Анализ причин обводненности добывающих скважин на нефтяных месторождениях

В процессе исследования рассмотрены причины преждевременного обводнения скважин, алгоритм подбора скважин-кандидатов для проведения водоизоляционных работ (ВИР), методы диагностики водопритоков, факторы, влияющие на эффективность ВИР и мероприятия по снижению обводненности скважинной продукции. Рассмотрен опыт применения технологии выравнивания профиля приемистости на месторождении АО "Газпромнефть-ННГ".During the research, the causes of premature well flooding, the algorithm for selecting candidate wells for water shutoff, methods for diagnosing water inflow, factors affecting the effectiveness of water shutoff and measures to reduce the water content of well products are considered. The experience of applying the technology of conformance control at the field of JSC Gazpromneft-NNG is considered

Разработка налоговой политики МУП «КРУ г.Юрги»

Объектом исследования является муниципальное унитарное предприятие "Комбинат ритуальных услуг г. Юрги". Цель работы – формирования налоговой политики муниципального унитарного предприятия "Комбинат ритуальных услуг г. Юрги". Актуальность работы определяется критическим влиянием налоговой политики на финансово-хозяйственную деятельность предприятия и повышение эффективности управления его налоговыми потоками. Для достижения поставленной цели решены следующие задачи: 1.Рассмотреть теоретическую базу проведения налогового анализа на микроуровне. 2.Выполнить анализ финансово-хозяйственной деятельности МУП КРУ г. Юрги. 3.Оценить влияние налоговых платежей на финансовый результат деятельности МУП КРУ г. Юрги. 4.Предложить рекомендации по оптимизации налоговых выплат.The purpose of the work is the formation of the tax policy of the municipal unitary enterprise "Combine of funeral services of Yurga". The relevance of the work is determined by the critical impact of tax policy on the financial and economic activities of the enterprise and improving the efficiency of managing its tax flows. To achieve this goal, the following tasks were solved: 1. Consider the theoretical basis for conducting tax analysis at the micro level. 2. To analyze the financial and economic activities of the municipal unitary enterprise of the switchgear of the city of Yurga. 3. To assess the impact of tax payments on the financial result of the activities of the municipal unitary enterprise of KRU of Yurga 4. To offer recommendations for optimizing tax payments

Combined activities of JNK1 and JNK2 in hepatocytes protect against toxic liver injury

Background & Aims: c-Jun N-terminal kinase (JNK)1 and JNK2 are expressed in hepatocytes and have overlapping and distinct functions. JNK proteins are activated, via phosphorylation, in response to acetaminophen- or CCl4-induced liver damage; the level of activation correlates with the degree of injury. SP600125, a JNK inhibitor, has been reported to block acetaminophen-induced liver injury. We investigated the role of JNK in drug-induced liver injury (DILI) in liver tissues from patients and in mice with genetic deletion of JNK in hepatocytes. Methods: We studied liver sections from patients with DILI (due to acetaminophen, phenprocoumon, non-steroidal anti-inflammatory drugs or autoimmune hepatitis), or patients without acute liver failure (controls), collected from a DILI Biobank in Germany. Levels of total and activated (phosphorylated) JNK were measured by immunohistochemistry and western blotting. Mice with hepatocyte-specific deletion ofJnk1 (Jnk1Δhepa) or combination of Jnk1 and Jnk2 (JnkΔhepa), as well as Jnk1-floxed C57BL/6 (control) mice, were given injections of CCl4 (to induce fibrosis) or acetaminophen (to induce toxic liver injury). We performed gene expression microarray, and phosphoproteomic analyses to determine mechanisms of JNK activity in hepatocytes.  Results: Liver samples from DILI patients contained more activated JNK, predominantly in nuclei of hepatocytes and in immune cells, than healthy tissue. Administration of acetaminophen to JnkΔhepa mice produced a greater level of liver injury than that observed in Jnk1Δhepa or control mice, based on levels of serum markers and microscopic and histologic analysis of liver tissues. Administration of CCl4 also induced stronger hepatic injury in JnkΔhepa mice, based on increased inflammation, cell proliferation, and fibrosis progression, compared to Jnk1Δhepa or control mice. Hepatocytes from JnkΔhepamice given acetaminophen had an increased oxidative stress response, leading to decreased activation of AMPK, total protein AMPK levels, and pJunD and subsequent necrosis. Administration of SP600125 before or with acetaminophen protected JnkΔhepaand control mice from liver injury. Conclusions: In hepatocytes, JNK1 and JNK2 appear to have combined effects in protecting mice from CCl4- and acetaminophen-induced liver injury. It is important to study the tissue-specific functions of both proteins, rather than just JNK1, in the onset of toxic liver injury. JNK inhibition with SP600125 shows off-target effects

