Maximum number of total born piglets in a parity and individual ranges in litter size expressed as specific characteristics of sows

( Gertraude Freyer ) 한국축산학회(구 한국동물자원과학회) 2018 한국축산학회지 Vol.60 No.5

Background: The objective of this study was to underline that litter size as a key trait of sows needs new parameters to be evaluated and to target an individual optimum. Large individual variation in litter size affects both production and piglet’s survival and health negatively. Therefore, two new traits were suggested and analyzed. Two data sets on 5509 purebred German Landrace sows and 3926 Large White and crossing sows including at least two parental generations and at least five parities were subjected to variance components analysis. Results: The new traits for evaluating litter size were derived from the individual numbers of total born piglets (TBP) per parity: In most cases, sows reach their maximum litter size in their fourth parity. Therefore, data from at least five parities were included. The first observable maximum and minimum of TBP, and the individual variation expressed by the range were targeted. Maximum of TBP being an observable trait in pig breeding and management yielded clearly higher heritability estimates (h²~ 0.3) than those estimates predominantly reported so far. Maximum TBP gets closer to the genetic capacity for litter size than other litter traits. Minimum of TBP is positively correlated with the range of TBP (r_p = 0.48, r_g > 0.6). The correlation between maximum of TBP and its individually reached frequency was negative in both data sets (r_p = - 0.28 and - 0.22, respectively). Estimated heritability coefficients for the range of TBP comprised a span of h² = 0.06 to 0.10. Conclusion: An optimum both for maximum and range of total born piglets in selecting sows is a way contributing to homogenous litters in order to improving the animal-related conditions both for piglets’ welfare and economic management in pig.

[S12-1] The Epidemiologic Evidence for a Role of Soy Foods in Reducing Breast and Prostate Cancer Risk

Gertraud Maskarinec 한국식품영양과학회 2007 한국식품영양과학회 학술대회발표집 Vol.2007 No.10

Bioimpedence to Assess Breast Density as a Risk Factor for Breast Cancer in Adult Women and Adolescent Girls

Maskarinec, Gertraud,Morimoto, Yukiko,Laguana, Michelle B,Novotny, Rachel,Guerrero, Rachael T Leon Asian Pacific Journal of Cancer Prevention 2016 Asian Pacific journal of cancer prevention Vol.17 No.1

Although high mammographic density is one of the strongest predictors of breast cancer risk, X-ray based mammography cannot be performed before the recommended screening age, especially not in adolescents and young women. Therefore, new techniques for breast density measurement are of interest. In this pilot study in Guam and Hawaii, we evaluated a radiation-free, bioimpedance device called Electrical Breast Densitometer$^{TM}$ (EBD; senoSENSE Medical Systems, Inc., Ontario, Canada) for measuring breast density in 95 women aged 31-82 years and 41 girls aged 8-18 years. Percent density (PD) was estimated in the women's most recent mammogram using a computer-assisted method. Correlation coefficients and linear regression were applied for statistical analysis. In adult women, mean EBD and PD values of the left and right breasts were $230{\pm}52$ and $226{\pm}50{\Omega}$ and $23.7{\pm}15.1$ and $24.2{\pm}15.2%$, respectively. The EBD measurements were inversely correlated with PD ($r_{Spearman}=-0.52$, p<0.0001); the correlation was stronger in Caucasians ($r_{Spearman}=-0.70$, p<0.0001) than Asians ($r_{Spearman}=-0.54$, p<0.01) and Native Hawaiian/Chamorro/Pacific Islanders ($r_{Spearman}=-0.34$, p=0.06). Using 4 categories of PD (<10, 10-25, 26-50, 51-75%), the respective mean EBD values were $256{\pm}32$, $249{\pm}41$, $202{\pm}46$, and $178{\pm}43{\Omega}$ (p<0.0001). In girls, the mean EBD values in the left and right breast were $148{\pm}40$ and $155{\pm}54{\Omega}$; EBD values decreased from Tanner stages 1 to 4 ($204{\pm}14$, $154{\pm}79$, $136{\pm}43$, and $119{\pm}16{\Omega}$ for stages 1-4, respectively) but were higher at Tanner stage 5 ($165{\pm}30{\Omega}$). With further development, this bioimpedance method may allow for investigations of breast development among adolescent, as well as assessment of breast cancer risk early in life and in populations without access to mammography.

