Microcavities filled with conjugated polymer active in strong light–matter interaction regime enable exciton-polariton condensates at room temperature. By imprinting lattices through nanostructuring and using a tunable platform, we can explore solid-state physics toy models.

An ensemble of emitters can behave significantly different from its individual constituents when interacting coherently via a common light field. After excitation, collective coupling gives rise to an intriguing many-body quantum phenomenon, resulting in short, intense bursts of light: so-called superfluorescence. Because it requires a fine balance of interaction between the emitters and their decoupling from the environment, together with close identity of the individual emitters, superfluorescence has thus far been observed only in a limited number of systems, such as atomic and molecular gases and semiconductor crystals, and could not be harnessed for applications. For colloidal nanocrystals, however, which are of increasing relevance in a number of opto-electronic applications, the generation of superfluorescent light was precluded by inhomogeneous emission broadening, low oscillator strength, and fast exciton dephasing. Using caesium lead halide (CsPbX3, X = Cl, Br) perovskite nanocrystals that are self-organized into highly ordered three-dimensional superlattices allows us to observe key signatures of superfluorescence: red-shifted emission with more than ten-fold accelerated radiative decay, extension of the first-order coherence time by more than a factor of four, photon bunching, and delayed emission pulses with Burnham-Chiao ringing behaviour at high excitation density. These mesoscopically extended coherent states can be employed to boost opto-electronic device performances and enable entangled multi-photon quantum light sources.

Background: The effects of acute excessive alcohol ingestion on echocardiographic parameters of left ventricular (LV) function are unclear.Methods: One hundred ninety-nine healthy subjects (44 6 5 years, 71% male) were prospectively examined within 6 hours after excessive alcohol ingestion as well as after 4 weeks with strict alcohol abstinence. Echocardiography was performed at baseline and follow-up for conventional parameters (left ventricular ejection fraction [LVEF], transmitral E and A Doppler flow velocities, E/A ratio, tissue Doppler velocity lateral and septal (e), E/e ratio, deceleration time of E, and isovolumic relaxation time) and myocardial deformation data (such as global radial and global and layer-specific circumferential [endo and epi global CS] and longitudinal [endo and epi global LS] strain). Multivariate regression was used to assess the impact of independent variables on echocardiographic parameters.Results: Alcohol levels were 1.2 +/- 0.3 g/ L at the time of drinking cessation. After alcohol ingestion endo CS (30% +/- 2% vs 37% +/- 3%, P = .008) and endo LS (27% +/- 4% vs 33% +/- 3%, P = .002) were significantly lower at baseline versus follow- up. Blood pressure, LVEF and heart rate, and other echocardiographic parameters did not differ between the two examinations. Alcohol levels were modestly, negatively associated with change in endo CS and endo LS (r = -0.54, 95% CI, -0.63 to -0.43, P < .001; and r = -0.26, 95% CI, -0.39 to -0.14; P < .003, respectively). Alcohol levels were the strongest predictor for endo CS (beta = -4.84; 95% CI, -6.31 to -3.37) and endo LS (beta= -2.50; 95% CI, -4.32 to -0.68).Conclusions: Acute alcohol ingestion effects endocardial CS and LS, suggesting an acute and transient toxic effect on myocardial deformation, an effect that remains undetected by conventional echocardiographic parameters. The current findings may help clinicians to gain more understanding into the mechanism of developing an alcohol cardiomyopathy and to detect early persistent alcohol-induced myocardial disturbances for an effective therapy in time to prevent harm. (J Am Soc Echocardiogr 2017; 30: 235-43.)

GLS was better than other risk scoring model (c-statistic 0.879, 95% CI 0.820-0.939,p<0.001).Figure 1.ROC curve for 30-day mortality.Conclusions: LV GLS is strong and independent predictor of 30-day mortality in patients with STEMI after primary PCI.Prognostic capacity of GLS is better than risk score model.

Recently, a report by Grim et al.1 highlighted the peculiar carrier dynamics in CdSe platelets as they were able to develop amplified spontaneous emission and lasing action under continuous wave (CW) conditions. An exciting prospect, yet remarkable as various literature reports , e.g. by Pelton et al.2, indicated the need for high exciton (X) densities of up to 50 X per platelet in order to observe any bleach of the band edge under pulsed excitation. Using transient absorption spectroscopy, we show that optical gain upon off-resonance (3.1 eV) pumping indeed only develops at exciton densities of up to 80 electron-hole (eh) pairs per platelet, a density suprisingly close to the Mott density. Reducing the excess energy per carrier by pumping the light-hole transition resonantly, we observe a decrease in the gain threshold to 20 eh-pairs. The observation of room-temperature lasing in the low density regime , the case of Grim et al. , can be matched with these observations if we assume a eh-plasma gain controlled by the temperature of the plasma itself. The latter can remain quite high due to surprisingly slow cooling. Remarkably, this scenario implies that the formation and existence of well-bound excitons is counterproductive for gain development as is evidenced by our data.

