They hold potential for detecting changes of low-volume, low-velo

They hold potential for detecting changes of low-volume, low-velocity blood flow in small vessels such as those of the synovium in arthritic joints [51]. Positron emission tomography [PET] is a technique that uses molecules labelled with isotopes that emit positrons from their nucleus. The most commonly used tracer is 2-deoxy-2-(18F) fluoro-p-deoxyglucose (FDG) [52]. After intravenous injection, FDG is taken up by the cells according to their level of glucose metabolism. Animal models have demonstrated that FDG uptake by tumours

is not only due to the tumour cells themselves, but also due to the inflammatory cells appearing in association with tumour growth or necrosis. Based on this concept, an on-going study (unpublished data) has demonstrated the feasibility of using PET to

detect arthritis-related inflammation prior to visualization by morphologic imaging in a rabbit model of blood-induced AZD5363 mouse arthritis. Preliminary results of this study showed that the number of bleeding events would influence the degree of inflammatory changes and consequently, the FDG uptake in affected knees. These data demonstrated that the increased glucose Venetoclax supplier metabolism of many inflammatory cell types and the FDG uptake by inflammatory tissues are the basis for the potential use of FDG-PET in the detection and monitoring of chronic arthropathic processes in haemophilia. Dual-echo steady-state imaging  Dual-echo steady-state (DESS) imaging results in images with higher T2* weighting, which has bright cartilage signal and bright synovial fluid. This technique has proved useful for assessing

cartilage morphology in osteoarthritis [53] and holds potential for the assessment of cartilage abnormalities in haemophilic arthropathy. Driven equilibrium Fourier transform and fluctuating equilibrium  Driven equilibrium Fourier transform (DEFT) and fluctuating equilibrium MRI SPTLC1 (FEMR) are techniques that depend on the ratio of T1/T2 in a given tissue [54,55]. These techniques produce contrast by enhancing the signal from synovial fluid rather than attenuation of cartilage signal as in T2-weighted sequences. DEFT and FEMR show much greater cartilage to fluid contrast than spoiled gradient-recalled (SPGR), proton-density spin-echo (PD-SE) or T2-weighted fast-spin-echo (FSE) sequences [56]. Sodium MRI  This technique is based on the ability of sodium imaging to depict regions of proteoglycan depletion [57]. High sodium concentration is seen throughout the normal cartilage. This method shows promise in being sensitive to early decreases in proteoglycan concentration in arthritis. T1 mapping  Gadolinium-DTPA-enhanced T1 imaging is also a technique sensitive to the cartilage proteoglycan content [58]. In this technique, the negative charge of the paramagnetic contrast agent distributes into the cartilage inversely to the fixed charge density of glycosaminoglycans [58].

The color of the glazed surfaces of the specimen was measured ove

The color of the glazed surfaces of the specimen was measured over a white (CIE L* = 96.68, Acalabrutinib supplier a* = −0.18, b* = −0.22) and a black (CIE L* = 1.15, a* = −0.11, b* = −0.50) background with a colorimeter (ShadeEye Ex, Shofu, Japan) in a viewing booth under D65 standard illumination. Before the experimental measurements, the colorimeter was calibrated according to the manufacturer’s instructions and positioned in the middle of each specimen. The L*a*b* color notation of each

specimen was measured consecutively three times, and the average of the three readings was calculated to give the initial color of the specimen. The TP was obtained by calculating the color difference between the specimen over the white background and that over the black background: TP = [(Lw−Lb)2 + (aw−ab)2 + (bw−bb)2]1/2 (b′ refers to the color coordinates over the black background, and the subscript DNA/RNA Synthesis inhibitor “w” refers to those over the white).[7,

8] Color measurements of the specimens were again performed under the same conditions after cementation and the aging test. The TP values of the specimens after aging process were calculated with the above formula. The specimens were subjected to artificial aging using an Atlas UV 2000 test machine (Material Testing Technology LLC, Chicago, IL). Aluminum plates were prepared in accordance with the specimen size, and the specimens were inserted into the mold of the plates and subjected to accelerated aging tests. All specimens were exposed to UV light and water spray for 300 hours in the test machine. The glazed surface of each specimen was continuously exposed to the light source. The back panel temperature varied between 38°C (dark) and 70°C (light), and the relative humidity was 95% (dark) and 50% (light). The dry bulb temperature was 38°C in the dark and 47°C in the light stage. The testing cycle consisted of 40 minutes of light only, 20 minutes of light with front water spray, 60 minutes of light only, and 60

