Polariton-polariton scattering in microcavities: A microscopic theory

We apply the fermion commutation technique for composite bosons to polariton-polariton scattering in semiconductor planar microcavities. Derivations are presented in a simple and physically transparent fashion. A procedure of orthogonolization of the initial and final two-exciton state wavefunctions is used to calculate the effective scattering matrix elements and the scattering rates. We show how the bosonic stimulation of the scattering appears in this full fermionic approach whose equivalence to the bosonization method is thus demonstrated in the regime of low exciton density. We find an additional contribution to polariton-polariton scattering due to the exciton oscillator strength saturation, which we analyze as well. We present a theory of the polariton-polariton scattering with opposite spin orientations and show that this scattering process takes place mainly via dark excitonic states. Analytical estimations of the effective scattering amplitudes are given.Comment: Theoretical paper on polariton-polariton scattering in planar microcavities. The new version contains a slightly modified abstract and a revised introduction. Typos have been corrected wherever spotted. 16 page

Resonant Fibonacci Quantum Well Structures

We propose a resonant one-dimensional quasicrystal, namely, a multiple quantum well (MQW) structure satisfying the Fibonacci-chain rule with the golden ratio between the long and short inter-well distances. The resonant Bragg condition is generalized from the periodic to Fibonacci MQWs. A dispersion equation for exciton-polaritons is derived in the two-wave approximation, the effective allowed and forbidden bands are found. The reflection spectra from the proposed structures are calculated as a function of the well number and detuning from the Bragg condition.Comment: 5 pages, 3 figures, submitted to Phys. Rev.

Fundamental collapse of the exciton-exciton effective scattering

The exciton-exciton effective scattering which rules the time evolution of two excitons is studied as a function of initial momentum difference, scattering angle and electron-to-hole mass ratio. We show that this effective scattering can collapse for energy-conserving configurations provided that the difference between the two initial exciton momenta is larger than a threshold value. Sizeable scatterings then exist in the forward direction only. We even find that, for an electron-to-hole mass ratio close to 1/2, the exciton-exciton effective scattering stays close to zero in all directions when the difference between the initial exciton momenta has a very specific value. This unexpected but quite remarkable collapse comes from tricky compensation between direct and exchange Coulomb processes which originates from the fundamental undistinguishability of the exciton fermionic components.Comment: Revised text version. Accepted for publication in Physical Review

Relationship between Persistent Gastrointestinal Symptoms and Duodenal Histological Findings after Adequate Gluten-Free Diet. A Gray Area of Celiac Disease Management in Adult Patients

A gluten-free diet (GFD) leads to a rapid improvement in gastrointestinal (GI) symptoms, biochemical alterations and duodenal histological damage in the majority of celiac disease (CD) patients. This study aimed to assess the frequency and factors associated with the persistence of GI symptoms/malabsorption signs and their relationship with duodenal histological findings among CD patients on an adequate GFD (mean duration 16 months, range 12-28 months). This longitudinal cohort study included 102 adult CD patients (median age 38.5 years, range 18-76 years, F = 71.6%) diagnosed between 2012 and 2018. A total of 36.3% of the included patients had persistent GI symptoms and/or malabsorption signs (Group 1), while the remaining patients had complete GI well-being without malabsorption signs (Group 2) at the time of histological re-evaluation. The persistence of GI symptoms/signs was associated with a long duration of symptoms/signs before CD diagnosis (>= 5 years) (OR 5.3; 95% CI 1.3-21.8) and the presence of constipation at the time of CD diagnosis (OR 7.5; 95% CI 1.3-42) while for other variables, including age at CD diagnosis, sex, duration of GFD, comorbidities, CD serology positivity and severity of duodenal damage at histological re-evaluation, no association was found. According to our results, the persistence of symptoms/signs is not associated with histological findings, and their relationship could be a gray area in CD management

Diabetes promotes invasive pancreatic cancer by increasing systemic and tumour carbonyl stress in Kras G12D/+mice

