By A.W. English
Particular subject factor: Cells Tissues Organs 2003, Vol. 174, No. 1-2 Temporomandibular (jaw) joint ailments and problems are anticipated to impact 10 million american citizens each year with the vast majority of these looking remedy being ladies of their childbearing years. Researchers in general agree that the commonest temporomandibular ailments and problems fall into 3 major different types: arthritis, inner derangement of the joint, and/or myofascial discomfort. This distinctive factor of Cells Tissues Organs is a variety of papers offered on the moment assembly of the Temporomandibular Joint organization held in might 2002. The assembly fascinated about the function that osteoarthritis and muscle mechanics play in temporomandibular joint ailments and issues. at present there aren't any validated remedies for temporomandibular joint stipulations, in order that the cures sufferers obtain regularly mirror the non-public perspectives and practices of the supplier. those papers will function a reference for medical and simple study during this box, in addition to a stimulus for destiny investigations. Clinicians facing continual musculoskeletal problems akin to arthritis will gain by means of increasing their point of view to incorporate new wisdom approximately their fields in addition to approximately comparable issues of the pinnacle and neck. easy and translational researchers within the similar fields should still learn those papers simply because we are hoping that this may inspire them to guage either the original and the generalized gains of analysis relating to temporomandibular problems.
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Additional resources for Joint and Muscle Dysfunction of the Temporomandibular Joint (Cells Tissues Organs (Formerly Acta Anatomica)) (v. 174, No. 1-2)
Thus, the prototypical IAP, namely XIAP, inhibited caspase-9 and caspase-3 via specific binding regions (BIR) that interact with mature caspases [Nicholson, 2001]. The structural relationship between XIAP and its antagonist, namely Smac/DIABLO, an apoptosis-promoting mitochondrial protein appears to regulate apoptosis dynamics [Nicholson, 2001]. , 2000; Yang and Li, 2000]. Thus, NF-ÎB is a repressor of apoptosis [Gupta, 2002]. , 2000]. Bcl-2 activity may also be regulated by phosphorylation. The activity of the proapoptosis Bcl-2 family members, namely Bax, Bak, Bad, Bin and Bim, often functions according to whether they are phosphorylated and where they are sequestered in the cell [Green and Reed, 1998].
1999]. , 1999]. Suppression of Bcl-2 may also result in additional changes in extracellular matrix proteins as well. Thus, Mechanical loading of joint cartilage may provide the primary environmental stimulus to initiate cartilage apoptosis during aging and in early OA. e. 3 MPa). , 2002]. , 2002]. , 2002]. DNA fragmentation was undetectable in nonloaded chondrocytes even after 4 h or after 30 min of pressure. The pattern of DNA fragment migration after 30 min of pressure was identical to nonloaded chondrocytes.
Mitochondrial changes and alterations in Bcl-2 are also characteristic of other cell types undergoing apoptosis [Adams and Cory, 1998; Green and Reed, 1998]. Studies of the structure and function of the Bcl-2 protein family indicate that all family members contain four conserved motifs (BH1, BH2, BH3 and BH4) which are homologous to Bcl-2. Most of the Bcl-2 family members that are affected by cytotoxic molecules contain the BH1 and BH2 motif, while those that are most similar to Bcl-2 contain all four domains [Adams and Cory, 1998].