Zero-Order Catalysis in TAML-Catalyzed Oxidation of Imidacloprid, a Neonicotinoid Pesticide.

Bis-sulfonamide bis-amide TAML activator [Fe{4-NO2 C6 H3 -1,2-(NCOCMe2 NSO2 )2 CHMe}]- (2) catalyzes oxidative degradation of the oxidation-resistant neonicotinoid insecticide, imidacloprid (IMI), by H2 O2 at pH 7 and 25 °C, whereas the tetrakis-amide TAML [Fe{4-NO2 C6 H3 -1,2-(NCOCMe2 NCO)2 CF2 }]- (1), previously regarded as the most catalytically active TAML, is inactive under the same conditions. At ultra-low concentrations of both imidacloprid and 2, 62 % of the insecticide was oxidized in 2 h, at which time the catalyst is inactivated; oxidation resumes on addition of a succeeding aliquot of 2. Acetate and oxamate were detected by ion chromatography, suggesting deep oxidation of imidacloprid. Explored at concentrations [2]≥[IMI], the reaction kinetics revealed unusually low kinetic order in 2 (0.164±0.006), which is observed alongside the first order in imidacloprid and an ascending hyperbolic dependence in [H2 O2 ]. Actual independence of the reaction rate on the catalyst concentration is accounted for in terms of a reversible noncovalent binding between a substrate and a catalyst, which usually results in substrate inhibition when [catalyst]≪[substrate] but explains the zero order in the catalyst when [2]>[IMI]. A plausible mechanism of the TAML-catalyzed oxidations of imidacloprid is briefly discussed. Similar zero-order catalysis is presented for the oxidation of 3-methyl-4-nitrophenol by H2 O2 , catalyzed by the TAML analogue of 1 without a NO2 -group in the aromatic ring.

[Progressive dyspnoea in two patients with carcinoid syndrome]. / Progrediente Dyspnoe bei Karzinoidsyndrom.

In patients with carcinoid syndrome, there has always to be considered cardiac impairment. We report about two patients with hepatic and bone metastases of a neuroendocrine tumor of the midgut, who suffered from progressive dyspnea. This was caused in both cases by a right-to-left atrial shunt, in case 1 based on a patent foramen ovale (PFO), in case 2 based on a secundum atrial septal defect. Symptoms were significantly reduced by percutaneous closure of PFO and ASD, respectively. Right-to-left atrial shunt was facilitated by right-sided carcinoid induced endocardial fibrosis with the consequence of severe tricuspid regurgitation, leading to an increase of right atrial pressure.

Aortic valve replacement for a patient with glucose-6-phosphate dehydrogenase deficiency and autoimmune hemolytic anemia.

Autoimmune hemolytic anemia and deficiency of glucose-6-phosphate deyhdrogenase (G6PD) result in severe hemolysis with different mechanisms. In patients with both pathologies, the effects of cardiopulmonary bypass on red blood cells and thrombocytes demand special care before and after open heart surgery. We evaluated the preoperative management and postoperative care of a patient with severe aortic insufficiency associated with G6PD deficiency and autoimmune hemolytic anemia who underwent aortic valve replacement.

A new experimental hypertrophic scar model in guinea pigs.

Many aspects of the biology and effective therapy of proliferative scars remain undefined, in part due to a lack of an accurate, practical, reproducible, and economical animal model for systematically studying hypertrophic scars. This study was designed to investigate whether hypertrophic scar formation could be induced in guinea pigs by removal of the panniculus carnosus alone, and by a combination of the removal of the panniculus carnosus with application of coal tar afterwards. Whole thickness skin excision or deep partial thickness injury was used to create the lesions on intact skin. Different anatomic locations were tested in different groups. Scars thus developed were examined morphologically by light microscopy and electron microscopy (TEM and SEM) and biochemically by measuring the activity of glucose-6-phosphate dehydrogenase (G6PD) to check whether these scars had morphological and biochemical properties specific to hypertrophic scars. The albino guinea pigs used in this study were divided into three groups. Removal of the panniculus carnosus was performed from the ventral aspect of the torso in animals in groups I and II. On the skin overlying the area of panniculectomy, circular skin excision was performed in group I, and deep partial thickness burn injury was inflicted in group II, to see whether wounds would heal with hypertrophic scars. In group III, dorsal aspect of the torso were used and wounds were produced by circular skin excisions followed by panniculectomy on both sides but coal tar was applied to only one side. Tissue samples were taken from the scars that were hypertrophic in appearance, and from normal scars and normal skin for comparison. Light and electron microscopic examinations and G6PD activity measurements were performed on these samples. While hypertrophic scar development was not seen in group I and group II, scars with morphological and biochemical properties specific to hypertrophic scars developed in one third of animals in group III after healing of the wounds treated with coal tar. In conclusion, it is shown that it is possible to develop experimental hypertrophic scars in guinea pigs with morphological and biochemical properties similar to those of human proliferative scars. Therefore this model is a new, practical, and economical experimental animal model to study proliferative scars, although improvements are needed to increase yield.