Background: Type 1 and 2 diabetes confer an increased risk of pancreatic cancer (PaC) of similar magnitude, suggesting a common mechanism. The recent finding that PaC incidence increases linearly with increasing fasting glucose levels supports a central role for hyperglycaemia, which is known to cause carbonyl stress and advanced glycation end-product (AGE) accumulation through increased glycolytic activity and non-enzymatic reactions. This study investigated the impact of hyperglycaemia on invasive tumour development and the underlying mechanisms involved. Methods: Pdx1-Cre;LSL-Kras G12D/+ mice were interbred with mitosis luciferase reporter mice, rendered diabetic with streptozotocin and treated or not with carnosinol (FL-926-16), a selective scavenger of reactive carbonyl species (RCS) and, as such, an inhibitor of AGE formation. Mice were monitored for tumour development by in vivo bioluminescence imaging. At the end of the study, pancreatic tissue was collected for histology/immunohistochemistry and molecular analyses. Mechanistic studies were performed in pancreatic ductal adenocarcinoma cell lines challenged with high glucose, glycolysis- and glycoxidation-derived RCS, their protein adducts AGEs and sera from diabetic patients. Results: Cumulative incidence of invasive PaC at 22 weeks of age was 75% in untreated diabetic vs 25% in FL-926-16-gtreated diabetic and 8.3% in non-diabetic mice. FL-926-16 treatment suppressed systemic and pancreatic carbonyl stress, extracellular signal-regulated kinases (ERK) 1/2 activation, and nuclear translocation of Yes-associated protein (YAP) in pancreas. In vitro, RCS scavenging and AGE elimination completely inhibited cell proliferation stimulated by high glucose, and YAP proved essential in mediating the effects of both glucose-derived RCS and their protein adducts AGEs. However, RCS and AGEs induced YAP activity through distinct pathways, causing reduction of Large Tumour Suppressor Kinase 1 and activation of the Epidermal Growth Factor Receptor/ERK signalling pathway, respectively. Conclusions: An RCS scavenger and AGE inhibitor prevented the accelerating effect of diabetes on PainINs progression to invasive PaC, showing that hyperglycaemia promotes PaC mainly through increased carbonyl stress. In vitro experiments demonstrated that both circulating RCS/AGEs and tumour cell-derived carbonyl stress generated by excess glucose metabolism induce proliferation by YAP activation, hence providing a molecular mechanism underlying the link between diabetes and PaC (and cancer in general)

The RNA-binding protein MEX3A is a prognostic factor and regulator of resistance to gemcitabine in pancreatic ductal adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer. Most patients present with advanced disease at diagnosis, which only permits palliative chemotherapeutic treatments. RNA dysregulation is a hallmark of most human cancers, including PDAC. To test the impact of RNA processing dysregulation on PDAC pathology, we performed a bioinformatics analysis to identify RNA-binding proteins (RBPs) associated with prognosis. Among the 12 RBPs associated with progression-free survival, we focused on MEX3A because it was recently shown to mark an intestinal stem cell population that is refractory to chemotherapeutic treatments, a typical feature of PDAC. Increased expression of MEX3A was correlated with higher disease stage in PDAC patients and with tumor development in a mouse model of PDAC. Depletion of MEX3A in PDAC cells enhanced sensitivity to chemotherapeutic treatment with gemcitabine, whereas its expression was increased in PDAC cells selected upon chronic exposure to the drug. RNA-sequencing analyses highlighted hundreds of genes whose expression is sensitive to MEX3A expression, with significant enrichment in cell cycle genes. MEX3A binds to its target mRNAs, like cyclin-dependent kinase 6 (CDK6), and promotes their stability. Accordingly, knockdown of MEX3A caused a significant reduction in PDAC cell proliferation and in progression to the S phase of the cell cycle. These findings uncover a novel role for MEX3A in the acquisition and maintenance of chemoresistance by PDAC cells, suggesting that it may represent a novel therapeutic target for PDAC

Chemotherapy resistance of glioblastoma stem cells [2]

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