Polariton Bose-Einstein condensate from a bound state in the continuum.

Bound states in the continuum (BICs)1-3 are peculiar topological states that, when realized in a planar photonic crystal lattice, are symmetry-protected from radiating in the far field despite lying within the light cone4. These BICs possess an invariant topological charge given by the winding number of the polarization vectors5, similar to vortices in quantum fluids such as superfluid helium and atomic Bose-Einstein condensates. In spite of several reports of optical BICs in patterned dielectric slabs with evidence of lasing, their potential as topologically protected states with theoretically infinite lifetime has not yet been fully exploited. Here we show non-equilibrium Bose-Einstein condensation of polaritons-hybrid light-matter excitations-occurring in a BIC thanks to its peculiar non-radiative nature, which favours polariton accumulation. The combination of the ultralong BIC lifetime and the tight confinement of the waveguide geometry enables the achievement of an extremely low threshold density for condensation, which is reached not in the dispersion minimum but at a saddle point in reciprocal space. By bridging bosonic condensation and symmetry-protected radiation eigenmodes, we reveal ways of imparting topological properties onto macroscopic quantum states with unexplored dispersion features. Such an observation may open a route towards energy-efficient polariton condensation in cost-effective integrated devices, ultimately suited for the development of hybrid light-matter optical circuits.

The quality of death certification practice in Greece.

BACKGROUND: Death certification represents an excellent source for mortality statistics and appropriate public health surveillance. Errors in reporting the cause of death impede the development of national health policies and, accordingly, allocation of resources. The aim of this study was to determine the frequency of errors in the cause of death and to identify factors that may be associated with inaccuracies in death certificates. METHODS: A cross-sectional study of all natural death certifications in a defined Greek region was conducted over the period 2006-2010. Specific criteria for major and minor errors were adopted for the evaluation of death certificates. RESULTS: A total of 5,828 death certificates due to natural causes were identified. Major errors were found in 64.6 % of them with almost every death certificate having a minor error. Major error rate did not differ per year (p =0.65). Most commonly encountered major errors were a non-acceptable cause of death (31.2 %) and an incorrect sequencing (16.8 %). Factors affecting their frequency were the age of the deceased (older than 80 years, p =0.025), the area of certificate completion (rural and semi-urban, p <0.001) and doctor's grade (consultant, p <0.026). CONCLUSIONS: High rate of recording errors at death certification influences the accuracy of the cause of death in a defined region in Southern Greece. Due to their impact on mortality statistics and health policies, standard practices of death certification should be established. Coordinated educational interventions are expected to play a significant role on this. Hippokratia 2016, 20(1): 19-25.

Immune responses during and after exercise of constant and alternating intensity above the lactate threshold.

AIM: Intense and prolonged exercise greatly affects circulating cytokine levels. The purpose of this study was to investigate the possible changes in tumour necrosis factor -a (TNF-a), interleukin 6 (IL-6) and cortisol concentrations during and after prolonged exercise of constant and alternating intensity of the same duration and total work performed. METHODS: Ten male subjects underwent two main cycling exercise trials lasting one hour each. On one occasion, exercise intensity was alternated between 46.5±1.9% of maximal oxygen uptake (VO2max ) for 40 s and 120% of VO2max for 20 s, so that the mean intensity corresponded to 105% of the lactate threshold. On the other occasion, exercise intensity was constant at 105% of the lactate threshold. Levels of TNF-a, IL-6 after lipo polysaccharide (LPS) stimulation as well as cortisol were measured at rest, 30 and 60 minutes of exercise and 1 hour after. RESULTS: No significant differences were observed in TNF-a concentrations between the two exercise protocols (P= 0.75), but there was a significant time effect (P<0.01). TNF-a was increased in both groups from a resting value of 436.1±102.5 to 649.5±187.7 pg/mL (P<0.05) at the end of exercise and was subsequently decreased 1 hour post exercise to 305.9±78.8 pg/mL (P<0.01). No significant difference in IL-6 and cortisol concentrations was observed between the two exercise protocols (P=0.13, P=0.10 accordingly). CONCLUSION: In conclusion, prolonged constant and alternating intensity exercise of the same mean intensity and duration seemed to provoke similar changes in aspects of immune response in healthy subjects.

