1,721,014 research outputs found
Short-term recall of usual diet and current cognitive difficulties in a cohort of free-living elderly people in southern Italy
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Moving the systemic evolutionary approach to cancer forward: Therapeutic implications
No full textWe have previously presented a new Systemic Evolutionary Theory of Cancer (SETOC) based on the failure of proper endosymbiosis in eukaryotic cells. Here, we propose that the progressive uncoupling of two endosymbiotic subsystems (information and energy) inside the cell, as a consequence of long-term injuries, gives rise to alterations (i) in tissue interactions and (ii) in cell organization. In the first case, we argue that the impairment of both the coherent state and the synergy between intercellular communications underpins the onset of tissue dysplasia, that usually evolves towards cancer development. In the second case, we suggest that the rupture of endosymbiosis drives a sort of cell regression towards a protist-like entity represented by the concept of “de-emergence” postulated in our systemic evolutionary approach to carcinogenesis. This conceptual association of the cancer cell with a protist-like organism could support the development of novel cancer therapeutic approaches. To this end, we propose a paradigm shift in cancer pharmacology since: i) our knowledge of cancer pathophysiology as a complex system is insufficient, despite a vast knowledge of molecular mechanisms underlying cancer; ii) current cancer pharmacology deals only with microvariables (e.g. gene or protein targets), which do not account for the integrated pathophysiology of cancer, rather than with macrovariables (e.g. pH, membrane potential, electromagnetic fields, cell communications and so on) and mesovariables (between micro and macro), such as the interaction between various cellular components including cellular organelles. This paradigm shift should allow cancer pharmacology to move forward from molecular treatments (focusing on single targets) to modular treatments that consider cancer-related processes (i.e. inflammation, coagulation, etc.) or even to a sort of ecosystemic treatment addressing the whole functioning of the “cancer ecosystem”. Examples of ecosystems treatment may be natural plant derivatives that act synergistically or pulsed electromagnetic fields which can act on particular biological processes in cancer cells. In addition, we need different working theoretical models on which to base new anticancer pharmacological approaches. Finally, we examine what value our systemic evolutionary approach could add to cancer treatments, in particular in liver cancer as a paradigm for developing potential applications
A systemic evolutionary approach to cancer: Hepatocarcinogenesis as a paradigm
No full textThe systemic evolutionary theory of cancer pathogenesis posits that cancer is generated by the de-emergence of the eukaryotic cell system and by the re-emergence of its archaea (genetic material and cytoplasm) and prokaryotic (mitochondria) subsystems with an uncoordinated behavior. This decreased coordination can be caused by a change in the organization of the eukaryote environment (mainly chronic inflammation), damage to mitochondrial DNA and/or to its membrane composition by many agents (e.g. viruses, chemicals, hydrogenated fatty acids in foods) or damage to nuclear DNA that controls mitochondrial energy production or metabolic pathways, including glycolysis. Here, we postulate that the two subsystems (the evolutionarily inherited archaea and the prokaryote) in a eukaryotic differentiated cell are well integrated, and produce the amount of clean energy that is constantly required to maintain the differentiated status. Conversely, when protracted injuries impair cell or tissue organization, the amount of energy necessary to maintain cell differentiation can be restricted, and this may cause gradual de-differentiation of the eukaryotic cell over time. In cirrhotic liver, for example, this process can be favored by reduced oxygen availability to the organ due to an altered vasculature and the fibrotic barrier caused by the disease. Thus, hepatocarcinogenesis is an ideal example to support our hypothesis. When cancer arises, the pre-eukaryote subsystems become predominant, as shown by the metabolic alterations of cancer cells (anaerobic glycolysis and glutamine utilization), and by their capacity for proliferation and invasion, resembling the primitive symbiotic components of the eukaryotic cell
Virus C hepatitis and type 2 diabetes: a cohort study in southern Italy.
No full textOBJECTIVES:The relationship between hepatitis C virus (HCV) infection and type 2 diabetes mellitus (DM 2) is still uncertain. The objective of this study was to evaluat. The association between HCV infection, measured as positivity to anti-HCV antibodies, an. The incidence of DM 2 in a cohort of subjects sampled fro. The general population and followed up for 20 years.METHODS:At baseline. The cohort consisted of a random sample of 2,472 subjects (72% response rate, age range 30-69 years) fro. The electoral register of a town in Southern Italy. The cohort subjects were examined three times: in 1985 (M1), in 1992 (M2), and in 2005 (M3). At M1, M2, and M3, each participant filled in a questionnaire and had a blood sample taken to measure blood glucose and other serum variables including glutamic pyruvic alanine aminotransferase (ALT). Anti-HCV antibodies were analyzed with standard techniques at M1 and M2. Diabetes type 2 diagnosis was a history of diabetes and/or serum glucose ≥126 mg/dl and/or treatment with insulin or hypoglycemic drugs. Logistic regression was used for multivariable data analysis.RESULTS:Diabetes prevalence was higher in subjects with positive anti-HCV antibodies at M1 and M2, and diabetes incidence was higher in subjects with baseline positive anti-HCV antibodies at M1-M2 and lower at M2-M3. In multivariable models, controlling for gender, age, and body mass index (BMI), there was no association between incident cases of diabetes and positive anti-HCV antibodies at baseline, either at M1-M2 (odds ratio (OR) 0.73, 95% confidence interval (CI) 0.43-1.22) or at M2-M3 (0.65, 0.41-1.04). HCV was associated with DM 2 only in subjects with elevated ALT (OR 0.58, 95% CI 0.31-1.08, if ALT normal; OR 1.47, 95% CI 1-2.16, if ALT elevated, controlling for age, gender, and BMI).CONCLUSIONS:Our findings, in a cohort study at population level, support an association betwee. The presence of anti-HCV antibodies at baseline and a higher incidence of type 2 diabetes i. The following 20 years only in subjects with elevated ALT
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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