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Pathophysiological mechanisms, subclinical abnormalities, and clinical manifestations of diabetic cardiomyopathy. AGEs, advanced glycation end-products; CMP, cardiomyopathy; EF, ejection fraction; HF, heart failure; LV, left ventricular; RAAS, renin-angiotensin-aldosterone system. *In patients with type-1 diabetes mellitus.

This is a sample power spectrum of the HRV signal from a subject breathing at an average rate of 7.5 breaths per minute (Fundamental Respiratory Frequency, FRF = 0.125 Hz). The method using HRV alone defines two fixed spectral regions for the low-frequency (LF) and high-frequency (HF) measure (dark gray and light gray, respectively). It is clear that the high-frequency (light gray) region includes very little area under the HRV spectral curve, suggesting very little parasympathetic activity. The great majority of the HRV spectral activity is under the low-frequency (dark gray) region suggesting primarily sympathetic activity. These representations are incorrect because the slow-breathing subject should have a large parasympathetic component reflective of the vagal activity. This parasympathetic component is represented correctly by the method using both HRV and respiratory activity which defines the red and blue regions of the spectrum in the graph. The blue region defined by the FRF represents purely parasympathetic activity whereas the remainder of the lower frequency regions (red region) represents purely sympathetic activity.

Regulation of testicular AMH production. Left: the onset of AMH expression is gonadotropin-independent and depends on SOX9 binding to the proximal AMH promoter. Subsequently, SF1, GATA4 and WT1 enhance AMH expression by binding to specific promoter sequences or by interacting with transactivating factors. DAX1 impairs GATA4 and SF1 binding to the AMH promoters, resulting in lower AMH expression levels. Right: Later in fetal and postnatal life, FSH regulates AMH production through the FSH receptor-Gsα protein-adenylate cyclase (AC)-cyclic AMP (cAMP) pathway, resulting in a stimulation of protein kinase A (PKA) activity. PKA mediates phosphorylation of the transcriptional regulators SOX9, SF1 and AP2, as well as of IκB which releases NFκB. In the nucleus these factors bind to their specific response elements in proximal (SOX9, SF1) or distal (AP2 and NFκB) regions of the AMH promoter.
Right figure reprinted from ref. (113): Lasala C, Schteingart HF, Arouche N, Bedecarrás P, Grinspon R, Picard JY, Josso N, di Clemente N, Rey RA. SOX9 and SF1 are involved in cyclic AMP-mediated upregulation of anti-Müllerian gene expression in the testicular prepubertal Sertoli cells SMAT1. American Journal of Physiology – Endocrinology and Metabolism 2011; 301: E539-E547, Copyright 2011 the American Physiological Society. http://ajpendo.physiology.org/content/301/3/E539.abstract?sid=3829d833-dfdf-4310-bd6f-e7481c62be06