A b s t r a c t. This work provides the values of both the static and the kinetic friction coefficients for chestnut (Castanea sativa Mill.) of Spanish origin. Knowledge concerning these coefficients has its main application in the study of agroindustrial structures and machinery with timber members in contact. This determination was developed taking into account the timber anisotropy to establish surfaces and directions of slipping. A modified direct shear test device was used to conduct the tests and reproduce the tribological system. This procedure was functional and reliable and considered suitable for standardizing the friction measurement between timber surfaces, since this device is widely distributed in geotechnical and materials laboratories and the European codes do not specify a procedure or device to carry it out. The average values obtained were 0.46 for the static coefficient and 0.33 for the kinetic one, without considering the surfaces and directions of slipping. These values ranged between 0.36 and 0.55 for the static friction coefficient and between 0.28 and 0.39 for the kinetic friction coefficient depending on the direction considered and also taking into account the anisotropy of the timber. A good correlation was obtained between both coefficients, thus allowing for the estimation of the kinetic coefficient from the static one.K e y w o r d s: wood, mechanical properties, friction coefficient, direct shear test

Background: Altered intracellular Ca 2+ homeostasis in neonatal platelets has been previously reported. This study aims to examine the changes in the Ca 2+ entry through the store-operated calcium entry (SOCE) mechanism in neonatal platelets. Methods: Human platelets from either control women, mothers, and neonates were isolated and, following, were fixed after being treated as required. Platelet samples were analyzed by Western blotting, qRT-PCR, and MALDITOF/TOF. Ca 2+ homeostasis was also determined. Culture cells were used as surrogated of platelets to overexpress the proteins of interest to reproduce the alterations observed in platelets. Results: Altered thapsigargin-evoked SOCE, alternative molecular weight form of STIM1 (stromal interaction molecule 1; s-STIM1 [short STIM1 isoform (478 aa)], around 60 kDa) and overexpression of SARAF (SOCE-associated regulatory factor [TMEM66]) were found in neonatal platelet as compared to maternal and control women platelets. s-STIM1 may result due to CAPN1 (calpain1)-dependent processing, as confirmed in platelets and MEG01 cells by using calpeptin and overexpressing CAPN1, respectively. In HEK293 (STIM1 and STIM2 [stromal interaction molecule 2] double knockout) cells transfected either with c-STIM1 (canonical STIM1 [685 aa]), s-STIM1 (478), STIM1B (540), and CAPN1 overexpression plasmids, we found s-STIM1 and c-STIM1, except in cells overexpressing s-STIM1 (478) that lacked CAPN1 target residues. These results and the in silico analysis, lead us to conclude that STIM1 is cleaved at Q496 by CAPN1. Ca 2+ imaging analysis and coimmunoprecipitation assay using MEG01 and HEK293 cells overexpressing SARAF together with s-STIM1 (478) reported a reduced slow Ca 2+ –dependent inactivation, so reproducing the Ca 2+ -homeostasis pattern observed in neonatal platelets. Conclusions: CAPN1 may cleave STIM1 in neonatal platelets, hence, impairing SARAF coupling after SOCE activation. S-STIM1 may avoid slow Ca 2+ –dependent inactivation and, subsequently, result in an enhanced thapsigargin-evoked SOCE as observed in neonatal platelets.

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