External validation of the relative fat mass (RFM) index in adults from north-west Mexico using different reference methods.

BACKGROUND: Analysis of body composition is becoming increasingly important for the assessment, understanding and monitoring of multiple health issues. The body mass index (BMI) has been questioned as a tool to estimate whole-body fat percentage (FM%). Recently, a simple equation described as relative fat mass (RFM) was proposed by Woolcott & Bergman. This equation estimates FM% using two anthropometric measurements: height and waist circumference (WC). The authors state that due to its simplicity and better performance than BMI, RFM could be used in daily clinical practice as a tool for the evaluation of body composition. The aim of this study was to externally validate the equation of Woolcott & Bergman to estimate FM% among adults from north-west Mexico compared with Dual-energy X-ray absorptiometry (DXA) as an alternative to BMI and secondly, to make the same comparison using air displacement plethysmography (ADP), Bioelectrical Impedance Analysis (BIA) and a 4-compartment model (4C model). METHODS: Weight, height and WC were measured following standard procedures. The RFM index was calculated for each of the 61 participating subjects (29 females and 32 males, ages 20-37 years). The RFM was then regressed against each of the four body composition methods for estimating FM%. RESULTS: Compared with BMI, RFM was a better predictor of FM% determined by each of the body composition methods. In terms of precision the best equation was RFM regressed against DXA (y = 1.12 + 0.99 x; R2 = 0.84 p<0.001). Accuracy (represented by the closeness to the zero-intercept) was 1.12 (95% CI: -2.44, to 4.68) and thus, not significantly different from zero. For the rest of the methods, precision in the prediction of FM% was improved compared to BMI, with significant increases in the R2 and reduction of the root mean squared error (RMSE). However, the intercepts of each regression did not show accuracy since they were different from zero, for ADP: -9.95 (95%CI: -15.7 to -4.14), for BIA: -12.6 (95%CI: -17.5 to -7.74) and for the 4C model: -13.6 (95%CI: -18.6 to -8.60). Irrespectively, FM% measured by each of the body composition methods was higher for DXA than the other three methods (p<0.001). CONCLUSIONS: This external validation proved that the performance of the RFM equation used in this study to estimate FM% was more consistent than BMI in this Mexican population, showing a stronger correlation with DXA than with the other body composition methods.

Id2 protein is selectively upregulated by UVB in primary, but not in immortalized human keratinocytes and inhibits differentiation.

Solar ultraviolet B (UVB) acts as both an initiator and promoter in models of multistage skin carcinogenesis. We found that, whereas UVB induces apoptosis in human papillomavirus-16 E6/7-immortalized keratinocytes, it inhibits markers of differentiation in human foreskin keratinocytes (HFK). Potential mechanisms for this differential response were examined by DNA microarray, which revealed that UVB alters the expression of three of the four human inhibitor of differentiation/DNA binding (Id) proteins that comprise a class of helix-loop-helix family of transcription factors involved in proliferation, differentiation, apoptosis, and carcinogenesis. These results were verified by RT-PCR and immunoblot analysis of control and UVB-irradiated primary and immortalized keratinocytes. Whereas Id1 was downregulated in both cell types, Id2 expression was upregulated in primary HFK, but not immortalized cells. In contrast, Id3 expression was significantly increased only in immortalized cells. The differential expression pattern of Id2 in response to UVB was recapitulated in reporter constructs containing the 5' regulatory regions of this gene. Id2 promoter activity increased in response to UVB in HFK, but not in immortalized cells. To identify the regulatory elements in the Id2 promoter that mediate transcriptional activation by UVB in HFK, promoter deletion/mutation analysis was performed. Deletion analysis revealed that transactivation involves a 166 bp region immediately upstream to the Id2 transcriptional start site and is independent of c-Myc. The consensus E twenty-six (ETS) binding site at -120 appears to mediate UVB transcriptional activation of Id2 because point mutations at this site completely abrogated this response. Chromatin immunoprecipitation and electrophoretic mobility-shift assays verified that the Id2 promoter interacts with known Id2 promoter (ETS) binding factors Erg1/2 and Fli1, but not with c-Myc; and this interaction is enhanced after UVB exposure. Similar to the effects of UVB exposure, ectopic expression of Id2 protein in primary HFK resulted in inhibition of differentiation, as shown by decreased levels of the terminal differentiation marker keratin K1 and inhibition of involucrin crosslinking. Reduction of Id2 expression by small interfering RNAs attenuated the UVB-induced inhibition of differentiation in these cells. These results suggest that UVB-induced inhibition of differentiation of primary HFK is at least, in part, due to the upregulation of Id2, and that upregulation of Id2 by UVB might predispose keratinocytes to carcinogenesis by preventing their normal differentiation program.

Disfunción de la articulación temporomandibular y su repercusión otológica / Disfunction of the temperomandibular articulation and otologic repercussion

La disfunción de la articulación témporomandibular (ATM) repercute a nivel del oído por su estrecha relación anatómica, siendo causa de signos y síntomas otológicos y de probable alteración en la audición. En el presente artículo se revisa la disfunción ATM y el mecanismo por el cual se produciría la otalgia, el tinnitus y el vértigo, así mismo su repercusión en la audición. Aunque dichos mecanismos no son bien conocidos, se mencionan las hipótesis de su etiopatogenia. Además se hace un alcance acerca de la terapia actual de la disfunción ATM incidiendo en la importancia de iniciarla haciendo conocer al paciente el origen de sus síntomas, con el fin de disminuir sus temores y stress; para luego proceder a calmarle el dolor mediante medidas generales y una terapia física coadyuvante, posteriormente el tratamiento definitivo es en base a la combinación de procedimientos oclusales y ortodoncia.