Heart disease in thalassemia intermedia.

Thalassemia intermedia (TI) presents with a clinical phenotype ranging between the severe, transfusion-dependent TM and the asymptomatic carrier state. Cardiovascular complications represent the primary cause of mortality both in TM and in TI. Several factors have been reported to interfere in the pathophysiology of cardiovascular abnormalities in TI, including high output state, vascular abnormalities, endothelial dysfunction, elastic tissue disorders, hypercoagulability, valvular abnormalities and, to a less extent, iron overload. These mechanisms end up affecting both left and right heart, hence leading to ventricular remodeling and finally heart failure.

Assessment and treatment of cardiac iron overload in thalassemia.

Cardiac disease remains the major cause of death in thalassemia major and iron overload is involved in heart failure development. Cardiac iron load and heart injury are evaluated by different means, among which CMR measurements remain the best method for estimation. In cases of heart iron overload, chelation treatment should be appropriately tailored in terms of intensification.

Severe aseptic inflammation caused by long distance running (246 km) does not increase procalcitonin.

BACKGROUND: The Spartathlon ultra distance running race (246 kilometres) is an exhausting physical exercise leading to a state of systemic inflammation associated with dramatic elevation of interleukin-6 and acute-phase reactants to levels seen only in critically ill or patients near death. We sought to study the effect of this severe inflammatory response on the levels of serum procalcitonin. MATERIALS AND METHODS: Fifteen healthy endurance-trained runners who participated in the 2006 Spartathlon were studied. Blood samples were taken the day before the race, within 15 min after the end of the race and 48 h after the end of the race. Serum interleukin-6, serum amyloid A protein, C-reactive protein, tumour necrosis factor-alpha and procalcitonin concentrations were determined. RESULTS: Serum interleukin-6, serum amyloid A protein and C-reactive protein were dramatically increased after the end of the race (150-, 116- and 10,470- fold increase of the mean values, respectively). Procalcitonin levels remained within normal range (mean +/- standard error of mean, 0.27 +/- 0.02 microg L(-1), 0.26 +/- 0.02 microg L(-1) and 0.27 +/- 0.02 microg L(-1) before, at the end, and 48 h after the race, respectively). Tumour necrosis factor-alpha measurements revealed no significant changes. CONCLUSIONS: This study provides strong evidence that Spartathlon, a prolonged endurance exercise resulting in severe stimulation of inflammatory mediators followed by muscle and liver damage, does not induce procalcitonin secretion. The findings cannot directly be applied to other causes of aseptic inflammation.

Changes in free radical generation and antioxidant capacity during ultramarathon foot race.

BACKGROUND: Exhaustive exercise has been implicated in the generation of reactive oxygen species, resulting in oxidative stress. We studied the effect of a long-distance, endurance exercise on oxidative stress parameters in athletes who participated in the ultramarathon race Spartathlon (246 km). MATERIALS AND METHODS: This study included 18 runners (16 men and 2 women) aged 42.8 +/- 1.4 years. Blood samples were obtained 24 h before (prerace), at the end (postrace) and 48 h after the end of the race (48 h postrace). We measured oxidative stress indices, including red cell glutathione, malonyldialdehyde and 8-iso-prostaglandin F(2a), as well as the total antioxidant capacity. RESULTS: 8-Iso-prostaglandin F(2a) level increased significantly at the end of the race, compared to prerace levels (up to 914.7 +/- 61.4 pg mL(-1) from 197.6 +/- 8.4 pg mL(-1)), and remained 2.5-fold increased over the baseline 48 h after the race (532.0 +/- 54.2 pg mL(-1), P < 0.000). The total antioxidant capacity of the athletes increased from a baseline of 289.6 +/- 9.0 micromol L(-1) to 358.7 +/- 11.0 micromol L(-1) immediately after the race and remained elevated 48 h later (350.6 +/- 7.6 micromol L(-1)) (P < 0.001). CONCLUSIONS: Prolonged exercise induces a marked response of oxidative stress biomarkers, which in part is compensated by serum ability to scavenge free radicals. Whether these changes have long-term negative effects in the organism needs further investigation.