minutes Carbohydrate in the dark with back water spray. The total exposure energy was 150 kJ/m[2]. These conditions are reported to be equivalent to 1 year of clinical service.[38] TP values of ceramics with the six resin shades were analyzed using ANOVA and Tukey’s tests, with significance set at p < 0.05. The mean values of TP before and after aging were compared using Paired Sample t-test. For all analyses, p-values < 0.05 were considered to indicate statistical significance. The mean TP values of ceramics and cemented ceramics before and after accelerated UV aging are given in Tables 2 and 3. Statistically significant differences were found among all tested resin cements after cementation for 0.5 mm thickness (p < 0.05). All the resin cements affected the TP values of 0.5-mm-thick ceramic, while RelyX Veneer Tr, Variolink II Tr, and Maxcem Clear did not affect the translucency of 1-mm-thick ceramics.

First, the authors mention that the relatively high misclassifica

First, the authors mention that the relatively high misclassification of the “gold standard” (liver biopsy) makes it impossible for noninvasive tests to achieve high concordances. This is indeed true for noninvasive tests whose development was independent from liver histology (e.g., elastography). However, serum markers have been calibrated with direct reference to sets of liver biopsies. Therefore, the perfect serum marker would replicate even the misclassifications of the “golden” histological standard and could theoretically reach an AUROC (area under the receiver operating characteristic curve) of 1. Second,

the explosive development and overenthusiastic acceptance of noninvasive markers is not always supported by sufficient evidence and validation. In our meta-analysis on Veliparib cell line elastography, we exposed issues such as invalidated stiffness cutoffs for specific liver disease stages and low methodological quality in

the vast majority of published studies.2 In numerous studies, the maximum interval between elastography and liver biopsy was >3-6 months; in such cases, there is an erroneous assumption that fibrosis remains stable over these periods of time. Furthermore, from all publications, only six studies had both optimal histological and elastography measurements.2 Third, the authors correctly state that liver biopsy is more of a reference standard than a gold standard for assessing fibrosis. As we have pointed out before, histological “scores” of fibrosis are ordinal categories that incorporate

both architectural changes and fibrosis, very and click here have no quantitative relationship between them.3 Therefore, using them as continuous variables is inappropriate.3 Validation of noninvasive markers of “fibrosis” should ideally use quantitative histological measures. We have described such a measure, namely, collagen proportionate area, and correlated it with hepatic venous pressure gradient.4 More importantly, we evaluated its prognostic value with respect to patient outcome.5 Notably, collagen proportionate area performed better than Ishak staging and hepatic venous pressure gradient for predicting decompensation (AUROC = 0.97).5 In conclusion, the way forward involves carefully designed studies that validate noninvasive fibrosis markers against quantitative histological measures and/or clinical outcomes. Because we are ultimately treating patients, the clinical consequences of false positive and false negative classifications should be incorporated in the validation processes. Emmanuel A. Tsochatzis M.D.*, Giacomo Germani M.D.*, Andrew Hall M.D.†, Pinelopi Manousou M.D.*, Amar P. Dhillon M.D.†, Andrew K. Burroughs M.D., F.Med.Sci.*, * The Royal Free Sheila Sherlock Liver Centre and University Department of Surgery, Royal Free Hospital and University College London, London, UK, † Department of Cellular Pathology, UCL Medical School, Royal Free Campus, Rowland Hill Street, London, UK.

The expression levels of LC3-II and P62 were increased by PA,

The expression levels of LC3-II and P62 were increased by PA,

suggesting that PA inhibits the autophagic process after autophagosome formation. PA also increased the expression level of Rubicon, a negative regulator of autophagosome-lysosome fusion. The inhibition of autophagy by PA was observed earlier (4h) than PA-induced apoptosis (8h). To examine the effect of https://www.selleckchem.com/products/z-vad-fmk.html PA’s autophagy inhibition on apoptosis, HepG2 cells were transfected with siRNA against Atg7 or Rubicon, followed by PA treatment. Autoph-agy inhibition by Atg7 konckdown exacerbated PA-induced apoptosis. Interestingly, Rubicon knockdown clearly abolished PA-induced inhibition of autophagic flux, reduced ER stress and ameliorated PA-induced apoptosis. Consistent with in vitro findings, mice on HFD for 3 months or more showed increased hepatocyte apoptosis compared with mice on control diet, evidenced by increase in serum ALT levels or caspase-activity and TUNEL-positive cells in the liver. Rubicon expression was increased for 1 month or more and increase of LC3-II and P62 were observed in murine livers on HFD for 2 months or more. Injection of PolyI:C into Mx1-Cre Atg7 fl/fl mice which had been given 1 month HFD inhibited liver autophagy and clearly induced live injury as evidenced by increase in serum ALT levels and TUNEL-positive hepatocytes

