began [34]. Working on the MCMDM–1VWD project was the turning point in investigating type 1 VWD. The criteria for correct diagnosis were bleeding history, low VWF activity and inheritance. For the first time a score was assigned for each bleeding symptom. Bleeding score was evaluated according to the age of the patient. Scores differed in affected and non-affected family members. Cutaneous bleeding, surgical bleeding and bleeding after minor wounds were predictable of VWD1, but oral bleeding and postpartum haemorrhage were less so (Fig. 4 [34]). The major article summarizing the most important selleck compound data published in 2007 gave details of the phenotype and genotype [35]. It was found that in the cohort of cases previously diagnosed as type 1 VWD a few patients had abnormal multimers and in these a mutation was found in the majority of cases. Among those cases with normal multimers there were some patients

with a mutation not easily detected. There was an association between the presence of mutations and VWF level in index cases. The study also looked at the quickest way to measure VWF, and this was the focus of an article Selleckchem Ceritinib published in 2010, which used the VWF–LIA test to determine VWF:Ag in patients with type 1 VWD [36]. Another paper computed the likelihood of having VWD as a function of the bleeding score, the VWF level and the number of first-degree family members with a reduced VWF level [37]. Castaman for the MCMDM–1VWD investigators looked at the response to DDAVP and how it is influenced by the genotype

and phenotype in type 1 VWD [38]. The aim of the study was to stratify responders, partial responders and non-responders. Response to DDAVP in these VWD patients seemed to be associated with the location of the causative mutation. The presence of subtle multimeric abnormalities did not hamper potential clinically useful responses, as in typical Avelestat (AZD9668) VWD1. With regard to management of patients with VWD1, in mild forms of VWD1 with baseline levels of VWF:RCo >30 U dL−1 and FVIII:C >40 U dL−1 all spontaneous bleeds usually occur rarely in agreement with their relatively low bleeding symptoms. Haematologists must suspect a mild form of VWD1 when unexpected bleeds occur and be ready to provide an appropriate therapy. DDAVP and/or VWF concentrates should be given when trauma or minor/major surgeries increase the risk of bleeding. Patients with VWD1 who are not well diagnosed and/or regularly followed up usually have the worst outcomes. Issues still to be addressed in the years 2012–2016 are determinants of bleeding, influence of VWF modifiers, benefit and limits of DDAVP and indications for VWF concentrates.

Very little is known on sea turtles, although this is one of the most ancient tetrapod groups JNK high throughput screening that successfully colonized the marine environments. Here, we investigated for the

first time the relationship between bone density and body size in the loggerhead turtle, Caretta caretta, with the aim to elucidate possible functional connections with the species’ aquatic habits. Humeri were extracted from the carcasses of 72 loggerhead turtles ranging in size from 7 to 89 cm (males = 18, females = 44, unknown = 10). Whole bone density was determined by Archimedes’ principle. Sexes exhibited comparable humerus densities (t-value = 0.49, P > 0.05). Mean humerus density (1.33 g cm−3) was intermediate within the range reported for marine mammals and suggested no extreme specialization towards an either pelagic or benthic lifestyle. Turtle size and humerus density were significantly correlated (Pearson’s correlation = 0.638, P < 0.01). Small juveniles had very light bones compared to adults in accordance with their stage specific pelagic diving and foraging behaviour. "
“The evolution CX-5461 cost of animal social dynamics and the origin of species through such interactions mediated

by sexual selection (i.e. sexual speciation) are major challenges in current evolutionary biology, and have therefore been the subject of intense debate. Given the evolutionary significance of these problems, major efforts to assess the reliability of the evidence have been made, with controversy standing firmly (Coyne & Orr, 2004; Ritchie, 2007; Kraaijeveld, Kraaijeveld-Smit & Maan, 2011). In a recent paper,

Labra (2011) suggested that the remarkable diversity of the lizard genus Liolaemus (220+ species) may be the result of speciation driven by chemical-based sexual selection. The problem of selection-driven speciation is particularly interesting in a model system like Liolaemus, as these lizards have achieved one of the most outstanding species diversities known for a single living vertebrate genus (Pincheira-Donoso, Scolaro & Sura, 2008c), which is mirrored by a remarkable ecological diversity (Schulte et al., 2004; Pincheira-Donoso et al., 2009) importantly caused by radiations across a substantial range of thermal and climatic conditions (Harmon et al., 2003; Phospholipase D1 Espinoza, Wiens & Tracy, 2004; Pincheira-Donoso, Hodgson & Tregenza, 2008b). Therefore, understanding the factors underlying such an extraordinary diversity can provide valuable insights into the evolutionary dynamics of active speciation rates taking place within prominent adaptive radiations. In her study, based on experimental observations of three Liolaemus species, Labra (2011) presents evidence suggesting that these lizards respond more actively to conspecific than to heterospecific scents secreted by male precloacal glands.