, 1984; Scheiner & Fisher, 2011). I am grateful to Alan McElligott, Megan Wyman, Anna Taylor and an anonymous referee for helpful comments on the manuscript. I acknowledge the financial support of the Swiss National Science Foundation and the Swiss Federal Veterinary Office. “
“Although competition between females is one of the cornerstones of the theory of natural selection, Selleckchem AZD1208 most studies of reproductive competition have focussed principally on mating competition in males. Here, we summarize our current understanding of adaptive tactics

used by competing females in social mammals, and assess the social mechanisms affecting competitive success and the evolutionary consequences of social competition between females. As well as emphasizing the importance of female–female

competition in social evolution, recent studies highlight the qualitative similarities in the operation of selection in females and males. Although competition between females is one of the cornerstones of the theory of natural selection, detailed studies of breeding competition have focussed largely on males (Darwin, 1871; Andersson, 1994). Compared to competition between males, female competition less frequently involves escalated contests and is less often associated with the evolution of exaggerated secondary sexual characters. Moreover, individual differences in breeding success among females are less obvious than among males: whereas measures of breeding success across a single season are sufficient to reveal large individual differences AUY-922 datasheet among males and to show that these are related to competitive ability, it is usually necessary to monitor the success many of females over several breeding attempts to appreciate the magnitude of individual

differences and to identify their causes (Clutton-Brock, 1983). As a result, only after long-term studies of individual life histories became available was it possible to assess the magnitude and consistency of individual differences in reproductive success and to measure the strength of selection operating on females in iteroparous organisms (Clutton-Brock, 1988). One of the consequences of delays in associating the extent of variation in female fitness and the factors that affect it was the perception that competition between females is weaker than between males, and that females compete principally for resources while males compete principally for females (Emlen & Oring, 1977; Clutton-Brock & Harvey, 1978, Clutton-Brock, Albon & Guinness 1989, Tobias, Montgomerie & Lyon, 2012). However, as more extensive studies of female life histories have become available, they have shown that the extent of individual differences in reproductive success among females and the intensity of intrasexual competition to breed can be as great or greater than in males (Hauber & Lacey, 2005; Clutton-Brock, 2009c) and have emphasized the qualitative similarities in the selection pressures operating on both sexes (Clutton-Brock, 2007).

As shown in Fig. 2, TGFβ1, and not starvation, significantly induced CD133 expression. In addition, we performed dose- and time-dependent experiments on the effect of TGFβ1 on CD133 expression. CD133− Huh7 cells were stimulated ICG-001 with up to 20 ng/mL TGFβ1 for 48 hours. As depicted in Fig. 3A, CD133 expression was induced by TGFβ1 in a dose-dependent manner up to 2.5

ng/mL, and dosages between 2.5 and 10 ng/mL had similar effects on CD133 expression induction. CD133− cells were then treated with 5 ng/mL TGFβ1 for up to 48 hours, followed by repeat treatment with 0 to 10 ng/mL TGFβ1 for an additional 24 hours. As shown in Fig. 3B, TGFβ1-induced CD133 expression was in a time-dependent fashion, and once CD133 expression was induced, the expression remained elevated even after TGFβ1 stimulation was removed. As CD133 is a CSC marker in Huh7 cells, we questioned if the TGFβ1-induced CD133+ Huh7 cells have the property of tumor initiation in vivo, comparable to native CD133+ Huh7 cells. Freshly isolated, untreated CD133+ and CD133− Huh7 cells were used as controls. Thirty

days after inoculation all of the mice transplanted with native CD133+ cells were sacrificed because the tumor size reached the endpoint according to our protocol (>3,500 mm3). As demonstrated in Fig. 4A, 6 and Protein Tyrosine Kinase inhibitor 12 hours of TGFβ1 stimulation increased CD133 expression in CD133− cells; 35 days after HSP90 inoculation in nude mice, TGFβ1-induced CD133+ cells were significantly more tumorigenic compared to native CD133− cells (Fig. 4B,C). Following activation of TGFβ receptors, Smad2 and Smad3 are phosphorylated and form a heterocomplex, Smad2/3/4, which