accompanied by JNK activation. siRNA-mediated in vivo knockdown of Rubicon ameliorated autophagy inhibition in livers of mice on HFD for 4 months. It inhibited ER stress and hepatocyte apoptosis. Conclusion: Increased expression

of Rubicon induced by HFD, as well as PA, suppresses Ulixertinib research buy autophagic flux and promotes hepatocyte apoptosis by increasing ER stress. Enhancement of autophagy by inhibiting Rubicon Methisazone may provide new approaches for treatment of NAFLD. Disclosures: Tetsuo Takehara – Grant/Research Support: Chugai Pharmaceutical Co., MSD K.K. The following people have nothing to disclose: Satoshi Tanaka, Hayato Hikita, Yasutoshi Nozaki, Yugo Kai, Tasuku Nakabori, Yoshinobu Saito, Ryotaro Saka-mori, Takuya Miyagi, Naoki Hiramatsu, Tomohide Tatsumi Obesity, insulin resistance, and diabetes have become the leading causes of renal and nonalcoholic fatty liver disease (NAFLD), and nonalcoholic steatohepatitis (NASH). Currently, there is no established therapy of NASH. Lifestyle alterations including diet and exercise often fail to prevent or reverse NASH. The purpose of the present study was to determine if in mice fed a Western (high fat, high sucrose, cholesterol) diet with established obesity, insulin resistance, NAFLD, and NASH, treatment with the dual agonist of the nuclear receptor the farnesoid X receptor (FXR) and the G protein coupled receptor TGR5, 6α-ethyl-3α,7α,23-trihydroxy-24-nor-5β-cholan-23-sulfate sodium salt (INT-767) decreases the progression of liver disease.

Adherent cells were used as intrahepatic APC) The IHL were resus

Adherent cells were used as intrahepatic APC). The IHL were resuspended in R-10. In each well of a 96-well round-bottomed plate, 2 × 106 IHL were incubated for

5 h at 37°C in R-10 containing 50 ng/mL phorbol myristate acetate (PMA; Sigma-Aldrich, St Louis, MI, USA), 1 μM ionophore A23187 (Sigma-Aldrich) and 1 μg/mL brefeldin-A (BD Biosciences). The cells were then washed twice with ice-cold PBS (−) and incubated for 10 min at 4°C with a rat antimouse CD16/CD32 monoclonal Ab (mAb; Fc Block; BD Biosciences) at a concentration of 1 μg/well. Following incubation, the cells were washed twice with ice-cold PBS (−) and stained with a PE-conjugated HCV-NS3 H-2Db tetramer (Tet-603; GAVQNEVTL; Medical and Biological Laboratories, Nagoya, Japan)[23] and peridinin chlorophyll selleckchem protein (PerCP)-conjugated rat antimouse CD8 MAb (clone 53-6.7; BD Biosciences) for 30 min at 4°C in staining buffer (PBS with 1% FCS and 0.1% NaN3). After the cells were washed twice, they were fixed and permeabilized by using a Cytofix/Cytoperm kit (BD Biosciences) and stained with a fluorescein isothiocyanate (FITC)-conjugated rat antimouse IFN-γ mAb (clone XMG1.2; BD Biosciences). After

the cells were washed, flow cytometric analyses were performed with a FACScanto II flow cytometer (Becton Dickinson, Franklin Lakes, NJ, USA), and the data were analyzed with FACSdiva software (Becton Dickinson). Intrahepatic lymphocytes were prepared and treated with an antimouse CD16/CD32 mAb as described above for intracellular IFN-γ staining and then stained find more with a PE-conjugated HCV-NS3 H-2Db tetramer, PerCP-conjugated anti-CD8a (BD Biosciences), FITC-conjugated anti-PD-1 (eBioscience, San Diego, CA, USA) and Alexa647-conjugated anti-Tim-3 (Biolegend, San Diego, CA, USA) for 30 min at 4°C. After the cells were washed twice, they were fixed with PBS containing 1% formaldehyde and 2% FCS and analyzed PLEK2 by flow cytometry. Intrahepatic APC were prepared and treated with an antimouse CD16/CD32 mAb as described above for intracellular IFN-γ staining and then stained