Background Two replicate, randomized, core Phase III trials (CLEAR 1 and 2) reported significantly more subjects treated with lesinurad 200 mg (LESU200) or 400 mg (LESU400) combined with allopurinol (ALLO) achieved target sUA <6.0 mg/dL at 6 and 12 months than ALLO+placebo (PBO) (P<0.0001). The safety profile of LESU200+ALLO was comparable to ALLO+placebo, except for higher rates of predominantly reversible serum creatinine (sCr) elevation. Objectives Assess long-term safety and efficacy of LESU+ALLO therapy in subjects enrolled in the CLEAR 1and 2 extension study (NCT01808131). Methods Efficacy was assessed for those completing the core study and either 1) continuing core LESU+ALLO treatment (200CONT, 400CONT) or 2) crossing over from core ALLO+PBO to either ALLO+LESU200 (200CROSS) or LESU400 (400CROSS). Core LESU200+ALLO or LESU400+ALLO subjects and 200CONT and 400CONT extension groups are reported for safety. Efficacy endpoints included proportions of subjects with target sUA <6.0 mg/dL and mean sUA levels (ITT–observed cases). Treatment-emergent adverse events (TEAEs) were calculated as exposure-adjusted incidence rates (EAIRs; events per 100 person-years [100-PY]). Results For efficacy, the 200CONT (n=239) and 400CONT (n=232) groups receiving treatment for up to 24 months, and 200CROSS (n=121) and 400CROSS (n=122) groups, receiving treatment for up to 12 months, were analyzed. Proportions of subjects with sUA <6.0 mg/dL during core and extension are shown (Figure). Mean (SD) sUA (mg/dL) for 200CONT, 200CROSS, 400CONT and 400CROSS groups, respectively, were 6.96 (1.14), 6.92 (1.33), 6.80 (1.20) and 6.99 (1.14) at baseline of the core studies, and 5.71 (1.80), 6.68 (1.57), 5.06 (1.94) and 6.68 (1.38) at the end of the 12-month core studies. After 12 months in the extension study when all patients received lesinurad, mean (SD) sUA was 5.75 (1.77), 5.78 (1.92), 5.01 (1.95), and 5.25 (1.77), respectively. For safety, pooled analysis on a total of 405 and 401 subjects (LESU200, LESU400 respectively), from the core studies and 239 and 232 (200CONT, 400CONT, respectively) from the extension studies, was conducted. EAIRs (per 100-PY) of TEAEs and serious TEAEs at any time during core or extension studies were 54.2 and 5.8 for LESU200 and 57.2 and 8.3 for LESU400. EAIRs of renal-related TEAEs and serious renal-related TEAEs were 7.4 and 0.5 for LESU200 and 14.2 and 0.8 for LESU400. EAIRs of kidney stone incidence rates were 0.5 and 2.0 per 100-PY for LESU200 and LESU400, respectively. EAIRs of sCr elevations ≥1.5x baseline was 7.8 and 17.0 per 100-PY for LESU200 and LESU400, respectively; resolution of sCr elevations by analysis cutoff occurred in 91.7% and 87.8% of cases, respectively. Conclusions Subjects treated with LESU+ALLO therapy through 2 years continued to be at sUA target; those crossing over from ALLO monotherapy had increased proportions reach target. Safety during continued treatment was consistent throughout the core and extension studies. Acknowledgement This study was funded by Ardea Biosciences/AstraZeneca. Disclosure of Interest K. Saag Grant/research support from: Ardea Biosciences, Inc., a member of the AstraZeneca Group; Crealta, Takeda, Consultant for: Ardea Biosciences Inc., a member of the AstraZeneca Group; AstraZeneca; Takeda, M. Becker Consultant for: Ardea Biosciences Inc., a member of the AstraZeneca Group; AstraZeneca; Takeda; Crealta; CymaBay; BioCryst; Pfizer, C. Storgard Employee of: Ardea Biosciences, Inc., a member of the AstraZeneca Group, M. Fung Employee of: Ardea Biosciences, Inc., a member of the AstraZeneca Group, N. Bhakta Employee of: Ardea Biosciences, Inc., a member of the AstraZeneca Group, S. Adler Employee of: AstraZeneca, J. Hu Employee of: Ardea Biosciences, Inc., a member of the AstraZeneca Group, T. Bardin Grant/research support from: Ipsen; Menarini, Consultant for: AstraZeneca; Ipsen; Menarini; Novartis; Savient; Sobi; Takeda