translocates to the nucleus to regulate responsive gene transcription.28 In order to test whether TGFβ induces CD133 expression through Smad-dependent pathways, we used inhibitory Smads, Smad6 and Smad7, which are able to block heterocomplex formation. Huh7 cells were transfected with Smad629 and Smad730 vectors, and 48 hours after transfection cells were stimulated with 5 ng/mL TGFβ1. In qPCR analysis, elevated CD133 mRNA induced by TGFβ1 was significantly attenuated by inhibitory Smads (Fig. 5A). This expression pattern was confirmed at the protein level (Fig. 5B). In colon cancer cells CD133 expression is regulated by promoter methylation. Compared with the parental HCT116 cell line, a double knockout line with disruption of DNA methyltransferases DNMT1 and DNMT3β demonstrates increased CD133 expression.8 To test if similar epigenetic regulation is involved in CD133 expression in liver cancer, a DNMT inhibitor (5-aza-2′-deoxycytidine, DAC) and a histone deacetylase inhibitor (trichostatin A, TSA) were introduced. As shown in Supporting Information Fig. 1, CD133 expression in CD133− Huh7 cells was up-regulated by DNMT inhibitor in a time- and dose-dependent manner.

” Dr. Mathew’s claim that 22 subjects did not present for a follow up is inaccurate. We operated on 91 patients and lost 2 patients during the first year follow up and an additional 10 patients in the ensuing 4 years, for a total of 12 patients not being available for a follow up at the end selleck chemicals of the 5th year. Again, I find his assumption that they were

potentially not included because we wanted to only include patients with favorable results very discourteous. I would understand if he would ask for an explanation. However, unashamedly stating that we may have excluded these patients because they had unfavorable outcomes is an insult to our team. We have included eight patients in the study who did not have a positive response (less than 50% improvement). For anyone who has not done a 5-year study, it would be difficult to understand how challenging it is to keep in

touch with close to 89 patients for 5 years. Of the possibilities MLN0128 molecular weight that he has outlined, the likely reason for losing these patients in follow up is that many of these patients were symptom free and they did not need care. Otherwise, these patients would have needed medication from our neurologists. Why would they not visit the neurologist and receive treatment without cost, had they had pain? But this is not what we claimed in the study nor do we claim it now. Articles and results should be about the facts, not suppositions. One inevitably loses a portion of the committed patients along the way, especially in a 5-year study, ASK1 and that is a fact. One more disrespectful statement from Dr. Mathew surrounds his conclusion

that our procedures are “self-promoting,” curative interventions. We have never stated during our presentations or publications that the surgery is a cure. To assign such a claim is totally unjustified and is self-serving on his part. Dr. Mathew writes “Commentary is then made about rebound headache, and subjects taking opiates, which is the only time the author comments on medications that are taken during the study. It is not surprising that the only medications noted by the author are those that may negatively impact study results (medication overuse headache), as there is no mention of preventative and abortive medications that can positively impact statistical analysis.” This is another misrepresentation of the facts to diminish the significance of the study. Had the glorification of the studies by referring to these medications been our aim, we would have referred to them more frequently and not just in the most recent study. The medication use was only elucidated on in our recent studies since we learned during the peer review process that this matter was important to our neurology colleagues. Dr.

The association of disease

factors and methotrexate use with significant fibrosis could not be demonstrated in the study. Further research is required to confirm our findings. Disclosures: The following people have nothing to disclose: Jamrus Pongpit, Saneerat Porntharukchareon, Wasana Stitchantrakul, Ammarin Thakkinstian, Piyaporn Kaewdoung, Kwannapa Promson, Supanna Petraksa, Natta Rajatanavin, Chomsri Kositchaiwat, Abhasnee Sobhonslidsuk “
“We aimed to elucidate the relationship between the contrast enhancement effect of gadolinium-ethoxybenzyl-diethylenetriamine pentaacetic GSK126 clinical trial acid (Gd-EOB-DTPA) on magnetic resonance imaging (MRI) of hepatocellular carcinomas (HCC) and the expressions of hepatocyte transporters (i.e. organic anion-transporting polypeptide [OATP]1B3, multidrug-resistant protein [MRP]2 and MRP3) and to clarify the characteristics of HCC with an MRI high-contrast enhancement effect. We retrospectively examined the relationship between the relative enhancement ratio (RER) of HCC, absolute and relative immunohistochemical

staining scores of hepatocyte transporters, and histological differentiation of 22 HCC from 21 patients who had undergone preoperative Gd-EOB-DTPA-enhanced MRI. RER had a significant correlation with OATP1B3 expression according to the absolute and relative scores (P = 0.016 vs 0.0006). The RER of HCC with high OATP1B3 and MRP2 selleck chemical expression levels was higher than that of HCC with low OATP1B3 or MRP2 expression levels (P = 0.0003). The RER of HCC with higher OATP1B3 rates