with a FITC-conjugated anti-CD11c (BD Biosciences) and PE-conjugated anti-PD-L1 (eBioscience) for 30 min at 4°C. After the cells were washed twice, they were fixed with PBS containing 1% formaldehyde and 2% FCS and analyzed by flow cytometry. For the detection of HCV core Ag in the liver, liver tissue samples isolated 7 and 14 days post-infection were homogenized in RIPA B buffer (50 mM Tris pH 7.5, 1% NP40, 0.15 M NaCl, 1 mM phenylmethylsulfonyl fluoride) to make 10% (w/v) extract. Liver tissue extracts were assessed using Lumispot Eiken HCV Ag assay kit (Lumispot-Ag; Eiken Chemical, Tokyo, Japan). Liver tissue samples isolated 7 and 14 days post-infection were used for histological studies. Paraffin sections (4-μm thick) were stained with hematoxylin–eosin safranin O.

Membrane mimics induced the formation of α-helix in Hpn The inte

Membrane mimics induced the formation of α-helix in Hpn. The interaction disrupts the LY2606368 integrity of the membrane mimics and leads to the release of inner calcein probe. The experiments involving the Laurdan and Prodan fluorescence indicated that increasing the total protein/lipid ratio leads to a less ordered and more hydrated lipid membrane structure close to the water/lipid interface of lipid bilayers modeling the mitochondrial inner membrane. The present data indicated that

Hpn may take part in the pathological roles of Helicobacter pylori through membrane interactions. “
“Background: Helicobacter pylori uses SabA to interact with sialyl-Lewis x on the gastric mucosal surface to establish persistent colonization. The number of CT repeats in sabA is variable and thus influences Kinase Inhibitor Library high throughput SabA translation, but the expression of SabA determined by Western blotting does not fully match with a CT sequence-based prediction. Furthermore, a homopolymeric thymidine (polyT) tract located upstream of sabA has been observed, but its role in regulating sabA expression is still unknown. Methods:  The transcriptional start site (TSS) of sabA in strains

J99 and Hp258 was determined by 5′ RACE. One hundred and fifteen clinical isolates were sequenced to analyze the distribution of the polyT tract length and promoter sequence. Finally, RT-PCR and an E. coli-lux reporter system were used to determine the sabA promoter activity with different lengths of the polyT tract. Results:  The TSS of sabA was located at 66 or 64 bp upstream of the translational start codon in J99 and Hp258, respectively. The polyT tract close to the −35 element varied from T10 to

T28 in 115 clinical isolates, and 70% of the isolates contained a stretch of 14–19 Ts. The sabA gene displayed slipped strand mispairing (SSM) of the polyT tract, generating varying genotypes in J99 (16–18 Ts) and Hp258 (14–15 Ts). Furthermore, J99 with lengths of T16 and T30, had higher sabA promoter activity than the common length of T18. Conclusion:  Our findings indicate that the sabA promoter region modulates its transcriptional activity through a variable polyT tract, and SSM generates mixed genotypes in the population. “
“Following Helicobacter pylori eradication Diflunisal in a placebo-controlled trial, the hypokinesia of idiopathic parkinsonism improved but flexor rigidity worsened. We surveyed the effect of all antimicrobial prescriptions in 66 patients with idiopathic parkinsonism over a median of 1.9 (interquartile range 0.4, 3.5) years. Initial Helicobacter screening was followed (where positive) by gastric biopsy. Serial lactulose hydrogen breath tests (364 tests) for small intestinal bacterial overgrowth monitored the need to encourage fluid intake and bulk/osmotic laxatives.

24 In addition, social factors, such as income, education, employ

24 In addition, social factors, such as income, education, employment, and access to health care, may contribute to disparities in survival. For example, a U.S. study of area-level median household income found better survival among treated HCC patients from high- versus low-income counties.19 In this study, the proportion of HCC diagnoses that were histologically confirmed decreased with time. Possible reasons could include changes in etiology or comorbidities of HCC cases.24 Histologic confirmation is also likely to be affected by guidelines Caspase inhibitor affirming the use of noninvasive diagnostic5 and clinical management procedures under specified circumstances.5,

