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《Expert Review of Clinical Immunology》2013,9(11):1031-1041
It has been proposed that changes in the composition of gut microbiota contribute to the development of diabetes Types 1, 2 and 3 (the latter known as Alzheimer’s disease). The onset of these diseases is affected by complex interactions of genetic and several environmental factors. Alterations in gut microbiota in combination with specific diets can result in increased intestinal permeability leading via a continuous state of low-grade inflammation to the development of insulin resistance. Since a change in composition of gut microbiota is also suggested to be the underlying factor for the development of obesity, it is obvious to link gut microbiota with the pathogenesis of diabetes. In addition, insulin resistance in the brain has been recently associated with Alzheimer’s disease. These new paradigms in combination with data from studies with prebiotics and probiotics may lead to a novel way to control and even prevent diabetes in general. 相似文献
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Within the NOD‐like receptor (NLR) family, there are several NLRP (NLR family, pyrin domain‐containing) proteins that are involved in the formation of inflammasomes. These multi‐protein complexes are a key part of the network of cellular events required for secretion of the pro‐inflammatory cytokines IL‐1β and IL‐18. The NLRP3 inflammasome is the best‐characterized member of the family and has recently been implicated in gut homeostasis and determining the severity of inflammation in inflammatory bowel disease (IBD) and inflammation‐associated colorectal cancer. This led to the discovery that NLRP6 and NLRP12 also contribute to the maintenance of intestinal homeostasis and modulation of the gut microbiota, which in turn influences the intestine and distant organs. In this review, we bring together the latest data on the potential roles of NLRP family members in gut health and disease and identify the most pressing questions that remain to be answered to further our understanding of human diseases including IBD, inflammation‐associated cancers, and metabolic syndromes linked with obesity. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. 相似文献
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The intricate interface between immune system and metabolism 总被引:4,自引:0,他引:4
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大量实验和数据表明炎症能导致肿瘤的发生。慢性炎症所形成的肿瘤微环境为肿瘤的发生和生长提供了条件,是肿瘤形成过程中必不可少的重要环节。髓系来源的抑制性细胞(MDSC)是一个重要的连接炎症与肿瘤的中介,MDSC通过多种机制抑制机体抗肿瘤免疫应答,从而促进肿瘤的生长。 相似文献
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McDonald P 《Explore (New York, N.Y.)》2008,4(2):148-153
Houston, we have a problem, and it involves the Apo E gene as it relates to heart disease, Alzheimer’s disease, and the environment that goes with an individual’s particular set of Apo E genes. This means the Apo E gene requires a gene-supportive environment in the form of the food chemistry of every meal, every day. Does the dietary environment of the individual matter to support cardiovascular health and neurovascular health? The answer seems to be a solid yes.And we also now know that the technological remedies of allopathic medicine don’t always get the job done. Integrative medicine brings a new paradigm of thinking that looks at all options for disease management and prevention. The new integrative medicine provider embraces all the clinical tools we have at our disposal to give a greater advantage to the patient.In addition, it’s important to utilize the cultural/traditional whole food diets we now realize are optimal for human health. We need to closely reexamine and place greater emphasis on the powerful role of the person’s environment by utilizing not just external food sources, but also examining their established internal feeding system based on their unique body composition. A person’s current body composition is likely very poor if the wrong nutritional input for their individual genetic expression has been chosen.Returning to the question I wondered about almost 30 years ago—as I walked slowly back across the famous square at St Bartholomew’s, stopping once again to check the ice in the fountain—I pondered the question even further: do people’s diets cause these horrible diseases? I am now asking the question again, and with some true clarity can say nutrition and diet are strongly connected. Are they the only cause? No, we don’t have the full picture yet, but I think we can say that diet is a powerful contributing factor.Once the medical field has a clearer understanding and acceptance of diet as a powerful tool, not just for prevention but also as a powerful treatment option, we will begin to change disease patterns by leaps and bounds. The climate is now ready for a strong, simple answer. As with most epidemics, the best outcomes are from the simplest, most fundamental remedies—practical processes clinicians on the front lines can use, such as good nutrition.
