Preliminary in vitro tests showed that ammonium bicarbonate, ammonium carbonate, potassium benzoate, potassium sorbate, sodium benzoate and sodium metabisulphite at 2% completely inhibited mycelial growth of the fungus. No significant differences were observed among these salts and disodium EDTA (P ≤ 0.05). However, the ED50, minimum

see more inhibition concentration (MIC), and minimum fungicidal concentration (MFC) values indicated that sodium metabisulphite was more toxic to Ilyonectria liriodendri than these other six salts. Soil bioassays showed that sodium metabisulphite, sodium benzoate and potassium sorbate at 0.25% completely inhibited mycelial growth of the fungus, whereas potassium benzoate reduced the mycelial growth of fungus Tanespimycin nmr by 90.30%; however, the differences in inhibitory effects were statistically insignificant (P ≤ 0.05). Moreover, there was no significant difference between 0.1% sodium metabisulphite and 0.5% ammonium carbonate, 0.75% ammonium bicarbonate and 1.5–2.0% disodium EDTA (P ≤ 0.05). Unlike disodium EDTA, complete inhibitory was observed with ammonium carbonate and ammonium bicarbonate at

higher concentrations. However, in root bioassays, applications of 2% ammonium bicarbonate, 1.5% ammonium carbonate and 2% disodium EDTA were phytotoxic to kiwifruit seedlings, but 0.25% four other salts were neither phytotoxic to kiwifruit seedlings nor did it adversely affect root length, root fresh weight and root dry weight of seedling. This study also showed I. liriodendri to be capable of growth in both acidic and basic environments. However, while the fungus showed uninhibited growth at pH values of 5–11, growth decreased significantly at both higher and lower pH values (P ≤ 0.05) and was completely inhibited at pH 12. “
“Anatomical observations of leaves infected by Taphrina deformans

were studied in tolerant peach trees (TPT) and in very susceptible (VSPT) ones. Leaves from the first sampling (2nd April) showed hyphae penetrating through the stomata or into the cuticle of the host tissue; anatomical structures of leaf sections were similar for both TPT and VSPT. The ultrastructure of the leaves of TPT showed seemingly normal mesophyll cells. In contrast, mesophyll cells of the VSPT showed important signs of degradation. Cells were organelle-free and the middle lamella was expanded and invaded by hyphae of Oxalosuccinic acid T. deformans. In some samples, the leaves of TPT showed deformed epidermal cells, loss of some spongy cells and increase of the intercellular spaces and division of the palisade cells. The pathogen proliferation in the leaves of the VSPT was considerably superior. In this case, stimulation of cell division occurred in the abaxial epidermis. Cells showed periclinal and oblique divisions, with an increased number of plasmodesmata; palisade or spongy cells were not differentiable. Leaves from TPT collected on 26th April showed hyphae with a non-cylindrical section and with a squashed aspect.

24 These results provided evidence that the PPARβ subtype interacted with the MAT2A PPRE sequence. Whether this interaction had a functional effect was determined in subsequent experiments. PPARβ exhibited enhanced binding to Selleckchem GSK1120212 PPREs 1, 2, 4, and 6 in activated HSCs from BDL livers compared with their quiescent counterparts from sham controls (Fig. 7A,B). PPARβ showed strong interaction with PPRE-5 in quiescent HSCs, and this binding was not enhanced

further during HSC activation (Fig. 7A,B). Knockdown of PPARβ in activated BSC cells (Fig. 7C,D, left panel) and primary rat HSCs (Fig. 7C,D, right panel) lowered the expression of both MAT2A mRNA and protein by 1.6- to two-fold. This also inhibited MAT2A promoter activity by two-fold compared with a negative control siRNA in activated BSC cells

(Fig. 7E). These results showed that in activated HSCs, PPARβ promoted MAT2A transcription. Forced expression of MAT2A vector resulted in a three- to four-fold increase Ceritinib of MAT2A protein in RSG-treated cells (Fig. 8A) that is comparable to endogenous expression of MAT2A in activated HSCs.15 This further resulted in a 55%-60% decrease in PPARγ and C/EBPβ protein expression (Fig. 8A) as well as a decrease in PPARγ mRNA (Fig. 8B) but not C/EBPβ (data not shown). The protein levels of PPARβ and α-SMA increased by two- to three-fold in MAT2A HSCs compared with vector control (Fig. 8A). A significant increase in α-SMA (Fig. 8B) but not PPARβ mRNA (data not shown) was observed after MAT2A overexpression. Lowering C/EBPβ reserves in RSG-treated BSC cells Depsipeptide mouse by siRNA resulted in a modest 1.3- to 1.4-fold increase in MAT2A mRNA and protein expression (Supporting Fig. 1A,B) and a similar increase in MAT2A promoter activity (Supporting Fig. 1C). However, overexpression of C/EBPβ in activated cells did not significantly alter MAT2A expression or promoter activity (data

