Excretal Near Infrared Reflectance Spectrometry to monitor the nutrient content of diets of grazing young ostriches (Struthio camelus)

Feeding systems in which young ostriches feed on pasture but have access to concentrates provide better welfare than confined systems but are sustainable only if nutrition is carefully controlled. This study was conducted to evaluate the potential of "excretal NIRS", a methodology that associates excretal spectral information in the near infrared (NIR) region with dietary attributes, in predicting dietary quality and nutrient intake in grazing ostrich chicks. Sixty sets of excretal and dietary information from chicks fed only concentrate or also grazing lucerne, barley, sulla or natural pastures, were used. The coefficient of determination (R2) and the standard error of cross validation (SECV) served to evaluate calibration quality. The prediction of dietary concentrate content ranging 420 to 1000 g/kg of DMI, was highly linear (R2 = 0.96), with SECV of 63 g/kg. Similar R2 values were noted for the dietary contents of crude protein (CP), acid detergent fibre (ADF) and ash; that for the prediction of neutral detergent fibre (NDF) was lower (0.87). Ash, CP, NDF and ADF were predicted with SECV values of 14.8, 5.0, 8.9 and 10.7 g/kg DM diet, respectively. The calibration for apparent total organic matter digestibility was of poor quality. Good (R2 = 0.95) and acceptable (R2 = 0.86) calibrations were obtained for the daily intakes of pasture and concentrate, respectively, with SECVs of 75 and 131 g/d. Predictions of ash (R2 = 0.85, SECV = 11 g/d) and ADF (R2 = 0.80, SECV = 19 g/d) intakes had mediocre accuracy, and calibrations for CP and NDF intakes were even poorer. These results suggest that excretal NIRS may be useful to predict dietary intake and composition for grazing ostriches when applied to a known nutritional environment attended with calibration standards. Keywords: Ratites, faecal NIRS, nutrition; pasture, herbivorySouth African Journal of Animal Science Vol. 36 (4) 2006: pp. 248-25

Social comparisons are associated with poorer and riskier financial decision making, no matter whether encounters are sporadic or repeated

Previous research suggests that social comparisons affect decision making under uncertainty. However, the role of the length of the social interaction for this relationship remains unknown. This experiment tests the effect of social comparisons on financial risk taking and how this effect is modulated by whether social encounters are sporadic or repeated. Participants carried out a computer task consisting of a series of binary choices between lotteries of varying profitability and risk, with real monetary stakes. After each decision, participants could compare their own payoff to that of a counterpart who made the same decision at the same time and whose choices/earnings did not affect the participants’ earnings. The design comprised three between-subjects treatments which differed in the nature of the social interaction: participants were informed that they would be matched with either (a) a different participant in each trial, (b) the same participant across all trials, or (c) a "virtual participant", i.e. a computer algorithm. Compared to the non-social condition (c), subjects in both social conditions (a and b) chose lotteries with lower expected value (z=-3.10, p<0.01) and higher outcome variance (z=2.13, p=0.03). However, no differences were found between the two social conditions (z=1.15, p=0.25 and z=0.35, p=0.73, respectively). These results indicate that social comparison information per se leads to poorer and riskier financial decisions, irrespective of whether or not the referent other is encountered repeatedly

C/EBP-β Regulates Endoplasmic Reticulum Stress–Triggered Cell Death in Mouse and Human Models

Endoplasmic reticulum (ER) stress elicits the unfolded protein response (UPR), initially aimed at coping with the stress, but triggering cell death upon further stress. ER stress induces the C/EBP-® variant Liver-enriched Activating Protein (LAP), followed by the dominant-negative variant, Liver Inhibitory Protein (LIP). However, the distinct role of LAP and LIP in ER stress is unknown. We found that the kinetics of the ER stress-induced expression of LIP overlapped with that of the cell death in mouse B16 melanoma cells. Furthermore, inducible over-expression of LIP augmented ER stress-triggered cell death whereas over-expression of LAP attenuated cell death. Similar results were obtained in human 293T cells. Limited vasculature in tumors triggers hypoxia, nutrient shortage and accumulation of toxic metabolites, all of which eliciting continuous ER stress. We found that LAP promoted and LIP inhibited B16 melanoma tumor progression without affecting angiogenesis or accelerating the cell cycle. Rather, LAP attenuated, whereas LIP augmented tumor ER stress. We therefore suggest that C/EBP-® regulates the transition from the protective to the death–promoting phase of the UPR. We further suggest that the over-expression of LAP observed in many solid tumors promotes tumor progression by attenuating ER stress–triggered tumor cell death

