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Michał Wiciński

Bio: Michał Wiciński is an academic researcher from Nicolaus Copernicus University in Toruń. The author has contributed to research in topics: Vascular smooth muscle & Phenylephrine. The author has an hindex of 14, co-authored 83 publications receiving 695 citations.


Papers
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Journal ArticleDOI
TL;DR: Many aspects of fasting are incorporated, mainly focusing on its effects on the cardiovascular system, involving atherosclerosis progression, benefits for diabetes mellitus type 2, lowering of blood pressure, and exploring other cardiovascular risk factors (such as lipid profile and inflammation).
Abstract: Intermittent fasting is a form of time restricted eating (typically 16 h fasting and 8 h eating), which has gained popularity in recent years and shows promise as a possible new paradigm in the approach to weight loss and the reduction of inflammation, and has many potential long term health benefits. In this review, the authors will incorporate many aspects of fasting, mainly focusing on its effects on the cardiovascular system, involving atherosclerosis progression, benefits for diabetes mellitus type 2, lowering of blood pressure, and exploring other cardiovascular risk factors (such as lipid profile and inflammation).

145 citations

Journal ArticleDOI
TL;DR: The mechanisms of action of HMOs in infants, such as their anti-adhesive properties, properties modulating the immune system, and impact on bacterial flora development are discussed.
Abstract: The first months of life are a special time for the health development and protection of infants. Breastfeeding is the natural and best way of feeding an infant, and positively influences their development and health. Breast milk provides the ideal balance of nutrients for the infant and contains countless bioactive ingredients such as immunoglobulins, hormones, oligosaccharides and others. Human milk oligosaccharides (HMOs) are a very important and interesting constituent of human milk, and are the third most abundant solid component after lactose and lipids. They are a structurally and biologically diverse group of complex indigestible sugars. This article will discuss the mechanisms of action of HMOs in infants, such as their anti-adhesive properties, properties modulating the immune system, and impact on bacterial flora development. Many health benefits result from consuming HMOs. They also may decrease the risk of infection by their interactions with viruses, bacteria or protozoa. The commercial use of HMOs in infant formula, future directions, and research on the use of HMOs as a therapy will be discussed.

131 citations

Journal ArticleDOI
TL;DR: Clozapine-induced agranulocytosis/granulocytopenia (CIAG) is an uncommon condition, but potentially fatal in consequences, and the current theory suggests reactive oxygen species – nitrenium ion as the most important factor of CIAG.
Abstract: Purpose of reviewClozapine-induced agranulocytosis/granulocytopenia (CIAG) is an uncommon condition, but potentially fatal in consequences. The pathogenesis, despite multiple experiments, is not fully elucidated. The current theory suggests reactive oxygen species – nitrenium ion as the most importa

58 citations

Journal ArticleDOI
TL;DR: It has been shown that T. forsythia may induce pro-inflammatory cytokines such as IL-1β and IL-6 by CD4 + T helper cells and TNF-α, and the role of P. gingivalis and T.forsythia in signaling pathways responsible for cancer development is described.
Abstract: Tannerella forsythia and Porphyromonas gingivalis are anaerobic, Gram-negative bacterial species which have been implicated in periodontal diseases as a part of red complex of periodontal pathogens. Esophageal cancer is the eight most common cause of cancer deaths worldwide. Higher rates of esophageal cancer cases may be attributed to lifestyle factors such as: diet, obesity, alcohol and tobacco use. Moreover, the presence of oral P. gingivalis and T. forsythia has been found to be associated with an increased risk of esophageal cancer. Our review describes the role of P. gingivalis and T. forsythia in signaling pathways responsible for cancer development. It has been shown that T. forsythia may induce pro-inflammatory cytokines such as IL-1β and IL-6 by CD4 + T helper cells and TNF-α. Moreover, gingipain K produced by P. gingivalis, affects hosts immune system by degradation of immunoglobulins and complement system (C3 and C5 components). Discussed bacteria are responsible for overexpression of MMP-2, MMP-2 and GLUT transporters.

