Inversion Ring in Chromonic Twisted Hedgehogs: Theory and Experiment

Twisted hedgehogs are defects in spherical cavities with homeotropic anchoring for the nematic director that arise when twist distortions are sufficiently less energetic than splay (and bend) distortions. They bear a characteristic inversion ring, where the director texture changes the sense it spirals about the center of the cavity. This paper applies a quartic twist theory recently proposed to describe the elasticity of chromonics to explain a series of inversion rings observed in aqueous solutions of SSY at two different concentrations. The theory features a phenomenological length a, whose measure is extracted from the data and shown to be fairly independent of the cavity radius, as expected for a material constant

Macrophage miR-210 induction and metabolic reprogramming in response to pathogen interaction boost life-threatening inflammation

Unbalanced immune responses to pathogens can be life-threatening although the underlying regulatory mechanisms remain unknown. Here, we show a hypoxia-inducible factor 1α–dependent microRNA (miR)–210 up-regulation in monocytes and macrophages upon pathogen interaction. MiR-210 knockout in the hematopoietic lineage or in monocytes/macrophages mitigated the symptoms of endotoxemia, bacteremia, sepsis, and parasitosis, limiting the cytokine storm, organ damage/dysfunction, pathogen spreading, and lethality. Similarly, pharmacologic miR-210 inhibition improved the survival of septic mice. Mechanistically, miR-210 induction in activated macrophages supported a switch toward a proinflammatory state by lessening mitochondria respiration in favor of glycolysis, partly achieved by downmodulating the iron-sulfur cluster assembly enzyme ISCU. In humans, augmented miR-210 levels in circulating monocytes correlated with the incidence of sepsis, while serum levels of monocyte/macrophage-derived miR-210 were associated with sepsis mortality. Together, our data identify miR-210 as a fine-tuning regulator of macrophage metabolism and inflammatory responses, suggesting miR-210–based therapeutic and diagnostic strategies

Risk factors in the development of dysphonia in childhood

Aim: Childhood dysphonia has an estimated incidence of 6–24%. Dysphonia may adversely impact the child’s communicative effectiveness, social and educational development, self-esteem and participation in school group activities. It is commonly believed that children become dysphonic due to vocal misuse behaviors, however there are no consistent data in the few studies published on this topic. Our aim was to evaluate the influence of some potential risk factors on the development of childhood dysphonia. Sources and methods: 33 consecutive dysphonic children with vocal folds nodules underwent a phoniatric examination in the Phoniatric Unit of the “Azienda Policlinico Umberto I Hospital” of Rome. The mean age was 10 years (Ds ± 2 ys). Several risk factor were examined, such as temperament, ENT pathologies, number of siblings, sport practices, scouting, extended school, singing activities, environmental noise in classrooms. Data were compared with a control group of 33 matched children without voice pathologies. Results: the incidence of allergy, sport practices and extended school was found significantly higher in the group of dysphonic children compared with the control group. Furthermore also a prevalence of extrovert and anxious personality in dysphonic children was found. Conclusions: data from our study on risk factors, that act in the development of dysphonia in childhood, stress the relevance of both personality and behavioral factors. It would be useful to encourage the diffusion of information to show the risks related to voice abuse in children, in order to prevent the development of pediatric dysphonia. It would also be necessary to develop instruments specifically designed to examine personality dispositions in dysphonic children

Inversion ring in chromonic twisted hedgehogs: theory and experiment

Twisted hedgehogs are defects in spherical cavities with homeotropic anchoring for the nematic director that arise when twist distortions are sufficiently less energetic than splay (and bend) distortions. They bear a characteristic inversion ring, where the director texture changes the sense it spirals about the centre of the cavity. This paper applies a quartic twist theory recently proposed to describe the elasticity of chromonics to explain a series of inversion rings observed in spherical microcavities containing aqueous solutions of SSY at two different concentrations. The theory features a phenomenological length a, whose measure is extracted from the data and shown to be fairly independent of the cavity radius, as expected for a material constant

Long-Term Stability of TiS₂–Alkylamine Hybrid Materials

Layered TiS2 intercalated with linear alkylamines has recently attracted significant interest as a model compound for flexible n-type thermoelectric applications, showing remarkably high power factors at room temperature. The thermal and, particularly, environmental stability of such materials is, however, a still an open challenge. In this paper, we show that amine-intercalated TiS2 prepared by a simple mechanochemical process is prone to chemical decomposition through sulfur exsolution, and that the presence of molecular oxygen is likely to mediate the decomposition reaction. Through computational analysis of the possible reaction pathways, we propose that Ti-N adducts are formed as a consequence of amine groups substituting for S vacancies on the internal surfaces of the S-Ti-S layers. These findings provide insights for possible future applications of similar hybrid compounds as devices operating in ambient conditions, and suggest isolating them from atmospheric oxygen