Data on the polarization observables T, P, and H for the reaction gamma p -> p pi(0) are reported. Compared to earlier data from other experiments, our data are more precise and extend the covered range in energy and angle substantially. The results were extracted from azimuthal asymmetries measured using a transversely polarized target and linearly polarized photons. The data were taken at the Bonn electron stretcher accelerator ELSA with the CBELSA/TAPS detector. Within the Bonn-Gatchina partial wave analysis, the new polarization data lead to a significant narrowing of the error band for the multipoles for neutral-pion photoproduction. (C) 2015 The Authors. Published by Elsevier B.V.

AimAssess influences of demographics and co-morbidities of gout patients with or without diabetes on safety and efficacy of urate-lowering agents.MethodsPost-hoc analysis of 312 diabetic and 1957 non-diabetic gout patients [baseline serum urate levels (sUA) 8.0mg/dl] enrolled in a 6-month randomized controlled trial comparing urate-lowering efficacy (ULE) and safety of daily xanthine oxidase inhibitors (XOIs) febuxostat (40mg or 80mg) and allopurinol (200mg or 300mg). We compared baseline demographic, gout and co-morbid characteristics, ULE, and safety of XOI treatment in diabetic and non-diabetic gout patients. ULE was measured by the proportion of diabetic and non-diabetic patients in each treatment group achieving final visit sUA<6.0mg/dl. Safety was monitored throughout the trial.ResultsDiabetic gout patients were older, more frequently female, and had longer gout duration. Co-morbidities were more frequent among diabetic patients: cardiovascular disease; impaired renal function; hyperlipidemia; and obesity (body mass index >30kg/m(2)) (p<0.001 for all comparisons). Febuxostat 80mg ULE exceeded that of febuxostat 40mg or allopurinol (p<0.050) at all levels of renal function, achieving sUA goal range in the majority of diabetic and non-diabetic patients. Diabetics and non-diabetics reported self-limiting diarrhoea and URIs as the most common adverse events.ConclusionsDespite higher co-morbidity rates in diabetic patients, febuxostat and allopurinol were safe in both groups at the doses tested. Febuxostat 80mg achieved sUA <6.0mg/dl more often than febuxostat 40mg or allopurinol at commonly prescribed doses.

Aim: Prospective, randomized study to examine the feasibility of an intraprocedural determination of myocardial viability (MV) by myocardial deformation imaging: patients with a relevant coronary stenosis and analogous severe myocardial dysfunction (MD) were studied within the Cath Lab (CL). Background: Evidence of residual MV in patients with ischemic MD has important therapeutic and prognostic implications. The benefit of revascularization for functional recovery depends on the presence of MV. At present patients with a relevant coronary stenosis and analogous severe regional MD are transfered to a two-step determination of MV by low-dose-dobutamin-echocardiography (DSE) or cardiovascular magnetic resonance (CMR). The myocardial deformation imaging by 2D Strain analysis allows a reliable determination of layer specific MV. Methods: Inclusion of 111 patients (pts) (62% men, age 59±8 years) with relevant coronary stenosis and analogous severe regional MD. Randomization in 2 groups: Group A: intraprocedural 2D Strain-Analysis within the CL after coronary angiogram, determination of residual MD by endocardial circumferential Strain (CS) > -20% (defined as optimal strain parameter/cut-off value by a pilot study in 55 pts compared to CMR), in case of positive MV immediate coronary intervention within one session. Group B: after coronary angiogram interruption of the session, two-step determination of MV by DSE or CMR, in case of positive MV anew session with coronary intervention. After 6 months analysis of the endpoints: primary: incidence of cardiovascular events, secondary: improvement of left ventricular (LV) function and comparison of costs. Results: Group A with 57 pts (79% with residual myocardial viability (CS>-20%) and coronary intervention within one session), group B with 54 Pt (82% with residual myocardial viability (increase of regional myocardial contractility by DSE or CMR) and coronary intervention at a second session). Cardiovascular events: group A 2.4% vs. group B 2.3%, p=0.224. Improvement of LV function: group A:+7% vs. group B:+6%, p=0.318. Costs: group A: 1.072 Euro vs. group B: 2.174 Euro, p<0.001. Conclusion: Intraprocedural determination of MV by myocardial deformation imaging within the CL is feasible and not inferior to the present approach of a two-step examination using DSE or CMR regarding cardiovascular events and improvement of LV function but superior regarding costs. Thus, the intraprocedural approach may be established generally to avoid hitherto existing procedure of two-step viability diagnostics with corresponding costs and patient exposure in this daily cohort.