Validation of Faecal NIRS for Monitoring the Diet of Confined and Grazing Goats

Goats are used for brush control and ecological management of Mediterranean grazing lands. Farmers are willing to cooperate with communities but they need an easy method to evaluate the daily intake of nutrients. A calibration of the chemical attributes of goats\u27 diets was set-up, based on faecal near infrared (NIR) spectra (Landau et al., 2004; Table 1). The accuracy of this methodology was estimated by using the standard error of cross-validation (SECV), which represents the variability in the difference between predicted and reference values when the equation is applied sequentially to subsets of data from the calibration data set. This procedure is justified in situations with calibration samples that are randomly selected from a natural population, but may give over-optimistic results, in particular if data are replicated. The standard error of prediction (SEP) represents the variability in the difference between predicted and reference values when the equation is applied to an external (i.e., not used in any step of the calibration) validation data set. (Naes et al., 2002). The aim of the present study was to test the robustness of predicting dietary CP, in vitro dry matter digestibility (IVDMD), and NDF percentages in goats\u27 diets, using faecal samples totally external to calibrations

Variations of X Chromosome Inactivation Occur in Early Passages of Female Human Embryonic Stem Cells

X chromosome inactivation (XCI) is a dosage compensation mechanism essential for embryonic development and cell physiology. Human embryonic stem cells (hESCs) derived from inner cell mass (ICM) of blastocyst stage embryos have been used as a model system to understand XCI initiation and maintenance. Previous studies of undifferentiated female hESCs at intermediate passages have shown three possible states of XCI; 1) cells in a pre-XCI state, 2) cells that already exhibit XCI, or 3) cells that never undergo XCI even upon differentiation. In this study, XCI status was assayed in ten female hESC lines between passage 5 and 15 to determine whether XCI variations occur in early passages of hESCs. Our results show that three different states of XCI already exist in the early passages of hESC. In addition, we observe one cell line with skewed XCI and preferential expression of X-linked genes from the paternal allele, while another cell line exhibits random XCI. Skewed XCI in undifferentiated hESCs may be due to clonal selection in culture instead of non-random XCI in ICM cells. We also found that XIST promoter methylation is correlated with silencing of XIST transcripts in early passages of hESCs, even in the pre-XCI state. In conclusion, XCI variations already take place in early passages of hESCs, which may be a consequence of in vitro culture selection during the derivation process. Nevertheless, we cannot rule out the possibility that XCI variations in hESCs may reflect heterogeneous XCI states in ICM cells that stochastically give rise to hESCs

Studying Early Lethality of 45,XO (Turner's Syndrome) Embryos Using Human Embryonic Stem Cells

Turner's syndrome (caused by monosomy of chromosome X) is one of the most common chromosomal abnormalities in females. Although 3% of all pregnancies start with XO embryos, 99% of these pregnancies terminate spontaneously during the first trimester. The common genetic explanation for the early lethality of monosomy X embryos, as well as the phenotype of surviving individuals is haploinsufficiency of pseudoautosomal genes on the X chromosome. Another possible mechanism is null expression of imprinted genes on the X chromosome due to the loss of the expressed allele. In contrast to humans, XO mice are viable, and fertile. Thus, neither cells from patients nor mouse models can be used in order to study the cause of early lethality in XO embryos. Human embryonic stem cells (HESCs) can differentiate in culture into cells from the three embryonic germ layers as well as into extraembryonic cells. These cells have been shown to have great value in modeling human developmental genetic disorders. In order to study the reasons for the early lethality of 45,XO embryos we have isolated HESCs that have spontaneously lost one of their sex chromosomes. To examine the possibility that imprinted genes on the X chromosome play a role in the phenotype of XO embryos, we have identified genes that were no longer expressed in the mutant cells. None of these genes showed a monoallelic expression in XX cells, implying that imprinting is not playing a major role in the phenotype of XO embryos. To suggest an explanation for the embryonic lethality caused by monosomy X, we have differentiated the XO HESCs in vitro an in vivo. DNA microarray analysis of the differentiated cells enabled us to compare the expression of tissue specific genes in XO and XX cells. The tissue that showed the most significant differences between the clones was the placenta. Many placental genes are expressed at much higher levels in XX cells in compare to XO cells. Thus, we suggest that abnormal placental differentiation as a result of haploinsufficiency of X-linked pseudoautosomal genes causes the early lethality in XO human embryos