Toxic and Potentially Toxic Mineral Elements of Edible Gastropods Land Snails (Mediterranean Escargot)

The meat of snails can be considered a high-quality food for the human diet and demand is already increasing across Europe. Due to the bioaccumulation of trace elements in their tissues, land snails can be a significant tool also for environmental pollution evaluation. In this study, 28 mineral elements (Ag, Al, As, B, Ba, Be, Bi, Cd, Co, Cr, Cu, Fe, Hg, K, Li, Na, Mg, Mn, Mo, Ni, Pb, Sb, Se, Sr, Ti, Tl, V, Zn) in both the edible part and the shell of edible land snails commercially available in Southern Italy belonging to Cernuella virgata, Helix aperta, Theba pisana species were investigated by ICP-MS and direct mercury analyser. The concentration of trace elements was variable among the samples. The variability demonstrates the close connection among the type of snail, the geographical origin, and the habitat in which the species grows. The edible part of the snails analysed in this study was found to be a good source of macro-nutrients. Toxic elements were detected in some samples, especially in shells; nevertheless, the values fell within the safety limits. Further investigations and monitoring of mineral contents in edible land snails are suggested both for human health and environmental pollution evaluation

Macrophage-derived glutamine boosts satellite cells and muscle regeneration

Muscle regeneration is sustained by infiltrating macrophages and the consequent activation of satellite cells1-4. Macrophages and satellite cells communicate in different ways1-5, but their metabolic interplay has not been investigated. Here we show, in a mouse model, that muscle injuries and ageing are characterized by intra-tissue restrictions of glutamine. Low levels of glutamine endow macrophages with the metabolic ability to secrete glutamine via enhanced glutamine synthetase (GS) activity, at the expense of glutamine oxidation mediated by glutamate dehydrogenase 1 (GLUD1). Glud1-knockout macrophages display constitutively high GS activity, which prevents glutamine shortages. The uptake of macrophage-derived glutamine by satellite cells through the glutamine transporter SLC1A5 activates mTOR and promotes the proliferation and differentiation of satellite cells. Consequently, macrophage-specific deletion or pharmacological inhibition of GLUD1 improves muscle regeneration and functional recovery in response to acute injury, ischaemia or ageing. Conversely, SLC1A5 blockade in satellite cells or GS inactivation in macrophages negatively affects satellite cell functions and muscle regeneration. These results highlight the metabolic crosstalk between satellite cells and macrophages, in which macrophage-derived glutamine sustains the functions of satellite cells. Thus, the targeting of GLUD1 may offer therapeutic opportunities for the regeneration of injured or aged muscles.status: publishe

Reprogramming of Amino Acid Transporters to Support Aspartate and Glutamate Dependency Sustains Endocrine Resistance in Breast Cancer

Endocrine therapy (ET) is the standard of care for estrogen receptor-positive (ER+) breast cancers. Despite its efficacy, ∼40% of women relapse with ET-resistant (ETR) disease. A global transcription analysis in ETR cells reveals a downregulation of the neutral and basic amino acid transporter SLC6A14 governed by enhanced miR-23b-3p expression, resulting in impaired amino acid metabolism. This altered amino acid metabolism in ETR cells is supported by the activation of autophagy and the enhanced import of acidic amino acids (aspartate and glutamate) mediated by the SLC1A2 transporter. The clinical significance of these findings is validated by multiple orthogonal approaches in a large cohort of ET-treated patients, in patient-derived xenografts, and in in vivo experiments. Targeting these amino acid metabolic dependencies resensitizes ETR cells to therapy and impairs the aggressive features of ETR cells, offering predictive biomarkers and potential targetable pathways to be exploited to combat or delay ETR in ER+ breast cancers.status: publishe

Reprogramming of Amino Acid Transporters to Support Aspartate and Glutamate Dependency Sustains Endocrine Resistance in Breast Cancer

Endocrine therapy (ET) is the standard of care for estrogen receptor-positive (ER+) breast cancers. Despite its efficacy, ∼40% of women relapse with ET-resistant (ETR) disease. A global transcription analysis in ETR cells reveals a downregulation of the neutral and basic amino acid transporter SLC6A14 governed by enhanced miR-23b-3p expression, resulting in impaired amino acid metabolism. This altered amino acid metabolism in ETR cells is supported by the activation of autophagy and the enhanced import of acidic amino acids (aspartate and glutamate) mediated by the SLC1A2 transporter. The clinical significance of these findings is validated by multiple orthogonal approaches in a large cohort of ET-treated patients, in patient-derived xenografts, and in in vivo experiments. Targeting these amino acid metabolic dependencies resensitizes ETR cells to therapy and impairs the aggressive features of ETR cells, offering predictive biomarkers and potential targetable pathways to be exploited to combat or delay ETR in ER+ breast cancers