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Masafumi Tetsuka and Misato Tanakadate

(PGE2) in cumulus cells ( 5 , 6 , 7 , 8 ). These hormones have been shown to play various roles in regulating the expression of many factors associated with oocyte maturation, fertilization and subsequent embryo development and cumulus expansion ( 8

Open access

M Axelstad, U Hass, M Scholze, S Christiansen, A Kortenkamp, and J Boberg

homeostasis is obtained, but during sexual development, exposure to certain chemicals can disturb this hormonal balance, and even short-term exposures can cause adverse and permanent changes to the reproductive system. The present study aimed at

Open access

Stavroula A Paschou, Nektaria Papadopoulou-Marketou, George P Chrousos, and Christina Kanaka-Gantenbein

) and located on chromosome 6. HLA complex polymorphic alleles are responsible for 40–50% of the genetic risk of T1DM development. The insulin gene (Ins-VNTR, IDDM 2) polymorphisms on chromosome 11 and the cytotoxic T lymphocyte-associated antigen-4 gene

Open access

Peter Wolf, Yvonne Winhofer, Martin Krššák, and Michael Krebs

). Furthermore, heart failure with preserved ejection fraction (HFpEF) has been accepted as an own condition, being linked to metabolic rather than atherosclerotic disturbances, further indicating the importance of considering metabolic changes in the development

Open access

Ningning Gong, Cuixia Gao, Xuedi Chen, Yu Wang, and Limin Tian

atherosclerosis (AS) was reported in a large population-based study ( 2 , 3 ). Multiple lines of evidence have shown that adipokines ( 4 ), endothelial dysfunction ( 5 ) and dyslipidemia ( 6 ) play a central role in the development of AS, but the relationship

Open access

Ling-Jun Li, Izzuddin M Aris, Lin Lin Su, Yap Seng Chong, Tien Yin Wong, Kok Hian Tan, and Jie Jin Wang

resistance) during pregnancy ( 4 , 5 ). After pregnancy, GDM mothers are susceptible to progressive worsening in chronic β-cell defects, which is believed to mediate the development of recurrent GDM in subsequent pregnancy and postpartum type 2 diabetes (T2D

Open access

Charlotte Höybye, Laia Faseh, Christos Himonakos, Tomasz Pielak, and Jesper Eugen-Olsen

). Elevated levels of suPAR have been associated with poor clinical outcomes of a number of infectious diseases and cancers ( 17 , 18 , 19 , 20 , 21 , 22 ). Furthermore, suPAR has also been shown to be prognostic for development of cancer, CVD and type 2

Open access

Robert A Hart, Robin C Dobos, Linda L Agnew, Neil A Smart, and James R McFarlane

lungs ( 19 ) leptin has been shown to regulate maturation and development. Leptin is also involved in the regulation of immune function ( 20 ) and may act to regulate appetite from the lumen of the digestive tract via the afferent vagus nerve ( 21 , 22

Open access

Chunliang Yang, Junyi Li, Fei Sun, Haifeng Zhou, Jia Yang, and Chao Yang

range. Genetic polymorphisms in 3′-UTR region of SGK1 are associated with the insulin secretion capacity and the risk of T2D development, suggesting a regulatory role of SGK1 in human β-cell function ( 25 ). Even though the mRNA transcripts of the human

Open access

Tingting Xia, Hongru Sun, Hao Huang, Haoran Bi, Rui Pu, Lei Zhang, Yuanyuan Zhang, Ying Liu, Jing Xu, Justina Ucheojor Onwuka, Yupeng Liu, Binbin Cui, and Yashuang Zhao

accumulating evidence suggests that sex hormones are relevant to its development ( 3 ). There is an observational phenomenon and clinical evidence suggesting that men tend to have a much higher risk of CRC than women of the same age ( 4 ). As one of the most