Bone marrow-derived c-jun N-terminal kinase-1 (JNK1) mediates liver regeneration

Liver regeneration is controlled by a complex network of signaling molecules, and a prominent role for c-jun N-terminal kinase has been suggested during this process. In the present study, we aimed to characterize and define the cell-type-specific contribution of JNK1 activation during liver regeneration. We used hepatocyte-specific JNK1 knockout mice (JNK1(Deltahepa)) using the cre/lox-P system. We performed partial hepatectomy (PH) in WT, JNK1(Deltahepa) and JNK1(-/-) animals and investigated time-points up to 72 h after PH. Additionally, bone marrow transplantation experiments were conducted in order to identify the contribution of hematopoietic cell-derived JNK1 activation for liver regeneration. Our results show that liver regeneration was significantly impaired in JNK1(-/-) compared to JNK1(Deltahepa) and WT animals. These data were evidenced by lower BrdU incorporation and decreased cell cycle markers such as Cyclin A, Cyclin D, E2F1 and PCNA 48 h after PH in JNK1(-/-) compared with JNK1(Deltahepa) and WT livers. In JNK1(-/-) mice, our findings were associated with a reduced acute phase response as evidenced by a lower activation of the IL-6/STAT3/SAA-1 cascade. Additionally, CD11b(+)Ly6G(+)-cells were decreased in JNK1(-/-) compared with JNK1(Deltahepa) and WT animals after PH. The transplantation of bone marrow-derived JNK1(-/-) into WT recipients caused significant reduction in liver regeneration. Interestingly, the transplantation of JNK1(-/-) into mice lacking JNK1 in hepatocytes only partially delayed liver regeneration. In summary, we provide evidence that (1) JNK1 in hematopoietic cells is crucial for liver regeneration, and (2) a synergistic function between JNK1 in hepatocytes and hematopoietic-derived cells is involved in the hepatic regenerative response

TNFR1 controls apoptosis and chronic liver disease in hepatocyte-specific IKKγ (Nemo) mice.

Death receptor-mediated hepatocyte apoptosis is implicated in a wide range of liver diseases including viral hepatitis, alcoholic hepatitis, ischemia/reperfusion injury, fulminant hepatic failure, cholestatic liver injury and cancer. Deletion of NF-ĸB essential modulator in hepatocytes (NemoΔhepa) causes the spontaneous development of hepatocellular carcinoma preceded by steatohepatitis in mice and thus serves as an excellent model for the progression from chronic hepatitis to liver cancer. In the present study we aimed to dissect the death-receptor mediated pathways that contribute to liver injury in NemoΔhepa mice. Therefore, we generated NemoΔhepa/TRAIL-/- and NemoΔhepa/TNFR1-/- animals and analyzed the progression of liver injury. NemoΔhepa/TRAIL-/- displayed a similar phenotype to NemoΔhepa mice characteristic of high apoptosis, infiltration of immune cells, hepatocyte proliferation and steatohepatitis. These pathophysiological features were significantly ameliorated in NemoΔhepa/TNFR1-/- livers. Hepatocyte apoptosis was increased in NemoΔhepa and NemoΔhepa/TRAIL-/- mice while NemoΔhepa/TNFR1-/- animals showed reduced cell death concomitant with a strong reduction in pJNK levels. Cell cycle parameters were significantly less activated in NemoΔhepa/TNFR1-/- livers. Additionally, markers of liver fibrosis and indicators of tumour progression were significantly decreased in these animals. The present data demonstrate that the death receptor TNFR1 but not TRAIL is important in determining progression of liver injury in hepatocyte-specific Nemo knockout mice