The typical features of eccentric exercise-induced muscle damage is prolonged loss of muscle strength and the most rapid structural change in the fibers is loss of immunostaining for the intermediate filament protein, desmin. In this study isolated perfused rat muscle was used to examine the direct effect of temperature changes on the eccentric contraction-induced force and desmin loss. The left medial gastrocnemius muscle was separated and the entire lower limb was transferred into a prewarmed (35oC) organ bath. Temperature was adjusted to 31 or 39oC during and after eccentric contractions. Maximal isometric force and desmin loss were measured after 15 isometric or eccentric contractions. According to our data, organ bath temperature changes during or after eccentric contractions had no significant effect on force loss. However, a strong correlation between desmin loss and temperature changes during (r=0.886, P<0.05) and a weak correlation between desmin loss and temperature changes after (r=0.699, P<0.05) eccentric contractions was observed. Our results suggest that cooling during eccentric contractions may decrease desmin loss but temperature changes after eccentric contractions have no effect on desmin loss.

In our own experiment, we studied microscopic changes in the anterior wall of the left ventricle of young, middle-aged, and old rats on the 30th day after exercising. Plasmorrhagia, edema, stasis, bruising, dystrophic-necrotic changes, and eventually atrophic and sclerotic changes with the proliferation of connective tissue, an expansion of fibroblasts, and collagen synthesis emerge against the backdrop of tissue hyperemia typical of general venous hyperemia. In contrast to the young rats, the middle-aged rats have more severe lesions, while the old rats exhibit lesser alterations than the first two age groups. Compared to the control, an immunohistochemical examination of Desmin expression indicated peculiar morphodynamics. Morphometric analysis revealed that the number of intercalated discs is stable in young rats compared to control groups, rises in middle-aged rats (24.17%), and decreases in older rats (23.67%) compared to control. The intercalated discs in all three cell types mostly undergo disintegration, fragmentation, and shortening with a decrease in size. Compared to older rats, the experiment shows that sustained physical strain initially triggers the onset of adaptive, compensatory hypertrophy processes in striated and smooth muscle tissues. The compensating mechanism is disrupted when there are morphological alterations like acute heart failure and myocardial infarction, risk factors for acute hyperemia, venous and capillary congestion, edema, hemorrhage, and dystrophic and necrotic changes with the destruction and reduction in the size of intercalated discs. These conditions also cause functional weakening, decreased myocardial contractility, and hypoxic damage and are risk factors for acute heart failure and myocardial infarction.

Uterine sarcomas, accounting for only 1% of malignant genital system tumors, present significant diagnostic and therapeutic challenges due to their rarity, small size, and diverse clinical manifestations. Leiomyosarcoma, a subtype of uterine sarcoma, is particularly difficult to differentiate from benign leiomyomas, as there are no distinct clinical or radiological criteria. The study aimed to identify specific structural changes in leiomyocytes of uterine leiomyomas that may indicate a high risk of developing leiomyosarcoma. Through histological and immunohistochemical analyses, including hematoxylin and eosin staining and markers such as Ki67, vimentin, and desmin, a detailed examination of operative materials from a single patient at two different times (2017 and 2023) was conducted. The initial histological diagnosis in 2017 suggested a leiomyoma with low malignant potential, but subsequent follow-up in 2023 revealed leiomyosarcoma with invasion into the sigmoid colon. This case emphasizes the diagnostic complexity of leiomyosarcoma, particularly when structural changes in leiomyocytes are present, and highlights the need for continuous monitoring of patients postoperatively, even in cases initially deemed to have low malignant potential. The study concludes that prognosis depends not on tumor size but on the degree of malignancy, with poorly differentiated sarcomas demonstrating a poor prognosis. These findings underscore the importance of histopathological evaluation and long-term follow-up to improve patient outcomes in uterine sarcoma cases.

