Reaction of tris(bipyridine)ruthenium(III) with hydroxide and its application in a solar energy storage system

Irradiation of Ru(bipy)₃²⁺ (bipy = 2,2′-bipyridine) with light below 560 nm results in the formation of a charge-transfer excited state potentially capable of reducing water to dihydrogen with concomitant production of Ru(bipy)₃³⁺. The latter may be reduced by hydroxide [Formula: see text] to form dioxygen and regenerate the starting complex. The use of these reactions in a cell designed to bring about the photochemical decomposition of water is proposed.     

Probing the Reaction Mechanisms of 3,5-Difluoro-2,4,6-Trinitroanisole (DFTNAN) through a Comparative Study with Trinitroanisole (TNAN)

To probe the thermal decomposition mechanisms of a novel fluorinated low-melting-point explosive 3,5-difluoro-2,4,6-trinitroanisole (DFTNAN), a comparative study with trinitroanisole (TNAN) was performed under different heating conditions. The thermal decomposition processes and initial reactions were monitored by DSC-TG-FTIR-MS and T-jump-PyGC-MS coupling analyses, respectively. The results show that fluorine decreased the thermal stability of the molecular structure, and the trigger bond was transferred from the ortho-nitro group of the ether to the para-nitro group. The possible reaction pathway of DFTNAN after the initial bond breakage is the rupture of the dissociative nitro group with massive heat release, which induces the ring opening of benzene. Major side reactions include the generation of polycyclic compounds and fluorine atom migration. Fluorine affects the thermal stability and changes the reaction pathway, and fluorinated products appear in the form of fluorocarbons due to the high stability of the C-F bond.     

Relevance of antithrombin III in thrombogenesis: the diagnosis and therapy of antithrombin III defects

Pathological and inconspicuous AT III measuring values were compared with the clinical findings (arterial occlusive diseases, postthrombotic syndromes, acute profound thrombosis of the pelvic veins and the leg veins, acute heparin tolerance in several basic diseases). After calculatory elaboration of all rightly positive and falsely positive, rightly negative and falsely negative laboratory results becomes evident that the positive power of prognosis of the AT III determination is unsatisfactory for a certain basic disease and the negative evidence in these questionings rather well satisfy for the functional measuring method. - The sensitivity of the functional AT III test for the recognition of increased heparin tolerances is quite satisfactory, and the test for the answer of this questioning also suitable and more sensitive than the immunological proof method. - The high percentage of rightly positive and rightly negative findings of all tested results of apparently healthy persons and the groups of patients represented makes clear, which role plays the AT III as a physiologic inhibitor against coagulation-active serine proteases particularly in DIC and in profound thrombosis of the pelvic and leg veins. - For the observation of the course in profound thrombosis of the pelvic and led veins, features of postthrombotic condition and the DIC at least the functional determination of AT III is decisively important.     

Observations and comments on the mechanism of epoxidation of alkenes by manganese(III) porphyrins with hypochlorite.

The kinetics of olefin epoxidation in a methylene chloride/water biphase containing a phase-transfer agent with hypochlorite as oxygen transfer reagent and manganese(III) tetraphenylporphyrin catalysts has been reinvestigated. The results do not support the accumulation of an intermediate composed of an alkene and a hypervalent metaloxo porphyrin. Second-order rate constants for oxygen transfer from hypochlorite to the manganese porphyrin, comproprotionation of the hypervalent manganese-oxo porphyrin with manganese(III) porphyrin, and olefin epoxidation by the hypervalent manganese-oxo porphyrin were obtained from experiments in a wet organic monophase.     

Apolipoprotein (a) phenotypes and lipoprotein (a) concentrations in patients with type III hyperlipoproteinaemia

Abstract. Objectives . The familial lipoprotein disorder type III hyperlipoproteinaemia (HLP) carries a marked increase in the risk of accelerated and premature atherosclerosis, but there is considerable variation amongst affected individuals in their susceptibility to cardiovascular disease (CVD). Therefore, it was the aim of our study to investigate the possible influence of lipoprotein (a) [Lp(a)] in the pathogenesis of type III HLP. Design . Apolipoprotein (a) [apo(a)] phenotypes and Lp(a) concentrations were determined in patients with the disease and in an appropriate control group. Setting . University out-patient lipid disorder clinic. Subjects . Seventy-six apoE-2 homozygous patients with type III HLP and 76 normolipidaemic and healthy age- and sex-matched controls. Main outcome measures . The frequencies of different apo(a) phenotypes and their correlations with Lp(a) serum concentrations were determined in patients and controls. Results . Lp(a) concentrations were not significantly different in type III HLP patients (14.1±19.1 mg dl^-1) as compared with the controls (13.3±16.2 mg dl^-1; P = 0.549, NS). In addition, there was no significant difference in apo(a) phenotype frequencies amongst both groups (0.2 > P > 0.1). Conclusions . We conclude that the apo(a) polymorphism does not participate (to a significant extent) in the phenotypical expression of type III HLP.     

