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1.
Einstein (Sao Paulo) ; 18: eAO4784, 2020.
Artigo em Inglês, Português | MEDLINE | ID: mdl-31553356

RESUMO

OBJECTIVE: To evaluate the effect of three types of muscular resistance training on adiposity, inflammation levels and insulin activity in Swiss mice with fat-rich diet-induced obesity. METHODS: Lean and obese male Swiss mice were selected and allocated to one of eight groups comprising eight mice each, as follows: standard diet + no training; standard diet + muscular resistance training; standard diet + hypertrophy training; standard diet + strength training; high-fat diet + no training; high-fat diet + muscular resistance training; high-fat diet + hypertrophy training; high-fat diet + strength training. The training protocol consisted of stair climbing for a 10-week period. Blood samples were collected for lactate analysis, glucose level measurement and insulin tolerance test. After euthanasia, adipose tissues were removed and weighed for adiposity index determination. Fragments of epididymal adipose tissue were then embedded for histological analysis or homogenized for tumor necrosis factor alpha level determination using the ELISA method. RESULTS: Ausency of differences in total training volume and blood lactate levels overall emphasize the similarity between the different resistance training protocols. Body weight loss, reduced adipocyte area and lower adiposity index were observed in trained obese mice, regardless of training modality. Different training protocols also improved insulin sensitivity and reduced inflammation levels. CONCLUSION: Resistance training protocols were equally effective in reducing body fat, inflammation levels and insulin resistance in obese mice.


Assuntos
Adiposidade/fisiologia , Hipertrofia/fisiopatologia , Inflamação/fisiopatologia , Resistência à Insulina/fisiologia , Exercícios de Alongamento Muscular/métodos , Obesidade/fisiopatologia , Condicionamento Físico Animal/fisiologia , Tecido Adiposo Branco/fisiopatologia , Animais , Glicemia/análise , Peso Corporal/fisiologia , Dieta Hiperlipídica , Ensaio de Imunoadsorção Enzimática , Masculino , Camundongos , Camundongos Obesos , Reprodutibilidade dos Testes , Treinamento de Resistência/métodos , Fatores de Tempo , Fator de Necrose Tumoral alfa/análise
2.
Adv Exp Med Biol ; 1175: 335-353, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31583594

RESUMO

Microglia are the most abundant immune cells in the central nervous system (CNS), where they interact with neurons and exhibit a wide array of functions in physiological and pathological conditions. Physiologically, microglia mediate synaptic pruning and remodeling crucial for neural circuits and brain connectivity. In pathological conditions such as neurodegeneration in the Parkinson's disease (PD), microglia are activated, migrated to the injury site, and prone to engulf debris, sense pathology, and secrete possible pro- and anti-inflammatory factors. Microglia mediate responses such as inflammation and phagocytosis associated with neurodegeneration and are pivotal players in exacerbating or relieving disease progression. This chapter provides an overview on microglial function in the neurodegenerative disease-Parkinson's disease (PD). An overview on the pathology of PD will first be given, followed by discussion on receptors and signaling pathways involved in microglia-mediated inflammation and phagocytosis. Mechanism of how microglia contribute to PD by inflammation, phagocytosis of α-Synuclein (α-Syn), and interaction with PD genes will also be discussed.


Assuntos
Microglia/citologia , Doença de Parkinson/fisiopatologia , Humanos , Inflamação/fisiopatologia , Fagocitose , Transdução de Sinais , alfa-Sinucleína
3.
Mol Biol (Mosk) ; 53(5): 790-798, 2019.
Artigo em Russo | MEDLINE | ID: mdl-31661478

RESUMO

Recently, much attention has been drawn to unraveling the mechanisms of neurodegenerative and neuroinflammatory disease pathogenesis. A special role in the development of neuropathologies is assigned to the interaction of the nervous and the immune systems. Microglia are the cells of the immune system that function as resident macrophages of the central nervous system (CNS) and are involved in the development of CNS, as well as in homeostatic interactions. Impaired microglia can contribute to neuroinflammation and neurodegeneration. With the help of genome editing technologies, the main paradigms in the development and functions of microglia have been addressed. At the same time, an understanding of the mechanisms of regulation of microglia in normal and pathological conditions is necessary to create an effective therapy aimed at treating various neurological diseases. This review focuses on recent findings on the origin of microglia, its regulatory role in the central nervous system, as well as its contribution to the development of neuroinflammation.


