Do children with primary nocturnal enuresis have a retarded bone age? A cross‐sectional study

OBJECTIVE: Nocturnal enuresis is a common pediatric problem, the etiology of which is unclear. In recent years, various studies have been published stating that children with nocturnal enuresis exhibit growth and skeletal maturation retardation. METHODS: In this cross-sectional study, we included 27 patients (16 boys, 11 girls) between the ages of 6 and 14 years who had presented with primary nocturnal enuresis (PNE) complaints. We included in the evaluation 19 healthy subjects (12 boys, 7 girls), who were the siblings of the children with PNE, as the control group. RESULTS: The patients in both groups were similar in chronological age, bone age, height and weight, with no significant difference between groups (P>0.05). CONCLUSION: The two groups in our study consisted of the same genetic background. Thus, our results were found to be different from the previous studies. We have concluded that there is no direct relationship between enuresis nocturnal and skeletal maturation.     

Mechanism of antithrombin III inhibition of factor VIIa/tissue factor activity on cell surfaces. Comparison with tissue factor pathway inhibitor/factor Xa-induced inhibition of factor VIIa/tissue factor activity

Recent studies have shown that antithrombin III (AT III)/heparin is capable of inhibiting the catalytic activity of factor VIIa bound either to relipidated tissue factor (TF) in suspension or to TF expressed on cell surfaces. We report studies of the mechanism of which by AT III inhibits factor VIIa bound to cell surface TF and compare this inhibitory mechanism with that of tissue factor pathway inhibitor (TFPI)-induced inhibition of factor VIIa/TF. AT III alone and AT III/heparin to a greater extent reduced factor VIIa bound to cell surface TF. Our data show that the decrease in the amount of factor VIIa associated with cell surface TF in the presence of AT III was the result of (1) accelerated dissociation of factor VIIa from cell surface TF after the binding of AT III to factor VIIa/TF complexes and (2) the inability of the resultant free factor VIIa-AT III complexes to bind effectively to a new cell surface TF site. Binding of TFPI/factor Xa to cell surface factor VIIa/TF complexes markedly decreased the dissociation of factor VIIa from the resultant quaternary complex of factor VIIa/TF/TFPI/factor Xa. Addition of high concentrations of factor VIIa could reverse the AT III-induced inhibition of cell surface factor VIIa/TF activity but not TFPI/factor Xa-induced inhibition of factor VIIa/TF activity.     

Acute intestinal infection caused by Escherichia coli

Clinical manifestations and autopsy findings on 23 patients who died of acute sepsis of Escherichia coli origin lead the authors to the conclusion on polymorphic clinical run of the disease. It varies with premorbid background (food intoxication, acute respiratory disease in decompensated diabetes mellitus, chronic somatic disorders) and risk factors (inadequate antibacterial therapy, nervous strain, fatigue). Inadequate antibacterial therapy promoting dysbacteriosis aggravated preexisting pathomorphological shifts in the intestine likely after toxic infection, diabetes-specific foci, contributed to the onset of intestinal sepsis.     

Fundamental signatures of short- and long-range electron transfer for the blue copper protein azurin at Au/SAM junctions

The blue copper protein from Pseudomonas aeruginosa, azurin, immobilized at gold electrodes through hydrophobic interaction with alkanethiol self-assembled monolayers (SAMs) of the general type [-S - (CH₂)_n - CH₃] (n = 4, 10, and 15) was employed to gain detailed insight into the physical mechanisms of short- and long-range biomolecular electron transfer (ET). Fast scan cyclic voltammetry and a Marcus equation analysis were used to determine unimolecular standard rate constants and reorganization free energies for variable n, temperature (2–55 °C), and pressure (5–150 MPa) conditions. A novel global fitting procedure was found to account for the reduced ET rate constant over almost five orders of magnitude (covering different n, temperature, and pressure) and revealed that electron exchange is a direct ET process and not conformationally gated. All the ET data, addressing SAMs with thickness variable over ca. 12 Å, could be described by using a single reorganization energy (0.3 eV), however, the values for the enthalpies and volumes of activation were found to vary with n. These data and their comparison with theory show how to discriminate between the fundamental signatures of short- and long-range biomolecular ET that are theoretically anticipated for the adiabatic and nonadiabatic ET mechanisms, respectively.