not shown). MAT1A and MAT2A genes exhibit differential expression within various cell types of the liver. Hepatocytes mainly express MAT1A, and Kupffer cells and endothelial cells express MAT1A with trace amounts of MAT2A, whereas normal HSCs exclusively express MAT2A.14 Despite the predominant expression of MAT1A in the differentiated liver, the small percentage of quiescent HSCs uses MAT2A rather than MAT1A for SAM biosynthesis.14 In rapidly dividing and dedifferentiated liver, a significant induction of MAT2A has been observed along with silencing of the MAT1A gene.9, 10, 20 It is intriguing that the pattern of MAT expression in HSCs from adult differentiated liver resembles that of actively growing hepatocytes, which have high MAT2A and low MAT1A expression. In light of these facts, it is logical to hypothesize that MAT2A would be tightly regulated in quiescent HSCs.

Based on the study by Jeng et al., the APASL stopping rule results in approximately 50% relapse within 1 year and also resulted in hepatic decompensation in 1 patient with cirrhosis. Therefore, this study, in our opinion, confirms earlier observations in studies performed with

lamivudine[12, 13] that finite duration of nucleos(t)ide analog treatment is not really feasible in the majority of HBeAg-negative HBV patients, even not with the usage of more-potent antiviral DMXAA cell line drugs and stringent cessation criteria. At this moment, long-term, if not lifelong, treatment may still be considered for the vast majority of patients. This recommendation definitely applies to patients who have already progressed to liver cirrhosis, because withdrawal hepatitis flares can result in

subsequent liver failure and death.[18] We also think that in future withdrawal studies, patients with cirrhosis should not be included until more data have become available from patients without advanced liver disease. Despite our concerns, the possibility that treatment cessation is feasible in a selected group of patients should drive LY2157299 manufacturer further research in this field. Unfortunately, it is currently unclear what criteria and which markers can be helpful to identify those patients in whom it may be safe to stop antiviral therapy with a low risk of relapse of disease. The usage of quantitative HBsAg levels[19] may help to find these patients who prevent the glass from becoming completely empty. Jurriën G.P. Reijnders, M.D., Ph.D.1 Mannose-binding protein-associated serine protease “
“Aim:  The diagnosis of Wilson disease is based on the results of several clinical and biochemical tests. This study aimed to clarify the clinical features and spectrum of Wilson disease, including severe Wilson disease. Methods:  Between 1985 and 2009, 10 patients with clinical, biochemical or histological evidence of Wilson disease were either diagnosed or had a previously established diagnosis confirmed at Fukuoka University Hospital. Severe Wilson disease was defined by a serum prothrombin time ratio of more than 1.5 or serum prothrombin activity of less than 50%. The 10 Wilson disease patients were divided into two groups, one

containing three non-severe patients and the other containing seven severe patients, and the biochemical features of the patients in these two groups were compared. Results:  The mean age at diagnosis was 21.5 ± 11.7 years (range, 7–39). Decreased serum ceruloplasmin, enhanced 24-h urinary copper excretion, presence of Kayser–Fleischer rings and histological signs of chronic liver damage were confirmed in 100%, 100%, 66.7% and 100% of patients, respectively. Severe Wilson disease patients had higher levels of serum ceruloplasmin and serum copper (P < 0.05, P < 0.05, respectively) than non-severe patients. Conclusion:  In severe Wilson disease patients, the serum ceruloplasmin and serum copper levels were higher than those in non-severe Wilson disease patients.

