Identification of the Causes of the Destruction of the Body of the Shut-off Valve

A study was made of the causes of the emergency destruction of the shut-off valve. The fracture surface was studied, the mechanical properties of the material and the structure of the metal were evaluated. The accident was caused by deviations from standard properties and equipment overload

STUDY OF DEFECTS OF LONGITUDINAL WELDED PIPE

A study of the defects of the longitudinal weld seam revealed by X-ray inspection was carried out. These defects were not detected by magnetic inspection. Erroneous identification of defects during X-ray inspection. Compliance of base metal and weld seam with regulatory documents.Работа выполнена в рамках государственного задания МИНОБРНАУКИ России (тема «Диагностика», № АААА-А18-118020690196-3)

FRACTOGRAPHIC STUDY OF FATIGUE FAILURE OF A HIGH-PRESSURE TURBINE ROTOR BLADE

The paper presents the results of studying the fracture surface of a high-pressure turbine rotor blade with a crack. The crack grew by a fatigue mechanism, with the formation of fan-shaped scars and grooves along the crack front in the fracture. Fatigue crack propagation caused emergency fracture.Работа выполнена в рамках государственного задания МИНОБРНАУКИ России (тема «Диагностика», № АААА-А18-118020690196-3)

USING OF HIGH-STRENGTH PROTECTIVE COATINGS, REDUCING THE RISK OF INITIATION AND DEVELOPMENT OF STRESS CORROSION CRACKING DEFECTS

The article is devoted to the application of new methods of protection of trunk pipelines with defects of SCC. New anti-corrosion coatings will significantly reduce the stress level in the pipeline being repaired, preventing the development of SCC defects.Работа выполнена в рамках государственного задания МИНОБРНАУКИ России (тема «Диагностика», Г.р.№ АААА-А18-118020690196-3)

Increased tumour dihydroceramide production after Photofrin-PDT alone and improved tumour response after the combination with the ceramide analogue LCL29. Evidence from mouse squamous cell carcinomas

Photodynamic therapy (PDT) has been proven effective for treatment of several types of cancer. Photodynamic therapy alone, however, attains limited cures with some tumours and there is need for its improved efficacy in such cases. Sphingolipid (SL) analogues can promote tumour response in combination with anticancer drugs. In this study, we used mouse SCCVII squamous cell carcinoma tumours to determine the impact of Photofrin-PDT on the in vivo SL profile and the effect of LCL29, a C6-pyridinium ceramide, on PDT tumour response. Following PDT, the levels of dihydroceramides (DHceramides), in particular C20-DHceramide, were elevated in tumours. Similarly, increases in DHceramides, in addition to C20:1-ceramide, were found in PDT-treated SCCVII cells. These findings indicate the importance of the de novo ceramide pathway in Photofrin-PDT response not only in cells but also in vivo. Notably, co-exposure of SCCVII tumours to Photofrin-PDT and LCL29 led to enhanced tumour response compared with PDT alone. Thus, we show for the first time that Photofrin-PDT has a distinct signature effect on the SL profile in vitro and in vivo, and that the combined treatment advances PDT therapeutic gain, implying translational significance of the combination

Mitochondrially targeted ceramide LCL-30 inhibits colorectal cancer in mice

The sphingolipid ceramide is intimately involved in the growth, differentiation, senescence, and death of normal and cancerous cells. Mitochondria are increasingly appreciated to play a key role in ceramide-induced cell death. Recent work showed the C16-pyridinium ceramide analogue LCL-30 to induce cell death in vitro by mitochondrial targeting. The aim of the current study was to translate these results to an in vivo model. We found that LCL-30 accumulated in mitochondria in the murine colorectal cancer cell line CT-26 and reduced cellular ATP content, leading to dose- and time-dependent cytotoxicity. Although the mitochondrial levels of sphingosine-1-phosphate (S1P) became elevated, transcription levels of ceramide-metabolising enzymes were not affected. In mice, LCL-30 was rapidly absorbed from the peritoneal cavity and cleared from the circulation within 24 h, but local peritoneal toxicity was dose-limiting. In a model of subcutaneous tumour inoculation, LCL-30 significantly reduced the proliferative activity and the growth rate of established tumours. Sphingolipid profiles in tumour tissue also showed increased levels of S1P. In summary, we present the first in vivo application of a long-chain pyridinium ceramide for the treatment of experimental metastatic colorectal cancer, together with its pharmacokinetic parameters. LCL-30 was an efficacious and safe agent. Future studies should identify an improved application route and effective partners for combination treatment

The Targeting of Plasmalemmal Ceramide to Mitochondria during Apoptosis

Ceramide is a key lipid mediator of cellular processes such as differentiation, proliferation, growth arrest and apoptosis. During apoptosis, ceramide is produced within the plasma membrane. Although recent data suggest that the generation of intracellular ceramide increases mitochondrial permeability, the source of mitochondrial ceramide remains unknown. Here, we determine whether a stress-mediated plasmalemmal pool of ceramide might become available to the mitochondria of apoptotic cells. We have previously established annexin A1—a member of a family of Ca2+ and membrane-binding proteins—to be a marker of ceramide platforms. Using fluorescently tagged annexin A1, we show that, upon its generation within the plasma membrane, ceramide self-associates into platforms that subsequently invaginate and fuse with mitochondria. An accumulation of ceramide within the mitochondria of apoptotic cells was also confirmed using a ceramide-specific antibody. Electron microscopic tomography confirmed that upon the formation of ceramide platforms, the invaginated regions of the plasma membrane extend deep into the cytoplasm forming direct physical contacts with mitochondrial outer membranes. Ceramide might thus be directly transferred from the plasma membrane to the mitochondrial outer membrane. It is conceivable that this “kiss-of-death” increases the permeability of the mitochondrial outer membrane thereby triggering apoptosis