Background. Osteoporosis is a disease characterized by decreased bone density and destruction of bone microarchitecture. Indicators for altered bone homeostasis are changes in the serum level of matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs). The purpose of the current study was to evaluate the effect of a 12‐week exercise program on enzyme activity of serum MMP‐9 and TIMP‐1 in postmenopausal osteoporotic patients. Materials and methods. Participants were randomized in two groups: exercise (EG) (N = 37) and control (CG) (N = 31). The exercise group completed a 12‐week supervised exercise program, while the control group did not take part in any physical activity. Enzyme activities of serum MMP‐9 and TIMP‐1 were detected by gelatin zymography and ELISA in both groups, respectively. Results. Significant differences between pretreatment and posttreatment enzyme activities of serum MMP‐9 (p = 0.009), TIMP‐1 (p ≤ 0.001), and MMP‐9/TIMP‐1 ratio (p ≤ 0.001) were detected in the exercise group. Exercises decreased the activity of serum MMP‐9 and increased the activity of TIMP‐1, while the enzyme activities of MMP‐9 (0.583) and TIMP‐1 (0.210) have not been significantly changed in CG. Patients from the exercise group had better treatment. Conclusion. Our results suggest that a 12‐week exercise program has an influence on enzyme activity of serum MMP‐9, revealing a possible role of MMPs in initiating training‐specific adaptation. Although measurements of circulating MMP‐9 and TIMP‐1 allowed us to detect effects of exercise, as of today, they have no real role in the diagnosis of osteoporosis and/or follow‐up of osteoporotic patient’s response to treatment. MMP‐9 might be used as an important prognostic marker for the evaluation of patient’s response to exercise. Larger‐randomized controlled studies need to be performed to expand this area of knowledge. This trial is registered with trial registration number: NCT03816449).

Purpose: Tunnel syndromes around the foot and ankle are underrecognized and frequently misdiagnosed nerve entrapments that can significantly impact patients' quality of life. This review aims to provide a comprehensive overview of the etiology, clinical presentation, diagnostic challenges, and management strategies for these syndromes, focusing on the sural nerve, deep peroneal nerve, tibial nerve, medial plantar nerve, and inferior calcaneal nerve. Methods: A thorough literature review was conducted, examining studies and case reports on nerve entrapments in the foot and ankle. The review covers the clinical assessment, differential diagnosis, and treatment options, including conservative and surgical interventions. Results: Tunnel syndromes of the foot and ankle can arise from various causes, including trauma, anatomical variations, repetitive strain, and systemic conditions. Clinical manifestations often include burning pain, tingling, and motor weakness, depending on the affected nerve. Accurate diagnosis relies on a detailed patient history, physical examination, and adjunctive tests such as electrodiagnostic and imaging. Conservative treatments, such as physical therapy, orthotics, and corticosteroid injections, are often effective, while surgical decompression is reserved for refractory cases. Conclusions: Recognizing and diagnosing tunnel syndromes in the foot and ankle is essential for effective management and preventing permanent nerve damage. A systematic approach that integrates clinical evaluation and appropriate imaging can improve patient outcomes. Timely intervention, whether conservative or surgical, is crucial for alleviating symptoms and restoring function.

Introduction: Febrile seizures (FS) are the most common neurological disease in childhood. The etiology of FS is the subject of numerous studies including studies regarding genetic predisposition. Aim: The aim of the study was to analyze the association of TRPV1 rs222747 and KCC2 rs2297201 gene polymorphisms with the occurrence of FS. Materials and Methods: The study included 112 patients diagnosed with FS classified as simple febrile seizures (SFS) or complex febrile seizures (CFS). We analyzed selected polymorphisms of KCC2 and TRPV1 genes using the Real-time PCR method. Results: The CT and TT genotypes of the rs2297201 polymorphism of the KCC2 gene are significantly more common in the group of children with FS than the control group (p = .002) as well as the allele T of this polymorphism (p = .045). Additionally, genotypes CT and TT of the rs2297201 polymorphism of the KCC2 gene were more frequent in the group of children with CFS compared to the control group (p < .001). Different genotypes and alleles of the rs222747 TRPV1 gene polymorphism were not associated with the occurrence of febrile seizures or epilepsy, nor were associated with the occurrence of a particular type of febrile seizure (p = .252). Conclusion: These results indicate that the CT and TT genotypes, as well as the T allele of rs2297201 polymorphism of the KCC2 gene, could be a predisposing factor for the FS, as well as the occurrence of CFS.

Febrile seizures (FS) are the most common neurological disorder in childhood and are a great stress for parents due to their dramatic clinical appearance. Using test for determination of homozygously recessive characteristics in humans (HRC test) we analyzed presence, distribution, and individual combination of 20 selected genetically controlled morphophysiological traits among FS patients (N=121) and control (N=121) to determine a possible deviation in the homozygosity level and genetic loads in the group of affected children and whether there is a predisposition to the occurrence of FS. The results of our study show a statistically significant difference in the mean values of the HRC tested (x¯HRC/20 CN = 3.2 ± 0.2; x¯HRC/20 FS = 4.6 ± 0.2, t= 5.74 , p< 0.0001), as well as in the distribution and variability of two studied samples (VC=55,3%, VFS= 39,6%), which indicates a complex polygenic difference among the tested groups of subjects. The differences in the degree of genetic homozygosity and variability are also present between the genders (t Cf/FSf = 4.12; t Cm/FSm = 3.98; p <0.0001) (VCf=56.9%, VFSf= 39.3%; VCm=54.1%, VFSm=40.1%). Obtained results indicate the enlargement of recessively homozygous genetic loads in the group of children with FS which may represent some kind of predisposition for expressivity of this type of seizures.