8 This study had strengths, including availability of trend data for stage and treatment as well as HCC survival data with sufficient counts to estimate survival within race and treatment subgroups. Caution is, however, recommended when interpreting the findings because of limited information on the method of diagnosis, as well as patient comorbidities, HCC etiology, and treatment. Though the favorable survival associated with curative therapy find more in this report is thought to be meaningful, lead-time bias resulting from earlier diagnosis should not be dismissed as a contributory factor.25 Furthermore, the SEER-13

registries include only 14% of the U.S. population, with racial and economic attributes that differ in several meaningful ways from those of the entire nation. For example, large Asian or Pacific selleck chemicals llc Islander populations are found in the Hawaii, Seattle, and California registries of SEER-13, whereas Hispanic populations in Florida and Texas are not. The SEER-13 population is more urban than the United States. Although SEER-13 contains 14% of the nation’s population, it contains 22% of U.S. liver transplant centers.26 Despite these limitations, the

findings suggest that HCC diagnosis and management are changing in the SEER-13 population, with favorable results on stage, treatment, and survival. In summary, the detection of early stage HCC among at-risk persons may enable the use of potentially curative therapies. This is likely to contribute to the improving survival described in this report. The small percentage of cases receiving either liver surgery or ablation therapy (22%) suggests that the potential exists for further improvement in survival, with ongoing implementation of the HCC control efforts already improving the prognoses of HCC cases. We thank Carol Johnson, Leon Sun, Kathleen Cronin, Carol Kosary, Lynn Ries, Jennifer Ruhl, Susan Devesa, Nadia Howlader (critical review), Neil Neyman (coding), the U.S. Census Bureau (population data), SEER registries (population-based surveillance) and IMS, Inc. (data file).

The number of diseased leaves and internodes (out of 15) per samp

The number of diseased leaves and internodes (out of 15) per sampling unit was better fitted by the beta-binomial than the binomial distribution in 67% and 91% of the cases, respectively. The index of aggregation was significantly >1 for 78% and 98% of the cases for

diseased leaves and internodes, respectively. These results indicated aggregation of this disease Tamoxifen chemical structure at an individual vine scale (or lower). Conversely, there was little evidence of aggregation at scales larger than a vine (e.g. disease foci extending beyond individual vines) for most vineyards based on Spatial Analysis by Distance IndicEs (SADIE). SADIE analysis suggested a random pattern of the count of diseased leaves and internodes in the majority (>86%) of the cases. Based on SADIE,

there was significant (P ≤ 0.05) evidence of association between leaf and internode selleck disease counts per vineyard in 75% of cases, indicating that the dispersal of inoculum from the previously infected wood tissues (canes) affected both leaf and internode in the same manner. In contrast, association of disease counts from one year to the next was only significant in approximately 15% of the cases, indicating the difficulty in predicting the level of disease in a section of a vineyard based on the previous year’s observations alone. “
“Eyespot disease caused by the soil-borne facultative fungi Oculimacula yallundae and O. acuformis is the major component of the stem-base disease complex of wheat in temperate regions of the world with a cool Thiamet G and wet climate. In this review, we focus on results of genetic studies concerning both partners of the host–pathogen interaction. This comprises analyses of genetic diversity of the pathogen and identification of particular genes within it, evaluation and screening methods for host resistance, resistance sources and genetics of these resistances, breeding of resistant cultivars in wheat, and application of genetic markers in tagging and tracking of eyespot resistance genes. We also attempt to foresee

some of the key issues and developments that may occur in future. The identification of markers tightly linked to eyespot resistance genes is the important research focus opening the door to marker-assisted selection of resistant varieties. “
“This study investigated the effect of silicon (Si) on the resistance of rice plants of the cv. ‘Primavera’ cultivar that were grown in a nutrient solution with 0 (−Si) or 2 mm (+Si) Si to leaf scald, which is caused by Monographella albescens. The leaf Si concentration increased in the +Si plants (4.8 decag/kg) compared to the −Si plants (0.9 decag/kg), contributing to a reduced expansion of the leaf scald lesions. The extent of the cellular damage that was caused by the oxidative burst in response to the infection by M. albescens was reduced in the +Si plants, as evidenced by the reduced concentration of malondialdehyde.