Prevalence and risk factors for carriage of multi-drug resistant Staphylococci in healthy cats and dogs

Paola Gandolfi-Decristophoris,Gertraud Regula,Orlando Petrini,Jakob Zinsstag,Esther Schelling 대한수의학회 2013 Journal of Veterinary Science Vol.14 No.4

We investigated the distribution of commensal staphylococcal species and determined the prevalence of multi-drug resistance in healthy cats and dogs. Risk factors associated with the carriage of multi-drug resistant strains were explored. Isolates from 256 dogs and 277 cats were identified at the species level using matrix-assisted laser desorption ionisation-time of flight mass spectrometry. The diversity of coagulase-negative Staphylococci (CNS) was high, with 22 species in dogs and 24 in cats. Multi-drug resistance was frequent (17%) and not always associated with the presence of the mecA gene. A stay in a veterinary clinic in the last year was associated with an increased risk of colonisation by multi-drug resistant Staphylococci (OR = 2.4, 95% CI: 1.1∼5.2, p value LRT = 0.04). When identifying efficient control strategies against antibiotic resistance, the presence of mechanisms other than methicillin resistance and the possible role of CNS in the spread of resistance determinants should be considered. We investigated the distribution of commensal staphylococcal species and determined the prevalence of multi-drug resistance in healthy cats and dogs. Risk factors associated with the carriage of multi-drug resistant strains were explored. Isolates from 256 dogs and 277 cats were identified at the species level using matrix-assisted laser desorption ionisation-time of flight mass spectrometry. The diversity of coagulase-negative Staphylococci (CNS) was high, with 22 species in dogs and 24 in cats. Multi-drug resistance was frequent (17%) and not always associated with the presence of the mecA gene. A stay in a veterinary clinic in the last year was associated with an increased risk of colonisation by multi-drug resistant Staphylococci (OR = 2.4, 95% CI: 1.1∼5.2, p value LRT = 0.04). When identifying efficient control strategies against antibiotic resistance, the presence of mechanisms other than methicillin resistance and the possible role of CNS in the spread of resistance determinants should be considered.

The gene encoding the hematopoietic stem cell regulator CCN3/NOV is under direct cytokine control through the transcription factors STAT5A/B.

Kimura, Akiko,Martin, Cyril,Robinson, Gertraud W,Simone, James M,Chen, Weiping,Wickre, Mark C,O'Shea, John J,Hennighausen, Lothar American Society for Biochemistry and Molecular Bi 2010 The Journal of biological chemistry Vol.285 No.43

<P>Cytokines control the biology of hematopoietic stem cells (HSCs) and progenitor cells in part through the transcription factors STAT5A/B. To investigate the target genes of STAT5A/B activated by cytokines in HSCs and progenitors, we performed microarray analyses using Lineage(-) Sca-1(+) c-Kit(+) (KSL) cells in the presence and absence of STAT5A/B. Stimulation with a mixture containing IL-3, IL-6, stem cell factor, thrombopoietin, and Flt3 ligand induced Ccn3/Nov mRNA over 100-fold in WT (control) but not Stat5a/b-null KSL cells. CCN3/NOV is a positive regulator of human HSC self-renewal and development of committed blood cells. Without stimulation, the Ccn3/Nov signal level was low in control KSL cells similar to Stat5a/b-null KSL cells. To determine which cytokine activates the Ccn3/Nov gene, we analyzed Lineage(-) c-Kit(+) (KL) and 32D cells using quantitative PCR and ChIP assays. Although stimulation with a mixture lacking IL-3 prevented the induction of Ccn3/Nov in control KL cells, IL-3 alone could induce Ccn3/Nov mRNA in control KL and 32D cells. ChIP assays using 32D cells revealed IL-3-induced binding of STAT5A/B to a γ-interferon-activated sequences site in the Ccn3/Nov gene promoter. This is the first report that Ccn3/Nov is directly induced by cytokines through STAT5A/B.</P>