We investigated the pattern and change of ox-stress parameters as well as glucose and lipid profile in NAFLD patients after a glucose versus lipid load and its impact on liver damage. Methods. We studied 44 patients with biopsy proven NAFLD during fasting and during a 4h oral glucose tolerance test (OGTT 75g, n=24 patients) or fat meal (200ml dairy cream plus an egg yolk, n=20 patients). We measured lipid profile, hormones and ox-stress parameters (oxLDLs, total anti-oxidative status (TAS), angptl4 and angptl6). Insulin resistance (IR) indices were derived from 4h double tracers infusion: hepatic-IR (hep-IR=EGP × fasting insulin), adipose tissue-IR

(adipo-IR=fasting lipolysis x fasting insulin). Results. During fasting, oxLDLs positively correlate with TG (r=0.398; P<0.01) and FFAs (r=0.313; P=0.04) while TAS positively correlate Selleck Panobinostat with angptl6 levels (r=0.404; P<0.01).

Angptl4 concentration positively correlate with FFAs (r=0.454; P<0.01) and adipo-IR (r=0.318; P<0.035). Among histological Cell Cycle inhibitor features, oxLDLs, angptl4 and angptl6 levels significantly correlate with steatosis (r=0.313, P=0.046; r=0.411, P=0.006 and r=0.422, P=0.004). TAS was significantly associated with NAS score (P=0.05). Of note, angptl4 increased according to the NAS score (P<0.01) and was significantly associated Wilson disease protein with severe fibrosis (F≥3). During meals, glucose and insulin curves were significantly higher in patients with F≥3 (all P<0.01) in both groups, and during OGTT showed a step-wise increase according to the degree of fibrosis. During lipid meal the large increase in plasma TG had no association with fibrosis while FFAs and oxLDLs levels were significantly higher in patients with F≥3 (P<0,01). Conclusion. Ox-stress-inducible factors are important mediators of necro-inflammation and fibrosis in patients with NAFLD. Metabolic changes occurring in the postprandial phase, particularly related to the increase of glucose, insulin and FFAs, further contribute

to liver damage. Funded by FP7/2007-2013 under grant agreement n° HEALTH-F2-2009-241762 for the project FLIP and by PRIN 2009ARYX4T. Disclosures: The following people have nothing to disclose: Lavinia Mezzabotta, Chiara Rosso, Ester Vanni, Roberto Gambino, Ramy Ibrahim Kamal Jouness, Francesca Saba, Federico Salomone, Melania Gaggini, Emma Buzzigoli, Chiara Sap-onaro, Fabrizia Carli, Gian Paolo Caviglia, Maria Lorena Abate, Antonina Smedile, Mario Rizzetto, Maurizio Cassader, Amalia Gastaldelli, Elisabetta Bugianesi Sequential use of noninvasive methods of predicting fibrosis has been proposed to evaluate fibrosis in subjects with nonalcoholic fatty liver disease (NAFLD) however, the accuracy of this approach has not been validated.

[122] The bulk of the expenses attributable to migraine derive from its high population prevalence and indirect costs due to occupational disability[123] rather than direct health care costs, which are lower for migraine than for the other neurological conditions. During the past few years, there has been a concerted effort to raise awareness of the enormous public health impact of migraine. In recognition of its high prevalence and burden,

as well as the limited devotion of research resources to migraine, the World Health Organization recently launched a global campaign to reduce the burden of headache (Lifting The Burden 2).[45] This review documents the initial success in terms of the rapid growth of information on the magnitude of migraine in areas of the world that had been previously underrepresented. Despite the high magnitude of disability associated Lenvatinib with migraine, DAPT chemical structure only approximately one half of those individuals who suffer from debilitating migraine seek professional help.[28, 113, 124] The gap in treatment is remarkably similar across the world despite variation in health systems across the world. Of those who do seek treatment, many do not continue in treatment. Only a minority of those with migraine in the general

population ever seek treatment with clinicians with expertise in headache. As expected, those who seek professional treatment are characterized by greater severity, longer duration, more disability, and more comorbidity.[5, 28] In light of the overwhelming evidence regarding the tremendous burden of migraine, leaders in the headache field have called for increased awareness of the availability of preventive efforts. Operational criteria for prevention have been developed based on headache frequency and attack-related disability, yet few of those with migraine have received preventive interventions.[113] For example, only 25% of those with migraine in the AMPP in the U.S. actually seek professional treatment and receive appropriate medications.[113] HA-1077 ic50 There has been substantial progress in the descriptive epidemiology of migraine

during the past decade. The introduction of the ICHD-II and increasing awareness of the high magnitude, burden, and impact of migraine have stimulated numerous studies of population-based data on the prevalence, correlates, and impact of migraine. In particular, there has been growing international research on migraine in children, and a greater focus on longitudinal studies of the stability, risk factors, and course of migraine. Although the bulk of population research has been conducted in Europe and the U.S., there is growing work on the epidemiology of migraine in Asia, the Middle East, and South America. Across the 19 studies of adults that employed the ICDH-II criteria, the aggregate weighted estimates of the 12-month prevalence of definite migraine are 11.

