Особливості девелопменту в реалізації інвестиційних проектів будівництва об’єктів різного функціонального призначення

The article considers the individual character of the development of investment projects implemented by construction companies in the construction market. The role of individual factors is determined, the significance of which varies depending on the functional purpose of the construction objects. The specificity of functions of development companies in the process of realizing housing construction projects, trade and office facilities is analyzed.В статті розглянуто індивідуальний  характер розвитку  інвестиційних   проектів,  що реалізуються  девелоперськими  компаніями  на  будівельному  ринку. Визначена роль  окремих факторів,  значимість  яких змінюється в залежності  від  функціонального призначення об’єктів будівництва. Проаналізовано  специфічність функцій  девелоперських  компаній в процесі реалізації  проектів  будівництва  житла, торгівельних  та  офісних  установ

Особливості економічної оцінки зведення будинків з низьким енергоспоживанням

The article deals with the problems of the economic evaluation of theconstruction of buildings with low power consumption. The classification of buildings according to the level of low energy consumption is given and it is recommended to differentiate the economic assessment according to the class. It is noted that when choosing an optimal investment option for energy-efficient construction, it is necessary to take into account the amount of capital investments and current operational costs.У статті  досліджуються проблеми економічної оцінки зведення будинків з низьким енергоспоживанням. Наведено класифікацію будинків за рівнем низького енергоспоживання,   рекомендовано диференціювати економічну оцінку відповідно до класу. Зазначено, що при виборі оптимального варіанта інвестування енергоефективного будівництва необхідно враховувати величину капітальних вкладень та поточні  експлуатаційні витрати

Deformation uniformity of additively manufactured materials on the example of austenitic stainless steel 321 and copper C11000

Structural studies and mechanical tests of additively manufactured samples from AISI 321 steel copper C110000 have been carried out. Mechanical tensile tests of 321 steel show slight differences in the ultimate tensile strength (up to 3-4%) and ductility (up to 10%) of test coupons tested along the material growth direction and along the layer deposition direction. The strength of C11000 copper samples is 9.4% higher in the layer deposition direction, but their ductility is 15.4% lower than that of samples deformed in the growth direction. The strain relief on the surface of the polished gage section of the steel test coupons demonstrates changes in the material structure with small elongated grains along the growth direction of the sample. The deformation relief of copper samples is mainly related to the deformation of large columnar grains stretched in the growth direction

Structure formation features of large block-shaped samples from the copper and aluminum alloy produced by the wire-feed electron-beam additive technology

In this work the study of the structure of samples made by the wire-feed electronbeam 3D printing from copper C11000 and aluminum alloy AA5056 was carried out. The presence of a dendritic structure typical of this method was revealed, as well as the presence of pores, cracks and other defects that occurred during printing. Mechanical properties of samples cut in the planar section are at a rather low level. The ultimate tensile strength of copper block samples varies between 165 and 187 MPa. The relative elongation of samples without pores is at 18%, but with the presence of pores it decreases sharply to 7%, while the strength is practically not decreased. The samples of alloy AA5056 demonstrate slightly higher mechanical properties: the strength is at the level of 190-192 MPa and the relative elongation is about 16-18%. In samples with defects such as large pores or discontinuities, the strength drops to almost zero

СЛУЧАЙ НЕТЯЖЕЛОГО ТЕЧЕНИЯ ВРОЖДЕННОГО НЕФРОТИЧЕСКОГО СИНДРОМА

Nephrotic syndrome is a severe renal disease that may result in the end-stage renal failure despite the extent of proteinuria. Prognosis and tactics of therapy of nephrotic syndrome depend both on the morphological diagnosis and on the cause of the disease. It ought to be considered that congenital nephrotic syndrome is resistant to immunosuppressive therapy. However, several foreign authors demonstrate cases of immunosuppressive therapy effectiveness (steroids and cyclosporine A) in a range of familial cases of nephroticsyndrome. Timely detection of children with genetically caused nephrotic syndrome allows to define the patient management tactics in each case on time. This clinical case represents non-severe course of congenital nephrotic syndrome caused by an NPHS2 gene mutation, which had not before been described neither in Russian nor in foreign literature. The authors deem introduction of the molecular genetic analysis to the routine clinical practice for all cases of congenital nephrotic syndrome and steroid-resistant nephrotic syndrome reasonable. Нефротический синдром — серьезное заболевание почек, исходом которого независимо от степени протеинурии может стать терминальная стадия почечной недостаточности. Прогноз и тактика терапии нефротического синдрома зависят как от морфологического диагноза, так и от причины возникновения данного заболевания. Следует учитывать тот факт, что врожденный нефротический синдром является резистентным к иммуносупрессивной терапии. Однако, ряд зарубежных авторов демонстрирует примеры эффективности применения иммуносупрессивных препаратов (стероиды и циклоспорин А) при некоторых семейных случаях нефротического синдрома. Своевременное выявление детей с генетически обусловленным нефротическим синдромом позволяет вовремя определиться с тактикой ведения пациента в каждом конкретном случае. Представленный в статье клинический пример описывает нетяжелое течение врожденного нефротического синдрома, причиной которого стала ранее не описанная в отечественной и зарубежной литературе мутация гена NPHS2. Авторы считают целесообразным введение молекулярно-генетического исследования в повседневную клиническую практику при всех случаях врожденного нефротического синдрома, а также при стероидрезистентном варианте нефротического синдрома.