Assuntos
Sistema Nervoso Central/citologia , Sistema Nervoso Central/fisiologia , Homeostase , Inflamação/patologia , Microglia/fisiologia , Doenças Neurodegenerativas/patologia , Sistema Nervoso Central/patologia , Sistema Nervoso Central/fisiopatologia , Humanos , Inflamação/fisiopatologia , Microglia/citologia , Microglia/patologia , Doenças Neurodegenerativas/fisiopatologia
4.
Expert Opin Investig Drugs ; 28(10): 871-889, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31566013

RESUMO

Introduction: Functional dyspepsia (FD), defined as the presence of chronic functional symptoms originating from the gastroduodenal, is one of the most common functional gastrointestinal disorders. FD is subdivided into postprandial distress syndrome (PDS), with meal-related symptoms such as postprandial fullness and early satiation, and epigastric pain syndrome (EPS), with meal-unrelated symptoms such as epigastric pain or burning. Therapeutic options for FD are very limited, probably reflecting the complex pathophysiology which comprises disorders of gastric sensorimotor function as well as low-grade duodenal inflammation.Areas covered: This review summarizes recent and ongoing drug development for FD as identifiedExpert opinion: Proton pump inhibitors (PPIs) are the traditional first-line therapy while potassiumcompetitive acid blockers are being studied. Ongoing drug development focuses on gastric motility with prokinetics (dopamine-2 antagonists and 5-HT4 agonists) and fundus relaxant therapies (acotiamide, azapirones), and on sensitivity with peripherally (guanylate cyclase and cannabinoid agonists) and centrally acting neuromodulators. Drugs under development for gastroparesis may be efficacious in PDS. There are emerging data with pro-and antibiotics and with phytotherapeutic agents. Duodenal low-grade inflammation is a newly emerging target which may respond also to PPIs, histamine and leukotriene receptor blockers.


Assuntos
Dispepsia/tratamento farmacológico , Fármacos Gastrointestinais/farmacologia , Gastroenteropatias/tratamento farmacológico , Dor Abdominal/etiologia , Desenvolvimento de Medicamentos/métodos , Dispepsia/fisiopatologia , Fármacos Gastrointestinais/administração & dosagem , Gastroenteropatias/fisiopatologia , Gastroparesia/tratamento farmacológico , Gastroparesia/fisiopatologia , Humanos , Inflamação/tratamento farmacológico , Inflamação/fisiopatologia , Inibidores da Bomba de Prótons/administração & dosagem , Inibidores da Bomba de Prótons/farmacologia
5.
Adv Exp Med Biol ; 1161: 27-35, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31562619

RESUMO

Surgery can be a life-saving procedure; however, significant complications may occur after routine procedures especially in older and more frail patients. Perioperative neurocognitive disorders (PNDs), including delirium and postoperative cognitive dysfunction, are the most common complications in older adults following common procedures such as orthopedic or cardiac surgery. The consequences of PNDs can be devastating, with longer in-hospital stay, poorer prognosis, and higher mortality rates. Inflammation is gaining considerable interest as a critical driver of cognitive deficits. In this regard, resolution of inflammation, once thought to be a passive process, may provide novel approaches to treat neuroinflammation and PNDs. Herein we review the role for impaired resolution after surgery and the growing role of specialized pro-resolving mediators (SPMs) in regulating postoperative neuroinflammation and neurological complications after surgery.