Sequential activation of genetic programs in mouse mammary epithelium during pregnancy depends on STAT5A/B concentration

Yamaji, Daisuke,Kang, Keunsoo,Robinson, Gertraud W.,Hennighausen, Lothar Oxford University Press 2013 Nucleic acids research Vol.41 No.3

<P>The transcription factors Signal Transducer and Activator of Transcription (STAT) 5A/B mediate prolactin-induced mammary development during pregnancy. However, it is not clear how the different processes, expansion and maturation of alveolar precursor cells and the differential induction of milk protein genes are regulated on a molecular level. We have used mouse genetics and genome-wide analyses to determine how altering concentrations of STAT5A and STAT5B impacts mammary epithelial development during pregnancy and the regulation of target genes. The presence of only a single <I>Stat5a</I> or <I>Stat5b</I> allele was sufficient for the establishment of histologically undifferentiated alveolar units and two alleles permitted the execution of a differentiation program similar to that found with all four alleles. While one copy of <I>Stat5</I> induced limited expression of target genes, two copies activated a lactation-like gene signature. Using ChIP-seq analyses on intact tissue under physiological conditions, we found that highly expressed and regulated genes were bound by STAT5 in their promoter proximal regions, whereas upstream binding had minor biological consequences. Remarkably, 80% of the genes bound by STAT5 <I>in vivo </I>were not under STAT5 control. RNA polymerase II intensity was directly proportional to STAT5 concentration only on STAT5 regulated genes providing mechanistic insight by which STAT5 activates mammary specific genes.</P>

The transcription factors signal transducer and activator of transcription 5A (STAT5A) and STAT5B negatively regulate cell proliferation through the activation of cyclin‐dependent kinase inhibitor 2b (<i>Cdkn2b</i>) and <i>Cdkn1a</i> expression

Yu, Ji Hoon,Zhu, Bing‐,Mei,Wickre, Mark,Riedlinger, Gregory,Chen, Weiping,Hosui, Atsushi,Robinson, Gertraud W.,Hennighausen, Lothar Wiley Subscription Services, Inc., A Wiley Company 2010 Hepatology Vol.52 No.5

<P><B>Abstract</B></P><P>Although the cytokine‐inducible transcription factor signal transducer and activator of transcription 5 (STAT5) promotes proliferation of a wide range of cell types, there are cell‐specific and context‐specific cases in which loss of STAT5 results in enhanced cell proliferation. Here, we report that loss of STAT5 from mouse embryonic fibroblasts (MEFs) leads to enhanced proliferation, which was linked to reduced levels of the cell cycle inhibitors p15<SUP>INK4B</SUP> and p21<SUP>CIP1</SUP>. We further demonstrate that growth hormone, through the transcription factor STAT5, enhances expression of the <I>Cdkn2b</I> (cyclin‐dependent kinase inhibitor 2B) gene and that STAT5A binds to interferon‐gamma–activated sequence sites within the promoter. We recently demonstrated that ablation of STAT5 from liver results in hepatocellular carcinoma upon CCl<SUB>4</SUB> treatment. We now establish that STAT5, like in MEFs, activates expression of the <I>Cdkn2b</I> gene in liver tissue. Loss of STAT5 led to diminished p15<SUP>INK4B</SUP> and increased hepatocyte proliferation. <I>Conclusion:</I> This study for the first time demonstrates that cytokines, through STAT5, induce the expression of a key cell cycle inhibitor. These experiments therefore shed mechanistic light on the context‐specific role of STAT5 as tumor suppressor. (HEPATOLOGY 2010;52:1808‐1818)</P>