Mineralogical, optical, geochemical, and particle size properties of four sediment samples for optical physics research

X-ray diffraction and spectroscopy were used to investigate the mineralogical and chemical properties of the Calvert, Ball Old Mine, Ball Martin, and Jordan Sediments. The particle size distribution and index of refraction of each sample were determined. The samples are composed primarily of quartz, kaolinite, and illite. The clay minerals are most abundant in the finer particle size fractions. The chemical properties of the four samples are similar. The Calvert sample is most notably different in that it contains a relatively high amount of iron. The dominant particle size fraction in each sample is silt, with lesser amounts of clay and sand. The indices of refraction of the sediments are the same with the exception of the Calvert sample which has a slightly higher value

Ruthenium-Phenothiazine Electron Transfer Dyads with a Photoswitchable Dithienylethene Bridge

A molecular ensemble composed of a phenothiazine (PTZ) electron donor, a photoisomerizable dithienylethene (DTE) bridge, and a Ru(bpy)32+ (bpy = 2,2′-bipyridine) electron acceptor was synthesized and investigated by optical spectroscopic and electrochemical means. Our initial intention was to perform flash-quench transient absorption studies in which the Ru(bpy)32+ unit is excited selectively (“flash”) and its 3MLCT excited state is quenched oxidatively (“quench”) by excess methylviologen prior to intramolecular electron transfer from phenothiazine to Ru(III) across the dithienylethene bridge. However, after selective Ru(bpy)32+1MLCT excitation of the dyad with the DTE bridge in its open form, 1MLCT → 3MLCT intersystem crossing on the metal complex is followed by triplet–triplet energy transfer to a 3π–π* state localized on the DTE unit. This energy transfer process is faster than bimolecular oxidative quenching with methylviologen at the ruthenium site (Ru(III) is not observed); only the triplet-excited DTE then undergoes rapid (10 ns, instrumentally limited) bimolecular electron transfer with methylviologen. Subsequently, there is intramolecular electron transfer with PTZ. The time constant for formation of the phenothiazine radical cation via intramolecular electron transfer occurring over two p-xylene units is 41 ns. When the DTE bridge is photoisomerized to the closed form, PTZ+ cannot be observed any more. Irrespective of the wavelength at which the closed isomer is irradiated, most of the excitation energy appears to be funneled rapidly into a DTE-localized singlet excited state from which photoisomerization to the open form occurs within picoseconds

Interview with Edna Bice

An interview with Edna Bice regarding her experiences in a one-room school house.https://scholars.fhsu.edu/ors/1198/thumbnail.jp

A Triarylamine-Triarylborane Dyad with a Photochromic Dithienylethene Bridge

A molecular triad composed of a triarylamine donor, a triarylborane acceptor, and a photoisomerizable dithienylethene bridge has been synthesized and explored by cyclic voltammetry, UV–vis, and luminescence spectroscopy. The effects of irradiation with UV light and fluoride addition on the electrochemical and optical spectroscopic properties of the donor–bridge–acceptor molecule were investigated. Photoisomerization of the dithienylethene bridge affects the triarylboron reduction potential, but not the triarylamine oxidation potential. UV–vis experiments reveal that the association constant for fluoride binding at the triarylborane site is independent of the isomerization state of the bridge. Irradiation of a THF solution of our donor–bridge–acceptor molecule with UV light, followed by F– addition, leads to a different color of the sample than UV irradiation alone or F– addition alone

Pre- and postconditioning the heart with hydrogen sulfide (H2S) against ischemia/reperfusion injury in vivo: a systematic review and meta-analysis

