Grating-based x-ray dark-field mammography: Assessing complementary imaging information in simple cystic lesions and typical fibroadenoma.

Background: A significant proportion of false positive recalls of mammography-screened women is due to benign breast cysts and simple fibroadenomas. These lesions appear mammographically as smooth-shaped dense masses and require the recalling of women for a breast ultrasound to obtain complementary imaging information. They can be identified safely by ultrasound with no need for further assessment or treatment.

Grating-based phase-contrast computed tomography for breast tissue at an inverse compton source.

The introduction of mammography screening programs has significantly reduced breast cancer mortality rates. Nevertheless, some lesions remain undetected, especially in dense breast tissue. Studies have shown that phase-contrast imaging can improve breast cancer diagnosis by increasing soft tissue contrast.

Hepatic noradrenergic innervation acts via CREB/CRTC2 to activate gluconeogenesis during cold.

Background And Aim: Although it is well established that hormones like glucagon stimulates gluconeogenesis via the PKA-mediated phosphorylation of CREB and dephosphorylation of the cAMP-regulated CREB coactivators CRTC2, the role of neural signals in the regulation of gluconeogenesis remains uncertain.

Methods And Results: Here, we characterize the noradrenergic bundle architecture in mouse liver; we show that the sympathoexcitation induced by acute cold exposure promotes hyperglycemia and upregulation of gluconeogenesis via triggering of the CREB/CRTC2 pathway. Following its induction by dephosphorylation, CRTC2 translocates to the nucleus and drives the transcription of key gluconeogenic genes.

Reduced sympathetic activity is associated with the development of pain and muscle atrophy in a female rat model of fibromyalgia.

Fibromyalgia (FM) is characterized by chronic widespread musculoskeletal pain accompanied by fatigue and muscle atrophy. Although its etiology is not known, studies have shown that FM patients exhibit altered function of the sympathetic nervous system (SNS), which regulates nociception and muscle plasticity. Nevertheless, the precise SNS-mediated mechanisms governing hyperalgesia and skeletal muscle atrophy in FM remain unclear.