52 citations

Journal ArticleDOI
29 Jul 2020
TL;DR: The study aimed to present the current state of knowledge about the role of intestinal microbiota in the development of obesity and the impact of supplementation with probiotic bacteria on the health of overweight and obese patients.
Abstract: The World Health Organization (WHO) reports that 400 million people are obese, and over 1.6 billion adults are overweight worldwide. Annually, over 2.8 million people die from obesity-related diseases. The incidence of overweight and obesity is steadily increasing, and this phenomenon is referred to as a 21st-century pandemic. The main reason for this phenomenon is an easy access to high-energy, processed foods, and a low-activity lifestyle. These changes lead to an energy imbalance and, as a consequence, to the development of body fat. Weight gain contributes to the development of heart diseases, skeletal system disorders, metabolic disorders such as diabetes, and certain types of cancer. In recent years, there have been many works linking obesity with intestinal microbiota. Experiments on germ-free animals (GFs) have provided much evidence for the contribution of bacteria to obesity. The composition of the gut microbiota (GM) changes in obese people. These changes affect the degree of energy obtained from food, the composition and secretory functions of adipose tissue, carbohydrate, and lipid metabolism in the liver, and the activity of centers in the brain. The study aimed to present the current state of knowledge about the role of intestinal microbiota in the development of obesity and the impact of supplementation with probiotic bacteria on the health of overweight and obese patients.

50 citations


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Journal Article
TL;DR: The highest amount of weekly exercise, with minimal weight change, had widespread beneficial effects on the lipoprotein profile, seen most clearly with the high amount of high-intensity exercise.
Abstract: BACKGROUND Increased physical activity is related to reduced risk of cardiovascular disease, possibly because it leads to improvement in the lipoprotein profile. However, the amount of exercise training required for optimal benefit is unknown. In a prospective, randomized study, we investigated the effects of the amount and intensity of exercise on lipoproteins. METHODS A total of 111 sedentary, overweight men and women with mild-to-moderate dyslipidemia were randomly assigned to participate for six months in a control group or for approximately eight months in one of three exercise groups: high-amount-high-intensity exercise, the caloric equivalent of jogging 20 mi (32.0 km) per week at 65 to 80 percent of peak oxygen consumption; low-amount-high-intensity exercise, the equivalent of jogging 12 mi (19.2 km) per week at 65 to 80 percent of peak oxygen consumption; or low-amount-moderate-intensity exercise, the equivalent of walking 12 mi per week at 40 to 55 percent of peak oxygen consumption. Subjects were encouraged to maintain their base-line body weight. The 84 subjects who complied with these guidelines served as the basis for the main analysis. Detailed lipoprotein profiling was performed by nuclear magnetic resonance spectroscopy with verification by measurement of cholesterol in lipoprotein subfractions. RESULTS There was a beneficial effect of exercise on a variety of lipid and lipoprotein variables, seen most clearly with the high amount of high-intensity exercise. The high amount of exercise resulted in greater improvements than did the lower amounts of exercise (in 10 of 11 lipoprotein variables) and was always superior to the control condition (11 of 11 variables). Both lower-amount exercise groups always had better responses than the control group (22 of 22 comparisons). CONCLUSIONS The highest amount of weekly exercise, with minimal weight change, had widespread beneficial effects on the lipoprotein profile. The improvements were related to the amount of activity and not to the intensity of exercise or improvement in fitness.

1,267 citations

Journal ArticleDOI
01 Nov 2020
TL;DR: The effects of probiotics on the F/B ratio that lead to weight loss or immunosuppression are reviewed, with a focus on probiotics from the genus Lactobacillus.
Abstract: The two most important bacterial phyla in the gastrointestinal tract, Firmicutes and Bacteroidetes, have gained much attention in recent years. The Firmicutes/Bacteroidetes (F/B) ratio is widely accepted to have an important influence in maintaining normal intestinal homeostasis. Increased or decreased F/B ratio is regarded as dysbiosis, whereby the former is usually observed with obesity, and the latter with inflammatory bowel disease (IBD). Probiotics as live microorganisms can confer health benefits to the host when administered in adequate amounts. There is considerable evidence of their nutritional and immunosuppressive properties including reports that elucidate the association of probiotics with the F/B ratio, obesity, and IBD. Orally administered probiotics can contribute to the restoration of dysbiotic microbiota and to the prevention of obesity or IBD. However, as the effects of different probiotics on the F/B ratio differ, selecting the appropriate species or mixture is crucial. The most commonly tested probiotics for modifying the F/B ratio and treating obesity and IBD are from the genus Lactobacillus. In this paper, we review the effects of probiotics on the F/B ratio that lead to weight loss or immunosuppression.