was greater than that of HCC with lower OATP1B3 rates (P = 0.0005). HCC histological differentiation showed a significant correlation with OATP1B3 expression and RER (P = 0.023 vs 0.0095). We found that coexpression of OATP1B3 and MRP2 influenced the high contrast enhancement of HCC on MRI. “
“Recent studies have demonstrated a bidirectional relationship between gastroesophageal reflux disease (GERD) and sleep where night-time reflux leads to sleep deprivation and sleep deprivation per se can exacerbate GERD by enhancing perception of intra-esophageal stimuli. Presently, treatment has primarily focused on reducing night-time reflux Phosphoprotein phosphatase and thus improving sleep quality. Future studies are needed to further explore the relationship between GERD and sleep and the potential of novel therapeutic options to interrupt the vicious cycle between GERD and sleep. Gastroesophageal reflux disease (GERD) is a chronic disorder and the most common disease that affects the esophagus. A population-based study estimated that 20% of the US adult population experience GERD-related symptoms at least once a week.1 GERD can lead to esophageal mucosal injury in a subset of patients as well as bothersome symptoms, such as heartburn and acid regurgitation, that may affect patients’ reported quality of life.

Mitochondrial extraction from liver tissue was performed using a Qproteome Mitochondrial Isolation kit (QIAGEN) according to the manufacturer’s instructions. The nuclear fraction from liver tissue was prepared using a Nuclear Extraction kit (Panomics, Fremont, CA, USA) according to the manufacturer’s instructions. Liver lysates and the mitochondrial and nuclear fractions from liver were separated by sodium dodecylsulfate polyacrylamide gel electrophoresis. The proteins were transferred to polyvinylidene difluoride membranes (Millipore, Bradford, MA, USA), blocked overnight at 4°C with 5% skim milk and 0.1% Tween-20 in Tris-buffered saline, and subsequently incubated for 1 h at room temperature

with goat antihuman SOD2 antibody (Santa Cruz Biotechnology, Santa Cruz, CA, USA), rabbit antihuman GPx1 see more antibody (Abcam, Cambridge, MA, USA), rabbit antihuman SIRT3 antibody (Abcam), rabbit antihuman Sorafenib ic50 peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α) antibody (Abcam), rabbit antihuman adenosine monophosphate-activated protein kinase-α (AMPKα) antibody (Cell Signaling Technology, Boston, MA, USA), rabbit antihuman phospho-AMPKα (Thr172) antibody (Cell Signaling Technology), rabbit antihuman mitochondrial heat shock protein 70 antibody (HSP70; Thermo Scientific, Rockford, IL, USA),

rabbit antihuman β-actin antibody (Cell Signaling Technology) or rabbit antimouse lamin B1 antibody (Abcam). The membranes were washed and incubated with horseradish peroxidase (HRP)-conjugated donkey antigoat immunoglobulin (Ig)G (Santa Cruz Biotechnology) or HRP-conjugated donkey antirabbit IgG (GE Healthcare Life Sciences, Pittsburgh, PA, USA). Quantitative values are expressed as mean ± standard deviation. Two groups among multiple groups were compared by the rank-based Kruskal–Wallis anova test followed by Scheffé’s test. The statistical significance of correlation was determined by the use of simple regression

analysis. P < 0.05 was considered to be significant. AS CONFIRMATION OF successful ovariectomy-induced suppression of endogenous estrogen production, the uterine weight of OVX mice was significantly decreased compared with that of sham-operated mice (Table 1). Dietary intake, bodyweight, liver weight and serum leptin levels were Methane monooxygenase significantly greater in OVX mice than in sham-operated mice regardless of whether they were transgenic or non-transgenic (Table 1). Interestingly, the serum alanine aminotransferase (ALT) level was significantly higher in OVX transgenic mice than in mice in the other three groups, but the levels were comparable in OVX non-transgenic and sham-operated non-transgenic mice (Table 1). To determine why OVX transgenic mice have a higher ALT level, we investigated the liver histology of the mice in the four groups (OVX transgenic, sham-operated transgenic, OVX non-transgenic and sham-operated non-transgenic mice).

