The Influence of Temperature on C153 Steady-State Absorption and Fluorescence Kinetics in Hydrogen Bonding Solvents

In a recent paper (J Fluoresc (2011) 21:1547–1557) a temperature induced modulation of Coumarin 153 (C153) fluorescence lifetime and quantum yield for the probe dissolved in the polar, nonspecifically interacting 1-chloropropane was reported. This modulation was also observed in temperature dependencies of the radiative and nonradiative rates. Here, we show that the modulation is also observed in another 1-chloroalkane—1-chlorohexane, as well as in hydrogen bonding propionitrile, ethanol and trifluoroethanol. Change in the equilibrium distance between S(0) an S(1) potential energies surfaces was identified as the source of this modulation. This change is driven by temperature changes. It leads to a modulation of the fluorescence transition dipole moment and it is the primary source of the experimental effects observed. Additionally, we have found that proticity of the solvent induces a rise in the fluorescence transition dipole moment, which leads to a shortening of the fluorescence lifetime. Hydrogen bonds are formed by C153 also with hydrogen accepting solvents like propionitrile. We show that while such bonds do not affect the transition probability, they do change the S(0) an S(1) energy gap which in turn implies a change in non-radiative transition rate in a similar way as in protic solvents, as well as in the fluorescence spectrum position. Finally, the influence of temperature on the energies of hydrogen bonds formed by C153 when acting as hydrogen donor or acceptor is reported

Effect of different diurnal blood pressure profiles on severity of the open-angle glaucoma in treated hypertensive patients

Wstęp Fizjologiczny spadek ciśnienia systemowego w trakcie snu i efekt hipotensyjny leków może prowadzić do obniżenia perfuzji w naczyniach gałki ocznej i rozwoju neuropatii nerwu wzrokowego. Celem pracy była ocena przepływu krwi w naczyniach gałki ocznej oraz zmian w nerwie wzrokowym u chorych z nadciśnieniem tętniczym i jaskrą pierwotną otwartego kąta. Materiał i metody Badanie przeprowadzono na grupie 69 chorych z jaskrą i leczonym, kontrolowanym nadciśnieniem tętniczym. U wszystkich chorych przeprowadzano badanie podmiotowe, przedmiotowe i dobowy pomiar ciśnienia tętniczego. W badaniu okulistycznym oceniono grubość włókien nerwowych oraz ubytki w polu widzenia. Wielokrotnie w ciągu doby badano ciśnienie śródgałkowe. W usg-doppler oceniono prędkość skurczową, końcowo- rozkurczową oraz indeks oporu naczyniowego w tętnicach: ocznej, środkowej siatkówki oraz rzęskowych tylnych krótkich. Ze względu na wartość nocnego spadku ciśnienia (NBPF) wydzielono dwie grupy: non-dippers (NBPF ≤ 10%) i dippers (NBPF > 10 %). Wyniki W grupie dippers wykazano istotnie niższe wartości ciśnienia perfuzji, mniejszą grubość włókien nerwowych oraz większy ubytek w polu widzenia. Wykazano istotne statystycznie zależności między przepływem skurczowym, rozkurczowym w tętnicy ocznej i środkowej siatkówki a ciśnieniem perfuzji nocnej, grubością włókien nerwowych i ubytkiem w polu widzenia. Wnioski Spadek nocny ciśnienia powyżej 10% wiąże się z większym ubytkiem pola widzenia i większą degeneracją włókien nerwu wzrokowego, co może wynikać ze zmniejszonej perfuzji w tętnicy ocznej i środkowej siatkówki. Do czynników ryzyka progresji jaskry można zaliczyć zbyt niskie ciśnienie perfuzji w nocy, minimalne ciśnienie rozkurczowe poniżej 45 mm Hg oraz zmniejszenie przepływu krwi w naczyniach gałki ocznej i oczodołu. Wykazane zależności nakazują unikanie nadmiernego obniżania ciśnienia tętniczego u chorych z jaskrą i nadciśnieniem tętniczym i wskazują na konieczność dalszych badań dotyczących określenia docelowych wartości ciśnienia systemowego w tej grupie chorych. Uzyskane wyniki wskazują na konieczność wykonywania w tej grupie chorych całodobowego pomiaru ciśnienia tętniczego i określenie wielkości spadku nocnego ciśnienia. Nadciśnienie Tętnicze 2010, tom 14, nr 2, strony 128-141.Background Physiological decrease in systemic blood pressure during sleep and the effect of antihypertensive drugs may lead to reduction in ocular perfusion and development of optic neuropathy. The aim of this study was to assess blood flow in the vessels of the eyeball and changes in the optic nerve among patients with hypertension and primary open-angle glaucoma. Material and methods The study was conducted on a group of 69 patients with glaucoma and treated, controlled hypertension. All patients in the survey have been examined both, subjectively and objectively. Additionally 24-h blood pressure records were taken. During ophthalmologic examination the thickness of the nerve fibers and the visual field defects were assessed. Many times during the day intraocular pressure was studied. The ultrasound-Doppler estimated peak systolic velocity, end-diastolic velocity and vascular resistance index in ophthalmic, central retinal and short posterior ciliary arteries. Because of the value of nocturnal blood pressure fall (NBPF) the patients were divided in two groups: non-dippers (NBPF ≥ 10%) and dippers (NBPF > 10%). Results In the group of dippers perfusion pressure was significantly lower and reduced thickness of the nerve fibers and a greater decrease in the visual field was observed. Statistically significant relationship between peak systolic, end-diastolic flow in ophthalmic and central retinal artery and night perfusion pressure, thickness of nerve fibers, loss in visual field was observed. Conclusion The night blood pressure fall > 10% is connected with more advanced loss in the visual field and greater degeneration of optic nerve fibers which may result from decrease perfusion in ophthalmic and central retinal artery. The risk factors for progression of glaucoma include low night-pressure perfusion, minimal diastolic blood pressure below 45 mm Hg and reduce ocular blood flow. The above presented correlations are shown to avoid excessive drops of blood pressure in patients with glaucoma and arterial hypertension and indicate the necessity of further research on determining the target value of blood pressure in these patients. The results indicate the necessity for this group of patients to perform the ambulatory blood pressure monitoring study and quantify the pressure drop in the night. Arterial Hypertension 2010, vol. 14, no 2, pages 128-141

