A new lectin was purified from larvae of the fly, Musca domestica L. (Diptera: Muscidae) (MLL-2, 38 kDa) using affinity chromatography and HPLC. Anti-tumor activity of MLL-2 was demonstrated by its inhibition of proliferation of human breast cancer (MCF-7) cells in a time-and dose-dependent manner. The results of acridine orange staining indicated that MLL-2 caused apoptosis in MCF-7 cells. DNA fragmentation in MCF-7 cells has been detected by TUNEL. Flow cytometric analysis also demonstrated that MLL-2 caused dose-dependent apoptosis of MCF-7 cells through cell arrest at G2/M phase. The MLL-2 induced a sustained increase in concentration of intracellular free calcium. Western blot revealed that MLL-2 induced apoptosis in MCF-7 cells was associated with typical apoptosis proteins in the mitochondrial pathway. In addition, the caspase-3 activity in MCF-7 cells treated with MLL-2 for 48 hours was significantly increased compared to controls (407.4 ± 3.0 vs. 1749.2 ± 6.0, P <0.01). Since MLL-2 induced apoptosis in MCF-7cells the mitochondrial pathway may be the main pathway of antitumor activity.

Mechanisms underlying ovarian cancer initiation and progression are unclear. Herein, we report that the Yes-associated protein (YAP), a major effector of the Hippo tumor suppressor pathway, interacts with ERBB signaling pathways to regulate the initiation and progression of ovarian cancer. Immunohistochemistry studies indicate that YAP expression is associated with poor clinical outcomes in patients. Overexpression or constitutive activation of YAP leads to transformation and tumorigenesis in human ovarian surface epithelial cells, and promotes growth of cancer cells in vivo and in vitro. YAP induces the expression of epidermal growth factor (EGF) receptors (EGFR, ERBB3) and production of EGF-like ligands (HBEGF, NRG1 and NRG2). HBEGF or NRG1, in turn, activates YAP and stimulates cancer cell growth. Knockdown of ERBB3 or HBEGF eliminates YAP effects on cell growth and transformation, whereas knockdown of YAP abrogates NRG1- and HBEGF-stimulated cell proliferation. Collectively, our study demonstrates the existence of HBEGF & NRGs/ERBBs/YAP/HBEGF & NRGs autocrine loop that controls ovarian cell tumorigenesis and cancer progression.

Sigma-1 receptor (σ1R) has been reported to be decreased in nigrostriatal motor system of Parkinson's disease patients. Using heterozygous and homozygous σ1R knockout (σ1R+/- and σ1R-/-) mice, we investigated the influence of σ1R deficiency on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-impaired nigrostriatal motor system. The injection of MPTP for 5 weeks in wild-type mice (MPTP-WT mice), but not in σ1R+/- or σ1R-/- mice (MPTP-σ1R+/- or MPTP-σ1R-/- mice), caused motor deficits and ~40% death of dopaminergic neurons in substantia nigra pars compacta with an elevation of N-methyl-d-aspartate receptor (NMDAr) NR2B phosphorylation. The σ1R antagonist NE100 or the NR2B inhibitor Ro25-6981 could alleviate the motor deficits and the death of dopaminergic neurons in MPTP-WT mice. By contrast, MPTP-σ1R+/- mice treated with the σ1R agonist PRE084 or MPTP-σ1R-/- mice treated with the NMDAr agonist NMDA appeared to have similar motor deficits and loss of dopaminergic neurons as MPTP-WT mice. The pharmacological or genetic inactivation of σ1R suppressed the expression of dopamine transporter (DAT) in substantia nigra, which was corrected by NMDA. The activation of σ1R by PRE084 enhanced the DAT expression in WT mice or σ1R+/- mice. By contrast, the level of vesicular monoamine transporter 2 (VMAT2) in σ1R+/- mice or σ1R-/- mice had no difference from WT mice. Interestingly, MPTP-WT mice showed the reduction in the levels of DAT and VMAT2, but MPTP-σ1R-/- mice did not. The inactivation of σ1R by NE100 could prevent the reduction of VMAT2 in MPTP-WT mice. In addition, the activation of microglia cells in substantia nigra was equally enhanced in MPTP-WT mice and MPTP-σ1R-/- mice. The number of activated astrocytes in MPTP-σ1R-/- mice was less than that in MPTP-WT mice. The findings indicate that the σ1R deficiency through suppressing NMDAr function and DAT expression can reduce MPTP-induced death of dopaminergic neurons and parkinsonism.