HDL level (>=40 male and >=50 female) and HbA1c level (<5.5) before OLT were significantly associated with better patient

survival(P=0.031 and 0.022). Conclusion: NAFLD recurrence rates after OLT are high(21.2%) and occur early at median of 15mos, but NASH recurrence rates are low(7.6%). Increased BMI post OLT, morbid obesity, and metabolic syndrome are not related to NAFLD or NASH recurrence. Better diabetes control before OLT may contribute to lower NAFLD recurrence and better patient survival. Disclosures: Norio Kawamura – Consulting: Novartis, Vital therapies; Grant/Research Support: Genzyme, Sanofi; Speaking and Teaching: Astellas John J. Fung – Advisory Committees or Review Panels: Astellas, Novartis; Consulting: Vital Therapies; Grant/Research Support: Sanofi Naim Alkhouri – Advisory Committees or Review Panels: Gilead Sciences The following people have nothing to disclose: Mustafa Nazzal, Galal El-Gaz-zaz, Mario Spaggiari, Masato Fujiki, Teresa Diago, Federico N. Aucejo, Koji Hashimoto, Cristiano Quintini, Charles Winans, Bijan Eghtesad, Charles M. Miller, Dympna Kelly Background: The prevalence of nonalcoholic fatty liver RXDX-106 datasheet disease (NAFLD) which is closely related to coronary atherosclerosis is continuously increasing worldwide. Controlled attenuation parameter (CAP) of transient elastography (TE) can assess the degree

of hepatic steatosis accurately. This study aimed to investigate the prevalence of TE-defined NAFLD and to identify factors which are associated with coronary artery calcification (CAC) in patients with NAFLD. Methods:

Between January 2012 and March 2014, a total of 385 asymptomatic subjects without chronic liver diseases, heavy alcohol consumption, or known heart diseases who underwent comprehensive medical health check-up including echocardiography, TE, carotid ultrasound, fat computed tomography (CT), and coronary CT were recruited. Of these, 144 (37.4%) subjects Metalloexopeptidase had TE-defined NAFLD (CAP ≥ 250 dB/m). Results: The median age of the whole study population (216 men and 169 women) was 56 (interquartile [IQR], 51-64) years. On multivariate analysis, subjects with NALFD were significantly older (mean 57 vs. 55 years) and had higher body mass index (BMI) (mean 25.7 vs. 23.0 kg/m2), higher alanine aminotransferase level (mean 26.2 vs. 20.0 IU/L), higher triglyceride (140 vs. 99 mg/dL), higher HOMA-IR (2.19 vs. 1.50), lower HDL-cholesterol (12.6 vs. 50.1 mg/dL), and higher amount of visceral fat area on CT (127.1 vs. 92.9 cm2) (all P<0.05). On multivariate analysis, higher BMI (odds ratio [OR] 3.76; 95% confidence interval [CI] 1.03-6.98; P<0.001), triglyceride (OR 2.25; 95% CI 1.28-3.95; P=0.005), higher amount of visceral fat area (OR 1.96; 95% CI 1.06-3.62; P=0.032) independently predicted the presence of NAFLD. In the sub-population with NAFLD (men 94 and women 50), the median age was 57 (IQR 51-64) years.

However, while he appears to be fumbling around and searching for genital openings that are not there, the subadult female, with a twisting lunge, makes a predatory attack and, when successful, the male becomes her prey (Jackson & Hallas, 1986). The subadult female practises aggressive

mimicry by Lorlatinib mouse behaving like an adult female and by indirectly controlling the behaviour of her prey, a mature conspecific male. She is physically incapable of mating, and yet we cannot rule out the possibility of entanglement between her predatory and mating strategies. A mating tactic often used by a Portia male is to cohabit in a web with a subadult female and then mate with her once she has moulted and become sexually mature.

A sexual-selection hypothesis we might propose is that subadults benefit from cohabiting and mating with males that can evade the lethal subadult-female behaviour. We should emphasize that there is currently no evidence supporting these sexual-selection hypotheses. We should also emphasize that these sexual-selection hypotheses are not simple alternatives to explaining BMS-777607 datasheet adult and subadult-female behaviour as being examples of aggressive mimicry. Entanglement with mating strategies notwithstanding, we still have predators (adult and subadult females) that use signals to control the behaviour of a specific kind of prey (adult conspecific males). When examining the cognitive implications of this predatory behaviour,

