Анализ технологии предварительной подготовки нефти на месторождении "Н" (Красноярский край)

Объектом исследования является технология предварительной подготовки нефти на "Н" нефтегазоконденсатном месторождении. Целью выпускной квалификационной работы является анализ технологии предварительной подготовки нефти и подбор аппарата для отделения воды. В процессе выполнения выпускной квалификационной работы были изучены причины образования нефтяной эмульсии и способы ее разрушения; рассмотрены наиболее распространение устройства для отделения воды. Собраны данные по характеристике месторождения, составам пластовой нефти, газа и воды, технологии предварительной подготовки обводненной нефти.The object of the study is the technology of preliminary oil treatment at the" N " oil and gas condensate field. The purpose of the final qualification work is to analyze the technology of preliminary preparation of oil and the selection of a device for separating water. In the course of the final qualification work, the reasons for the formation of an oil emulsion and the methods of its destruction were studied; the most common devices for separating water were considered. Data on the characteristics of the field, the composition of reservoir oil, gas and water, and the technology of preliminary preparation of watered oil are collected

Expression of a constitutively active mutant of heat shock factor 1 under the control of testis-specific hst70 gene promoter in transgenic mice induces degeneration of seminiferous epithelium.

Heat shock activates in somatic cells a set of genes encoding heat shock proteins which function as molecular chaperones. The basic mechanism by which these genes are activated is the interaction of the specific transcription factor HSF1 with a regulatory DNA sequence called heat shock element (HSE). In higher eukaryotes HSF1 is present in unstressed cells as inactive monomers which, in response to cellular stress, aggregate into transcriptionally competent homotrimers. In the present paper we showed that the expression of a transgene encoding mutated constitutively active HSF1 placed under the control of a spermatocyte-specific promoter derived from the hst70 gene severely affects spermatogenesis. We found the testes of transgenic mice to be significantly smaller than those of wild-type males and histological analysis showed massive degeneration of the seminiferous epithelium. The lumen of tubules was devoid of spermatids and spermatozoa and using the TUNEL method we demonstrated a high rate of spermatocyte apoptosis. The molecular mechanism by which constitutively active HSF1 arrests spermatogenesis is not known so far. One can assume that HSF1 can either induce or repress so far unknown target genes involved in germ cell apoptosis

Transcriptional Activation of the cAMP-responsive Modulator Promoter in Human T Cells Is Regulated by Protein Phosphatase 2A-mediated Dephosphorylation of SP-1 and Reflects Disease Activity in Patients with Systemic Lupus Erythematosus*

Systemic lupus erythematosus (SLE) is a complex autoimmune disease with numerous abnormalities recorded at the cellular, molecular, and genetic level. Expression of the basic leucine zipper transcription factor cAMP-responsive element modulator (CREM)α was reported to be abnormally increased in T cells from SLE patients. CREMα suppresses IL-2 and T cell receptor ζ chain gene transcription by direct binding to the respective promoters. Here, we show that increased CREM expression is the result of enhanced promoter activity. DNA binding analyses reveal direct binding of transcription factor specificity protein-1 (SP-1) to the CREM promoter resulting in enhanced transcriptional activity and increased CREM expression. Protein phosphatase 2A is known to activate SP-1 through dephosphorylation at its serine residue 59. Our results show that nuclei from SLE T cells contain lower levels of Ser59-phosphorylated SP-1 protein and a stronger SP-1 binding to the CREM promoter. We conclude that protein phosphatase 2A accounts for enhanced SP-1 dephosphorylation at Ser59 in SLE T cells. More importantly, CREM promoter activity mirrors reliably disease activity in SLE patients, underscoring its potential role as a biomarker for the prediction of flares in SLE patients