These results suggest that chaetocin has therapeutic potential for the control of solid tumors, including hepatoma. Furthermore, our findings suggest that HIF-1α pre-mRNA splicing should also be viewed as a therapeutic Trichostatin A chemical structure target. The thiodioxopiperazine moiety of chaetocin has chirality opposite to that of chetomin. Chetomin has been reported to directly

inhibit the interaction between HIF-1α and p300 and, thus, to repress HIF-1-driven gene expression.21 A recent report demonstrated that despite structural differences, three thiodioxopiperazines commonly inhibit the p300 binding in vitro and reduce VEGF secretion in HCT116 cells.22 However, as HIF-1α expression had not been determined, we examined whether chetomin, like chaetocin, down-regulates HIF-1α. Although chetomin LBH589 chemical structure repressed the transcriptional activity of HIF-1α, it had no effect on HIF-1α expression or pre-mRNA splicing (Supporting Information Fig. 7). These results indicate that chaetocin and chetomin inhibit HIF-1α in different ways. Indeed, we could not check the effect of chaetocin on p300-HIF-1α binding because HIF-1α disappeared. Nevertheless, because HIF-1α synthesis precedes p300-HIF-1α binding, the anticancer effect of chaetocin might be primarily

due to HIF-1α suppression. VEGF acts in a paracrine manner on endothelial cells to increase numbers of blood and lymphatic vessels, and also in an autocrine manner activates the VEGF receptor-mediated survival pathway. Therefore, antibodies

and peptides that antagonize VEGF or its receptors have been developed as anticancer therapies.23, 24 We found that chaetocin inhibits VEGF production in hepatoma cells and grafts, and that vessels were poorly developed in chaetocin-treated tumors. These results suggest that the VEGF suppression underlies the antiangiogenic and anticancer action of chaetocin. To correct ATP depletion and subsequent acidosis in hypoxia, HIF-1α facilitates ATP generation by up-regulating very a number of glycolytic enzymes, but it inhibits oxidative phosphorylation by inducing PDK1, which blocks the trichloroacetic acid (TCA) cycle.25 HIF-1α also corrects acidosis by inducing CA9, which generates HCO.26 Accordingly, suppression of these metabolic genes by chaetocin may contribute to its cytotoxicity to hepatoma cells cultured under severe hypoxic conditions. Many small molecules that inhibit HIF-1 have been reported in the literature. Some functionally inhibit HIF-1α by blocking its binding to p300 or DNA,21, 27 and others down-regulate HIF-1α by destabilizing it or by inhibiting its translation.28, 29 However, to the best of our knowledge, no agent has been previously reported to inhibit HIF-1α at the mRNA splicing level. Then, how does chaetocin inhibit HIF-1α pre-mRNA splicing? Spliceosome consists of small nuclear ribonucleoproteins and a host of associated proteins.

All laboratory tests were performed for each patient just before initiation of IFN therapy. Blood cell counts, serum alanine transaminase, gamma-glutamyl transpeptidase, hemoglobin A1c, total bilirubin, albumin, prothrombin time, and alpha-fetoprotein (AFP) were measured using commercially available assays. The HCV genotype was determined using polymerase chain reaction with the HCV Genotype Primer Kit (Institute of Immunology Co., Ltd., Tokyo, Japan) and classified as genotype 1, genotype 2, or other, according to Simmonds’ classification system. Serum HCV viral load

was determined using quantitative reverse transcription polymerase chain reaction using the COBAS TaqMan HCV Test (Roche Diagnostics, Branchburg, NJ, USA). The treatment protocol for CHC patients consisted of 1.5 μg/kg of pegylated RO4929097 manufacturer IFN-α-2b or 180 μg of pegylated IFN-α-2a once a week, combined with ribavirin at an oral dose of 600–1000 mg/day. Duration of the treatment was 48–72 weeks for those with HCV genotype 1 AZD2014 manufacturer and a serum HCV viral load > 5 log IU/mL. For all other patients, treatment lasted for 24 weeks. SVR was defined as undetectable serum HCV-RNA at 24 weeks after the end of treatment. Measurement of liver stiffness by transient elastography was performed using FibroScan (Echosens, Paris, France) within a week before treatment initiation. Technical