Long-term exposure to hypoxia inhibits tumor progression of lung cancer in rats and mice

<p>Abstract</p> <p>Background</p> <p>Hypoxia has been identified as a major negative factor for tumor progression in clinical observations and in animal studies. However, the precise role of hypoxia in tumor progression has not been fully explained. In this study, we extensively investigated the effect of long-term exposure to hypoxia on tumor progression <it>in vivo.</it></p> <p>Methods</p> <p>Rats bearing transplanted tumors consisting of A549 human lung cancer cells (lung cancer tumor) were exposed to hypoxia for different durations and different levels of oxygen. The tumor growth and metastasis were evaluated. We also treated A549 lung cancer cells (A549 cells) with chronic hypoxia and then implanted the hypoxia-pretreated cancer cells into mice. The effect of exposure to hypoxia on metastasis of Lewis lung carcinoma in mice was also investigated.</p> <p>Results</p> <p>We found that long-term exposure to hypoxia a) significantly inhibited lung cancer tumor growth in xenograft and orthotopic models in rats, b) significantly reduced lymphatic metastasis of the lung cancer in rats and decreased lung metastasis of Lewis lung carcinoma in mice, c) reduced lung cancer cell proliferation and cell cycle progression <it>in vitro</it>, d) decreased growth of the tumors from hypoxia-pretreated A549 cells, e) decreased Na⁺-K⁺ATPase α1 expression in hypoxic lung cancer tumors, and f) increased expression of hypoxia inducible factors (HIF1α and HIF2α) but decreased microvessel density in the lung cancer tumors. In contrast to lung cancer, the growth of tumor from HCT116 human colon cancer cells (colon cancer tumor) was a) significantly enhanced in the same hypoxia conditions, accompanied by b) no significant change in expression of Na⁺-K⁺ATPase α1, c) increased HIF1α expression (no HIF2α was detected) and d) increased microvessel density in the tumor tissues.</p> <p>Conclusions</p> <p>This study demonstrated that long-term exposure to hypoxia repressed tumor progression of the lung cancer from A549 cells and that decreased expression of Na⁺-K⁺ATPase was involved in hypoxic inhibition of tumor progression. The results from this study provide new insights into the role of hypoxia in tumor progression and therapeutic strategies for cancer treatment.</p

Molecular Determinants and Dynamics of Hepatitis C Virus Secretion

The current model of hepatitis C virus (HCV) production involves the assembly of virions on or near the surface of lipid droplets, envelopment at the ER in association with components of VLDL synthesis, and egress via the secretory pathway. However, the cellular requirements for and a mechanistic understanding of HCV secretion are incomplete at best. We combined an RNA interference (RNAi) analysis of host factors for infectious HCV secretion with the development of live cell imaging of HCV core trafficking to gain a detailed understanding of HCV egress. RNAi studies identified multiple components of the secretory pathway, including ER to Golgi trafficking, lipid and protein kinases that regulate budding from the trans-Golgi network (TGN), VAMP1 vesicles and adaptor proteins, and the recycling endosome. Our results support a model wherein HCV is infectious upon envelopment at the ER and exits the cell via the secretory pathway. We next constructed infectious HCV with a tetracysteine (TC) tag insertion in core (TC-core) to monitor the dynamics of HCV core trafficking in association with its cellular cofactors. In order to isolate core protein movements associated with infectious HCV secretion, only trafficking events that required the essential HCV assembly factor NS2 were quantified. TC-core traffics to the cell periphery along microtubules and this movement can be inhibited by nocodazole. Sub-populations of TC-core localize to the Golgi and co-traffic with components of the recycling endosome. Silencing of the recycling endosome component Rab11a results in the accumulation of HCV core at the Golgi. The majority of dynamic core traffics in association with apolipoprotein E (ApoE) and VAMP1 vesicles. This study identifies many new host cofactors of HCV egress, while presenting dynamic studies of HCV core trafficking in infected cells