Assuntos
Mediadores da Inflamação , Transtornos Neurocognitivos , Complicações Pós-Operatórias , Humanos , Inflamação/fisiopatologia , Mediadores da Inflamação/metabolismo , Transtornos Neurocognitivos/fisiopatologia , Período Perioperatório , Complicações Pós-Operatórias/fisiopatologia
6.
Adv Exp Med Biol ; 1161: 193-217, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31562631

RESUMO

Headache is a common complaint after mild traumatic brain injury (mTBI). Changes in the CNS lipidome were previously associated with acrolein-induced headache in rodents. mTBI caused similar headache-like symptoms in rats; therefore, we tested the hypothesis that mTBI might likewise alter the lipidome. Using a stereotaxic impactor, rats were given either a single mTBI or a series of 4 mTBIs 48 h apart. 72 h later for single mTBI and 7 days later for repeated mTBI, the trigeminal ganglia (TG), trigeminal nucleus (TNC), and cerebellum (CER) were isolated. Using HPLC/MS/MS, ~80 lipids were measured in each tissue and compared to sham controls. mTBI drove widespread alterations in lipid levels. Single mTBI increased arachidonic acid and repeated mTBI increased prostaglandins in all 3 tissue types. mTBI affected multiple TRPV agonists, including N-arachidonoyl ethanolamine (AEA), which increased in the TNC and CER after single mTBI. After repeated mTBI, AEA increased in the TG, but decreased in the TNC. Common to all tissue types in single and repeated mTBI was an increase the AEA metabolite, N-arachidonoyl glycine, a potent activator of microglial migration. Changes in the CNS lipidome associated with mTBI likely play a role in headache and in long-term neurodegenerative effects of repeated mTBI.


Assuntos
Lesões Encefálicas Traumáticas , Sistema Nervoso Central , Cefaleia , Inflamação , Lipídeos , Neoplasias , Animais , Lesões Encefálicas Traumáticas/fisiopatologia , Sistema Nervoso Central/fisiopatologia , Cefaleia/fisiopatologia , Inflamação/fisiopatologia , Lipídeos/química , Lipídeos/genética , Lipídeos/fisiologia , Neoplasias/fisiopatologia , Ratos
7.
Isr Med Assoc J ; 21(7): 460-463, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31507121

RESUMO

BACKGROUND: Inflammation is the basic mechanism leading to many pathological processes, including degenerative diseases, atherosclerosis, and cancer. We found an interesting link connecting rheumatoid arthritis and atherosclerosis that may explain the high cardiovascular event rate among patients with rheumatoid arthritis, but also may lead to a new way of thinking and a better understanding of atherosclerosis. Rheumatoid arthritis could serve as a model of accelerated atherosclerosis. Understanding the basic mechanisms of rheumatoid arthritis may solve some of the complexity of atherosclerosis.


Assuntos
Artrite Reumatoide/fisiopatologia , Aterosclerose/fisiopatologia , Inflamação/fisiopatologia , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/fisiopatologia , Humanos , Fatores de Risco
8.
Adv Exp Med Biol ; 1161: 45-64, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31562621

RESUMO

After myocardial infarction, splenic leukocytes direct biosynthesis of specialized pro-resolving mediators (SPMs) that are essential for the resolution of inflammation and tissue repair. In a laboratory environment, after coronary ligation of healthy risk free rodents (young adult mice) leukocytes biosynthesize SPMs with induced activity of lipoxygenases and cyclooxygenases, which facilitate cardiac repair. Activated monocytes/macrophages drive the biosynthesis of SPMs following experimental myocardial infarction in mice during the acute heart failure. In the presented review, we provided the recent updates on SPMs (resolvins, lipoxins and maresins) in cardiac repair that may serve as novel therapeutics for future heart failure therapy/management. We incorporated the underlying causes of non-resolving inflammation following cardiac injury if superimposed with obesity, hypertension, diabetes, disrupted circadian rhythm, co-medication (painkillers or oncological therapeutics), and/or aging that may delay or impair the biosynthesis of SPMs, intensifying pathological remodeling in heart failure.