details of the examination and procedure have been reported previously.[17] Ten validated measurements were made on each patient, and results were expressed in kilopascals (kPa). Only procedures with 10 validated measurements and a success rate of at least 60% were considered reliable, and the median value was considered representative of the liver

elastic modulus. Serum AFP was measured every month, and ultrasonography or computed tomography were performed at least every 3–6 months for HCC surveillance during and after treatment, with a minimum follow-up duration of 6 months after the initiation of IFN therapy. HCC was diagnosed by histological examination and/or triphasic computerized tomography, in Mannose-binding protein-associated serine protease which hyperattenuation in the arterial phase with washout in the late phase is pathognomonic for HCC.[20] The status of patients enrolled in this study was confirmed as of March 2012. All analyses were conducted using IBM SPSS version 19 (IBM SPSS, Chicago, IL, USA), and P values less than 0.05 were considered statistically significant. Continuous variables and categorical variables were summarized as median (range) and percentage, respectively. Mann–Whitney U and chi-square tests were used when appropriate. The strength of the association between LSM and the histological fibrosis stage was estimated using the Spearman’s rank correlation coefficient.

The average age was Selleck Belinostat 50.3 years, ranging from 12 to 69 years. type B was the most commonly observed type of biliary

obstruction after liver transplantation, accounting for 47.3% (44/93), and type A was the least commonly observed type of biliary obstruction after liver transplantation, accounting for 9.7% (9/93). And type C accounted for 23.7% (22/93)and type D accounted for 19.3% (18/93). Conclusion: A new endoscopic classification of biliary obstruction after liver transplantation is proposed that might help in determining the proper candidates for treatment. Key Word(s): 1. Biliary obstruction; 2. Liver; 3. classification; 4. transplantation; Presenting Author: HONG CHANG Additional Authors: YONGHUI HUANG, WEI YAO, LI ZHANG, YUAN LI Corresponding Author: YONGHUI HUANG Affiliations: Peking University Third Hospital Objective: To evaluate

the feasibility and efficacy of Applications of a small -caliber transnasal endoscopy PF 01367338 for percutaneous endoscopic gastrostomy and gastrostomy tube replacement in patients with motor neuron disease (MND) or severe esophageal diseases. Methods: Between June 2005 and March 2012, in Peking University Third Hospital, 118 persom-times underwent percutaneous endoscopic gastrostomy (PEG) with the ‘pull’ method using conventional gastroscopy (69 cases) or a small-caliber transnasal endoscopy (49 cases), 44 persom-times underwent gastrostomy tube replacement using conventional endoscopy (37 cases) or through the abdominal-wall stoma with a small-caliber transnasal endoscopy (7 cases). Indications for PEG included MND, esophageal stricture, esophagotracheal Fistula, and anorexia nervosa. Results: PEG by ‘pull’ method achieved in 47 of 49 cases (95.92%) with small-caliber transnasal endoscopy (one faied becaused of dyspnea, one becaused of puncture failure), which achieved in 66 of 69 cases (95.65%) with traditionary endoscopy (3 patients failed because of dyspnea), There were no significant differences in the average procedure time between the two groups, but Vasopressin Receptor the patients in group of small-caliber transnasal endoscopy reported less discomfort

associated with the procedure. There were no complications of major hemorrhage, perforation or aspiration. Gastrostomy tube replacement achieved in 44 of 44 cases (100%). 7 of these underwent with a small-caliber transnasal endoscopy through the abdominal-wall stoma, and colonoscopy position made the procedure quick and easy, the average procedure time was 7 ± 1.5 min. Conclusion: Small -caliber transnasal endoscope reduces the discomfort of the procedure and is safer than conventional gastroscopy for PEG. Gastrostomy tube replacement through the abdominal-wall stoma with a small-caliber transnasal endoscopy was feasible, safe and simple procedure and reduced the pain and stress of patients. Key Word(s): 1. transnasal endoscopy; 2. PEG; 3.