P. labiata’s mating and predatory strategy is as relevant as any of the other aggressive-mimicry examples we have considered. Anglerfish, caudal-luring snakes and femmes fatales are all examples of predators indirectly manipulating their prey’s behaviour by providing stimuli to the prey, with the prey’s response being advantageous to the predator, but not necessarily to the prey. Adopting a first-principles approach to understanding communication (Dawkins & Krebs, 1978), we can say that all of these are examples of communication and that there is no pressing need to begin with an emphasis on information. However, we should not ignore the things information might explain. ‘Information’ and ‘correlation’ are sister concepts and identifying correlations learn more between signals and factors that matter to the receiver can be a critical step towards understanding the receiver’s predisposition to respond in some particular way to the signal. When considering aggressive mimicry as communication, we can substitute the term ‘misinformation’ for ‘information’. This is a way of expressing that the stimulus provided by the signal resembles a stimulus for which the elicited response is usually advantageous to the receiver. The term ‘mimicry’ predisposes us to expect an easily specifiable model and, for aggressive mimicry, we can envisage ‘model’ and ‘misinformation’ as meaning much the same thing.

2 Patients with reflux during sleep are more likely to develop esophageal inflammation, peptic stricture, esophageal ulceration, Barrett’s esophagus and even adenocarcinoma of the esophagus.3,4 In addition, these patients have a higher prevalence of oropharyngeal, laryngeal and pulmonary manifestations.5,6 Poor quality of sleep and a variety of sleep disturbances

have been recently added to the growing list of extra-esophageal manifestations of GERD. Recent studies have suggested a bidirectional relationship between GERD and sleep (Fig. 1).7 GERD has been shown to adversely affect sleep by awakening patients from sleep during the night or more commonly by leading to multiple short amnestic arousals, PLX4032 nmr resulting in sleep fragmentation. At the same time, sleep deprivation per se can adversely affect GERD by enhancing perception of intra-esophageal acid (esophageal hypersensitivity).7 In fact, there is a potential ‘vicious cycle’ BAY 80-6946 in vivo in which GERD leads to poor quality of sleep,

which then in turn enhances perception of intra-esophageal stimuli that further exacerbates GERD.8 Overall, the epidemiology of nocturnal gastroesophageal reflux is not well studied. According to a Gallup Poll from 1988 in which 1000 GERD patients completed a survey, 79% of the respondents reported nocturnal heartburn.9 In a study by Farup et al., 74% of the GERD subjects with frequent GERD symptoms reported nocturnal GERD symptoms.10 In contrast, Locke et al. found in a community-based selleck screening library survey that 47% and 34% of the GERD sufferers reported nocturnal heartburn and nocturnal acid regurgitation, respectively.1 However, in the first two studies, only 57% and 54% of the patients, respectively, reported heartburn that awakened them from sleep during the night. Fass et al. in a large prospective, cohort study of subjects evaluated for sleep disturbances demonstrated that 24.9% reported heartburn during sleep.11 Recently, it was demonstrated that heartburn that

awakens patients from sleep during the night is highly predictive for GERD.12 This effect was further accentuated in morbidly obese subjects. In the aforementioned national survey of 1000 subjects with GERD, 75% of the participants reported that GERD symptoms affected their sleep, and 63% believed that heartburn negatively affected their ability to sleep well.9 Additionally, 42% stated that they were unable to sleep through a full night, 39% had to take naps during the day and 34% were sleeping in a seated position. Interestingly, 27% reported that their heartburn-induced sleep disturbances kept their spouse from having a good night’s sleep. The prevalence of sleep disturbances among respondents increased with increase in frequency of the night-time heartburn episodes during the week.

The majority (82%) of post HEV-IgG and all seroconverters samples were tested for HEV RNA. Borderline positive and negative samples were designated as positive and negative, respectively.

Donor specimens were not available for testing. Results: Among the 255 pre-LT samples 97 (38%, 95% CI 32-44%) were anti-HEV-IgG positive and none were positive for anti-HEV IgM. Age, gender, race, and etiology of cirrhosis were not significantly different in patients with or without anti-HEV. All 97 patients with anti-HEV IgG before transplant remained positive on the post-LT sample and 1 was IgM anti-HEV positive 4 yrs post-LT. Among the158 LT recipients who tested negative for IgG anti-HEV before transplant, 3 (1.9%, 95% CI: 0.4-5.4%) VX-770 order became anti-HEV IgG positive during follow up (median 114 days, IQR 85-133), one of whom was also anti-HEV IgM positive. The 3 incident infection cases were all females, median age 57 yrs, Hispanic White (n=2) or Black (N=1), received deceased (N=1) or living (N=2) donors and were transplanted for non-viral causes of cirrhosis. All 3 cases were HEV RNA negative. Conclusions: In this geographically diverse LT population, prevalent HEV infection was common among

