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Sex hormones and their receptors play a crucial role in human sexual dimorphism and have been traditionally associated with hormone-dependent cancers like breast, prostate, and endometrial cancer. However, recent research has broadened our understanding by revealing connections with other types of cancers, such as lung cancer, where the androgen receptor has been found to be particularly significant. This review aims to explore the molecular mechanisms of androgen action in lung cancer pathogenesis and progression, highlighting the potential of inhibiting the androgen receptor signaling pathway as a therapeutic strategy for lung cancer treatment.

Endocannabinoids act as a stress response system simultaneously the modulation of this system has emerged a novel approach for the therapy of cardiovascular disorders. We investigated the protective effects of the chronic administration of the fatty acid amide hydrolase (FAAH) inhibitor URB597 on morphology, pro-inflammatory and anti-inflammatory cytokine, the cytoplasm-nuclear distribution of JAK2/STAT3, NF-kB, and Nrf2/HO-1 signaling in the left ventricle of female and male rats exposed to chronic unpredictable stress. Our results show that URB597 treatment exhibits an antidepressant-like effect, decreases the heart/body weight ratio, prevents the hypertrophy of cardiomyocytes, and reduces the increased level of IL-6 in the wall of the left ventricle of stressed female and male rats. The phosphorylation levels of JAK2 and STAT3 in the ventricle of male rats treated with URB597 declined, whereas in female rats the decrease of STAT3 was observed. In addition, URB597 reduced increased NF-κB in both females and males and increased the expression of Nrf2 and HO-1 protein in the cytosol of male rats whereas did not affect their levels in females. The cardioprotective effects of URB597 could be linked to the ability to inhibit the JAK2 in males and the STAT3 inflammatory signaling pathways in both females and males.

An increasing body of evidence shows significant sex differences in the mammalian brain in multiple behaviours and psychiatric and neurological diseases and as well as that the endocannabinoid system may differ between males and females. In this study we investigated sex differences in working, short-term and long-term memory and the expression of β

After radioiodine therapy of differentiated thyroid cancer (DTC) patients, whole body scintigraphy (WBS) is standard procedure before releasing the patient from the hospital. A common problem is the precise localization of regions where the iod-avide tissue is located. Sometimes is practically impossible to perform precise topographic localization of such regions.In order to face this problem, we have developed a low-cost Vision-Fusion system for web-camera image acquisition simultaneously with routine scintigraphic whole body acquisition including the algorithm for fusion of images given from both cameras. For image acquisition in the gamma part of the spectra we used e.cam dual head gamma camera (Siemens, Erlangen, Germany) in WBS modality, with matrix size of 256×1024 pixels and bed speed of 6cm/min, equipped with high energy collimator. For optical image acquisition in visible part of spectra we have used web-camera model C905 (Logitech, USA) with Carl Zeiss® optics, native resolution 1600×1200 pixels, 34We tested our system for 10 patients with DTC who received radioiodine therapy (8 women and two men, with average age of 50.10±12.26 years). Five patients received 5.55Gbq, three 3.70GBq and two 1.85GBq. Whole-body scintigraphy and optical image acquisition were performed 72 hours after application of radioiodine therapy.Based on our first results during clinical testing of our system, we can conclude that our system can improve diagnostic possibility of whole body scintigraphy to detect thyroid remnant tissue in patients with DTC after radioiodine therapy.

Baseline sympathetic activity was found to be elevated in rheumatoid arthritis (RA) patients and it is related to increased cardiovascular risk in these patients. Although many studies have highlighted the association between RA and increased cardiac sympathetic activity, the underlying mechanistic links remain unclear. The aim of the present study was to understand how diseases-triggered changes in gene expression may result in maladaptive physiological changes. Our results suggest that the equilibrium between noradrenaline synthesis, release and reuptake was disrupted in the ventricles of arthritic rats. In the acute phase of the arthritic process, decreased gene expression of MAO-A might lead to accumulation of noradrenaline in myocardial interstitial space, whereas increased gene expression of NET protected cardiomyocytes from the deleterious effects of enhanced noradrenaline. During the chronic phase, reduced expression of beta(1)-adrenoceptor and decreased efficiency of noradrenaline reuptake contribute to progressive damage of the myocardium and limits heart efficiency.