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- Häggman Henrikson, Birgitta, et al.
(författare)
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Temporomandibular Disorder Pain After Whiplash Trauma: A Systematic Review
- 2013
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Ingår i: Journal of Orofacial Pain. - : Quintessence. - 1064-6655 .- 1945-3396. ; 27:3, s. 217-226
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Forskningsöversikt (refereegranskat)abstract
- Aims: To assess, by systematic review of the literature, (1) the prevalence and incidence of temporomandibular disorder (TMD) pain after whiplash trauma, and (2) whether treatment modalities commonly used for TMD are equally effective in patients with solely TMD pain and those with TMD/whiplash-associated disorders (WAD) pain. Methods: A systematic literature search of the PubMed, Cochrane Library, and Bandolier databases was conducted from January 1966 through October 2012. The systematic search identified 125 articles. After an initial screening of abstracts, 45 articles were reviewed in full text. Two investigators evaluated the methodological quality of each identified study. Results: Eight studies on prevalence/incidence of TMD pain in WAD and four studies on interventions in TMD pain and WAD met the inclusion criteria. The reported median prevalence of TMD pain after whiplash trauma was 23% (range 2.4% to 52%) and the incidence ranged from 4% to 34%. For healthy controls, the reported median prevalence was 3% (range 2.5% to 8%) and the incidence ranged from 4.7% to 7%. For patients with a combination of TMD pain and WAD, treatment modalities conventionally used for TMD, such as jaw exercises and occlusal splints, had less of an effect (median improvement rate of 48%, range 13% to 68%) compared to TMD patients without a whiplash injury (75%, range 51% to 91%). Conclusion: There is some evidence that prevalence and incidence of TMD pain is increased after whiplash trauma. The poorer treatment outcome suggests that TMD pain after whiplash trauma has a different pathophysiology compared to TMD pain localized to the facial region.
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| 2. |
- Storm, Petter, et al.
(författare)
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A Unifying Mechanism for Cancer Cell Death through Ion Channel Activation by HAMLET.
- 2013
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Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:3
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Tidskriftsartikel (refereegranskat)abstract
- Ion channels and ion fluxes control many aspects of tissue homeostasis. During oncogenic transformation, critical ion channel functions may be perturbed but conserved tumor specific ion fluxes remain to be defined. Here we used the tumoricidal protein-lipid complex HAMLET as a probe to identify ion fluxes involved in tumor cell death. We show that HAMLET activates a non-selective cation current, which reached a magnitude of 2.74±0.88 nA within 1.43±0.13 min from HAMLET application. Rapid ion fluxes were essential for HAMLET-induced carcinoma cell death as inhibitors (amiloride, BaCl2), preventing the changes in free cellular Na(+) and K(+) concentrations also prevented essential steps accompanying carcinoma cell death, including changes in morphology, uptake, global transcription, and MAP kinase activation. Through global transcriptional analysis and phosphorylation arrays, a strong ion flux dependent p38 MAPK response was detected and inhibition of p38 signaling delayed HAMLET-induced death. Healthy, differentiated cells were resistant to HAMLET challenge, which was accompanied by innate immunity rather than p38-activation. The results suggest, for the first time, a unifying mechanism for the initiation of HAMLET's broad and rapid lethal effect on tumor cells. These findings are particularly significant in view of HAMLET's documented therapeutic efficacy in human studies and animal models. The results also suggest that HAMLET offers a two-tiered therapeutic approach, killing cancer cells while stimulating an innate immune response in surrounding healthy tissues.
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