Decreased levels of soluble ubiquitin carboxy-terminal hydrolase L1 (UCHL1) have been reported in the brains of sporadic Alzheimer's disease (AD) patients, and the introduction of UCHL1 rescued the synaptic and cognitive function of AD model mice. Obviously, a reduction in the levels of UCHL1 may play a role in the pathogenesis of AD. However, the mechanisms underlying the regulation of UCHL1 levels in AD have not been fully elucidated. MicroRNAs (miRs) have been shown to participate in the process of AD. In our study, we discovered that microRNA-922 decreased the levels of UCHL1. Neurofibrillary tangles (NFTs) mainly consisting of the hyperphosphorylated microtubule-associated protein tau are the defining pathological features of AD. In the present study, we found the levels of UCHL1 affected the levels of phosphorylated tau: the phosphorylated tau levels increased after knockdown of UCHL1 expression, and the phosphorylated tau levels decreased when UCHL1 was overexpressed. Furthermore, overexpression of microRNA-922 increased the phosphorylated tau levels. In conclusion, miR-922 increasing the levels of phosphorylated tau by regulating UCHL1 levels contributed to the pathogenesis of AD. Our study partly explained one of the mechanisms underlying the downregulation of UCHL1 levels in AD patients and could enrich the content of tau pathology in the pathogenesis of AD.

Acute myeloid leukemia (AML) is recognized as a complex disease of hematopoietic stem cell disorders, but its pathogenesis mechanisms, diagnosis, and treatment remain unclear. General histone deacetylase (HDAC) inhibitors have been used in blood cancers including AML, but the lack of gene specificity greatly limits their anti-cancer effects and clinical applications. Here, we found that HDAC1 expression was negatively correlated with that of Krüppel-like factor 4 (Klf4) and that AML patients with lower HDAC1 level had better prognosis. Further, knockdown of HDAC1 in leukemia cells K562, HL-60, and U937 significantly increased Klf4 expression and inhibited cell cycle progression and cell proliferation, similar results were found for HDAC inhibitors (VPA and mocetinostat). Moreover, overexpression or knockdown of Klf4 could markedly block the effects of HDAC1 overexpression or knockdown on leukemia cells in vitro and in vivo, respectively. Mechanistic analyses demonstrated that HDAC1 and Klf4 competitively bound to the promoter region of Klf4 and oppositely regulated Klf4 expression in myeloid leukemia. We identified HDAC1 as a potential specific target for repressing cell proliferation and inducing cell cycle arrest through interplay and modulation of Klf4 expression, suggests that HDAC1 and Klf4 are potential new molecular markers and targets for clinical diagnosis, prognosis, and treatment of myeloid leukemia.

Whole brain volume (WBV) estimates in patients with multiple sclerosis (MS) correlate more robustly with clinical disability than traditional, lesion-based metrics. Numerous algorithms to measure WBV have been developed over the past two decades. We compare Structural Image Evaluation using Normalisation of Atrophy-Cross-sectional (SIENAX) to NeuroQuant and MSmetrix, for assessment of cross-sectional WBV in patients with MS.

Apoptosis has a critical role in both physiological and pathological processes, and therefore probes that enable direct and fast visualization for apoptosis in vitro and in vivo have great significance for evaluation of therapeutic effects, disease monitoring and drug screening. We report here a novel apoptotic marker heat shock protein 60 (HSP60)-based apoptosis imaging probe, P17. In this study, we show that P17 can label multiple drug-induced apoptotic cells in vitro, and the difference in binding intensities between apoptotic and viable cells by fluorescent P17 is more than 10-fold in six cell lines measured by flow cytometry and proportional to the apoptotic level of the cells. We further visualized the apoptosis in the subcutaneous tumor of mice by vein injection of P17 using in vivo fluorescent imaging. P17 was identified to bind specifically to HSP60 accumulated in apoptotic cells by pull-down experiments and mass spectrometry. Furthermore, the P17 binding was correlated with the apoptotic feature of phosphatidylserine (PS) exposure and caspase-3 activation. We also clarify that P17 labels the cells in late stage apoptosis by double staining with different stage markers, unveiling that HSP60 may be involved with late stage of apoptosis. Overall, this study has demonstrated that P17 is a novel apoptosis probe targeting HSP60 and promising for the detection of apoptosis in vitro and in vivo.