Objective: Sertoli cell tumor (SCT) is common in dogs, affecting mainly old or cryptorchid animals. During maturation from fetal to adult testis, SCs undergo a process of differentiation whereby the expression of some cytoskeletal markers is maintained, while other markers disappear and others are acquired. Human fetal Sertoli cells (SCs) have shown transient expression of cytokeratin (CK) and desmin (DES) that is replaced after birth by expression of vimentin (VIM). Human Sertoli cell tumours (SCTs) are characterized by re-expression of CK and DES.Materials and Methods: Neoplastic Samples from mature dogs (n=14) and Normal testicular tissue from two adult dogs, one 6-month-old puppy and two neonatal pups were obtained. For each sample, sections (5mm) were stained with haematoxylin and eosin (HE) and Immunohistochemical labelling was performed using the avidin-biotinperoxidase complex (ABC) procedure.Results: VIM was expressed in the stroma of all testes examined. Samples those from adult and puppy expressed VIM, while those of neonates were negative. All SCTs strongly expressed VIM. SCs did not express CK and DES. But were expressed only by some SCTs.Conclusion: The SCs of adult dogs expressed VIM, confirming that expression of this molecule may be reliable marker for dogs. Canine SCs do not express VIM at the time of birth but man and rodent, SCs express VIM before birth. SCs in dogs did not express DES and CK. This result is similar to in man and rodents, where only transient expression of these proteins in early fetal stages and is lost in the early phases of gestation, so expression of these molecules by canine SCTs may be because of neoplastic regressing of canine SCs to an undifferentiated immunophenotype.Thus Canine SCTs may express CK and DES, suggesting that the neoplastic cells undergo de-differentiation during transformation.

Objective (s): Occlusal trauma is one of the most common forms of oral biting dysfunction. Long‐term occlusal trauma could weaken the stomatognathic system; especially damage one’s masticatory muscle. Through using the rat model, this study investigated the trophic effect of ciliary neurotrophic factor (CNTF) on injured masseter muscle.Materials and Methods: Male Wistar rats (n=36) were randomly divided into five experimental groups and one control group (6 rats per group). Animals in the experimental group were cemented modified crowns on their mandibular first molars to artificially induce occlusal trauma in 1, 3, 7, 14, and 28 days. Control group was sham‐treated with forced mouth‐opening for about 5 min, while no crowns were placed. After 28 days of treatment, all rats were euthanized and their masseter muscle was collected. Through immunofluorescence and real‐time quantitative PCR, the expression of desmin, CNTF, and CNTFRa was investigated in rat masseter muscle. The microstructure of masseter muscle was observed by transmission electron microscope.Results: The expression of desmin showed a time‐dependent decrease on traumatic and non‐traumatic sides masseter, until reached the nadir at the 14th day, then restored to its normal level at the 28th day; however, the expression of CNTF and CNTFRa on the traumatic and non‐traumatic sides increased from day 7, reached the peak at the 14th day, and returned to normal level on the 28th day.Conclusion: CNTF, as an important neurotrophic factor, was tightly associated to the restoring of rat injured masseter muscle, which provides new target and treatment method for clinical application.

Rhabdomyosarcoma is a rare soft tissue malignant neoplasm with striated muscle differentiation often found in the head and neck region. In our case a 33-year-old man presented with a bulging mass near his right mandibular second molar tooth, identified as a unilocular destructive lesion on an X-ray. An incisional biopsy confirmed rhabdomyosarcoma, leading to a hemi-mandibulectomy. Histopathologic findings showed spindle and rhabdoid cells with positive immunoreactivity to Desmin, myogenin and myoD1. In conclusion, it is crucial to differentiate rhabdomyosarcoma from other more common intraosseous malignancies, and using Desmin staining as part of the initial immunohistochemical panel can aid in the diagnosis process.

Introduction: Numerous studies have shown that enriched plasma protects myocardial cells against ischemia. The aim of this study was to evaluate the effect of rat enriched plasma by preconditioning, ischemia, and reperfusion on the differentiation of bone marrow mesenchymal stem cells (BMMSC) into cardiomyocytes. Methods: In this experimental and laboratory study, BMMSCs were extracted from the femur bone of male Wistar rats weighting 250-300 g. BMMSCs of the third passage were divided into six groups according to the type of plasma received: 1) control, 2) azacytidine, 3) azacytidine and non-ischemic plasma recipient, 4) azacytidine and preconditioned plasma recipient, 5) azacytidine and ischemic plasma recipient 6) azacytidine and plasma reperfusion recipient groups. In all groups except group 1, to initiate cardiomyocyte differentiation, BMMSCs were exposed to azacytidine (10 μ, M) for 24 hours. Plasma (25 μ, g / ml) was added to the culture medium each time the culture medium was changed. After 21 days, the expression level of myocardial β, MHC, desmin, and troponin I genes was assessed using qRT-PCR. Results: The expression of myocardial β, MHC, desmin, and troponin I genes was significantly increased in all groups received azacytidine (groups 2 to 6) (P<0. 01). There was no significant difference in the expression of myocardial β, MHC, desmin, and troponin I genes, the doubling time, and migration between the plasma receiving groups (groups 3 to 6) compared to the group 2 (P>0. 05). Conclusion: The findings of present study showed that the plasma collected during ischemia, ischemiareperfusion, and ischemia preconditioning had no effect on the differentiation of BMMSCs into cardiomyocytes in the presence of azacytidine.