Technological and economic features of growing organic soybeans and winter wheat forage

This article is devoted to research of technological processes of cultivation of soybeans and winter wheat forage by the organic standards for the period of 4 years that provides observance of the crop rotation and satisfies the existing demand for organic agricultural products abroad. In this paper technological cards of cultivation of the specified crops are developed and their economic profitableness is proved due to lower expenses for fuel and biological preparations and higher prices for organic products. It is proved that economic efficiency of cultivation: soybeans by the organic standards makes in the first year 233%, and in the third 565%; winter wheat in the second year 260%, and in the fourth 513%. The cash flows calculated for four years testify about economic profitableness of the organic agriculture and its prospects in the modern conditions. On the basis of the conducted researches the risks of cultivation of soybeans and winter wheat forage by the organic standards are defined which can be minimized in 3 years by observance of the main principles of organic agriculture, being guided by the practice of I.Ovsinsky and M.Kurdyumov. The demand for grown organic agricultural products has stable dynamics to growth both within the country and abroad which ensures profitability for agricultural producer

CHEMICAL STUDY OF SNOW OF VLADIVOSTOK CITY AND RUSSKY ISLAND

In the paper thefirst results of mass and spectrometer research of snow cover of the largest city in the Far East - Vladivostok (mainland and Island Russky), dropped-out on the November 19 2012, are presented. To exclude secondary pollution by anthropogenous aerosols we used the top layer (5-10 cm) of just dropped-out snow placed in the 3-liter sterile containers. In a couple of hours, when snow in containers thawed, 10 ml of liquid were gained from each sample and were analyzed on a mass spectrometer of high resolution with inductive-connected plasma (MS-ICP) Element XR (Thermo Scientific). Measurements were carried out with use of a technique of TsV3.18.05-2005 Fr.1.31.2005.01714. Tests were selected in 20 points: 16 points - Vladivostok, 3 points - Island Russky (DVFU campus, the bridge, the settlement) and a comparison point - the bay Hero in the southwest of Peter the Great Bay. For the first time application of the most highly sensitive chemical method for an applied ecological task is shown today. Distribution of Pb, Cr, Mn, Fe, Co, Ni, Cu and Zn in areas of Vladivostok different by anthropogenous loading and on Russian Island is revealed. In districts of Vladivostok with high transport loading high contents of metals (Mn, Cu, Zn) which source is motor transport (exhaustgases, autopaint, catalysts) are fixed also. Tests from districts of the Academic Town have traces of influence of the sea coast (halite and potassium-containing minerals) and railroad tracks (a microparticle of iron and its oxides) that strongly pollutes environment iron because of continuous movement of trains. In the tests taken on the Eagle hill, the highest point of Vladivostok, high concentrations of Mn (the highest concentration from all tests) and Cu (the third concentration from all tests) are recorded. This point of selection is in the downtown and, apparently, isn't ecologically clear. It should be noted that height above sea level in an urban environment isn't in sufficient condition for ecological safety. Russian Island is a pure zone with low background contents of heavy metals. The raised maintenance of Cu, Ni and Zn in snow cover of the bay Hero is shown

A promyelocytic leukemia protein-thrombospondin 2 axis and the risk of relapse in neuroblastoma

Purpose. Neuroblastoma is a childhood malignancy originating from the sympathetic nervous system with a complex biology, prone to metastasize and relapse. High-risk, metastatic cases are explained in part by amplification or mutation of oncogenes such as MYCN and ALK and loss of tumour suppressor genes in chromosome band 1p. However, it is fundamental to identify other pathways responsible for the large portion of neuroblastomas with no obvious molecular alterations. Experimental design. Neuroblastoma cell lines were used for assessment of tumour growth in vivo and in vitro. Protein expression in tissues and cells was assessed using immunofluorescence and immunohistochemistry. The association of PML expression with neuroblastoma outcome and relapse was calculated using log-rank and Mann-Whitney tests, respectively. Gene expression was assessed using chip microarrays. Results: PML is detected in the developing and adult sympathetic nervous system, whereas it is not expressed or low in metastatic neuroblastoma tumours. Reduced PML expression in patients with low-risk cancers - i.e. localized and negative for the MYCN protooncogene - is strongly associated with tumour recurrence. PML-I, but not PML-IV, isoform suppresses angiogenesis via upregulation of thrombospondin-2 (TSP-2), a key inhibitor of angiogenesis. Finally, PML-I and TSP-2 expression inversely correlates with tumour angiogenesis and recurrence in localized neuroblastomas. Dvorkina et al. A promyelocytic leukaemia protein-thrombospondin 2 axis and the risk of relapse in neuroblastoma 3 Conclusions: Our work reveals a novel PML-I-TSP2 axis for regulation of angiogenesis and cancer relapse, which could be used to identify patients with low-risk, localized tumours that might benefit from chemotherapy

ATR is a MYB regulated gene and potential therapeutic target in adenoid cystic carcinoma