Conditioning-like infarct limitation by enhanced level of hydrogen sulfide (H2S) has been demonstrated in many animal models of myocardial ischemia/reperfusion injury (MIRI) in vivo. We sought to evaluate the effect of H2S on myocardial infarction across in vivo pre-clinical studies of MIRI using a comprehensive systematic review followed by meta-analysis. Embase, Pubmed and Web of Science were searched for pre-clinical investigation of the effect of H2S on MIRI in vivo. Retained records (6031) were subjected to our pre-defined inclusion criteria then were objectively critiqued. Thirty-two reports were considered eligible to be included in this study and were grouped, based on the time of H2S application, into preconditioning and postconditioning groups. Data were pooled using random effect meta-analysis. We also investigated the possible impact of different experimental variables and the risk of bias on the observed effect size. Preconditioning with H2S (n = 23) caused a significant infarct limitation of − 20.25% (95% CI − 25.02, − 15.47). Similarly, postconditioning with H2S (n = 40) also limited infarct size by − 21.61% (95% CI − 24.17, − 19.05). This cardioprotection was also robust and consistent following sensitivity analyses where none of the pre-defined experimental variables had a significant effect on the observed infarct limitation. H2S shows a significant infarct limitation across in vivo pre-clinical studies of MIRI which include data from 825 animals. This infarct-sparing effect is robust and consistent when H2S is applied before ischemia or at reperfusion, independently on animal size or sulfide source. Validating this infarct limitation using large animals from standard medical therapy background and with co-morbidities should be the way forward

Cardioprotection afforded by targeting guanylyl cyclase during early reperfusion

Guanylyl cyclase - cyclic guanosine monophosphate (cGMP) signalling has been demonstrated to play an important role in the endogenous cardioprotective signalling of the myocardium during early reperfusion. It is proposed that infarct limitation is afforded by elevating cGMP and activating protein kinase G and its distal targets. It was hypothesised that increasing the activity of soluble guanylyl cyclase (sGC) would limit myocardial ischaemia-reperfusion injury. Primarily using the rat isolated perfused heart method, the experiments reported in this thesis investigate the role of exogenous targeting of sGC during early reperfusion, specifically exploring targeting different redox states of the enzyme and their effects on myocardial infarct size. The novel sGC stimulator BAY 41-2272 and activator BAY 60-2770 were selected to investigate this hypothesis. Both administration of BAY 41-2272 and BAY 60-2770 during early reperfusion significantly limited infarct size compared to controls. This was associated with elevated total tissue cGMP levels. Inhibition of nitric oxide could not completely abrogate this protection, but exogenous perfusion of nitric oxide along with BAY 41-2272 showed synergistic action. Oxidation of the prosthetic haem group by ODQ abrogated the protection afforded by BAY 41-2272 but potentiated the protection afforded by BAY 60-2770. Targeting both the reduced and oxidised forms of sGC together did not afford additive protection, in fact it reduced the protection afforded compared to the individual treatments. Preliminary data also suggest that targeting the particulate form of guanylyl cyclase increases activity of Akt signalling during early reperfusion suggesting common signalling between soluble and particulate guanylyl cyclase. These data suggest that targeting sGC during early reperfusion can afford cardioprotection by limiting infarct size. The relationship between cGMP elevation and infarct size needs to be investigated further. Nevertheless, these studies suggest that sGC may be a tractable target for the therapeutic management of acute myocardial infarction

Nitric oxide treatments as adjuncts to reperfusion in acute myocardial infarction: a systematic review of experimental and clinical studies

Unmodified reperfusion therapy for acute myocardial infarction (AMI) is associated with irreversible myocardial injury beyond that sustained during ischemia. Studies in experimental models of ischemia/reperfusion and in humans undergoing reperfusion therapy for AMI have examined potential beneficial effects of nitric oxide (NO) supplemented at the time of reperfusion. Using a rigorous systematic search approach, we have identified and critically evaluated all the relevant experimental and clinical literature to assess whether exogenous NO given at reperfusion can limit infarct size. An inclusive search strategy was undertaken to identify all in vivo experimental animal and clinical human studies published in the period 1990–2014 where NO gas, nitrite, nitrate or NO donors were given to ameliorate reperfusion injury. Articles were screened at title and subsequently at abstract level, followed by objective full text analysis using a critical appraisal tool. In twenty-one animal studies, all NO treatments except nitroglycerin afforded protection against measures of reperfusion injury, including infarct size, creatinine kinase release, neutrophil accumulation and cardiac dysfunction. In three human AMI RCT’s, there was no consistent evidence of infarct limitation associated with NO treatment as an adjunct to reperfusion. Despite experimental evidence that most NO treatments can reduce infarct size when given as adjuncts to reperfusion, the value of these interventions in clinical AMI is unproven. Our study raises issues for the design of further clinical studies and emphasises the need for improved design of animal studies to reflect more accurately the comorbidities and other confounding factors seen in clinical AMI