Development of Direct Antiglobulin Reaction Accompanying Alloimmunization in a Patient with Rhd (D,Category III) Phenotype1

Abstract. New examples of the Rh^d (D, category III) red cell phenotype are described in three siblings. One of these individuals who had previously been transfused, received three units of Rh_o(D) positive blood several years later and developed a high titer anti-Rh^D antibody. This anamnestic response was associated with the development of an autoantibody which persisted for a period of at least 8 months. This observation represents another example of autoimmunization which has rarely been observed to accompany alloimmunization.     

The pH dependence of the mechanism of reaction of hydrogen peroxide with a nonaggregating, non-mu-oxo dimer-forming iron (III) porphyrin in water.

The reaction of hydrogen peroxide with 5, 10,15,20-tetrakis(2,6-dimethyl-3-sulfonatophenyl)porphinato- iron(III) hydrate [(P)FeIII(H2O)] has been investigated in water between pH 1 and pH 12. The water-soluble (P)FeIII(H2O) neither aggregates nor forms a mu-oxo dimer. The pH dependence and rate-limiting second-order rate constants (kly) for oxygen transfer from H2O2 and HO2- to the iron(III) porphyrin were determined by trapping of the resultant higher-valent iron-oxo porphyrin species with 2,2'-azinodi(3-ethylbenzthiazoline)-6-sulfonate (ABTS). Reactions were monitored spectrophometrically by following the appearance of the radical ABTS.+. From a plot of the logarithm of the determined second-order rate constants for reaction of hydrogen peroxide with iron(III) porphyrin vs. pH, the composition of the transition states can be assigned for the three reactions that result in oxygen transfer to yield a higher-valent iron-oxo porphyrin species. The latter not only reacts with ABTS to provide ABTS.+ in a peroxidase-type reaction but also reacts with hydrogen peroxide to provide O2 in a catalase-type reaction. The nitrogen base 2,4,6-collidine serves as a catalyst for oxygen transfer from hydrogen peroxide to the (P)FeIII-(H2O) and (P)FeIII(HO) species. The preferred mechanism involves a 1,2-proton shift concerted with heterolytic cleavage of the peroxide O-O bond. An analogous mechanism is believed to occur in the peroxidase enzymes.     

Successful renal transplantation in a patient with anaphylactic reaction to Solu-Medrol (methylprednisolone sodium succinate)

Following the intravenous infusion of Solu-Medrol^® (methylprednisolone sodium succinate), anaphylactic shock developed in a 41 year old man on two consecutive occasions, six weeks apart. Intracutaneous testing with different components of the Solu-Medrol Mix-O-Vial^® demonstrated that the patient was allergic to methylprednisolone sodium succinate but not to other ingredients. In view of the recent increase in the popularity of steroid pulse therapy, we believe that all clinicians should be aware of this unusual and potentially fatal reaction to Solu-Medrol.     

Picosecond photochemistry of a cofacial diporphyrin containing iron(III) and zinc(II): Mimicking electron transfer between cytochrome c and the primary electron donor in reaction centers of photosynthetic bacteria

Comparison of picosecond kinetic and spectroscopic data for Zn octaethylporphine and Fe(III)Cl octaethylporphine with that for Zn—Fe(III)Cl, a cofacial diporphyrin composed of a Zn porphyrin covalently bound to an Fe(III)Cl porphyrin with two chains of five atoms each, supports the assignment of a light-driven electron transfer (k > 10¹¹s^-1) within Zn—Fe(III)Cl to form [Zn⁺·—Fe(II)]Cl. The kinetics (k ≈ 10¹⁰s^-1) and thermodynamics of the reverse electron transfer are compared to those of a similar electron transfer in bacterial photosynthesis, the reduction of an oxidized bacteriochlorophyll dimer, (BChl)₂⁺·, by Fe(II) cytochrome c.     