patients undergoing LT — present in 38%. Incident infections after LT were rare, with only 1.9% (3 cases) identified and none with persistent click here infection. This natural history contrasts sharply with the reports from Europe and suggests unique epidemiologic risks in Europe. We conclude that HEV is not a major cause of unexplained chronic hepatitis in US liver transplant populations. Disclosures: Norah Terrault – Advisory Committees or Review Panels: Eisai, Biotest; Consulting: BMS, Merck; Grant/Research Support: Eisai, Biotest, Vertex, Gilead, AbbVie, Novartis, Merck The following people have nothing to disclose: Ronald E. Engle, Jennifer L. Dodge, Chris

Freise, Averell H. Sherker, Patrizia Farci, Robert H. Purcell Background: Hepatitis selleck chemicals E virus (HEV) is an emerging cause of autochthonous infections among immunocompromised individuals in developed nations. Among solid organ transplant (SOT) recipients, HEV infection has been associated with acute hepatitis, liver graft dysfunction, cirrhosis, and chronic infection in up to 65% of cases. While thrombocytopenia, leukopenia, and tacrolimus use have been associated with the development of chronic HEV infection among SOT recipients in Europe, risk factors for HEV infection among SOT recipients in North America have not been previously characterized. Methods: We conducted a nested case-control study of 16 SOT recipients at our institution with evidence of post-transplant HEV infection (evidenced by anti-HEV IgM, IgG seroconversion, or positive PCR at 6 months post-transplant), to determine risk factors for HEV infection following SOT. Categorical variables included age (by quartile), gender, immunosuppressive regimen, leukopenia (WBC< 4.

nov. Both species formed minute coccoid cells with an irregular globular outline, a smooth cell wall, and a single parietal chloroplast without a pyrenoid. The two species, described herein as J. perforata and J. minuta, differed in chloroplast morphology and cell wall structure. Phylogenetic analyses

of 18S rRNA gene sequences showed a firm relationship between the two species and placed the Jenufa lineage in an unresolved position within the CS clade (Chlamydomonadales + Sphaeropleales) of the class Chlorophyceae, although possible affinities to the genus Golenkinia were suggested both by maximum-likelihood (ML) and Bayesian methods. Furthermore, two almost mTOR inhibitor identical environmental 18S rDNA sequences from an endolithic microbial community occurring in dolomite rock in the central Alps turned out to be specifically related to, yet apparently distinct from, the sequence of J. minuta, indicating the existence of an undescribed Jenufa species occurring in the temperate zone. “
“Photosynthetic Venetoclax characteristics of four Porphyra yezoensis Ueda [a taxonomic synonym of Pyropia yezoensis (Ueda) M. S. Hwang et H. G. Choi] strains in conchocelis phase were investigated and compared with one wildtype of P. yezoensis and two strains of Porphyra haitanensis T. J. Chang et B. F. Zheng [a taxonomic synonym of Pyropia haitanensis (T. J. Chang

et B. F. Zheng) N. Kikuchi et M. Miyata]. Results showed that experimental strains had higher contents of chl a and carotenoids, but a lower content of total phycobiliproteins than the wildtype. Meanwhile, photochemical efficiency of PSII was measured using pulse amplitude modulation (PAM) fluorometry technology. The value of PSII photosynthetic parameters of P. yezoensis strains were all higher than the wild strain, and the maximal quantum yields (Fv/Fm), effective quantum yields Y(II), and relative photosynthetic electron transport learn more rates

(rETR) of P. haitanensis were higher than those of P. yezoensis. The present study verified the possibility of selective breeding of P. yezoensis using the filamentous sporophyte instead of the gametophytic thallus, the advantages being (i) nonrequirement of control of life cycle and (ii) direct and rapid cultivar improvement by artificial selection. We consider the method to be a promising technique for selective breeding of P. yezoensis cultivars. “
“Eukaryotes such as plants and the unicellular green alga Chlamydomonas reinhardtii P. A. Dang. produce and secrete compounds that mimic N-acyl homoserine lactone (AHL) bacterial quorum-sensing (QS) signals and alter QS-regulated gene expression in the associated bacteria. Here, we show that the set of C. reinhardtii signal-mimic compounds that activate the CepR AHL receptor of Burkholderia cepacia are susceptible to inactivation by AiiA, an AHL lactonase enzyme of Bacillus.