Dramatic reduction of erythrocyte glucose-6-phosphate dehydrogenase activity in athletes participating in the ultradistance foot race "Spartathlon".

OBJECTIVE: To investigate the effect of a long-distance endurance exercise "Spartathlon" on erythrocyte glucose-6-phosphate dehydrogenase (G(6)PD) activity. MATERIAL AND METHODS: The study comprised 15 male runners, median age 36.5 years. Blood samples were obtained in the 15 min before the race and again within 15 min after the end of the race. Erythrocyte glutathione (GSH and GSSG) and plasma malonyldialdehyde were measured with HPLC methods, and total antioxidant capacity (TAC), total hyperoxides and G(6)PD activity with commercial kits. Lipids, uric acid and total bilirubin were determined with a clinical chemistry analyser. RESULTS: Total hyperoxides were found statistically reduced, whereas total bilirubin was measured elevated post-race. Interestingly, GSSG levels were found increased (167.3+/-12.0 versus 219.5+/-20.3 micromol/L; p<0.005) as well as GSSG/GSH ratio (16.0+/-1.3 versus 20.60+/-1.65; p<0.05) post-race. In contrast, G(6)PD activity was found remarkably decreased (8.72+/-3.10 versus 3.8+/-2.5 U/g Hb; p<0.0001) pre versus post the event. CONCLUSION: Red blood cell G(6)PD activity in athletes may be reduced post-race as a consequence of the modulation of NADP/NADPH levels and elevation of the erythrocyte GSSG, and especially GSSG/GSH ratio, resulting in an impairment of the hexose monophosphate shunt.

Hypocalcemic heart failure in thalassemic patients.

Hypocalcemic cardiomyopathy in primary or secondary hypoparathyroidism is usually refractory to conventional treatment of cardiac failure. We report the case of a thalassemic patient with severe cardiac failure that might have been attributed to several factors, such as hemosiderosis, hypomagnesemia, and hypocalcemia, refractory to conventional cardiac therapy. Cardiac echocardiography showed impaired biventricular performance, and laboratory analyses revealed hypoparathyroidism due to hemosiderosis. When concomitant treatment of heart failure and calcium supplementation was initiated, correction of hypocalcemia resulted in clinical and laboratory improvement, providing strong evidence in support of our hypothesis about hypocalcemic myocardiopathy.

Transfusional hemosiderosis and combined chelation therapy in sickle thalassemia.

Although the indications for transfusions in sickle cell syndromes are well listed, and chronic transfusion has become practicable since the recent advances in chelation therapy have essentially eliminated the risk of secondary iron overload, multi-transfused, non-compliant to long-term chelation therapy patients confront the complication of iron overload and secondary hemosiderosis. In thalassemia major patients, combined therapy with desferrioxamine and deferiprone has maximized tissue iron removal and may reduce the overall occurrence of hemosiderotic heart failure. Despite this, safety and contradictions of chelating agents are still controversial. The aim of this report is to present the results of this combination in a long-term transfused sickle beta-thalassemic patient suffering from severe heart failure and liver dysfunction.

Prevalence of inducible clindamycin resistance in macrolide-resistant Staphylococcus spp.

Between January 2002 and December 2003, macrolide-resistant isolates of Staphylococcus aureus (n = 45) and coagulase-negative staphylococci (CoNS; n = 75) from a Greek hospital were examined phenotypically for inducible clindamycin resistance. The constitutive macrolide resistance phenotype predominated (60%) in S. aureus, followed by the inducible (35%) and the clindamycin-susceptible (5%) phenotypes. In CoNS, the inducible phenotype was more common than the constitutive phenotype (50% vs. 41%). There was a significant incidence of inducible clindamycin resistance, and screening of all staphylococci is necessary in order to differentiate inducibly resistant isolates from those that are truly sensitive.

