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World Population 1800-2050 [6]. 

World Population 1800-2050 [6]. 

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In the first article published in 4open, the journal’s Editor-in-Chief, Björn LDM Brücher discusses several important aspects relating to scientific publishing in a modern, digital world.

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... the global population increases and ages ( Fig. 1) [6], work in geriatric medicine and geriatric science will increase and become common during the next decades. Chronic diseases, which occur mainly in the elderly [7], exact a high cost from society, as DeVol and Bredroussian have shown: "The overall economic impact of absenteeism and presenteeism from common chronic diseases exceeded ...
Context 2
... in the way certain scientific publications dominate Leydesdorff et al. point to the rapid and dynamic growth in China's position in scientific publications compared to Europe and the United States ( Fig. 1 in J Informetr 2014, not shown) [32]. Although we assume that China will lead the pack over the next decade, The International Scientific Journal & Country Ranking (SJR) provides a less robust view, with data that include journal- and country-specific scientific indicators obtained from the Scopus ® database (Elsevier B.V.) [33]. Table ...

Citations

... No as both are also economic factors. Science has power and with power comes responsibility and also here silence is also not an option in the war against the Ukraine [6]. Many Russians of various professions opposed this war, even though this meant being regarded as a threat by their government [7][8][9]. ...
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Science should not stigmatize in regard to origin, citizenship, gender, religion or color and many aspects are of importance in this regard. We at the 4open Life Sciences – Medicine Editorial Board care primarily about science, and distance ourselves from war, and support humanitarian initiatives, but reject any attempt at alienating anyone (government or policies) and/or global citizens or scientists of a country, as well as any kind of racism and/or anti-Semitism and/or prejudices based on ethnic, religion, language, politics, gender, sex or age and therefore reject the wholesale stigmatizing of one profession from one country. Editors should not abuse their authority to play on the political stage. If politics successfully coopts science, then science would be lost.
... Unfortunately, a common trend for most of researchers is to adhere to the third benefit of research, seeking quantity rather than quality in their publication; hence, favoring merely personal credit. The advent of predatory journals and publishers that rapidly publish biased and/or poor study designs with no peer review imposed a big threat to the integrity of scientific research and became "the dark dangerous force" of publishing (7) . Many thanks to the first attempt carried out by the American librarian Dr. Jeffrey Beall to preserve the academic research from this big deal of fake and predatory journals and publishers (8) . ...
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In our modest point of view "research is not a paper published to increase the biography of an academic, nor a tool for getting fund, promotion and job. Research adds a great value to the society's life and can change the world; besides its reflection on a long-lasting impression of an academic, being his/her surviving wealth". To preserve science and society all over the world, we should ban fake research, fake journals and publishers. Finally, selecting prestigious journals for publishing scientific research is an issue of honesty.
... As reported recently "Although science belongs to no oneand to everyone, property (science) obliges" and "Our responsibility as scientists is to insure that the generations that follow us cannot write, Science and research, especially within biotechnology and molecular biology, promised so much and delivered so little" [334]. This knowledge provides various opportunities for science and research as well as for primary preventive interventions on the onset of cancer as a disease and, to mitigate metastases. ...
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Abstract It is increasingly evident that carcinogenesis, in the vast majority of cancers, cannot be explained simply through an accumulation of somatic mutations, or epigenetics, the stem cell theory, or the Warburg effect. Here, decades of thinking based on incorrect assumptions has resulted in an incorrect hypothesis on the origin of cancer. Many papers studying DNA, genetics, RNA, miRNA, proteomics, and epigenetics have increased our understanding of biology. Our paradigm, though more complex, is more reliable and plausible. It states that cancer originates from a disruption of homeostasis. This essential biological phenomenon, homeostasis, maintains the interrelationships of various signaling pathways and induced crosstalk which modify cellular functions together with the interactions of surrounding cells and structures such that the equilibrium lies towards the optimal health of the organism. This Special Issue “Disruption of signaling homeostasis induced crosstalk in the carcinogenesis paradigm Epistemology of the origin of cancer” provides compelling evidence that carcinogenesis is explained by a six-step sequence of events for the vast majority of cancers. These six steps include, (1) a pathogenic stimulus followed by (2) chronic inflammation, from which develops (3) fibrosis with associated remodeling in the cellular microenvironment. From these changes a (4) pre-cancerous niche develops which triggers the deployment of (5) a chronic stress escape strategy, and when this fails to resolve, and (6) the transition of a normal cell to a cancer cell occurs. This paradigm provides opportunities to move away from a symptom-oriented understanding of cancer and is much closer to a cause-based understanding, which opens the door for early preventative strategies to mitigate cancer as a disease, and to interdict metastases. This is underpinned by the fact that an independent recently published proof of this paradigm showed how a stimulus trigger the proposed multi-sequence cascade of events as abrupt involution-induced chronic inflammation, followed by fibrosis with remodeling, which describes the pre-cancerous niche followed by hyperplasia, metaplasia, and cancer.
