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In this study, we described the dynamics of land-cover and gross carbon stocks and emissions (C) in 55 settlements in Legal Amazon, located in northern Mato Grosso state, between 2008 and 2016 and discussed their implications for climate change policies. C estimates were based on land-cover changes, obtained with Spot, Sentinel and Landsat image processing and field visits, and secondary data of mean carbon values ​​per vegetation class. The 55 settlements were originally covered by 685,000 ha of native vegetation (103 Tg C). Deforestation by 2016 was over 65%. Most of it (77%) occurred by 2008. Although restoration of consolidated areas (areas deforested before July 2008) is not mandatory, it can generate revenue from carbon credits, environmental reserve quotas, forest management and agroforestry. The deforested area per settlement by 2008 was strongly related to the deforestation per settlement between 2008 and 2016. This suggests that those who deforested a lot until 2008 tend to continue to do so until 2016. The annual deforestation rate between 2008 and 2016 was 12.7 thousand ha /year. If it remains the same, all native vegetation will have been suppressed in less than two decades. In general, the Sustainable-Development-Project settlements had less deforestation, which indicates that it is possible to associate agrarian reform and economic and social development with the conservation of the Amazon rainforest. However, it is necessary to strengthen policies toward payment for ecosystem services and forest management products (low-impact forest management and non-timber forest products). In order to do so, the integration of federal, state and local governments and market efforts is paramount.

Aim. To find out the relationship of particular blood cells (BC) and their ratios with lipid metabolism in patients with essential hypertension (EH), with (EH-1) and without kinesiotherapy (EH-2).Material and methods. The study included 30 healthy women (control group) and 72 women with EH, which were divided into 2 groups: group 1 (EH-1) — 37 women with stage II (target organ damage classification) hypertension who receive antihypertensive therapy; group 2 (EH-2) — 35 women who underwent antihypertensive therapy and kinesiotherapy (3-4 courses for 2-3 years).Results. Correlation analysis revealed that the studied relationships in healthy women, EH-1 and EH-2 women can be either direct or inverse. In healthy women, we observed negative association of monocytes (MON) with atherogenic index (AI), a positive association of basophils (BAS) with high density lipoproteins (HDL) and its negative association with low density lipoproteins (LDL), very low density lipoproteins (VLDL) and AI and red blood cells/platelets (RBC/PLT ratio) with HDL. Negative associations of lymphocytes (LYM)/BAS ratio with triglyceride (TG) and eosinophils (EOS)/BAS ratio with LDL were also detected. Patients with EH-1 had a direct relationship between LYM/EOS ratio and TG. In patients with EH-2, a negative relationship was found between PLT and HDL, MON and HDL, neutrophils (NEU)/MON ratio and TAG, and a positive — between white blood cells (WBC), NEU, MON and AI, LYM and TAG, MON and TAG, as well as AI.Conclusion. The obtained data indicate that all BC and their ratios in women with/without EH and with/without kinesiotherapy affect the lipid metabolism.

The article presents the results of long-term clinical, molecular-biological and laboratory studies on combined poly-stage treatment of patients with colon cancer with liver metastases. The cytotoxicity of various chemotherapeutic agents for colorectal carcinoma in the lines of HT 29 and NMG 64/84 cells was studied by analysis of human colony-forming tumor (HTCA). In vitro studies on the suspension of tumor cells from remote liver metastases were carried out to determine the most effective chemotherapeutic agents for intra-arterial hepatic infusion (HAI). Individual choice of the scheme of systemic chemotherapy depends on the level of thymidylate synthetase (TS) in the tumor tissue. Long-term own clinical experience and analysis of world literature allow authors to state that stage resection of the liver (STR) in combination with regional (HAI) and systemic chemotherapy is the method of choice in the treatment of patients with colorectal cancer with unresectable liver metastases. In comparison with other treatment methods (ALPPS and TSH), STR has the least negative consequences and is beneficial from the tumor-biological point of view.

Abstract Failure to precisely repair DNA damage in self-renewing Hematopoietic Stem and early Progenitor Cells (HSPCs) can disrupt normal hematopoiesis and promote leukemogenesis. Although HSPCs are widely considered a target of ionizing radiation (IR)-induced hematopoietic injury, definitive data regarding cell death, DNA repair, and genomic stability in these rare quiescent cells are scarce. We found that irradiated HSPCs, but not lineage-committed progenitors (CPs), undergo rapid ATM-dependent apoptosis, which is suppressed upon interaction with bone-marrow stroma cells. Using DNA repair reporters to quantify mutagenic Non-Homologous End Joining (NHEJ) processes, we found that HSPCs exhibit reduced NHEJ activities in comparison with CPs. HSPC-stroma interactions did not affect the NHEJ capacity of HSPCs, emphasizing its cell autonomous regulation. We noted diminished expression of multiple double strand break (DSB) repair transcripts along with more persistent 53BP1 foci in irradiated HSPCs in comparison with CPs, which can account for low NHEJ activity and its distinct control in HSPCs. Finally, we documented clonal chromosomal aberrations in 10% of IR-surviving HSPCs. Taken together, our results revealed potential mechanisms contributing to the inherent susceptibility of human HSPC to the cytotoxic and mutagenic effects of DNA damage.

Summary: The tumor suppressor p53 limits tumorigenesis by inducing apoptosis, cell cycle arrest, and senescence. Although p53 is known to limit inflammation during tumor development, its role in regulating chronic lung inflammation is less well understood. To elucidate the function of airway epithelial p53 in such inflammation, we subjected genetically modified mice, whose bronchial epithelial club cells lack p53, to repetitive inhalations of lipopolysaccharide (LPS), an exposure that leads to severe chronic bronchitis and airway senescence in wild-type mice. Surprisingly, the club cell p53 knockout mice exhibited reduced airway senescence and bronchitis in response to chronic LPS exposure and were significantly protected from global lung destruction. Furthermore, pharmacological elimination of senescent cells also protected wild-type mice from chronic LPS-induced bronchitis. Our results implicate p53 in induction of club-cell senescence and correlate epithelial cell senescence of chronic airway inflammation and lung destruction. : Sagiv et al. find that senescence and p53 in bronchial epithelial cells promote chronic lung inflammation and COPD-like disease. Genetic or pharmacological reduction in senescent cell number blunts chronic inflammation and limits disease progression. Keywords: cellular senescence, p53, bronchitis, inflammation, club cells