Reversal of heart failure in thalassemia major by combined chelation therapy: a case report.

In patients with thalassemia major (TM) who are non-compliant with long-term desferrioxamine (DFO) chelation, survival is limited mainly because of cardiac complications of transfusional hemosiderosis. Combined chelation therapy with DFO and deferiprone has maximized the efficacy of the therapy and reduced cardiological complications. The aim of this report is to present the results of this combination in a desperate case of heart failure.

Exercise-induced myocardial perfusion abnormalities in sickle beta-thalassemia: Tc-99m tetrofosmin gated SPECT imaging study.

PURPOSE: To determine the mechanism of myocardial ischemia in patients with sickle beta-thalassemia, we performed a scintigraphic evaluation of myocardial perfusion during exercise. SUBJECTS AND METHODS: We studied 30 patients with sickle beta-thalassemia, (mean [+/-SD] age, 37 +/- 10 years) who had no electrocardiographic (ECG), radiographic, or echo-Doppler signs of pulmonary hypertension, left ventricular hypertrophy, or impaired contractility. All patients had a hemoglobin level greater than 7 g/dL. Treadmill exercise test was performed according to the Bruce protocol. Myocardial perfusion was assessed by single-photon emission computed tomography, using Tetrofosmin Tc-99 m Myoview as radiotracer, at peak exercise and again 4 hours later. RESULTS: Eight patients (27%) developed stress-induced scintigraphic perfusion abnormalities that were reversible in all but 1 patient. Subsequent coronary angiograms were normal in all 8 patients. ST segment depression was seen during exercise in 5 of the 7 patients who had reversible perfusion defects. Except for a significantly greater white blood cell count, these 5 patients did not differ from the rest of patients by sex, age, hemoglobin level, percentage hemoglobin F, beta-thalassemia genotype, or risk factors for coronary artery disease. Three of the 5 patients with perfusion and ECG abnormalities (and another with only perfusion defects) developed a stress-induced sickling crisis. CONCLUSION: Physical stress may induce myocardial ischemia in sickle beta-thalassemia patients with normal coronary arteries and elicit painful crises. The sickling process, activated by exercise, could be the common underlying mechanism.

Arterial calcifications in beta-thalassemia.

The purpose of this study was to define the incidence of arterial calcifications in patients with beta-thalassemia. Beta-thalassemia patients have been shown to present a high prevalence of angioid streaks and skin lesions characteristic of pseudoxanthoma elasticum (PXE). Given the fact that vascular involvement in the form of arterial calcifications is also a common manifestation of PXE, the authors investigated radiographically the presence of arterial calcifications in beta-thalassemia patients. They studied 40 patients with beta-thalassemia over 30 years of age. Forty healthy, age- and sex-matched subjects were chosen as a control group. Radiographs of the tibias were performed in order to disclose arterial calcifications. The occurrence of PXE skin lesions and of angioid streaks (AS) was also investigated. Arterial calcifications were detected in the posterior tibial artery in 22 (55%) beta-thalassemia patients and in six (15%) controls (P < 0.01 for the comparison). PXE skin lesions and AS were found in eight (20%) and 21 (52%) patients respectively. A total of 34 patients (85%) had at least one of the three lesions, namely, arterial calcifications, angioid streaks, and/or PXE-like skin lesions. Stepwise logistic regression analysis did not reveal prognostic value in independent variables such as transfusions, chelation therapy, pseudoxanthoma elasticum skin lesions and/or angioid streaks, diabetes, hemoglobin, serum ferritin, and uric acid. It was concluded that arterial calcifications are common in older beta-thalassemia patients. This finding could be a manifestation of an acquired PXE syndrome associated with beta-thalassemia, and consequently, vascular events complicating PXE should be expected in these patients.