Physical therapy involves a set of factors and methods that affect the biological processes in the body. It is widely used, relatively inexpensive, non-invasive, and easy to apply. Physiotherapy is also used in the treatment of patients with carpal tunnel syndrome (CTS). This syndrome represents the most common compressive mononeuropathy of the upper limb and leads to significant disability. Hence, its successful treatment leads to significant benefits for both the patient and society. There is no established algorithm for the use of physical therapy in these patients. In this publication, we present the physiotherapeutic methods used for the treatment of CTS both before and after surgical treatment.

Hypertension-induced cardiac remodeling is a complex process driven by interconnected molecular and cellular mechanisms that culminate in hypertensive myocardium, characterized by ventricular hypertrophy, fibrosis, impaired angiogenesis, and myocardial dysfunction. This review discusses the histomorphometric changes in capillary density, fibrosis, and mast cells in the hypertensive myocardium and delves into the roles of key regulatory systems, including the apelinergic system, vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) pathways, and nitric oxide (NO)/nitric oxide synthase (NOS) signaling in the pathogenesis of hypertensive heart disease (HHD). Capillary rarefaction, a hallmark of HHD, contributes to myocardial ischemia and fibrosis, underscoring the importance of maintaining vascular integrity. Targeting capillary density (CD) through antihypertensive therapy or angiogenic interventions could significantly improve cardiac outcomes. Myocardial fibrosis, mediated by excessive collagen deposition and influenced by fibroblast growth factor-2 (FGF-2) and transforming growth factor-beta (TGF-β), plays a pivotal role in the structural remodeling of hypertensive myocardium. While renin–angiotensin–aldosterone system (RAAS) inhibitors show anti-fibrotic effects, more targeted therapies are needed to address fibrosis directly. Mast cells, though less studied in humans, emerge as critical regulators of cardiac remodeling through their release of pro-fibrotic mediators such as histamine, tryptase, and FGF-2. The apelinergic system emerges as a promising therapeutic target due to its vasodilatory, anti-fibrotic, and cardioprotective properties. The system counteracts the deleterious effects of the RAAS and has demonstrated efficacy in preclinical models of hypertension-induced cardiac damage. Despite its potential, human studies on apelin analogs remain limited, warranting further exploration to evaluate their clinical utility. VEGF signaling plays a dual role, facilitating angiogenesis and compensatory remodeling during the early stages of arterial hypertension (AH) but contributing to maladaptive changes when dysregulated. Modulating VEGF signaling through exercise or pharmacological interventions has shown promise in improving CD and mitigating hypertensive cardiac damage. However, VEGF inhibitors, commonly used in oncology, can exacerbate AH and endothelial dysfunction, highlighting the need for therapeutic caution. The NO/NOS pathway is essential for vascular homeostasis and the prevention of oxidative stress. Dysregulation of this pathway, particularly endothelial NOS (eNOS) uncoupling and inducible NOS (iNOS) overexpression, leads to endothelial dysfunction and nitrosative stress in hypertensive myocardium. Strategies to restore NO bioavailability, such as tetrahydrobiopterin (BH₄) supplementation and antioxidants, hold potential for therapeutic application but require further validation. Future studies should adopt a multidisciplinary approach to integrate molecular insights with clinical applications, paving the way for more personalized and effective treatments for HHD. Addressing these challenges will not only enhance the understanding of hypertensive myocardium but also improve patient outcomes and quality of life.

The use of medical ultrasound as an imaging modality in the evaluation of the carpal tunnel syndrome has been growing. Technical progress and the introduction of new, high-quality devices and ultra-high frequency transducers with smaller dimensions have led to a better quality of acquired images and the development of new examination methodologies. The sonographic method has a number of advantages: available, non-invasive, cheaper, and allows an easier and faster evaluation and diagnosis of carpal tunnel syndrome, along with the possibility to assess various parameters of the median nerve, including its size, blood flow, and mobility. In addition, medical ultrasound may be used to detect anatomical variations and space-occupying lesions in the carpal tunnel to monitor the therapeutic response in patients suffering from carpal tunnel syndrome and to evaluate median nerve injuries. Herein, we present a review of the pertinent literature with regard to the diagnostic potential of medical ultrasound in the evaluation of pathological changes in the carpal tunnel.

The azygos lobe is a rare anatomical variant, most often encountered in the right lung. Its etiology is related to a defect of the migration of the azygos vein during the embryonic development. Here, we describe a rare case of an azygos lobe of the right lung, diagnosed incidentally on a computed tomography (CT) scan in a 40-year-old male patient who presented with chest pain, shortness of breath, and fever. The initial differential diagnosis included acute myocardial infarction, aortic dissection, and myocarditis. Chest CT with contrast matter demonstrated a peculiar finding in the right lung which was recognized as an azygos vein passing through the upper lobe and separating an azygos lobe with its mesoazygos. The azygos lobe may be rarely associated with neoplastic processes or spontaneous pneumothorax and its differential diagnosis on imaging studies includes various conditions. Knowledge of this variation is important to avoid misdiagnosis or complications during thoracic surgery.

Angiogenesis, the natural mechanism by which fresh blood vessels develop from preexisting ones, is altered in arterial hypertension (AH), impacting renal function. Studies have shown that hypertension-induced renal damage involves changes in capillary density (CD), indicating alterations in vascularization. We aimed to elucidate the role of the apelin receptor (APLNR), neuronal nitric oxide synthase (nNOS), and vascular endothelial growth factor (VEGF) in hypertension-induced renal damage. We used two groups of spontaneously hypertensive rats aged 6 and 12 months, representing different stages of AH, and compared them to age-matched normotensive controls. The kidney tissue samples were prepared through a well-established protocol. All data analysis was conducted with a dedicated software program. APLNR was localized in tubular epithelial cells and the endothelial cells of the glomeruli, with higher expression in older SHRs. The localization of nNOS and VEGF was similar. The expression of APLNR and nNOS increased with AH progression, while VEGF levels decreased. CD was lower in young SHRs compared to controls and decreased significantly in older SHRs in comparison to age-matched controls. Our statistical analysis revealed significant differences in molecule expression between age groups and varying correlations between the expression of the three molecules and CD.