Gastric lactobezoar - a rare disorder?

Gastric lactobezoar, a pathological conglomeration of milk and mucus in the stomach of milk-fed infants often causing gastric outlet obstruction, is a rarely reported disorder (96 cases since its first description in 1959). While most patients were described 1975-1985 only 26 children have been published since 1986. Clinically, gastric lactobezoars frequently manifest as acute abdomen with abdominal distension (61.0% of 96 patients), vomiting (54.2%), diarrhea (21.9%), and/or a palpable abdominal mass (19.8%). Respiratory (23.0%) and cardiocirculatory (16.7%) symptoms are not uncommon. The pathogenesis of lactobezoar formation is multifactorial: exogenous influences such as high casein content (54.2%), medium chain triglycerides (54.2%) or enhanced caloric density (65.6%) of infant milk as well as endogenous factors including immature gastrointestinal functions (66.0%), dehydration (27.5%) and many other mechanisms have been suggested. Diagnosis is easy if the potential presence of a gastric lactobezoar is thought of, and is based on a history of inappropriate milk feeding, signs of acute abdomen and characteristic features of diagnostic imaging. Previously, plain and/or air-, clear fluid- or opaque contrast medium radiography techniques were used to demonstrate a mass free-floating in the lumen of the stomach. This feature differentiates a gastric lactobezoar from intussusception or an abdominal neoplasm. Currently, abdominal ultrasound, showing highly echogenic intrabezoaric air trapping, is the diagnostic method of choice. However, identifying a gastric lactobezoar requires an investigator experienced in gastrointestinal problems of infancy as can be appreciated from the results of our review which show that in not even a single patient gastric lactobezoar was initially considered as a possible differential diagnosis. Furthermore, in over 30% of plain radiographs reported, diagnosis was initially missed although a lactobezoar was clearly demonstrable on repeat evaluation of the same X-ray films. Enhanced diagnostic sensitivity would be most rewarding since management consisting of cessation of oral feedings combined with administration of intravenous fluids and gastric lavage is easy and resolves over 85% of gastric lactobezoars. In conclusion, gastric lactobezoar is a disorder of unknown prevalence and is nowadays very rarely published, possibly because of inadequate diagnostic sensitivity and/or not yet identified but beneficial modifications of patient management

Evaluation of the effects of establishing of consalidated groups of taxpayers for Russian groups of companies

One of the most important decisions in the field of tax policy is the possibility of establishing consolidated groups of taxpayers. In this article we consider the ambiguity of influence of establishing such groups on the revenues of budgets of subjects of Russia. Besides we will find out the reasons of this influence

Электроснабжение Международного аэропорта Сабетты, ЯНАО

В процессе выполнения выпускной квалификационной работы была спроектирована система электроснабжения здания ангара и предприятия в целом. При расчете использовался метод коэффициента расчетной мощности и метод коэффициента мощности. Были рассмотрены вопросы ресурсоэффективности и социальной ответственности проектируемой системы. Основные конструктивные, технологические и эксплуатационные характеристики: предприятие включает четырнадцать зданий 1 и 2 категорий, напряжение питающей линии -35 кВ, напряжение внутризаводской сети – 10 кВ, напряжение зданий – 0.4 кВIn the course of the final qualifying work, the power supply system of the hangar building and the enterprise as a whole was designed. In the calculation we used the method of ratio calculation method of power and power factor. The issues of resource efficiency and social responsibility of the designed system were considered. The basic constructive, technological and operating characteristics: the company includes fourteen buildings 1 and 2 categories, the line voltage of -35 kV, the voltage of the in-plant network of 10 kV, voltage-buildings – 0.4 k

Mutations in GDF5 Reveal a Key Residue Mediating BMP Inhibition by NOGGIN

Signaling output of bone morphogenetic proteins (BMPs) is determined by two sets of opposing interactions, one with heterotetrameric complexes of cell surface receptors, the other with secreted antagonists that act as ligand traps. We identified two mutations (N445K,T) in patients with multiple synostosis syndrome (SYM1) in the BMP–related ligand GDF5. Functional studies of both mutants in chicken micromass culture demonstrated a gain of function caused by a resistance to the BMP–inhibitor NOGGIN and an altered signaling effect. Residue N445, situated within overlapping receptor and antagonist interfaces, is highly conserved among the BMP family with the exception of BMP9 and BMP10, in which it is substituted with lysine. Like the mutant GDF5, both BMPs are insensitive to NOGGIN and show a high chondrogenic activity. Ectopic expression of BMP9 or the GDF5 mutants resulted in massive induction of cartilage in an in vivo chick model presumably by bypassing the feedback inhibition imposed by endogenous NOGGIN. Swapping residues at the mutation site alone was not sufficient to render Bmp9 NOG-sensitive; however, successive introduction of two additional substitutions imparted high to total sensitivity on customized variants of Bmp9. In conclusion, we show a new mechanism for abnormal joint development that interferes with a naturally occurring regulatory mechanism of BMP signaling

NOG insensitivity of rhN445T GDF5 in vitro.

<p>(A) ALP activity induced in C2C12 myoblastic mouse cells overexpressing the Bmpr1b receptor (C2C12-Bmpr1b) after three days of stimulation. All BMPs show dose-dependent induction of ALP activity. (B) Inhibition of rhBMP-induced ALP activity in the C2C12-Bmpr1b cell line by rhNOG. ALP activity was measured after co-stimulation of 5 nM rhGDF5, rhN445T GDF5, rhBMP2, and 0.05 nM rhBMP9 with up to 40 nM rhNOG (rhBMP9 up to 0.4 nM). RhBMP2 is strongly inhibited by rhNOG. In contrast to rhGDF5 the mutant rhN445T GDF5 shows no response to rhNOG inhibition.</p

Biacore interaction analysis (n = 6) showed no binding differences for rhGDF5 and rhN445T GDF5 with BMPR1Aecd and BMPR1Becd.

<p>Biacore interaction analysis (n = 6) showed no binding differences for rhGDF5 and rhN445T GDF5 with BMPR1Aecd and BMPR1Becd.</p