CD44, a transmembrane glycoprotein expressed in a variety of cells and tissues, has been implicated in tumour metastasis. But the molecular mechanisms of CD44-mediated tumour cell metastasis remain to be elucidated.

Most genetic variants identified for type 2 diabetes have been discovered in European populations. We performed genome-wide association studies (GWAS) in a Chinese population with the aim of identifying novel variants for type 2 diabetes in Asians.

Abnormal gene regulation as a consequence of flawed epigenetic mechanisms may be central to the initiation and persistence of many human diseases. However, the association of epigenetic dysfunction with disease and the development of therapeutic agents for treatment are slow. Developing new methodologies used to visualize chromatin-modifying enzymes and their function in the human brain would be valuable for the diagnosis of brain disorders and drug discovery. We provide an overview of current invasive and noninvasive techniques for measuring expression and functions of chromatin-modifying enzymes in the brain, emphasizing tools applicable to histone deacetylase (HDAC) enzymes as a leading example. The majority of current techniques are invasive and difficult to translate to what is happening within a human brain in vivo. However, recent progress in molecular imaging provides new, noninvasive ways to visualize epigenetics in the human brain. Neuroimaging tool development presents a unique set of challenges in order to identify and validate CNS radiotracers for HDACs and other histone-modifying enzymes. We summarize advances in the effort to image HDACs and HDAC inhibitory effects in the brain using positron emission tomography (PET) and highlight generalizable techniques that can be adapted to investigate other specific components of epigenetic machinery. Translational tools like neuroimaging by PET and magnetic resonance imaging provide the best way to link our current understanding of epigenetic changes with in vivo function in normal and diseased brains. These tools will be a critical addition to ex vivo methods to evaluate - and intervene - in CNS dysfunction.

The paper presents studies of Bose-Einstein Correlations (BEC) for pairs of like-sign charged particles measured in the kinematic range [Formula: see text] 100 MeV and [Formula: see text] 2.5 in proton collisions at centre-of-mass energies of 0.9 and 7 TeV with the ATLAS detector at the CERN Large Hadron Collider. The integrated luminosities are approximately 7 [Formula: see text]b[Formula: see text], 190 [Formula: see text]b[Formula: see text] and 12.4 nb[Formula: see text] for 0.9 TeV, 7 TeV minimum-bias and 7 TeV high-multiplicity data samples, respectively. The multiplicity dependence of the BEC parameters characterizing the correlation strength and the correlation source size are investigated for charged-particle multiplicities of up to 240. A saturation effect in the multiplicity dependence of the correlation source size parameter is observed using the high-multiplicity 7 TeV data sample. The dependence of the BEC parameters on the average transverse momentum of the particle pair is also investigated.

New-onset diabetes after liver transplantation (NODALT) is a frequent complication with an unfavorable outcome. We previously demonstrated a crucial link between donor graft genetics and the risk of NODALT. We selected 15 matched pairs of NODALT and non-NODALT liver recipients using propensity score matching analysis. The donor liver tissues were tested for the expression of 10 microRNAs (miRNAs) regulating human hepatic glucose homeostasis. The biological functions of potential target genes were predicted using gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Both miR-103 and miR-181a were significantly highly expressed in the NODALT group as compared to the non-NODALT group. The predicted target genes (e.g. Irs2, Pik3r1, Akt2, and Gsk3b) were involved in glucose import and the insulin signaling pathway. We also observed dysregulation of miRNAs (e.g. let-7, miR-26b, miR-145, and miR-183) in cultured human hepatocytes treated with tacrolimus or high glucose, the two independent risk factors of NODALT identified in this cohort. The hepatic miRNA profiles altered by tacrolimus or hyperglycemia were associated with insulin resistance and glucose homeostatic imbalance as revealed by enrichment analysis. The disease susceptibility miRNA expressive pattern could be imported directly from the donor and consolidated by the transplant factors.

