Spiropyran Sulfonates for Photo- and pH-Responsive Air-Water Interfaces and Aqueous Foam.

Responsive foams and interfaces are interesting building blocks for active materials that respond and adapt to external stimuli. We have used the photochromic reaction of a spiropyran sulfonate surfactant to render interfacial, rising bubbles as well as foaming properties active to light stimuli. In order to address the air-water interface on a molecular level, we have applied sum-frequency generation (SFG) spectroscopy which has provided qualitative information on the surface excess and the interfacial charging state as a function of light irradiation and solution pH. Under blue light irradiation, the surfactant forms a closed ring spiro form (SP), whereas under dark conditions the ring opens and the merocyanine (MC) form is generated. Using SFG spectroscopy, we show that at the interface, different pH conditions of the bulk solution lead to changes in the interfacial charging state. We have exploited the fact that the MC surfactant's O-H group can be deprotonated as a function of pH and used that to tune the molecules net charge at the interface. In fact, SFG spectroscopy shows that with increasing pH the intensity of the O-H stretching band from interfacial water molecules increases, which we associate to an increase in surface net charge. At a pH of 5.3, irradiation with blue light leads to a reversible decrease of O-H intensities, whereas the C-H intensities were unchanged compared to the corresponding intensities under dark conditions. These results are indicative of changes in the surface net charge with light irradiation, which are also expected to influence the foam stability via changes in the electrostatic disjoining pressure. In fact, measurements of the foam stabilities are consistent with this hypothesis and show higher foam stability under dark conditions. At pH 2.7 this behavior is reversed as far as the surface tension and surface charging as well as the foam stability are concerned. This is corroborated by rising bubble experiments, which demonstrated an unprecedented reduction of ∼30% in bubble velocity when the bubbles were irradiated with blue light compared to the velocity of bubbles with the surfactants in the dark state. Clearly, the light-triggered changes can be used to control foams, rising bubbles, and fluid interfaces on a molecular level which renders them active to light stimuli.

Low triiodothyronine syndrome and serum selenium status in the course of acute myocardial infarction.

Both glutathione peroxidase and deiodinases are selenoproteins requiring selenium. Oxidative stress accompanying acute myocardial infarction (MI) may lead to activation of peroxidase and relative selenium deficiency. That may impair conversion of tetraiodothyronine (T4) to triiodothyronine (T3). AIM: The aim of the study was the evaluation of the prevalence of low T3 syndrome in MI, in relation to selenium deficiency. MATERIALS AND METHODS: The study group consisted of 59 consecutive patients hospitalized due to STEMI or NSTEMI, treated with primary percutaneous coronary intervention. Exclusion criteria: thyroid dysfunction, severe systemic disease, treatment with amiodarone, steroids or propranolol. Group A consisted of 7 patients with low fT3 concentration, Group B consisted of remaining 52 patients with normal fT3 levels. RESULTS: The prevalence of low T3 syndrome was 11.9%. The prevalence of selenium deficiency was 71.2%. Patients with low T3 syndrome had higher heart rate at admission and more often needed intravenous diuretics or inotropic agents. Low fT3 group presented higher levels of NT-proBNP, hsCRP, WBC, admission CKMB levels. There was a nonsignificant trend towards lower selenium levels in A group. We demonstrated correlations between fT3 and hsTnT, CKMB, NT-proBNP, hsCRP, MAPSE but we did not find correlation between fT3 and selenium or LVEF. CONCLUSIONS: Selenium deficiency was found in majority of MI patients, while low T3 was identified in 11.9% of patients. fT3 levels correlate with markers of infarction severity and inflammatory markers. Se deficiency alone does not explain the reason of low fT3 concentration.

Correction to: Low triiodothyronine syndrome and selenium deficiency - undervalued players in advanced heart failure? A single center pilot study.

After publication of the original article [1], the authors have notified us of a typing error in spelling Dr. Kabat's name. The original publication has been corrected.

Low triiodothyronine syndrome and selenium deficiency - undervalued players in advanced heart failure? A single center pilot study.

BACKGROUND: The function of deiodinases - selenoproteins converting thyroid hormones may be disturbed by oxidative stress accompanying heart failure. Selenium (Se) may be used by glutathione peroxidase, leading to a lack of deiodinase and triiodothyronine (T3). The aim of the study was the evaluation of the prevalence and clinical significance of low T3 syndrome in heart failure and the assessment of the association of low fT3 and Se deficiency. METHODS: The study group consisted of 59 consecutive patients hospitalized due to decompensated HFrEF NYHA III or IV. Exclusion criteria were: thyroid dysfunction, severe systemic disease, treatment with amiodarone, steroids or propranolol. Group A included 9 patients with low free T3 (fT3) concentration below 3.1 pmol/L. Group B consisted of the remaining 50 patients with normal fT3 levels. RESULTS: The prevalence of low T3 syndrome was 15.3%. The prevalence of Se deficiency was 74.6%. We demonstrated correlations between fT3 and main clinical variables (i.e. NT-proBNP, LVEF, hsCRP), but we did not find correlation between fT3 and the Se level. Kaplan-Meier survival analysis showed lower survival probability in patients with low fT3 (p < 0.001). CONCLUSIONS: Low T3 syndrome is frequently found in patients with HFrEF and is associated with a poor outcome. We did not identify any significant correlation between Se and fT3 level.

Selenium deficiency and the dynamics of changes of thyroid profile in patients with acute myocardial infarction and chronic heart failure.

BACKGROUND: Selenium (Se) is incorporated in 25 enzymes, for example, glutathione peroxidase (activatedb by oxidative stress) and deiodinases (converting thyroid hormones). Oxidative stress present in heart failure (HF) and myocardial infarction (MI) might cause Se deficiency and decreased thyroxine to triiodothyronine conversion. AIMS: We sought to evaluate Se levels in Polish patients with MI, HF, and healthy volunteers in relation to thyroid hormone levels. METHODS: The study group consisted of 143 participants: 54 patients with MI, 59 patients with decompensated HF, and 30 healthy matched volunteers. The patients underwent echocardiography and laboratory tests on admission and 5 months later. RESULTS: Se levels were lower in patients with MI and HF than in controls (median [interquartile range, IQR], 65.9 [55.2-76.1] µg/l and 59.7 [47.7-70.7] µg/l vs 93.2 [84.2-99.1] µg/l, respectively; P <0.001). The Se deficiency was very common in patients with MI and HF, while it was rare in controls (70.37% and 74.58% vs 10%, respectively; P <0.001). Patients with MI and HF presented lower free triiodothyronine (FT3) levels and lower FT3 to free thyroxine (FT4) ratio in comparison with controls (median [IQR], 3.90 [3.60-4.38] pmol/l and 4.25 [3.57-4.60] pmol/l vs 4.92 [4.50-5.27] pmol/l; P <0.001; and 0.25 [0.23-0.29] and 0.25 [0.21-0.28] vs 0.32 [0.29-0.37]; P <0.001, respectively). There was a weak to moderate correlation between Se level, FT3 level, and the FT3/FT4 ratio. At follow­up, the FT3/FT4 ratio tended to normalize in patients with MI and remained decreased in patients with HF (mean [SD], 0.31 [0.06] vs 0.27 ([0.05]; P <0.001. CONCLUSIONS: Se deficiency is very common in Polish patients with MI and HF. Thyroid hormones disturbances were more transient in patients with MI, but more chronic in those with HF.