Reduced empathic concern leads to utilitarian moral judgments in trait alexithymia

Recent research with moral dilemmas supports dual-process model of moral decision making. This model posits two different paths via which people can endorse utilitarian solution that requires personally harming someone in order to achieve the greater good (e.g., killing one to save five people): (i) weakened emotional aversion to the prospect of harming someone due to reduced empathic concern for the victim; (ii) enhanced cognition which supports cost-benefit analysis and countervails the prepotent emotional aversion to harm. Direct prediction of this model would be that personality traits associated with reduced empathy would show higher propensity to endorse utilitarian solutions. As per this prediction, we found that trait alexithymia, which is well-known to have deficits in empathy, was indeed associated with increased utilitarian tendencies on emotionally aversive personal moral dilemmas and this was due to reduced empathic concern for the victim. Results underscore the importance of empathy for moral judgments in harm/care domain of morality

Efeito da aplicação de lodo de ETE sobre a acarofauna edáfica em áreas de plantio de Pinus taeda L. (Pinaceae).

IV SIBAC. Resumo

Universal photonic processors in a glass-based femtosecond laser writing platform

Femtosecond laser writing (FLW) can open new perspectives on universal photonic processors (UPPs). We propose here two building blocks for the realization of FLW-UPPs and we show the preliminary results obtained on a 6-mode device

Universal photonic processors fabricated by femtosecond laser writing

Universal photonic processors (UPPs) are reconfigurable photonic integrated circuits able to implement arbitrary unitary transformations on an input photonic state. Femtosecond laser writing (FLW) allows for rapid and cost-effective fabrication of circuits with low propagation losses. A FLW process featuring thermal isolation allows for a dramatic reduction in dissipated power and crosstalk in integrated thermally-reconfigurable Mach-Zehnder interferometers (MZIs), especially when operated in vacuum, with 0.9 mW dissipation for full reconfiguration and 0.5% crosstalk at 785 nm wavelength. To demonstrate the potential of this technology we fabricated and characterized a 6-mode FLW-UPP in a rectangular MZI mesh with 30 thermal shifters

The Araucaria dendrochronological network: growth patterns and climatic signals of paraná-pine on the Southern Brazilian plateau.

Ameridendro

Diabetes Causes Bone Marrow Autonomic Neuropathy and Impairs Stem Cell Mobilization via Dysregulated p66Shc and Sirt1

Diabetes compromises the bone marrow (BM) microenvironment and reduces circulating CD34 + cells. Diabetic autonomic neuropathy (DAN) may impact the BM, because the sympathetic nervous system (SNS) is prominently involved in BM stem cell trafficking. We hypothesize that neuropathy of the BM affects stem cell mobilization and vascular recovery after ischemia in diabetes. We report that, in patients, cardiovascular DAN was associated with fewer circulating CD34 + cells. Experimental diabetes (STZ and Ob/Ob ) or chemical sympathectomy in mice resulted in BM autonomic neuropathy, impaired Lin - cKit + Sca1 + (LKS) cell and endothelial progenitor cells (EPC, CD34 + Flk1 + ) mobilization and vascular recovery after ischemia. DAN increased expression of p66Shc and reduced expression of Sirt1 in mice and humans. p66Shc KO in diabetic mice prevented DAN in the BM, and rescued defective LKS cell and EPC mobilization. Hematopoietic Sirt1 KO mimicked the diabetic mobilization defect, while hematopoietic Sirt1 overexpression in diabetes rescued defective mobilization and vascular repair. Through p66Shc and Sirt1 , diabetes and sympathectomy elevated the expression of various adhesion molecules, including CD62L . CD62L KO partially rescued the defective stem/progenitor cell mobilization. In conclusion, autonomic neuropathy in the BM impairs stem cell mobilization in diabetes with dysregulation of the lifespan regulators p66Shc and Sirt1

Quantifying n -Photon Indistinguishability with a Cyclic Integrated Interferometer

We report on a universal method to measure the genuine indistinguishability of n photons - a crucial parameter that determines the accuracy of optical quantum computing. Our approach relies on a low-depth cyclic multiport interferometer with N=2n modes, leading to a quantum interference fringe whose visibility is a direct measurement of the genuine n-photon indistinguishability. We experimentally demonstrate this technique for an eight-mode integrated interferometer fabricated using femtosecond laser micromachining and four photons from a quantum dot single-photon source. We measure a four-photon indistinguishability up to 0.81±0.03. This value decreases as we intentionally alter the photon pairwise indistinguishability. The low-depth and low-loss multiport interferometer design provides an original path to evaluate the genuine indistinguishability of resource states of increasing photon number

The Peritoneum as a Natural Scaffold for Vascular Regeneration

Objective: The peritoneum has the same developmental origin as blood vessels, is highly reactive and poorly thrombogenic. We hypothesize that parietal peritoneum can sustain development and regeneration of new vessels. Methods and Results: The study comprised two experimental approaches. First, to test surgical feasibility and efficacy of the peritoneal vascular autograft, we set up an autologous transplantation procedure in pigs, where a tubularized parietal peritoneal graft was covered with a metal mesh and anastomosed end-to-end in the infrarenal aorta. Second, to dissect the contribution of graft vs host cells to the newly developed vessel wall, we performed human-to-rat peritoneal patch grafting in the abdominal aorta and examined the origin of endothelial and smooth muscle cells. In pig experiments, the graft remodeled to an apparently normal blood vessel, without thrombosis. Histology confirmed arterialization of the graft with complete endothelial coverage and neointimal hyperplasia in the absence of erosion, inflammation or thrombosis. In rats, immunostaining for human mitochondri revealed that endothelial cells and smooth muscle cells rarely were of human origin. Remodeling of the graft was mainly attributable to local cells with no clear evidence of c-kit+ endothelial progenitor cells or c-kit+ resident perivascular progenitor cells. Conclusions: The parietal peritoneum can be feasibly used as a scaffold to sustain the regeneration of blood vessels, whic

Dynamic Regulation of TWIST1 Expression during Chondrogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells

Human bone marrow-derived mesenchymal stem cells (BMSCs) are clinically promising to repair damaged articular cartilage. This study investigated TWIST1, an important transcriptional regulator in mesenchymal lineages, in BMSC chondrogenesis. We hypothesized that downregulation of TWIST1 expression is required for in vitro chondrogenic differentiation. Indeed, significant downregulation of TWIST1 was observed in murine skeletal progenitor cells during limb development (_N_ = 3 embryos), and during chondrogenic differentiation of culture-expanded human articular chondrocytes (_N_ = 3 donors) and isolated adult human BMSCs (_N_ = 7 donors), consistent with an inhibitory effect of TWIST1 expression on chondrogenic differentiation. Silencing of TWIST1 expression in BMSCs by siRNA, however, did not improve chondrogenic differentiation potential. Interestingly, additional investigation revealed that downregulation of TWIST1 in chondrogenic BMSCs is preceded by an initial upregulation. Similar upregulation is observed in non-chondrogenic BMSCs (_N_ = 5 donors); however, non-chondrogenic cells fail to downregulate TWIST1 expression thereafter, preventing their chondrogenic differentiation. This study describes for the first time endogenous TWIST1 expression during in vitro chondrogenic differentiation of human BMSCs, demonstrating dynamic regulation of TWIST1 expression whereby upregulation and then downregulation of TWIST1 expression are required for chondrogenic differentiation of BMSCs. Elucidation of the molecular regulation of, and by, TWIST1 will provide targets for optimization of BMSC chondrogenic differentiation culture