... Like blockchain, science is architecturally (research infrastructures do not have a single point of failure) and politically (research is not governed by a single scientific authority) decentralized [15]. Science is, however, logically centralized (the scientific community must agree on one state-scientific truth) through "a process that does lead to a broadly shared consensus. ...
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Scholarly communication is today immersed in publish-or-perish culture that propels non-cooperative behavior in the sense of strategic games played by researchers. Here we introduce and describe a blockchain based platform for decentralized scholarly communication. The design of the platform rests on community driven publishing reviewing processes and implements cryptoeconomic incentives that promote cooperative user behavior. The key to achieve cooperation in blockchain based scholarly communication is to transform today’s static research paper into a modifiable research paper under continuous peer review process. We introduce and discuss the implementation of a modifiable research paper as a smart contract on the blockchain.
... According to the World Health Organization (WHO), the proportion of people over 60 years of age will increase to about 2 billion by 2050 [2]. Epidemiologically, cancer is an age-related disease which will be a major burden to healthcare worldwide along with neurologic, cardiovascular diseases, and diabetes [3]. While more advanced cancer stages reveal significantly lower survival rates [1] they may just represent clinical empiricism [4,5] and do not explain the origin of cancer. ...
Article
Full-text available
The vast majority of anticancer strategies are symptomatic but in order to achieve some tangible progress, we need to identify the cause(s) of the majority of cancers. There is a kind of zeitgeist that findings in genetics, namely somatic mutations, are reflexively viewed as being causative for carcinogenesis, although some 80% of all cancers are presently termed "sporadic" (i.e., with no proven cause). The observation that one inch of cancerous liver tissue can have more than 100 000 000 mutations and an identical mutation can result in different phenotypes, depending on the environment surrounding that mutation, makes it very unlikely that mutations by themselves are causative of most cancers. 4open debuts its Special Issue series with papers that provide strong evidence that carcinogenesis consists of a 6-step sequence (1) a pathogenic stimulus followed by (2) chronic inflammation from which develops (3) fibrosis with associated remodeling of the extracellular microenvironment, and from these changes a (4) precancerous niche (PCN), a product of fibrosis with remod-eling by persistent inflammation develops which triggers the deployment of (5) a chronic stress escape strategy and when this fails to be resolved it results in (6) the normal cell to cancerous cell transition. This Special Issue contains separate papers discussing undervalued ubiquitous proteins, chronic inflammation, eicosanoids, microbiome and morbid obesity, PCN, cell transition, followed by altered signaling induced by Metformin, NF-jB signaling and crosstalk during carcinogenesis, and a brief synopsis. In essence, the available evidence, both in vitro and in vivo, lends credence to the proposition that the majority of cancers occur from a disruption of homeostasis-induced signaling and crosstalk in the carcinogenesis paradigm "Epistemology of the origin of cancer".
... The proportion of people above 60 years old will increase from 841 million at present to an estimated 2 billion by 2050 according to the World Health Organization [1]. This will increase the burden of age-related chronic diseases such as cancer, neurologic and cardiovascular diseases and T2D as the global costs for healthcare worldwide [2]. The increase in metabolic syndrome, defined by three out of five medical conditions, which include obesity, elevated blood pressure, insulin resistance, elevated fasting plasma glucose, high serum triglycerides, and low levels of high-density cholesterol (HDL), is a risk factor for T2D [3] and explains the parallel increase of T2D prevalence in the US [4], Asia [5], Europe [6], and the Middle East [7] reflecting global healthcare liabilities. ...
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The anti-hyperglycemic drug, Metformin, is effective in treating early stages of diabetes and has been associated with a 37% decrease in cancer incidence. While the precise mechanisms for the anti-cancer effects of Metformin remain to be elucidated, this review shows the multiplicity of its effects on interdicting signaling and crosstalk, anti-inflammatory effects and in restoring homeostasis, which, taken together, go beyond its well-known anti-hyperglycemic effect that serves as the basis for its use in type 2 diabetes. Met-formin is much more than a one-trick pony. The recent discovery of several signaling pathways influenced by Metformin appears to have potential value in cancer therapy. Based on what we know at present, Metformin promotes beneficial effects attributed to its anti-inflammatory and anti-fibrotic effects largely demonstrated in vitro. Metformin activates or upregulates while it simultaneously inhibits or downregulates multiple signal-ing pathways of cell-cycle arrest and apoptosis accompanied by oxidative stress, which are in accordance with the 6-step sequence of carcinogenesis. Furthermore, in vivo studies in laboratory animals and in cancer patients are beginning to address the magnitude of the anti-cancer effects and delineate its anti-cancer effects. In this context, results from prior pancreatic and non-pancreatic cancer trials, which contained a significant proportion of the patient population treated with Metformin, will have to be reexamined in light of the observed anti-cancerous effects to gain additional insights. The detailed exploration of Metformin in the context of the "Disruption of signaling homeostasis induced crosstalk in the carcinogenesis paradigm Epistemology of the origin of cancer" can provide helpful insights into the anti-proliferative mechanisms and could play a relevant role in anti-cancer therapy in the future.