496 citations

Journal ArticleDOI
Wen-Jun Tu1, Hong Wang1, Song Li1, Qiang Liu1, Hong Sha1 
TL;DR: The redox-sensitive signaling system Keap1/Nrf2/ARE plays a key role in the maintenance of cellular homeostasis under stress, inflammatory, carcinogenic, and pro-apoptotic conditions, which allows us to consider it as a pharmacological target.
Abstract: Oxidative stress is defined as an imbalance between production of free radicals and reactive metabolites or [reactive oxygen species (ROS)] and their elimination by through protective mechanisms, including (antioxidants) This Such imbalance leads to damage of cells and important biomolecules and cells, with hence posing a potential adverse impact on the whole organism At the center of the day-to-day biological response to oxidative stress is the Kelch-like ECH-associated protein 1 (Keap1) - nuclear factor erythroid 2-related factor 2 (Nrf2)- antioxidant response elements (ARE) pathway, which regulates the transcription of many several antioxidant genes that preserve cellular homeostasis and detoxification genes that process and eliminate carcinogens and toxins before they can cause damage The redox-sensitive signaling system Keap1/Nrf2/ARE plays a key role in the maintenance of cellular homeostasis under stress, inflammatory, carcinogenic, and pro-apoptotic conditions, which allows us to consider it as a pharmacological target Herein, we review and discuss the recent advancements in the regulation of the Keap1/Nrf2/ARE system, and its role under physiological and pathophysiological conditions, eg such as in exercise, diabetes, cardiovascular diseases, cancer, neurodegenerative disorders, stroke, liver and kidney system, etc and such

338 citations

Journal ArticleDOI
TL;DR: Soehnlein et al. as discussed by the authors consider a gamut of attractive possibilities for modifying inflammation in atherosclerosis, including targeting pivotal inflammatory pathways such as the inflammasomes, inhibiting cytokines, manipulating adaptive immunity and promoting pro-resolution mechanisms.
Abstract: Atherosclerosis, a dominant and growing cause of death and disability worldwide, involves inflammation from its inception to the emergence of complications. Targeting inflammatory pathways could therefore provide a promising new avenue to prevent and treat atherosclerosis. Indeed, clinical studies have now demonstrated unequivocally that modulation of inflammation can forestall the clinical complications of atherosclerosis. This progress pinpoints the need for preclinical investigations to refine strategies for combatting inflammation in the human disease. In this Review, we consider a gamut of attractive possibilities for modifying inflammation in atherosclerosis, including targeting pivotal inflammatory pathways such as the inflammasomes, inhibiting cytokines, manipulating adaptive immunity and promoting pro-resolution mechanisms. Along with lifestyle measures, pharmacological interventions to mute inflammation could complement traditional targets, such as lipids and hypertension, to make new inroads into the management of atherosclerotic risk. The contribution of inflammation to atherosclerosis is substantial, and is just beginning to be understood. In this Review, Soehnlein and Libby discuss how inflammation promotes atherosclerosis and its consequences, and how such processes could be targeted therapeutically. The potential pitfalls of targeting immune processes — namely the increased potential for infections — are also discussed, along with ways to modulate cardiovascular therapies in time and space to make them more effective.

287 citations

01 Jan 2008
TL;DR: In this article, the sterol-regulatory element binding protein-1 (SREBP-1) was found to increase the promoter activity of Proprotein convertase subtilisin/kexin type 9.
Abstract: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a member of the subtilases that promotes the internalization and degradation of LDL receptor in liver and thereby controls the level of LDL cholesterol in plasma. Here, we show that the expression of PCSK9 in HepG2 cells is completely dependent on the absence or presence of sterols. The minimal promoter region of the PCSK9 gene contains a sterol-regulatory element (SRE), which makes the transcription of PCSK9 dependent on sterols. Expression of nuclear forms of sterol-regulatory element binding protein-1 (SREBP-1) and SREBP-2 dramatically increased the promoter activity of PCSK9. In vitro-translated nuclear forms of SREBPs showed interactions with SRE, whereas mutations in SRE abolished their binding. In vivo studies in mice showed that Pcsk9 protein and mRNA were decreased significantly by fasting and increased by refeeding. However, supplementation with 2% cholesterol in the diet prevented the increase in Pcsk9. The amounts of Pcsk9 mRNA in livers of refed mice showed correlated regulation by the changes in the nuclear form of Srebp-2. In summary, it is suggested that the expression of PCSK9 is regulated by sterol at the transcriptional level in HepG2 cells and that both SREBP-1 and SREBP-2 can transcriptionally activate PCSK9 via SRE in its proximal promoter region in vitro. However, in vivo, it is suggested that the sterol-dependent regulation of PCSK9 is mediated predominantly by SREBP-2.

269 citations