Autoantibodies to extractable nuclear antigens (ENAs) pattern in rheumatoid arthritis patients: Relevance and clinical implications

ObjectivesTo study the frequency of different autoantibodies to extractable nuclear antigens (ENAs) in rheumatoid arthritis (RA) patients and to correlate findings with clinical manifestations, disease activity and radiological damage.MethodsA total of 230 RA patients were included and 75 healthy controls. In all patients rheumatological assessment was done and routine laboratory investigations and immune profile were performed in both patients and controls, including: RF, ACPA, ANA and anti-ENAs (Ro/SSA, La/SSB, U1-RNP, anti-Jo-1 and anti-Sm). Radiological damage was scored using Sharp/van der Heijde, and disease activity was evaluated by DAS28-ESR and DAS28-CRP.ResultsRF was positive in 101 (43.9%), ACPA in 220 (95.7%), ANA in 58 (25.2%), anti Ro in 31 (13.5%), anti-La in 10 (4.3%), anti-Jo1 in 5 (2.2%) and anti-RNP in 2 (0.9%). Anti-Ro/SSA positively correlated with sicca symptoms (p = .02), RF titer (p < .001), ANA (p < .001), DAS28-ESR (p = .026), and DAS28-CRP (p = .003). Anti-La antibodies correlated positively with SJC (p = .001), TJC (p = .001), ANA (p < .001), DAS-28 ESR (p = .007). Anti-Jo-1 correlated positively with interstitial lung disease (ILD) (p ≤ .001), RF titer (p = .037) and ANA (p ≤ .001). Anti-RNP antibodies correlated positively with disease duration (p ≤ .001), ACPA titer (p ≤ .001) and ANA (p = .014). In the controls ANA was positive in two (2.7%), anti-Ro in three (4%), and none of the controls tested positive for other autoantibodies.ConclusionsIn RA patients, positive ANA is frequent and positively associated with anti-Ro, anti-La and anti-Jo1 autoantibodies. Screening for autoantibodies against other anti-ENAs seems mandatory in RA patients especially when ANA is positive. RA cases with positive Anti-Jo-1 may develop anti synthetase syndrome and ILD.     

Severe hepatotoxic reaction with progression to cirrhosis after use of a novel retinoid (acitretin)

We report the case of a 50-year-old female who suffered from severe palmar and plantar pustulosis. During treatment with acitretin, a novel oral retinoid, which is the main derivative of etretinate, the patient developed a severe hepatotoxic reaction. Subsequent histological studies strongly suggested the development of liver cirrhosis. Reversible elevation of serum aminotransferase values during treatment with acitretin has been reported. However, the present observation indicates that severe hepatotoxic injury may also follow treatment with this agent.     

Covalent attachment of metal chelates to proteins:the stability in vivo and in vitro of the conjugate of albumin with a chelate of 111indium.

Human serum albumin has been conjugated to 1-(p-bnezenediazonium)-(ethylenedinitrilo)tetraacetic acid, a powerful chelating agent, and radioactive 111indium ions have been added specifically to the chelating groups. The product, with a specific radioactivity of about 1 mCi/mg of protein, was employed as a radiotracer in scintillation scanning studies with human volunteers. Results show that 48 hr after injection, practically all of the label remains attached to albumin. This is confirmed by electrophoresis of serum proteins; 7 days after injection, 85% of the radioactivity in the serum is still in the albumin fraction. These observations agree with in vitro studies of the labeled albumin in human serum, where loss of the metal ion from the chelating group to the protein transferrin amounts to less than 3% after 1 week and less than 5% after 2 weeks. Measurements of the distribution of label in mice up to 23 days after injection suggest that metabolism of the labeled protein does not lead to binding of indium ions by transferrin. The binding of indium and other metal ions by transferrin has previously posed a major impediment to the use of metal chelates for in vivo diagnostic procedures. Demonstration of the kinetic inertness of the chelate in these experiments suggests the use of related chelates as physical probes of biological systems.     

Desensitization to co-trimoxazole (trimethoprim-sulphamethoxazole) in HIV-infected patients: is patch testing a useful predictor of reaction?

OBJECTIVE: To establish the safety and efficacy of desensitization to co-trimoxazole in hypersensitive HIV-infected subjects. To assess if delayed hypersensitivity (type IV) to co-trimoxazole predicts those unable to be desensitized. METHOD: desensitization to co-trimoxazole, comprising trimethoprim (T) 0.4 mg and sulphamethoxazole (S) 2 mg initially with doubling dose daily, full strength co-trimoxazole (T/S 160 mg/800 mg) at 10 days. Patch testing with 4.5% and 9% co-trimoxazole in yellow soft paraffin, CMI Multitest. RESULTS: nineteen patients, 18 male and one female, were recruited and completed the desensitization regime. Of these 80%(15) achieved successful desensitization. Three of those who reacted did so within 18 days. All patients were successfully managed in an outpatient setting. There were no major adverse reactions. Of those reacting none gave a positive patch test to co-trimoxazole and all showed absent delayed type hypersensitivity reactions to recall antigens. CONCLUSIONS: co-trimoxazole desensitization is a safe and efficacious procedure, with a success rate of 80% using the above regime. Patch testing with co-trimoxazole gives no useful information about those that reacted.