Conclusions
I know I am not alone in this search for answers. Many of you are asking the same questions as I am. The goal is to work with what we know and provide what is safe for the individual. The individual has to eat. Guiding people to make better choices around diet and nutrition is the key to helping. Exploring why people consume the foods they consume can be helpful. For example, people like hot beverages in the morning, yet is it the coffee they like or is it the hot fluid, the pretty warm cup, and the time they give themselves to drink a warm, nurturing beverage? Changing from coffee to green tea is not too much of a shift, yet the health benefits can be enormous.Keeping an open mind to new science and treatment options regarding genes and diet, simple steps can be incorporated into current medical practices that can help in a big way. One interesting way to understand how powerful this is: try it for yourself. There is no substitute for personal experience. 相似文献8.
During the last few decades we have become accustomed to the idea that viruses can cause tumors. It is much less considered and discussed, however, that most people infected with oncoviruses will never develop cancer. Therefore, the genetic and environmental factors that tip the scales from clearance of viral infection to development of cancer are currently an area of active investigation. Microbiota has recently emerged as a potentially critical factor that would affect this balance by increasing or decreasing the ability of viral infection to promote carcinogenesis. In this review, we provide a model of microbiome contribution to the development of oncogenic viral infections and viral associated cancers, give examples of this process in human tumors, and describe the challenges that prevent progress in the field as well as their potential solutions. 相似文献
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《Mucosal immunology》2021,14(1):4-13
Food allergies are a major public health concern due to their widespread and rising prevalence. The increase in food allergy is partially due to Western lifestyle habits which deplete protective commensal microbiota. These microbial perturbations can result in adverse host–microbe interactions, altering the phenotype of various immune cells and instigating allergic sensitization. Although B cells are critical to allergic pathology, microbial influences on B cells have been somewhat overlooked. Here, we focus on direct and indirect interactions between bacteria and B cells and how such interactions regulate B-cell phenotype, namely antibody production (IgA, IgE, IgG1, and IgG4) and regulatory B-cell (Breg) function. Understanding how microbes modulate B-cell activity in the context of food allergies is critical to both tracing the development of disease and assessing future treatment options. 相似文献
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K. D. Salzmann 《The British journal of general practice》1981,31(223):97-98
Eight hundred and eighty women having their first baby were asked whether they had had dysmenorrhoea; 61 per cent had and 39 per cent had not. Eleven per cent of the former had to have forceps, ventouse or caesarean section, compared with twice as many (20·8 per cent) of the latter (p = 0·001). Those with severe dysmenorrhoea had a greater need for operative interference (not statistically significant). I suggest, after 21 years of observation, that the level of prostaglandin activity may be different in these women, and that a history of no dysmenorrhoea or severe dysmenorrhoea might be considered as a risk factor for a complicated delivery. 相似文献
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Aging, cancer and nutrition: the DNA methylation connection 总被引:7,自引:0,他引:7
Liu L Wylie RC Andrews LG Tollefsbol TO 《Mechanisms of ageing and development》2003,124(10-12):989-998
Cancer and aging are two coupled developmental processes as reflected by the higher incidence of cancer in the elderly human population group. Genetic mutations accumulate in somatic cells with age, which may explain in part the association of age with cancer. Epigenetic mechanisms are also frequently involved in controlling gene functions during development and tumorigenesis. A common molecular feature associated with both aging and tumorigenesis is global hypomethylation of the genomic DNA. The contributing mechanisms underlying this hypomethylation are not yet well understood. Epigenetic investigation of cancer and aging has recently emerged as a fruitful area of study and has added exciting insights into some of the mysteries surrounding aging and cancer. Recent studies have also shown that dietary factors can modulate DNA methylation and thereby contribute to aging and tumorigenesis. Thus, DNA methylation provides an important common link between aging, cancer and nutrition. 相似文献
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Diet and colonic cancer: putting the puzzle together 总被引:1,自引:0,他引:1
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Amiran Dzutsev Romina S. Goldszmid Sophie Viaud Laurence Zitvogel Giorgio Trinchieri 《European journal of immunology》2015,45(1):17-31