... It may be argued that the benchmarking in healthcare already is more related to the prestige of the hospital rather than a criterion of excellence. The reasons for the "businessization", a term coined by Michele Pagano in 2017 [3,4], of healthcare are complex, but one observable condition in both science and healthcare, is the increased misuse of mathematical variables, such as benchmarking. ...
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The shortage of nursing staff in Germany compromises public healthcare in deference to profits explaining why this is on the daily political and media agenda. In Germany, over a 22 year period, significant savings were achieved by decreases in: (1) hospital beds by À29.3% saving 119 000 beds, (2) patient care and treatment days by À23% saving 43.1 million patient days, and (3) length of hospital stay in days by À39% saving 4.7 days. This occurred together with the parallel increase of treated patient cases by +26.5% with an additional burden of 4.1 million patients. Since 2010, as birth rates increase again treatment cases will also increase. In parallel, the percentage of total nurses has decreased (À2.1%) as well as that of registered nurses in hospitals between 1999 (325 539) and 2009 (324 337) have decreased (À0.4%), in conjunction with nurses employed in preventive and rehabilitation facilities (+15.1%) and/or in outpatient care facilities (+41.1%) and/or nursing homes (+24.8%) and/or nurses working in retirement homes (+77.9%). This "profititis" endangers both patient care and detracts from people joining the nursing profession. It might even be a shortsighted tightrope act which, in the end, might counteract the marketing strategy of "patient safety" by risking quality of patient care. Maybe healthcare politics would be well-advised to rethink the fact that as the population gets older and as birth rates and immigration increases, these factors could result in increased patient caseloads in hospitals which need to be addressed now so as to avert a future crisis.
... According to the World Health Organization (WHO), the proportion of people over 60 years of age will increase to about 2 billion by 2050 [2]. Epidemiologically, cancer is an age-related disease which will be a major burden to healthcare worldwide along with neurologic, cardiovascular diseases, and diabetes [3]. While more advanced cancer stages reveal significantly lower survival rates [1] they may just represent clinical empiricism [4,5] and do not explain the origin of cancer. ...
Article
Full-text available
The vast majority of anticancer strategies are symptomatic but in order to achieve some tangible progress, we need to identify the cause(s) of the majority of cancers. There is a kind of zeitgeist that findings in genetics, namely somatic mutations, are reflexively viewed as being causative for carcinogenesis, although some 80% of all cancers are presently termed “sporadic” (i.e., with no proven cause). The observation that one inch of cancerous liver tissue can have more than 100 000 000 mutations and an identical mutation can result in different phenotypes, depending on the environment surrounding that mutation, makes it very unlikely that mutations by themselves are causative of most cancers. 4open debuts its Special Issue series with papers that provide strong evidence that carcinogenesis consists of a 6-step sequence (1) a pathogenic stimulus followed by (2) chronic inflammation from which develops (3) fibrosis with associated remodeling of the extracellular microenvironment, and from these changes a (4) precancerous niche (PCN), a product of fibrosis with remodeling by persistent inflammation develops which triggers the deployment of (5) a chronic stress escape strategy and when this fails to be resolved it results in (6) the normal cell to cancerous cell transition. This Special Issue contains separate papers discussing undervalued ubiquitous proteins, chronic inflammation, eicosanoids, microbiome and morbid obesity, PCN, cell transition, followed by altered signaling induced by Metformin, NF-κB signaling and crosstalk during carcinogenesis, and a brief synopsis. In essence, the available evidence, both in vitro and in vivo, lends credence to the proposition that the majority of cancers occur from a disruption of homeostasis-induced signaling and crosstalk in the carcinogenesis paradigm “ Epistemology of the origin of cancer ”.
... As stated by Poincare "Science is built of facts the way a house is built of bricks: but an accumulation of facts is no more science than a pile of bricks is a house". Also, the "foundation of science is trust, which is earned, not given" [18]. ...
... This characteristic of gold (author-pays) open-access has opened the door to crookedness in science, and it's not just the publishers that lack integrity. Academic evaluation systems that still merely look at the number of published articles by a given scientist also help drive the corruption [8]. ...
... The honor system no longer guarantees that publishing ethics will be followed, so to be successful, academic journals must have safeguards built in that ensure integrity. Moreover, to succeed and gain broad acceptance, open-access needs to resolve the predatory publisher problem as such are "the dark dangerous force" of publishing [8]. It needs to earn respect and demonstrate that it's worthy of serving as a vehicle for communicating and preserving research knowledge. ...