Infectious hematopoietic necrosis virus is a highly contagious disease of juvenile salmonid species. From the IHNV HLJ-09 isolated in China, two recombinant viruses were generated by reverse genetics using the RNA polymerase II transcription system. The recombinant viruses were confirmed by RT-PCR, indirect immunofluorescence assay and electron microscopy. They were referred to as rIHNV HLJ-09 and rIHNV-EGFP. rIHNV HLJ-09 and rIHNV-EGFP could stably replicate in EPC cell lines and had the same cellular tropism as wtIHNV HLJ-09. But the titer of rIHNV-EGFP was significantly lower than rIHNV HLJ-09 and wtIHNV HLJ-09. rIHNV-EGFP strain could express EGFP stably at least in 20 passages, and the fluorescence could be observed clearly. To assess the virulence and pathogenicity of the recombinant viruses in vivo, juvenile rainbow trout were challenged by intraperitoneal injection with 20μl of rIHNV HLJ-09, rIHNV-EGFP or wtIHNV HLJ-09 (1×10(6)pfuml(-1)). Fish challenged with rIHNV HLJ-09 and wtIHNV HLJ-09 exhibited clinical signs typical of IHN disease and both produced 90% cumulative percent mortality, whlie rIHNV-EGFP produced only 5%. Pathological sectioning results showed that the tissues (liver, kidney, heart muscle, back muscle) of the fish infected with rIHNV HLJ-09 exhibited pathological changes, with the exception of cerebral neurons and the cheek. However, no lesions of liver, kidney, heart, muscle, brain in rainbow trout of rIHNV-EGFP or the control group were observed. Indirect ELISA results showed that a high level of serum antibody was detected in the experimental fish challenged with rIHNV HLJ-09, just as the same as wtIHNV HLJ-09, while a lower titer was detecred in the fish infected with rIHNV-EGFP. This indicated that the recombinant viruses could induce humoral immune response in the experimental fish. The recombinant viruses had unique genetic tags and could be used for genetic engineering, laying new ground for further investigation of IHNV pathopoiesis molecular mechanism, host tropism and the development of novel vaccines against IHN.

Radiotherapy is the standard therapy for nasopharyngeal carcinoma (NPC); however, radioresistance can hinder successful treatment. Here we report that microRNA (miR)-24 acts as a tumor suppressor and radiosensitizer in NPC cells and xenografts by targeting Jab1/CSN5. Although accumulating evidence has shown that Jab1/CSN5 functions as an oncoprotein in human cancers, its regulation through miRs has not been described. In this study, we found that Jab1/CSN5 functioned in a manner opposite to that of miR-24 in NPC tumorigenesis and radioresistance. We demonstrated that miR-24 inhibits Jab1/CSN5 translation via direct binding to its 3' untranslated region (3'UTR) and 5'UTR, leading to tumor growth inhibition, and sensitizes NPC tumors to radiation in vivo. Furthermore, silencing Jab1/CSN5 phenocopied the function of miR-24 in NPC cells after ionizing radiation treatment, resulting in increased apoptosis. Finally, we analyzed 50 paired samples of primary and matched recurrent NPC tissues from 25 NPC patients and subjected them to high-throughput genomic quantitative nuclease protection assay for quantifying simultaneously miR and mRNA levels. Our results showed that miR-24 levels were significantly decreased in recurrent NPC and that levels of Jab1/CSN5, as its target, were higher than those in primary NPC. Together, our findings indicate that miR-24 inhibits NPC tumor growth and increases NPC radiosensitivity by directly regulating Jab1/CSN5 and that both miR-24 and Jab1/CSN5 can serve as prognostic markers for NPC recurrence; this, in turn, may provide a promising therapeutic strategy for reversing NPC radioresistance.

The magnitude of spike-responses of neurons in the mammalian visual system to sine-wave luminance-contrast-modulated drifting gratings is modulated by the temporal frequency of the stimulation. However, there are serious problems with consistency and reliability of the traditionally used methods of assessment of strength of such modulation. Here we propose an intuitive and simple tool for assessment of the strength of modulations in the form of standardized F1 index, zF1. We define zF1 as the ratio of the difference between the F1 (component of amplitude spectrum of the spike-response at temporal frequency of stimulation) and the mean value of spectrum amplitudes to standard deviation along all frequencies in the spectrum. In order to assess the validity of this measure, we have: (1) examined behavior of zF1 using spike-responses to optimized drifting gratings of single neurons recorded from four 'visual' structures (area V1 of primary visual cortex, superior colliculus, suprageniculate nucleus and caudate nucleus) in the brain of commonly used visual mammal - domestic cat; (2) compared the behavior of zF1 with that of classical statistics commonly employed in the analysis of steady-state responses; (3) tested the zF1 index on simulated spike-trains generated with threshold-linear model. Our analyses indicate that zF1 is resistant to distortions due to the low spike count in responses and therefore can be particularly useful in the case of recordings from neurons with low firing rates and/or low net mean responses. While most V1 and a half of caudate neurons exhibit high zF1 indices, the majorities of collicular and suprageniculate neurons exhibit low zF1 indices. We conclude that despite the general shortcomings of measuring strength of modulation inherent in the linear system approach, zF1 can serve as a sensitive and easy to interpret tool for detection of modulation and assessment of its strength in responses of visual neurons.