Commensal microorganisms colonize barrier surfaces of all multicellular organisms, including those of humans. For more than 500 million years, commensal microorganisms and their hosts have coevolved and adapted to each other. As a result, the commensal microbiota affects many immune and nonimmune functions of their hosts, and de facto the two together comprise one metaorganism. The commensal microbiota communicates with the host via biologically active molecules. Recently, it has been reported that microbial imbalance may play a critical role in the development of multiple diseases, such as cancer, autoimmune conditions, and increased susceptibility to infection. In this review, we focus on the role of the commensal microbiota in the development, progression, and immune evasion of cancer, as well as some modulatory effects on the treatment of cancer. In particular, we discuss the mechanisms of microbiota‐mediated regulation of innate and adaptive immune responses to tumors, and the consequences on cancer progression and whether tumors subsequently become resistant or susceptible to different anticancer therapeutic regiments. 相似文献
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The ROS-NOX connection in cancer and angiogenesis 总被引:1,自引:0,他引:1
Initially viewed as dangerous byproducts of aerobic life, reactive oxygen species (ROS) nowadays appear to be essential secondary messengers of many signaling cascades and cellular functions. The establishment of ROS as important signaling molecules has been confirmed by the existence of specialized ROS producing complexes expressed in nonphagocytic cells, the NADPH oxidase complex (NOX). Because of the diversity of their proteic targets (besides lipids and DNA), ROS have multiple and sometimes contradictory functions. In the present review, we focus on several different signaling pathways influenced by ROS and NOX in tumorigenesis, focusing on proliferation and angiogenesis. We review the ROS targets regulating proliferation, including cellular signaling (phosphatases, AP1, and nuclear factor-kappa B [NF-kappaB]) and cell cycle targets (CDC25, cyclin D, and forkhead proteins), and the role of NOX during proliferation. Finally, we review the direct and indirect involvement of ROS and NOX in (tumor) angiogenesis through the regulation of different biologic systems such as vascular endothelial growth factor, angiotensin II, hypoxia-inducible factor, AP1, and inflammation. 相似文献
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Introduction
Attachment theory offers an evolutionary explanation for the occurrence of panic states. The distance between a mother and child causes the sensation of fear. The experience of feared annihilation, an intense fear reaction (panic), is presented as a threat to the individual’s cohesiveness, disrupting the mental representation of self-consciousness, specifically self-unity. Alterations in self-consciousness in schizophrenia are so important that they are mostly included among Kurt Schneider’s first-ranked symptoms.Hypotheses
Based on clinical trials, case reports, and brain imaging and pharmacological studies, a paradigm is proposed to explain the relationship between panic anxiety and psychosis.Conclusion
The psychosis-anxiety pathophysiology explanation needs further investigation into the brain areas that integrate self-monitoring with fear areas, but it seems possible to note the importance of the anterior cingulate cortex. 相似文献18.
Stephen Seely 《Medical hypotheses》1982,8(4):349-354
Phytoestrogens are estrogen mimics produced mainly by leguminous plants, like clover, lucerne and soya beans, but also by some grasses and other plants. They are isoflavones and other plant phenols, bearing no resemblance to natural estrogens, but somewhat similar to non-steroidal synthetic estrogens, like diethylstilbestrol. Normally they have little ill effect on herbivors, but in large doses they can result in prolonged periods of estrus. It is suggested that when consumed by lactating cows, the estrogenic substance appears in their milk and transferred to the human consumer, on whom the effect could be similar to that of diethylstilbestrol — a substance with well substantiated atherogenic properties. This could be the explanation of the strong positive correlation between the consumption of milk and mortality from coronary disease reported in previous papers of the writer and other authors, and also of the differences between male and female mortality from coronary disease.When phytoestrogens are consumed directly in plants like soya beans, they appear to be correlated with cerebrovascular disease. 相似文献
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The paper presents an epidemiological study of breast cancer mortality in relation to food consumption. It was found that younger and older women (possibly pre- and post-menopausal women) differ with respect to such correlations. In older women a strong correlation was found between breast cancer mortality and sugar consumption (correlation coefficient = 0.9), and a weaker correlation, possibly of marginal interest, with fat consumption (correlation coefficient = 0.7). In younger women the correlation with diet seems weak. A possible connecting link between sugar consumption and breast cancer is insulin. This is an absolute requirement for the proliferation of normal mammary tissue and experimental mammary tumours may regress in its absence. Insulin secretion occurs in response to blood glucose level and could be excessive if the regulatory mechanism is overtaxed by large sugar intake. The same mechanism might account for the increased risk of mammary cancer in diabetics. 相似文献