Two out of three diseases of the prostate gland affect aging men worldwide. Benign prostatic hyperplasia (BPH) is a noncancerous enlargement affecting millions of men. Prostate cancer (PCa) in turn is the second leading cause of cancer death. The factors influencing the occurrence of BPH and PCa are different; however, in the course of these two diseases, the overexpression of heat shock proteins is observed. Heat shock proteins (HSPs), chaperone proteins, are known to be one of the main proteins playing a role in maintaining cell homeostasis. HSPs take part in the process of the proper folding of newly formed proteins, and participate in the renaturation of damaged proteins. In addition, they are involved in the transport of specific proteins to the appropriate cell organelles and directing damaged proteins to proteasomes or lysosomes. Their function is to protect the proteins against degradation factors that are produced during cellular stress. HSPs are also involved in modulating the immune response and the process of apoptosis. One well-known factor affecting HSPs is the androgen receptor (AR)—a main player involved in the development of BPH and the progression of prostate cancer. HSPs play a cytoprotective role and determine the survival of cancer cells. These chaperones are often upregulated in malignancies and play an indispensable role in tumor progression. Therefore, HSPs are considered as one of the therapeutic targets in anti-cancer therapies. In this review article, we discuss the role of different HSPs in prostate diseases, and their potential as therapeutic targets.

Background: Temporomandibular disorder (TMD) is a collective term covering acute or chronic musculoskeletal and neuromuscular pain associated with the masticatory muscles, temporomandibular joint, and the associated structures. The surface electromyography (sEMG) test represents clinical potential as an additional diagnostic tool. The purpose of this study was to evaluate differences in masseter and temporalis muscle activity (in sEMG) in subjects with TMD compared to a control group. Methods: The TMD group included 45 people qualified according to the diagnostic criteria for temporomandibular disorder (DC/TMD). In the control group, there were 30 subjects. All participants underwent detailed examinations including sEMG diagnosis of the masseter and temporalis muscles. The sEMG was measured both at rest and during maximal voluntary contraction (MVC). Amplitude root mean square (A_RMS) values for the analysis were determined. Results: No differences were shown in the value of the results between TMD and control group in RS A_RMS transformed data values (p = 0.086) and in the MVC A_RMS transformed data values (p = 0.536). The presence of TMD has no significant effect on the symmetry index value for the temporalis (p = 0.42) and masseter muscles (p = 0.379). Conclusions: Analysis of both raw and normalized sEMG signals is insufficient to differentiate TMD patients from healthy individuals.