Using the PorcineSNP80 BeadChip, we performed a genome-wide association study for seven reproductive traits, including total number born, number born alive, litter birth weight, average birth weight, gestation length, age at first service and age at first farrowing, in a population of 1207 Large White pigs. In total, we detected 12 genome-wide significant and 41 suggestive significant SNPs associated with six reproductive traits. The proportion of phenotypic variance explained by all significant SNPs for each trait ranged from 4.46% (number born alive) to 11.49% (gestation length). Among them, 29 significant SNPs were located within known QTL regions for swine reproductive traits, such as corpus luteum number, stillborn number and litter size, of which one QTL region associated with litter size contained the ALGA0098819 SNP for total number born. Subsequently, we found that 376 functional genes contained or were near these significant SNPs. Of these, 14 genes-BHLHA15, OCM2, IL1B2, GCK, SMAD2, HABP2, PAQR5, GRB10, PRELID2, DMKN, GPI, GPIHBP1, ADCY2 and ACVR2B-were considered important candidates for swine reproductive traits based on their critical roles in embryonic development, energy metabolism and growth development. Our findings contribute to the understanding of the genetic mechanisms for reproductive traits and could have a positive effect on pig breeding programs.

The seasonality of individual influenza subtypes/lineages and the association of influenza epidemics with meteorological factors in the tropics/subtropics have not been well understood. The impact of the 2009 H1N1 pandemic on the prevalence of seasonal influenza virus remains to be explored. Using wavelet analysis, the periodicities of A/H3N2, seasonal A/H1N1, A/H1N1pdm09, Victoria and Yamagata were identified, respectively, in Panzhihua during 2006-2015. As a subtropical city in southwestern China, Panzhihua is the first industrial city in the upper reaches of the Yangtze River. The relationship between influenza epidemics and local climatic variables was examined based on regression models. The temporal distribution of influenza subtypes/lineages during the pre-pandemic (2006-2009), pandemic (2009) and post-pandemic (2010-2015) years was described and compared. A total of 6892 respiratory specimens were collected and 737 influenza viruses were isolated. A/H3N2 showed an annual cycle with a peak in summer-autumn, while A/H1N1pdm09, Victoria and Yamagata exhibited an annual cycle with a peak in winter-spring. Regression analyses demonstrated that relative humidity was positively associated with A/H3N2 activity while negatively associated with Victoria activity. Higher prevalence of A/H1N1pdm09 and Yamagata was driven by lower absolute humidity. The role of weather conditions in regulating influenza epidemics could be complicated since the diverse viral transmission modes and mechanism. Differences in seasonality and different associations with meteorological factors by influenza subtypes/lineages should be considered in epidemiological studies in the tropics/subtropics. The development of subtype- and lineage-specific prevention and control measures is of significant importance.