Reactive stroma and trastuzumab resistance in HER2-positive early breast cancer

We investigated the value of reactive stroma as a predictor for trastuzumab resistance in patients with early HER2-positive breast cancer receiving adjuvant therapy. The pathological reactive stroma and the mRNA gene signatures that reflect reactive stroma in 209 HER2-positive breast cancer samples from the FinHer adjuvant trial were evaluated. Levels of stromal gene signatures were determined as a continuous parameter, and pathological reactive stromal findings were defined as stromal predominant breast cancer (SPBC; >= 50% stromal) and correlated with distant disease-free survival. Gene signatures associated with reactive stroma in HER2-positive early breast cancer (N = 209) were significantly associated with trastuzumab resistance in estrogen receptor (ER)-negative tumors (hazard ratio [HR] = 1.27 p interaction = 0.014 [DCN], HR = 1.58, p interaction = 0.027 [PLAU], HR = 1.71, p interaction = 0.019 [HER2STROMA, novel HER2 stromal signature]), but not in ER-positive tumors (HR = 0.73 p interaction = 0.47 [DCN], HR = 0.71, p interaction = 0.73 [PLAU], HR = 0.84; p interaction = 0.36 [HER2STROMA]). Pathological evaluation of HER2-positive/ER-negative tumors suggested an association between SPBC and trastuzumab resistance. Reactive stroma did not correlate with tumor-infiltrating lymphocytes (TILs), and the expected benefit from trastuzumab in patients with high levels of TILs was pronounced only in tumors with low stromal reactivity (SPBCPeer reviewe

So pretty! The neural correlates of self-other vs familiar-other attractiveness comparisons

Previous research has demonstrated that comparing two persons activates a frontoparietal network associated with numbers and nonsocial magnitudes. However, it is unclear whether this network is also recruited by comparisons involving the self. Self-reflection engages self-serving motivations (e.g., the maintenance of a positive self-image) and is associated with specific brain structures, such as the medial prefrontal cortex (MPFC), the anterior insula (AI) and the anterior cingulate cortex (ACC). Self-other comparisons may thus rely on distinct neural activity. To clarify this question, we used fMRI and asked female participants to compare their own attractiveness (or the attractiveness of a familiar woman) to pictures of unknown women. Participants were slower for comparisons with targets whose attractiveness was similar to their own (or their familiar other). Yet although this behavioral result resembles the distance effect reported for nonsocial magnitudes, at the brain level, it was linked to the activity of the AI, the ACC and the MPFC. The effect of distance in these regions was stronger for self-other than familiar-other comparisons. We interpret these results in relation to previous literature in social psychology and social neuroscience

A Novel SALL4/OCT4 Transcriptional Feedback Network for Pluripotency of Embryonic Stem Cells

Background: SALL4 is a member of the SALL gene family that encodes a group of putative developmental transcription factors. Murine Sall4 plays a critical role in maintaining embryonic stem cell (ES cell) pluripotency and self-renewal. We have shown that Sall4 activates Oct4 and is a master regulator in murine ES cells. Other SALL gene members, especially Sall1 and Sall3 are expressed in both murine and human ES cells, and deletions of these two genes in mice lead to perinatal death due to developmental defects. To date, little is known about the molecular mechanisms controlling the regulation of expressions of SALL4 or other SALL gene family members. Methodology/Principal Findings: This report describes a novel SALL4/OCT4 regulator feedback loop in ES cells in balancing the proper expression dosage of SALL4 and OCT4 for the maintenance of ESC stem cell properties. While we have observed that a positive feedback relationship is present between SALL4 and OCT4, the strong self-repression of SALL4 seems to be the “break” for this loop. In addition, we have shown that SALL4 can repress the promoters of other SALL family members, such as SALL1 and SALL3, which competes with the activation of these two genes by OCT4. Conclusions/Significance: Our findings, when taken together, indicate that SALL4 is a master regulator that controls its own expression and the expression of OCT4. SALL4 and OCT4 work antagonistically to balance the expressions of other SALL gene family members. This novel SALL4/OCT4 transcription regulation feedback loop should provide more insight into the mechanism of governing the “stemness” of ES cells