Assuntos
Insuficiência Cardíaca , Mediadores da Inflamação , Animais , Insuficiência Cardíaca/fisiopatologia , Insuficiência Cardíaca/terapia , Humanos , Inflamação/fisiopatologia , Mediadores da Inflamação/metabolismo , Mediadores da Inflamação/uso terapêutico , Leucócitos , Infarto do Miocárdio
9.
Adv Exp Med Biol ; 1161: 65-75, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31562622

RESUMO

Inflammation is a fundamentally protective process that guards the host from invading pathogens and is central in the repair and regeneration of damaged tissue. However, when uncontrolled, the overzealous response leads to tissue damage and malaise. Indeed, this process is now appreciated to be at the center of many chronic inflammatory diseases including vascular disease and arthritis. Studies investigating the mechanisms through which acute inflammation is actively turned off allowing tissues to regain function demonstrated that the essential fatty acids, arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are enzymatically converted to bioactive mediators. These autacoids carry distinct structures and biological actions, actively reprogramming the inflammatory reaction to promote its termination by counter-regulating the production of pro-inflammatory mediators and regulate leukocyte trafficking as well as phenotype. Recently we found that n-3 docosapentaenoic acid (DPA), which was until then only regarded as a biosynthetic intermediate in the formation of DHA from EPA, is also converted to structurally distinct bioactive mediators that reprogram the host immune response. In the present review we will discuss the evidence underpinning the biological actions of these novel n-3 DPA-derived autacoids in particular as they pertain to the vascular system.


Assuntos
Vasos Sanguíneos , Inibidores de Hidroximetilglutaril-CoA Redutases , Mediadores da Inflamação , Inflamação , Vasos Sanguíneos/efeitos dos fármacos , Vasos Sanguíneos/fisiologia , Ácidos Docosa-Hexaenoicos/química , Humanos , Inibidores de Hidroximetilglutaril-CoA Redutases/química , Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia , Inflamação/tratamento farmacológico , Inflamação/fisiopatologia , Mediadores da Inflamação/química , Mediadores da Inflamação/metabolismo , Leucócitos/efeitos dos fármacos
10.
Adv Exp Med Biol ; 1161: 149-167, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31562629

RESUMO

Inflammation is a common underlying factor in a diversity of ocular diseases, ranging from macular degeneration, autoimmune uveitis, glaucoma, diabetic retinopathy and microbial infection. In addition to the variety of known cellular mediators of inflammation, such as cytokines, chemokines and lipid mediators, there is now considerable evidence that sphingolipid metabolites also play a central role in the regulation of inflammatory pathways. Various sphingolipid metabolites, such as ceramide (Cer), ceramide-1-phosphate (C1P), sphingosine-1-phosphate (S1P), and lactosylceramide (LacCer) can contribute to ocular inflammatory diseases through multiple pathways. For example, inflammation generates Cer from sphingomyelins (SM) in the plasma membrane, which induces death receptor ligand formation and leads to apoptosis of retinal pigment epithelial (RPE) and photoreceptor cells. Inflammatory stress by reactive oxygen species leads to LacCer accumulation and S1P secretion and induces proliferation of retinal endothelial cells and eventual formation of new vessels. In sphingolipid/lysosomal storage disorders, sphingolipid metabolites accumulate in lysosomes and can cause ocular disorders that have an inflammatory etiology. Sphingolipid metabolites activate complement factors in the immune-response mediated pathogenesis of macular degeneration. These examples highlight the integral association between sphingolipids and inflammation in ocular diseases.


Assuntos
Oftalmopatias , Inflamação , Esfingolipídeos , Apoptose , Células Endoteliais/citologia , Células Endoteliais/patologia , Oftalmopatias/fisiopatologia , Humanos , Inflamação/fisiopatologia , Esfingolipídeos/metabolismo
11.
Adv Exp Med Biol ; 1161: 169-191, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31562630

RESUMO

Ceramides are bioactive sphingolipids that support the structure of the plasma membrane and mediate numerous cell-signaling events in eukaryotic cells. The finding that ceramides act as second messengers transducing cellular signals has attracted substantial attention in several fields of Biology. Since all cells contain lipid plasma membranes, the impact of various ceramides, ceramide synthases, ceramide metabolites, and other sphingolipids has been implicated in a vast range of cellular functions including, migration, proliferation, response to external stimuli, and death. The roles of lipids in these functions widely differ among the diverse cell types. Herein, we discuss the roles of ceramides and other sphingolipids in mediating the function of various immune cells; particularly dendritic cells, neutrophils, and macrophages. In addition, we highlight the main studies describing effects of ceramides in inflammation, specifically in various inflammatory settings including insulin resistance, graft-versus-host disease, immune suppression in cancer, multiple sclerosis, and inflammatory bowel disease.