Adenoid cystic carcinoma (ACC) is a rare cancer that preferentially occurs in the head and neck, breast, as well as in other sites. It is an aggressive cancer with high rates of recurrence and distant metastasis. Patients with advanced disease are generally incurable due to the lack of effective systemic therapies. Activation of the master transcriptional regulator MYB is the genomic hallmark of ACC. MYB activation occurs through chromosomal translocation, copy number gain or enhancer hijacking, and is the key driving event in the pathogenesis of ACC. However, the functional consequences of alternative mechanisms of MYB activation are still uncertain. Here, we show that overexpression of MYB or MYB-NFIB fusions leads to transformation of human glandular epithelial cells in vitro and results in analogous cellular and molecular consequences. MYB and MYB-NFIB expression led to increased cell proliferation and upregulation of genes involved in cell cycle control, DNA replication, and DNA repair. Notably, we identified the DNA-damage sensor kinase ATR, as a MYB downstream therapeutic target that is overexpressed in primary ACCs and ACC patient-derived xenografts (PDXs). Treatment with the clinical ATR kinase inhibitor VX-970 induced apoptosis in MYB-positive ACC cells and growth inhibition in ACC PDXs. To our knowledge, ATR is the first example of an actionable target downstream of MYB that could be further exploited for therapeutic opportunities in ACC patients. Our findings may also have implications for other types of neoplasms with activation of the MYB oncogene.Adenoid Cystic Carcinoma Research Foundation; Swedish Cancer Society; BioCARE – a National Strategic Cancer Research Program at the University of Gothenburg; AG-Fon

The tumour-suppressive function of CLU is explained by its localisation and interaction with HSP60

The product of the CLU gene promotes or inhibits tumourigenesis in a context-dependent manner. It has been hypothesised that different CLU isoforms have different and even opposing biological functions, but this theory has not been experimentally validated. Here we show that molecules involved in survival pathways are differentially modulated by the intracellular or secreted forms of CLU. Secreted CLU, which is selectively increased after transformation, activates the survival factor AKT, whereas intracellular CLU inhibits the activity of the oncogenic transcription factor nuclear factor kappa B. Furthermore, intracellular CLU is inactivated by the pro-proliferative and pro-survival activity of the chaperone protein HSP60 in neuroblastoma cells by forming a physical complex. Thus, localisation is key for CLU physiology, explaining the wide range of effects in cell survival and transformation

CLU blocks HDACI-mediated killing of neuroblastoma

Clusterin is a ubiquitously expressed glycoprotein with multiple binding partners including IL-6, Ku70, and Bax. Clusterin blocks apoptosis by binding to activated Bax and sequestering it in the cytoplasm, thereby preventing Bax from entering mitochondria, releasing cytochrome c, and triggering apoptosis. Because increased clusterin expression correlates with aggressive behavior in tumors, clusterin inhibition might be beneficial in cancer treatment. Our recent findings indicated that, in neuroblastoma cells, cytoplasmic Bax also binds to Ku70; when Ku70 is acetylated, Bax is released and can initiate cell death. Therefore, increasing Ku70 acetylation, such as by using histone deacetylase inhibitors, may be therapeutically useful in promoting cell death in neuroblastoma tumors. Since clusterin, Bax, and Ku70 form a complex, it seemed likely that clusterin would mediate its anti-apoptotic effects by inhibiting Ku70 acetylation and blocking Bax release. Our results, however, demonstrate that while clusterin level does indeed determine the sensitivity of neuroblastoma cells to histone deacetylase inhibitor-induced cell death, it does so without affecting histone deacetylase-inhibitor-induced Ku70 acetylation. Our results suggest that in neuroblastoma, clusterin exerts its anti-apoptotic effects downstream of Ku70 acetylation, likely by directly blocking Bax activation

Lineage-Specific Restraint of Pituitary Gonadotroph Cell Adenoma Growth

Although pituitary adenomas are usually benign, unique trophic mechanisms restraining cell proliferation are unclear. As GH-secreting adenomas are associated with p53/p21-dependent senescence, we tested mechanisms constraining non-functioning pituitary adenoma growth. Thirty six gonadotroph-derived non-functioning pituitary adenomas all exhibited DNA damage, but undetectable p21 expression. However, these adenomas all expressed p16, and >90% abundantly expressed cytoplasmic clusterin associated with induction of the Cdk inhibitor p15 in 70% of gonadotroph and in 26% of somatotroph lineage adenomas (p = 0.006). Murine LβT2 and αT3 gonadotroph pituitary cells, and αGSU.PTTG transgenic mice with targeted gonadotroph cell adenomas also abundantly expressed clusterin and exhibited features of oncogene-induced senescence as evidenced by C/EBPβ and C/EBPδ induction. In turn, C/EBPs activated the clusterin promoter ∼5 fold, and elevated clusterin subsequently elicited p15 and p16 expression, acting to arrest murine gonadotroph cell proliferation. In contrast, specific clusterin suppression by RNAis enhanced gonadotroph proliferation. FOXL2, a tissue-specific gonadotroph lineage factor, also induced the clusterin promoter ∼3 fold in αT3 pituitary cells. As nine of 12 pituitary carcinomas were devoid of clusterin expression, this protein may limit proliferation of benign adenomatous pituitary cells. These results point to lineage-specific pathways restricting uncontrolled murine and human pituitary gonadotroph adenoma cell growth