br Experimental design materials and

Experimental design, materials and methods
Acknowledgements This work was supported by the Maurice Wilkins Centre for Molecular Biodiscovery and a Marsden Grant from the Royal Society of New Zealand. G.M.C. was supported by a James Cook Fellowship from the Royal Society of New Zealand. MP was supported by a University of Otago Doctoral Scholarship, the Webster Center for Infectious Diseases and the Otago School of Medical Sciences.
Data The data represents the genomic polymorphisms of Mycoplasma gallisepticum clones after infection and isolation from HD3 cells. Table 1 represent data obtained during acute (24h) infection. Table 2 represent data obtained during chronic (7 weeks) infection. In analysis were taken 10 different colonies of mycoplasma isolated from HD3 vesicular monoamine transporter after acute infection, 10 different colonies of mycoplasma isolated from HD3 cells after chronic infection and 12 different colonies of control laboratory strain.
Experimental design, materials and methods
Acknowledgements We are grateful to professor S. V. Razin (Institute of Gene Biology, Russian Academy of Sciences) for donating HD3 cells, professor M. A. Lagarkova for culturing the HD3 cell. The work was funded by Russian Science Foundation, Russia Grant 14-24-00159 (Systems research of minimal cell on a Mycoplasma gallisepticum model).
Experimental design, materials and methods
Data Congenital Adrenal Hyperplasia is an autosomal recessive disorder mainly caused by defects in 21-Hydroxylase gene (CYP21A2) which codes for 21-Hydroxylase enzyme [2]. Figs. 1–3 and Table 1 indicate ratio of patients (males and females) in classical (SW, SV) and non classical CAH and the associated level of 17-α-OHP which is the substrate of 21-Hydroxylase enzyme. The major disease-causing mutations in CYP21A2 (functional gene) are transferred from CYP21A1P (pseudogene) due to unequal crossing over during meiosis or apparent gene conversion events [3], macro or microconversion events [4]. Tables 1–5 elucidate the age of the CAH patients in the classical and nonclassical CAH, the primer sequences which were used for detection of the common mutations, polymorphisms and novel mutations in the CYP21A2 gene. The novel mutations were detected at the frequency of 3%–5% when large cohorts were investigated [5] (Table 6).
Experimental design
Acknowledgments We express our sincere gratitude to Science & Engineering Research Board (SERB), New Delhi, India for funding the project (Sanction number: SR/SO/HS/0045/2010) and Indian Council of Medical Research, New Delhi for ICMR-JRF and SRF (Reference number: 3/1/3/JRF-2011/HRD-3). We are also thankful to all the patients included in this study.
Data To examine the differences in the mitochondrial and inflammatory response gene expressions between GPER-knockout and intact cardiomyocytes, microarray data were loaded into GSEA 2.0.1 software using GSEA gene sets “MITOCHONDRION (including 314 genes)” and “HALLMARK_INFLAMMATORY_RESPONSE (including 193 genes)” [1,2]. The altered individual mitochondrial and inflammatory genes in GPER knockout versus intact cardiomyocytes from both sexes are presented in Tables 1–4.
Experimental design, materials and methods
Acknowledgments The GPER knockout mouse strain was generated with the help of the KOMP Repository (WWW.KOMP.org) and the Mouse Biology Program (www.mousebiology.org) at the University of California Davis. We appreciate the assistance of Ms. Lou Craddock at Wake Forest University Comprehensive Cancer Center Microarray facility in running the microarray. This work was funded by the National Institutes of Health, USA Grants AG-042758 (L.G.), AG-033727 (L.G.), and HL-051952 (C.M.F.).
Data The data presented in this paper provides additional physico-chemical information on tested fat-micelles with six liquid formulations of commercial pine-derived phytosterol (CPP) and bile salt effect on cholesterol micelles size with monoglyceride (MG) and oleic acid (OA). Table 1 shows micelle size and zeta potential of CPP mixture with fat micelles. Fig. 1 shows the bile salt effect on the size of cholesterol micelles with MG and OA.