Assuntos
Ceramidas , Inflamação , Esfingolipídeos , Ceramidas/imunologia , Ceramidas/metabolismo , Humanos , Inflamação/fisiopatologia , Sistemas do Segundo Mensageiro , Transdução de Sinais , Esfingolipídeos/imunologia
12.
Adv Exp Med Biol ; 1161: 243-253, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31562634

RESUMO

Flavonoids are plant secondary metabolites that act as protectants against harmful effects of UV-B radiation inasmuch as biotic stress, conferring at the same time pigmentation of fruits and leaves [67]. The term "flavonoid" refers to phenolics having a basic skeleton of diphenylpropane (C6-C3-C6), which consists of two aromatic rings linked through three carbons that usually form an oxygenated heterocycle [25, 52]. Flavonoids are broken down into several different sub-categories based on their chemical structure. The main subclasses commonly found in food items are: flavonols, flavones, flavanones, flavan-3-ols, proanthocyanidins, and anthocyanins [44, 67]. Figure 19.1 depicts the major classification of flavonoids according to their chemical structure. Their occurrence in food matrices has been extensively reviewed [39, 44], and has been subject of extensive research in the last decades. Table 19.1 contains a few examples of compounds from each of the subcategory, with the fruit (berry) in which they are commonly found. The monomeric unit of flavonoids can dimerize and polymerize to form other important high molecular weight molecules; this is the case of proanthocyanidins, that are polymers of flavan-3-ols or flavanols. Not only do these compounds act as plant protectants, but they can also be very beneficial to human health. Cohorts studies performed in the early '90 have shown that dietary consumption of flavonoids was inversely associated with morbidity and mortality from coronary heart disease [31, 32]. These findings have opened an intensive field of research on the effects of flavonoids and flavonoids-rich food extracts in cardiovascular diseases (CVD) progression, particularly in the modulating CVD-associated oxidative stress and inflammation. In this short review, we will summarize the current findings in flavonoids beneficial effects in preventing CVD through inhibition of initial stages of CVD progression. Given the magnitude of scientific literature in the field, we will focus on two strictly mechanistic aspects: inhibition of chemical-induced LDL oxidation, and the effect of flavonoids in the monocyte/macrophages activation pathways.


Assuntos
Colesterol , Flavonoides , Metabolismo dos Lipídeos , Colesterol/metabolismo , Dieta , Flavonoides/metabolismo , Humanos , Inflamação/fisiopatologia , Oxirredução
13.
Life Sci ; 235: 116838, 2019 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-31493482

RESUMO

AIMS: This work aimed to evaluate the regulatory function of IL-10-producing B cells in viral myocarditis (VMC). MAIN METHODS: We adoptively transferred purified IL-10-producing B cells to VMC mice via the tail vein. We observed the inflammatory responses and cardiac lesions by histological analysis, examined the proportions of spleen Th1 and T17 cells by flow cytometry and expression levels of related transcription factors (T-bet and RORγt) by reverse transcription polymerase chain reaction (RT-PCR), and calculated the cardiac pathological scores and the mean survival times. KEY FINDINGS: IL-10-producing B cells were found to be T cell-dependent in the pathogenesis of VMC. They mainly downregulated T-bet and RORγt mRNA levels to decrease the proportions of Th1 and Th17 cells, thereby restraining the inflammation and damage in the myocardium in B cell-deficient VMC mice. Adoptive transfer of IL-10-producing B cells before VMC induction also normalized the inflammatory responses and prolonged the survival time in wild-type (WT) VMC mice. While the transfer of IL-10-producing B cells on day 3 of VMC alleviated the severity of disease, it did not extend the mean survival time of VMC mice. By contrast, IL-10-producing B cells showed no effect on day 7 of VMC. In conclusion, IL-10-producing B cells downregulate the proportion of Th1 and Th17 cells to alleviate inflammatory damage in the myocardium during VMC before the induction or the early phase of disease. SIGNIFICANCE: These findings suggest that IL-10-producing B cells may be a new therapeutic target for modulating the immune response in VMC.


