A Photoelastic Assessment of Residual Stresses in Zirconia-Veneer Crowns

Residual stresses within the veneer are linked to the high prevalence of veneer chipping observed in clinical trials of zirconia prostheses. We hypothesized that the thermal mismatch between the zirconia infrastructure and the veneer porcelain, as well as the rate used for cooling zirconia-veneer crowns, would be directly proportional to the magnitude of residual stresses built within the veneer layer. Two porcelains with different coefficients of thermal expansion were used to veneer zirconia copings, to create high or low thermal mismatches. The crowns were cooled according to a fast- or a slow-cooling protocol. The retardation of polarized light waves was used to calculate the residual stress magnitude and distribution across the veneer, according to the photoelasticity principle, in 1.0-mm-thick crown sections. While thermal mismatch was an important factor influencing the maximum stress development in the veneer, cooling rate had a minor role. Curved surfaces were preferential sites for stress concentration regardless of thermal mismatch or cooling rate

Nanowire Metal-Insulator-Metal Plasmonic Devices

In this paper we theoretically study the responsivity of Metal-Insulator-Metal nanostructures to light illumination over a broad wavelength band (1 - 25 microns) and we examine the role of a local field enhancement and electrostatic field on the responsivity

Renin angiotensin aldosterone system altered in resistant hypertension in Sub-Saharan African diabetes patients without evidence of primary hyperaldosteronism

Background The renin-angiotensin-aldosterone system may be altered in patients with resistant hypertension. This study aimed to evaluate the relation between renin-angiotensin-aldosterone system activity and resistant hypertension in Cameroonian diabetes patients with resistant hypertension. Methods We carried out a case-control study including 19 diabetes patients with resistant hypertension and 19 diabetes patients with controlled hypertension matched to cases according to age, sex and duration of hypertension since diagnosis. After collection of data, fasting blood was collected for measurement of sodium, potassium, chloride, active renin and plasma aldosterone of which the aldosterone-renin ratio was derived to assess the activity of renin-angiotensin-aldosterone system. Then, each participant received 2000 ml infusion of saline solution after which plasma aldosterone was re-assayed. Results Potassium levels were lower among cases compared to controls (mean: (4.10 ± 0.63 mmol/l vs. 4.47 ± 0.58 mmol/l), though nonsignificant (p = 0.065). Active renin, plasma aldosterone both before and after the dynamic test and aldosterone-renin ratio were comparable between cases and controls (all p values > 0.05). Plasma aldosterone significantly decreased after the dynamic test in both groups (p 280 pmol/l. We found a significant negative correlation between potassium ion and plasma aldosterone (ρ = −0.324; p  = 0.047), the other correlations being weak and unsignificant. Conclusion Although this study failed to show an association between RH and primary hyperaldosteronism in our context, there was a hyperactivity of renin-angiotensin-aldosterone system. Moreover, this study confirms the importance of potassium dosage when screening the renin-angiotensin-aldosterone system

Rare type 1-like and type 2-like calreticulin mutants induce similar myeloproliferative neoplasms as prevalent type 1 and 2 mutants in mice.

Frameshift mutations in the calreticulin (CALR) gene are present in 30% of essential thrombocythemia and myelofibrosis patients. The two most frequent mutations are CALR del52 (type 1, approximately 60%) and CALR ins5 (type 2, around 30%), but many other rarer mutations exist accounting each for less than 2% of all CALR mutations. Most of them are structurally classified as type 1-like and type 2-like CALR mutations according to the absence or presence of a residual wild-type calcium-binding motif and the modification of the alpha-helix structure. Yet, several key questions remain unanswered, especially the reason of such low frequencies of these other mutations. In an attempt to investigate specific pathogenic differences between type 1-like and type 2-like CALR mutations and del52 and ins5, we modeled two type 1-like (del34 and del46) and one type 2-like (del19) mutations in cell lines and in mice. All CALR mutants constitutively activate JAK2 and STAT5/3/1 in a similar way in the presence of the thrombopoietin receptor (MPL) and induced cytokine-independent cell growth but to a lesser extent with rare mutants over time. This correlates with reduced expression levels of rare CALR mutants compared to del52 and ins5. Lethally irradiated mice that were engrafted with bone marrow transduced with the different CALR mutations developed thrombocytosis, but to a much lesser extent with ins5 and the type 2-like CALR mutation. In contrast to type 2-like mice, type 1-like mice developed marked myelofibrosis and splenomegaly 10 months after engraftment. Similar to del52, type 1-like CALR mutations induced an expansion at an early stage of hematopoiesis compared to ins5 and type 2-like mutation. Thus, type 1-like and type 2-like CALR mutants structurally and functionally resemble del52 and ins5 mutants, respectively