Articular chondrocytes respond to mechanical forces by alterations in gene expression, proliferative status, and metabolic functions. Little is known concerning the cell signaling systems that receive, transduce, and convey mechanical information to the chondrocyte interior. Here, we show that ex vivo cartilage compression stimulates the phosphorylation of ERK1/2, p38 MAPK, and SAPK/ERK kinase-1 (SEK1) of the JNK pathway. Mechanical compression induced a phased phosphorylation of ERK consisting of a rapid induction of ERK1/2 phosphorylation at 10 min, a rapid decay, and a sustained level of ERK2 phosphorylation that persisted for at least 24 h. Mechanical compression also induced the phosphorylation of p38 MAPK in strictly a transient fashion, with maximal phosphorylation occurring at 10 min. Mechanical compression stimulated SEK1 phosphorylation, with a maximum at the relatively delayed time point of 1 h and with a higher amplitude than ERK1/2 and p38 MAPK phosphorylation. These data demonstrate that mechanical compression alone activates MAPK signaling in intact cartilage. In addition, these data demonstrate distinct temporal patterns of MAPK signaling in response to mechanical loading and to the anabolic insulin-like growth factor-I. Finally, the data indicate that compression coactivates distinct signaling pathways that may help define the nature of mechanotransduction in cartilage.

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The classical hyperthermia effect is based on well-focused energy absorption targeting the malignant tissue. The treatment temperature has been considered as the main technical parameter. There are discussions about the mechanism and control of the process because of some doubts about the micro-mechanisms. The main idea of the extracellular hyperthermia is to heat up the targeted tissue by means of electric field, keeping the energy absorption in the extracellular liquid. This produces a temperature gradient and connected heat flow through the cell membrane, which initializes numerous nonequilibrium thermal microprocesses to destroy the cell membrane. Furthermore, before the heat shock activates the intracellular heat shock protein (HSP) mechanisms, the cell membrane has been already compromised, therefore the HSP synthesis in the cells starts secondarily only after the membrane damage. The process could explain why the nonuniform and basically unsatisfactorily high temperature locoregional hyperthermia could be effective.

Comparison of thermal noise limits and the effects of low frequency electromagnetic fields (LFEMF) on the cellular membrane have important implications for the study of bioelectro-magnetism in this regime. Over a decade ago, Weaver and Astumian developed a model to show that thermal noise can limit the efficacy of LFEMF. A recent report by Kaune [Kaune (2002) Bioelectromagnetics 23:622-628], however, contradicted their findings. Kaune assumes that the conductance noise current of cell membrane can be decomposed into two components, where one of them is identical regarding all segments (coherent), while the other is different (incoherent). Besides, this decomposition is not unequivocal and contradicts to the statistical independence of the segment noise currents, and therefore to the second law of thermodynamics as well. We suggest the procedure based on the method of symmetrical components, by the means of which we can re-interpret the result of Kaune in a correct way.