Assuntos
Linfócitos B/metabolismo , Enterovirus Humano B/imunologia , Inflamação/fisiopatologia , Interleucina-10/fisiologia , Miocardite/fisiopatologia , Células Th1/imunologia , Células Th17/imunologia , Transferência Adotiva , Animais , Infecções por Coxsackievirus/imunologia , Infecções por Coxsackievirus/virologia , Regulação para Baixo , Interleucina-10/biossíntese , Masculino , Camundongos , Miocardite/metabolismo , Miocardite/patologia , Miocardite/virologia , Miocárdio/patologia , Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/biossíntese , Taxa de Sobrevida , Proteínas com Domínio T/biossíntese
14.
Braz Oral Res ; 33: e060, 2019 Jul 29.
Artigo em Inglês | MEDLINE | ID: mdl-31365705

RESUMO

This study evaluated the effect of hypertension on tissue response and biomineralization capacity of white Mineral Trioxide Aggregate (MTA), High-plasticity MTA (MTA HP), and Biodentine® (BDT) in rats. Polyethylene tubes filled with MTA, MTA HP, BDT, and the control group (empty tubes) were placed into the dorsal subcutaneous tissue of 32 male rats (16 normotensive (NT) and 16 hypertensive rats - 8 per group). After 7 and 30 days, the polyethylene tubes surrounded by connective tissue were removed, fixed, and embedded in histological resin. The mean number of inflammatory cells was estimated in HE-stained sections, biomineralization was quantified as area (µm2) by Kossa (VK) staining, and examination by polarized light (LP) microscopy was performed. The differences amongst the groups were analyzed statistically by the Mann-Whitney or Student's t test, according to Shapiro-Wilk test of normality (p < 0.05). The inflammatory responses to all materials were greater in hypertensive rats than in NT rats (p < 0.05). Positive VK staining in MTA and BDT were more pronounced in NT rats at 7 and 30 days (p < 0.05). Birefringent structures in LP for MTA, MTA HP, and BDT were more pronounced in NT rats at 7 days (p<0.05). In rats, hypertension was able to increase inflammatory infiltrate and decrease biomineralization of the tested materials.


Assuntos
Compostos de Alumínio/farmacologia , Materiais Biocompatíveis/farmacologia , Biomineralização/fisiologia , Compostos de Cálcio/farmacologia , Hipertensão/fisiopatologia , Óxidos/farmacologia , Silicatos/farmacologia , Tela Subcutânea/efeitos dos fármacos , Tela Subcutânea/fisiopatologia , Animais , Combinação de Medicamentos , Hipertensão/complicações , Inflamação/patologia , Inflamação/fisiopatologia , Masculino , Teste de Materiais , Microscopia de Polarização , Ratos Wistar , Reprodutibilidade dos Testes , Tela Subcutânea/patologia , Fatores de Tempo
15.
BMC Public Health ; 19(1): 1076, 2019 Aug 09.
Artigo em Inglês | MEDLINE | ID: mdl-31399027