Weak temperature dependence of P (+) H A (-) recombination in mutant Rhodobacter sphaeroides reaction centers

International audienceIn contrast with findings on the wild-type Rhodobacter sphaeroides reaction center, biexponential P (+) H A (-) → PH A charge recombination is shown to be weakly dependent on temperature between 78 and 298 K in three variants with single amino acids exchanged in the vicinity of primary electron acceptors. These mutated reaction centers have diverse overall kinetics of charge recombination, spanning an average lifetime from ~2 to ~20 ns. Despite these differences a protein relaxation model applied previously to wild-type reaction centers was successfully used to relate the observed kinetics to the temporal evolution of the free energy level of the state P (+) H A (-) relative to P (+) B A (-) . We conclude that the observed variety in the kinetics of charge recombination, together with their weak temperature dependence, is caused by a combination of factors that are each affected to a different extent by the point mutations in a particular mutant complex. These are as follows: (1) the initial free energy gap between the states P (+) B A (-) and P (+) H A (-) , (2) the intrinsic rate of P (+) B A (-) → PB A charge recombination, and (3) the rate of protein relaxation in response to the appearance of the charge separated states. In the case of a mutant which displays rapid P (+) H A (-) recombination (ELL), most of this recombination occurs in an unrelaxed protein in which P (+) B A (-) and P (+) H A (-) are almost isoenergetic. In contrast, in a mutant in which P (+) H A (-) recombination is relatively slow (GML), most of the recombination occurs in a relaxed protein in which P (+) H A (-) is much lower in energy than P (+) H A (-) . The weak temperature dependence in the ELL reaction center and a YLH mutant was modeled in two ways: (1) by assuming that the initial P (+) B A (-) and P (+) H A (-) states in an unrelaxed protein are isoenergetic, whereas the final free energy gap between these states following the protein relaxation is large (~250 meV or more), independent of temperature and (2) by assuming that the initial and final free energy gaps between P (+) B A (-) and P (+) H A (-) are moderate and temperature dependent. In the case of the GML mutant, it was concluded that the free energy gap between P (+) B A (-) and P (+) H A (-) is large at all times

PYROLYSIS JET SPECTROSCOPY: THE ROTATIONALLY RESOLVED ELECTRONIC SPECTRUM OF DICHLOROCARBENE

Author Institution: Department of Chemistry, University of Kentucky; Quantum Electronics Laboratory, Institute of Physics, A. Mickiewicz UniversityRotationally cold spectra of the 600 nm band system of $CCl_{2}$ have been observed by LIF. The transient species was produced by pyrolysis of trichloromethyltrimethylsilane in the throat of a continuous supersonic jet expansion. The pyrolysis products are probed downstream of the nozzle with a cw scanning ring dye laser, producing high resolution, rotationally resolved spectra. Deatils of the vibrational and rotational analysis, isotope effects and derived geometries will be presented

Transient states and the role of excited state self-quenching of indoline dyes in complete dye-sensitized solar cells

The photo behaviour of indoline dye D149 on different metal oxide nanoparticles in functioning solar cells is investigated by time-resolved studies in the time range from 100 fs to several ns. The cells are also characterized by standard photovoltaic measurements. The electron injection is found to occur on the time scales fro