Background: This study sought to determine the time sequence of post systolic thickening as marker of myocardial ischemia measured by ultrasonic strain for an endocardial and epicardial myocardial layer in acute ischemia as well as subsequent reperfusion. Methods: In 15 patients (age 61±10 years) 2D echocardiography was performed continuously during PCI of a proximal large coronary artery for 30 seconds of acute myocardial ischemia as well as the subsequent 30 seconds of myocardial reperfusion. Layer specific myocardial deformation analysis was performed at 5 sec intervals using speckle tracking echocardiography to assess peak systolic longitudinal strain and post-systolic strain index (PSI) of an endocardial and epicardial layer. The Time-to-peak strain index as a parameter of post systolic shortening was calculated as: time-to-peak strain/R-R interval duration. Ischemic segments were compared with the opposing myocardial segments. Results: The onset of post systolic thickening was similar in endocardial as well as epicardial layer. PSI increased significantly at the end of the induced ischemia in the endocardial compared with the control segment (0.17 vs. -0.83, p<0.05) as well as in the epicardial layer (0.23 vs. -0.89, p<0.05). At the end of reperfusion the PSI returned to normal values in the endocardial as well as epicardial layer. Time to post systolic thickening at the onset of ischemia was similar in the segment at risk as well as in the control segment (0.48±0.08%; 0.46±0.07% ns). At 10 seconds after onset of ischemia the time-to-peak strain index increased (0.58±0.09%, 0.45±0.05%, p<0.05) continuing at 20 seconds after ischemia (0.58±0.1%, 0.45±0.07%, p<0.05) as well as at 30 seconds (0.57±0.07%, 0.46±0.05%, p<0.05). 10 seconds after the beginning of reperfusion the time-to-peak strain index was still increased (0.57±0.06%, 0.48±0.06%, p<0.05) following near normal values at 20 seconds (0.54±0.09%, 0.5±0.08%, ns) as well as 30 seconds after reperfusion (0.45±0.18%, 0.44±0.17%, ns). Conclusion: Post systolic thickening occurs simultaneously in endocardial and epicardial layers during acute ischemia due to short total blockage of a coronary artery and subsequent reperfusion. The time-to-peak strain index increased during ischemia, following a normalisation during reperfusion. This finding indicates simultaneous onset of ischemia in the endocardial and epicardial myocardial layer.

Background The tophus is a pathognomonic feature of chronic gout and may cause disability and joint damage. Accordingly, OMERACT has endorsed tophus measurement as a key domain in clinical trials of chronic gout. The approval of febuxostat (FEB) in 2009 and pegloticase (PGL) in 2010 has been accompanied by publications describing clinical trials of urate-lowering therapies (ULTs). These trials also provide detailed data, not previously available, on change in tophus burden in response to treatment in defined gout populations. Objectives We compared tophus resolution in published clinical trials of ULTs that included such measurements. Methods A PubMed search using the terms “gout” and “tophi OR tophus” was performed with the following limits applied: clinical trial, humans, and English. The 15 articles retrieved were evaluated for appropriateness and used to identify additional publications/abstracts. Six trials met the analysis criteria. Results Conclusions Clinical trials of ULTs have not used consistent methods or timepoints to evaluate tophus response. Nevertheless, pegloticase treatment results in more robust and rapid resolution of tophi compared to treatment with febuxostat or allopurinol. References Wallace et al. Arth Rheum 1977;20:895-900. Disclosure of Interest M. Becker Grant/Research support from: Savient, Takeda, Consultant for: Savient, Takeda, Ardea, BioCryst, Regeneron, URL/Mutual/Metabolex/Chugai, R. Yood Grant/Research support from: Savient, Takeda, F. Perez-Ruiz Consultant for: Ardea, Menarini, Novartis, Savient, Speakers Bureau: Ardea, Menarini, Novartis, Savient, N. Dalbeth Grant/Research support from: Fonterra, Consultant for: Takeda, Ardea, Novartis, Abbott, Roche