The placenta is a vitally important organ in the regulation of embryonic development. That is why extensive calcium deposition [also named as pathological placental calcifi cation (PPC)] could have serious negative consequences for the adequate growth of embryos. The nature and mechanism of PPC development has not been defi ned as yet. In the present investigation, we have tested the hypothesis that the molecular basis of PPC development consists of nanobacteria-induced calcifi cation in infected female placenta. Electron microscopy fi ndings support this hypothesis. The initial stage of micro-calcifi cation may originate from the external surface of individual nanobacteria-like particles found mainly in placental extracellular matrix, where initial calcium deposition occurs as a needle surface deposition or as an amorphous-like surface precipitate. Further calcifi c propagation in placenta takes place in the newly formed macro-cavities, which are characterized by low electron density, possibly refl ecting its liquid content around calcium deposition. The micro-cavities contain free nanobacterial-like particles, which may relate to atypical Gram-negative bacteria but not to apoptotic bodies by morphological characters and DNA/RNA distribution. We hypothesize that the increased placental calcifi cation might be caused, at least in part, by nanobacterial infection. [Agababov R M, Abashina T N, Suzina N E, Vainshtein M B and Schwartsburd P M 2007 Link between the early calcium deposition in placenta and its nanobaсterial-like infection;
Unrestricted cancer growth requires permanent supply of glucose that can be obtained from cancer-mediated reprogramming of glucose metabolism in the cancer-bearing host. The pathological mechanisms by which cancer cells exert their negative influence on host glucose metabolism are largely unknown. This paper proposes a mechanism of metabolic and hormonal changes that may favor glucose delivery to tumor (not host) cells by creating a cancer-host “vicious cycle” whose prolonged action drives cancer progression and promotes host cachexia. To verify this hypothesis, a feedback model of host-cancer interactions that create the “vicious cycle” via cancer-induced reprogramming of host glucose metabolism is proposed. This model is capable of answering some crucial questions as to how anabolic cancer cells can reprogram the systemic glucose metabolism and why these pathways were not observed in pregnancy. The current paper helps to better understanding a pathogenesis of cancer progression and identify hormonal/metabolic targets for anti-cancer treatment.
Maintenance of glucose homeostasis during circadian behavioral cycles is critical. The processes controlling the switch between predominant lipolysis/fatty oxidation during fasting and predominant lipid storage/glucose oxidation following feeding are determined principally by insulin. Chronic elevated threshold of insulin resistance (IR) is a key pathological feature of obesity, Type 2 diabetes, sepsis and cancer cachexia; however, a temporal reduced threshold of IR is widely met in fasting/hibernation, pregnancy, antibacterial immunity, exercise and stress. Paradoxically, some of these cases are associated with catabolic metabolism, whereas others are related to anabolic pathways. This article considers the possible causes of circadian disorders in glucose and lipid metabolism that act as a driving force for obesity-promoted development of Type 2 diabetes. This is intended to provide improved insight into the pathogenesis of chronic circadian disorders that increase the risk of diabetes, and consider new targets for its metabolic and drug correction.
Local chronic inflammation can act as a high cancer risk factor. The basis of this pathogenic effect is under investigation. This review examines the evidence that chronic inflammation is capable of inducing the complex of microenvironmental changes similar to those seen around growing cancer cells. The changes include: enhanced oxidative cell resistance against apoptosis; switch to glycolytic metabolism, neovasculogenesis and vasorelaxation which provide nutrient delivery but restrict the immune/inflammatory cell recruiting. These synergistic changes can act as a counter balancing force to self-limit the cytotoxic response by normally acute inflammation. However, the duration and intensity of this force can become insufficient to restrict the prolonged cytotoxic response by chronic inflammation. The hypothetic model of the latter effects is presented as a result of discoordinated feedback regulation among heme-, prostaglandin E2-, nitric oxide-, carbon monoxide-, and polyamine-dependent enzymatic pathways in the growth inhibiting (cytotoxic) and growth promoting (regenerative) stages of acute or chronic inflammatory response. According to this model, chronic inflammation is capable of generating a potentially 'vicious self-sustaining loop(s)' which are resulted in the pro-cancer microenvironment favorable for survival of tumor cells and their growth.
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