4 % Men are affected more than twice as often compared to women

4 %. Men are affected more than twice as often compared to women and the median age of patients with double pylorus is 59.6 years. The genesis of acquired double pylorus is usually a transmural peptic ulcer creating a fistula between the duodenal bulb and antrum commonly localized on the lesser curvature of the antrum without perforation and fluid leakage into the abdominal cavity. Alternatively, double pylorus can involve penetrations into the pancreas, bile ducts,

liver, colon and spleen. The size of these gastroduodenal fistulas varies from a couple of mm up to several cm. In general, double pylorus is identified by upper GI-endoscopy. Intake of NSAIDs and chronic diseases are encountered in patients with double pylorus. The clinical presentation of the peptic ulcer penetration and formation of double pylorus is unspecific and discrete. The primary therapeutic BGJ398 datasheet procedure is conservative with high-dose proton pump inhibitor and eradication of Helicobacter pylori. Surgical intervention should be only considered in patients with therapy refractory complaints, recurrent ulcers or other complications. The healing rates of acquired double pylorus are low despite adequate medical therapy. Only in some cases is spontaneous fistula occlusion observed. In the presented case, we assume that the history of peptic ulcer in the upper GI tract is the cause of the double pylorus. In conclusion,

double pylorus is a rare complication of peptic ulcers associated with Helicobacter pylori infection and anti-inflammatory medication as well as chronic diseases, and should ALK tumor be managed with medical therapy although there is a high-rate of persisting fistula. Contributed by “
“Regurgitation is common and usually benign, although often a source of concern for families. Vomiting has a wide differential diagnosis, including many disease states outside of the GI tract. This chapter offers an approach to assessment and management strategies for gastro-oesophageal reflux. “
“We read with

interest the article by Si-Tayeb et al., in Janus kinase (JAK) which they generated human hepatocyte-like cells from human induced pluripotent stem cells (iPSCs) with four transcription factors (Oct3/4, Sox2, Nanog, and LIN28).1 They use viral transgenes for the establishment of the human iPSCs,1 and it is thought that the use of viral transgenes would contribute to the increase in tumorigenicity of iPSCs.2 Yet, as their colleagues develop vector and/or transgene-free human iPSCs,2 they could generate hepatocyte-like cells derived from the human iPSCs in the near future. However, the associations between the use of viral transgenes and the tumorigenicity of human iPSCs are as-yet not clear. Therefore, by using our previous methods,3 we investigated microvessel density (MVD) within teratomas between the vector and/or transgene-free human iPSCs established according to the methods of Yu et al.

) Some bizarre structures in extinct dinosaurs may have threatene

) Some bizarre structures in extinct dinosaurs may have threatened rivals, but this is difficult Selleckchem Fulvestrant to test without direct knowledge of behaviors that are not preserved in the fossil record. (ii) Intersexual: The principal means of intersexual display is display for

mates, traditionally called sexual display. Sexual display usually implies sexual selection, and explanations of sexual selection must be evaluated much like those for mechanical adaptations. In contemporary populations, sexual selection often acts on minor features and elaborates them (Mendelson & Shaw, 2005); intense sexual selection can result in runaway selection (Futuyma, 2009) and (or) divergent selection (Kroodsma et al., 1985; Price, 1998). Evolutionary theory holds that this kind of divergence can result in speciation (Futuyma, 2009), and that like natural selection, sexual selection can be responsible for patterns of sorting in clades (Vrba, 1984; Sampson, 1999). This could be shown if the characters subject to sexual selection show non-random trends in clades (though the variation of the trends themselves does not have to be directional or trendlike). A problem with invoking sexual display Selleckchem RO4929097 as the explanation of bizarre structures can be traced to Darwin’s (1871) original formation of the problem of sexual selection. Darwin emphasized that sexual selection could only apply when one sex bears structures used in

intersexual display (or agonistic behavior in intrasexual interaction). In other words, sexual selection cannot be invoked without discrete, qualitative features of sexual dimorphism. (We acknowledge that many neobiologists [apparently originating with West-Eberhard's, 1983 conflation

of the concepts] feel that sexual dimorphism is not necessary 4-Aminobutyrate aminotransferase for sexual selection, but Darwin defined the concept in this way and by definition he cannot be wrong. This does not deny that various other phenomena associated with competition for mates and reproductive success are interesting and important; but they are not strictly part of sexual selection.) Unfortunately, this degree of sexual dimorphism, typical of birds and some mammals, has not been sufficiently established for dinosaurs. (iii) Social selection: This concept (West-Eberhard, 1983) was recently applied to dinosaurs by Hieronymus et al. (2009), who argued persuasively that the nasal cornifications of centrosaurine ceratopsians were progressively selected for larger size and broader display. According to them, ‘social selection occurs when there is differential success in within-species competition for any limited resource.’ Two problems with this definition, as applied to fossils, are that within-species phenomena can almost never be observed, and competition is particularly difficult to establish in extinct forms (Benton, 1996). On the other hand, it is possible to identify structures that can plausibly have functioned only in social interaction (as opposed to food gathering, thermoregulation, etc.