Introduction Congenital hypogonadotropic hypogonadism (CHH) is characterised by partial or complete lack of pubertal development, secondary to deficient gonadotropin-releasing hormone (GnRH)-induced gonadotropin secretion ( 1 ). Diagnosis is
Catarina I Gonçalves, José M Aragüés, Margarida Bastos, Luísa Barros, Nuno Vicente, Davide Carvalho, and Manuel C Lemos
Jana Ernst, Katharina Gert, Frank Bernhard Kraus, Ulrike Elisabeth Rolle-Kampczyk, Martin Wabitsch, Faramarz Dehghani, and Kristina Schaedlich
influence during early development (i.e. preconceptional up to 1000 days of postnatal life) can program the unborn/newborn for metabolic dysfunctions later in life. Apart from environmental factors maternal diseases such as overweight or excessive weight
Maria Stelmachowska-Banaś and Izabella Czajka-Oraniec
should not delay hormonal workup and treatment initiation, which mostly depend on clinical presentation and demonstration of hypopituitarism ( 6 , 50 ). On the other hand, pituitary MRI abnormalities can precede the development of pituitary deficiency
Iben Katinka Greiber, Casper P Hagen, Alexander Siegfried Busch, Mikkel Grunnet Mieritz, Lise Aksglæde, Katharina Main, Kristian Almstrup, and Anders Juul
assess the effect of genetic variation of AMH signaling ( AMH rs10407022 T>G and AMHR2 rs11170547 C>T) on circulating hormone levels in boys and girls during pubertal development. Our findings support recent GWAS results in young adults and expand
Kristin Ottarsdottir, Margareta Hellgren, David Bock, Anna G Nilsson, and Bledar Daka
-sectional studies have found an inverse association between levels of SHBG and insulin resistance in men ( 9 , 10 ) and women ( 11 , 12 ). Only few studies have investigated whether levels of SHBG can predict the development of insulin resistance, and there are no
Kjell Oberg, Eric Krenning, Anders Sundin, Lisa Bodei, Mark Kidd, Margot Tesselaar, Valentina Ambrosini, Richard P Baum, Matthew Kulke, Marianne Pavel, Jaroslaw Cwikla, Ignat Drozdov, Massimo Falconi, Nicola Fazio, Andrea Frilling, Robert Jensen, Klaus Koopmans, Tiny Korse, Dik Kwekkeboom, Helmut Maecke, Giovanni Paganelli, Ramon Salazar, Stefano Severi, Jonathan Strosberg, Vikas Prasad, Aldo Scarpa, Ashley Grossman, Annemeik Walenkamp, Mauro Cives, Irene Virgolini, Andreas Kjaer, and Irvin M Modlin
with reproducibility and accurate delineation of metastatic disease, particularly extra-liver disease. The development of new lesions is probably the most powerful indicator of disease progression. Functional imaging with somatostatin receptor
Xuan Luo, Tingting Zheng, Chaoming Mao, Xin Dong, Xiao Mou, Chengcheng Xu, Qingyan Lu, Baocui Liu, Shengjun Wang, and Yichuan Xiao
. Importantly, IL-1β was also highly expressed in the tissues of the HT patients, suggesting that there is an interaction between MRP14 and IL-1β in the development of HT. Notably, our results showed that IL-1β induced the expression of not only chemokines in
Juan Carlos Juárez-Cruz, Miriam Daniela Zuñiga-Eulogio, Monserrat Olea-Flores, Eduardo Castañeda-Saucedo, Miguel Ángel Mendoza-Catalán, Carlos Ortuño-Pineda, Ma Elena Moreno-Godínez, Sócrates Villegas-Comonfort, Teresita Padilla-Benavides, and Napoleón Navarro-Tito
, which further enhances the predisposition of developing breast tumors ( 4 ). Among these molecules, leptin is one of the most important adipokines involved in the development and progression of mammary tumors ( 5 ). Leptin is a hormone with a molecular
Fabian Eichelmann, Cornelia Weikert, Romina di Giuseppe, Ronald Biemann, Berend Isermann, Matthias B Schulze, Heiner Boeing, and Krasimira Aleksandrova
-scale prospective population-based studies exist to support or refute generated hypothesis on chemerin involvement in disease development. Important prerequisite for planning biomarker assessment in a prospective study is the assessment of whether single biomarker
Selina Mäkinen, Yen H Nguyen, Paulina Skrobuk, and Heikki A Koistinen
to ROS production ( 18 ), we next analysed if development of insulin resistance of glucose uptake is related to ROS. Human myotubes were exposed for 12 h to palmitate, oleate or their combination. Mitochondrial ROS production was significantly