Note the difference in units for HBV DNA levels. In the current Guidelines and in Japan in general, HBV DNA is expressed as copies/mL, but elsewhere the unit IU/mL is used (IU stands for international units). The AASLD, EASL and APASL guidelines all use IU/mL. Table 10 shows conversion rates between IU/mL and copies/mL. For example, the general treatment cutoff of 2000 IU/mL is equivalent to 4.07 log copies/mL (conversion rate 5.82) using the TaqMan method (Roche). Note that conversion rates may differ between real-time PCR methods; for example,

the same treatment standard would be 3.83 log copies/mL (conversion rate 3.41) using the AccuGene method (Abbott). Further research is required into these discrepancies. TaqMan (Roche) (×5.82) 116 9.9×108 AccuGene (Abbott) (×3.41) 34 3.4×109 Recommendation Real-time PCR is recommended for HBV DNA quantification in the clinical setting. Ixazomib nmr HBsAg is an antigen within the HBV envelope that is present within the blood as the Dane particle as well as empty particles, small spherical particles and tubular particles, all of which are generated from covalently closed FDA approved Drug Library price circular DNA (cccDNA) in the hepatocytes, as shown in Figure 2. Qualitative reagents have traditionally been used for measuring HBsAg and for the diagnosis of hepatitis B. But recent

years have seen the development of a number of new quantitative reagents with considerable

potential for prognosis and evaluation of therapeutic effects.[64, Y-27632 nmr 65] Table 11 lists reagents used for measuring HBsAg. Mono (two types) Mono (two types) Mono (various) Mono (two types) Mono (two types) Mono (various) Mono (two types) 0.1∼2000 C.O.I. 0.05∼250 IU/mL (manual/auto dilution) 0.03∼2500 IU/mL (auto dilution) 0.005∼150 IU/mL (auto dilution) Observations generated by qualitative reagents are expressed in terms of a cut-off index (COI), where a value of 1.0 or higher is deemed positive and higher measurements are semiquantitative, used for reference purposes. Common quantitative reagents include Architect (Abbott) and HISCL (Sysmex). Table 11 shows the threshold criteria and measurement ranges in IU/mL. Quantification covers a wide range through dilution. A newly developed quantitative reagent for HBsAg called Lumipulse HBsAg-HQ claims ten times the sensitivity of conventional reagents, and shows considerable potential for clinical settings. HBsAg levels vary in accordance with factors such as age, HBV DNA levels and HBV genotype.[66] HBV DNA is considered unsuitable for evaluating therapeutic effects because the HBV DNA levels often falls below the limit of detection shortly after the commencement of antiviral treatment. Several reports therefore recommend monitoring the HBsAg levels over time instead.

Some of the best evidence of the effects of resource competition on females comes from studies of the effects of increasing group size, which commonly depress fecundity and increase mortality of females and their offspring (Clutton-Brock, Albon & Guinness, 1982, van Schaik et al., 1983; Clutton-Brock, 2009b, 2009b, Silk, 2007a; Clutton-Brock, Hodge & Flower, 2008). Very similar patterns of resource competition occur in males, where breeding activity can also have high energetic

costs (Lane et al., 2010), and individuals compete both for direct access to resources Sunitinib and for access to feeding territories (Clutton-Brock, 2007), and survival is often sensitive to food shortages (Clutton-Brock, Major & Guinness, 1985). As well as competing for access to resources, females, like males, often compete to breed and, as in males, the structure of social groups intensifies conflicts of interest between group members (West-Eberhard, 1983, 1984). In some mammals, females compete to become sexually mature and, in extreme cases, one female suppresses the sexual development of all other females, evicting individuals that attempt BI 6727 clinical trial to breed (Creel & Creel, 2002; Clutton-Brock et al., 2006; Clutton-Brock, 2009b).

In others, females compete for access to mates, even though operational sex ratios (the ratio of males to females that are ready to mate at a given time) are biased towards males. For example, in some ungulates where males defend groups of females during a well-defined mating season, there is often more than one receptive female in a male’s harem on the same day, and females commonly compete for the attentions Progesterone of males (Bro-Jørgensen, 2002, 2011). Female competition may help females to ensure that they are mated by one or more males

within the time frame of their reproductive cycles (Parker & Ball, 2005), for the sperm supplies of successful males can become depleted (Dewsbury, 1982; Preston et al., 2001, Wedell, Gage & Parker 2002) or popular males may strategically conserve sperm for subsequent mating opportunities (Parker et al., 1996, Wedell et al., 2002). As would be expected, the frequency of overt female competition for mating partners increases in populations where adult sex ratios are strongly biased towards females (Milner-Gulland et al., 2003, Cheney, Silk & Seyfarth, 2012), where there is a high degree of reproductive synchrony (Emlen & Oring, 1977; Stockley & Bro-Jorgensen, 2011), or where females mate with multiple partners (Charlat et al., 2007).