Programmed cell death 4 (Pdcd4), a tumor invasion suppressor, is frequently downregulated in colorectal cancer and other cancers. In this study, we find that loss of Pdcd4 increases the activity of mammalian target of rapamycin complex 2 (mTORC2) and thereby upregulates Snail expression. Examining the components of mTORC2 showed that Pdcd4 knockdown increased the protein but not mRNA level of stress-activated-protein kinase interacting protein 1 (Sin1), which resulted from enhanced Sin1 translation. To understand how Pdcd4 regulates Sin1 translation, the SIN1 5' untranslated region (5'UTR) was fused with luciferase reporter and named as 5'Sin1-Luc. Pdcd4 knockdown/knockout significantly increased the translation of 5'Sin1-Luc but not the control luciferase without the SIN1 5'UTR, suggesting that Sin1 5'UTR is necessary for Pdcd4 to inhibit Sin1 translation. Ectopic expression of wild-type Pdcd4 and Pdcd4(157-469), a deletion mutant that binds to translation initiation factor 4A (eIF4A), sufficiently inhibited Sin1 translation, and thus suppressed mTORC2 kinase activity and invasion in colon tumor cells. By contrast, Pdcd4(157-469)(D253A,D418A), a mutant that does not bind to eIF4A, failed to inhibit Sin1 translation, and consequently failed to repress mTORC2 activity and invasion. In addition, directly inhibiting eIF4A with silvestrol significantly suppressed Sin1 translation and attenuated invasion. These results indicate that Pdcd4-inhibited Sin1 translation is through suppressing eIF4A, and functionally important for suppression of mTORC2 activity and invasion. Moreover, in colorectal cancer tissues, the Sin1 protein but not mRNA was significantly upregulated while Pdcd4 protein was downregulated, suggesting that loss of Pdcd4 might correlate with Sin1 protein level but not mRNA level in colorectal cancer patients. Taken together, our work reveals a novel mechanism by which Pdcd4 inhibits Sin1 translation to attenuatemTORC2 activity and thereby suppresses invasion.

Tongue cancer resistance-related protein 1 (TCRP1) gene was first cloned from the multidrug resistance tongue cancer cell (Tca8113/pingyangmycin) in our lab. Our precious studies demonstrated that TCRP1 was involving in chemotherapy and radiotherapy resistance of tongue cancer cells, lung cancer cells and ovarian cancer cells. In this study, we showed that TCRP1 overexpression promotes cell transformation and tumorigenesis through hyperphosphorylation of the oncogenic kinase 3-phosphoinositide-dependent protein kinase-1 (PDK1) and AKT1, whereas inhibition of PDK1 by OSU-03012 or PDK1 small interfering RNA reversed TCRP1-mediated cell transformation. Importantly, TCRP1 was able to directly interact with PDK1, and 93-107 amino-acid and 109-124 amino-acid sites of TCRP1 were the common binding domain of PDK1. Moreover, in line with its oncogenic activity, we found that TCRP1 is often overexpressed in human in lung cancer, glioma, ovarian cancer, thyroid cancer, nasopharyngeal carcinoma, pancreatic cancer, stomach cancer and tongue carcinoma tissues. Spearman correlation analysis showed that the expression of TCRP1 has a positive correlation with p-PDK1, as well as p-AKT1 in lung cancer and gliomas tissues. Thus, TCRP1 may be a candidate as human oncoprotein that promotes cancer development by activation of PDK1/AKT1 signaling.

This study was conducted to determine the effect of feeding frequency on growth performance, carcass traits, and apparent nutrient digestibility in geese from 28 to 70 D of age. In experiment 1, a total of 240 geese were distributed in a completely randomized design into 4 treatments and 6 replicates of 10 birds each. The treatments were free access to the feeder (ad libitum) and access to the feeder 3, 4, and 5 times daily. Geese fed 3 times daily had a lower (P < 0.05) BW, ADG, and ADFI and a higher (P = 0.064) feed conversion ratio (FCR) from 28 to 41 D of age compared with the other groups. Geese fed 4 times daily had a higher (P < 0.05) ADG and ADFI and a lower (P < 0.05) FCR from 42 to 55 D of age compared with ad libitum fed geese. Geese fed 3 times daily had a higher (P < 0.05) ADG from 56 to 69 D of age than geese fed ad libitum and 4 times daily. No differences (P > 0.05) in BW, ADFI, ADG, and FCR were observed between ad libitum and feeding frequency groups from 28 to 69 D of age. Carcass traits and gastrointestinal development were not affected (P > 0.05) by feeding frequency. In experiment 2, the apparent nutrient digestibility in geese from 71 to 77 D of age fed using different feeding frequencies was determined using the total fecal collection method. Feeding frequency did not affect (P > 0.05) the apparent digestibility of DM, CP, crude ash, calcium, phosphorous, or ether extract in geese. Our study demonstrates for the first time that compensatory growth can be gained by enhancing feed intake when a lower feeding frequency is imposed on geese. Both ad libitum feeding and fixed feeding frequency for 3 to 5 times daily are suitable for geese from 28 to 70 D of age to achieve optimum production.