RESUMO

BACKGROUND: Chronic inflammation contributes to the risk of osteoporosis and fracture. Dietary Inflammatory Index (DII), a novel method appraising the inflammatory potential of diet, has been utilized to examine the association between diet and bone health among postmenopausal women or the elderly. However, its relationship with bone density (BD) in lactating women has not been studied. METHODS: The prospective study was conducted to assess the possible association between DII and maternal BD during lactation. We enrolled 150 lactating women in the cohort. Participants were measured ultrasonic BD as baseline values at 1 month postpartum. After five-month follow up, the participants' BD were measured again. DII scores were calculated from semi-quantitative food frequency questionnaires (FFQ) and divided into tertiles. We compared the differences in the changes of BD at 6 months postpartum without or with adjustment for potential covariates across the tertiles. RESULTS: The women in Q1 of DII scores had less bone mass loss than those in Q2 and Q3 without adjustment for any covariates (p < 0.01); after adjusting demographic characteristics such as BMI (kg/m2) at 6 months postpartum, educational level, metabolic equivalent (MET), daily energy intake (kcal/d), we found that participants in the highest tertile of DII scores had much more bone loss than those in the lowest tertile (p = 0.038). However, in the test for trend, no significant association between DII and the changes of maternal BD at 6 months postpartum was observed. CONCLUSIONS: Chinese lactating women with higher DII scores have more bone mass loss; however significant differences and trends are attenuated and/or disappear depending on covariates and confounders that are taken into account in statistical analysis. The further study should be conducted in larger population to explore whether the significant association between DII and BD exists in Chinese lactating women.


Assuntos
Densidade Óssea/fisiologia , Dieta/efeitos adversos , Inflamação/fisiopatologia , Lactação/fisiologia , Adulto , China , Feminino , Humanos , Estudos Longitudinais , Período Pós-Parto , Estudos Prospectivos
16.
Life Sci ; 233: 116707, 2019 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-31374234

RESUMO

The epidemiological investigations and animal model experiments have confirmed the impact of obesity on the brain, behavior, and cognition. However, the mechanism by which obesity affects cognitive function is not fully understood. With the development of an aging society, there is an increase in the economic and social burden caused by the decline in cognitive function. This manuscript reviews the effects of inflammation and endoplasmic reticulum stress (ERS) on the hypothalamus, hippocampus, and the possible impact on cognitive impairment. These findings provide new insights into the pathophysiological mechanisms that lead to the development of cognitive impairment in the context of obesity.


Assuntos
Disfunção Cognitiva/etiologia , Estresse do Retículo Endoplasmático , Inflamação/fisiopatologia , Obesidade/complicações , Animais , Disfunção Cognitiva/patologia , Humanos
17.
Curr Urol Rep ; 20(9): 54, 2019 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-31377881

RESUMO

PURPOSE OF REVIEW: The purpose of this review is to summarize the role and significance of inflammation as a putative additional factor contributing to lower urinary tract symptoms and the progression of benign prostatic hyperplasia. We review (1) the histologic definition of prostatic inflammation and its prevalence, (2) the effects inflammation in the prostate including on risk of acute urinary retention, and (3) the effects of systemic inflammation on the prostate and on voiding. RECENT FINDINGS: Inflammation is a highly prevalent finding in the prostate, both on a histological and biochemical level. Men with inflammation have higher IPSS scores and increased prostate size; however, these differences appear to be imperceptibly small. Men with inflammation do experience a significantly increased risk of developing acute urinary retention, an event that is associated with significant morbidity. Recently, attempts have been made to identify more specific biochemical markers of local inflammation, and to identify regional patterns of inflamed tissue within the prostate which may be associated with higher IPSS scores, accelerated progression, and AUR. The effects of systemic inflammatory states, most notably MetS, and their role in LUTS have also been examined. Inflammation is a common finding in prostates of aging men, but its contribution to lower urinary tract symptoms and benign prostatic hyperplasia progression appears to be small when considered as a clinically relevant entity. Advances in the understanding of different forms of inflammation, and their impact when experienced in different locations within the prostate, may refine this knowledge. Systemic inflammation affects voiding, including in the absence of a prostate, but again significant effects of systemic inflammation on the prostate itself are also difficult to demonstrate. Prostatic inflammation is associated with a significantly increased risk of acute urinary retention.


Assuntos
Inflamação/fisiopatologia , Sintomas do Trato Urinário Inferior/fisiopatologia , Hiperplasia Prostática/fisiopatologia , Prostatite/fisiopatologia , Doença Aguda , Progressão da Doença , Humanos , Sintomas do Trato Urinário Inferior/etiologia , Masculino , Hiperplasia Prostática/etiologia , Prostatite/complicações , Retenção Urinária/etiologia , Retenção Urinária/fisiopatologia
18.
Health Psychol ; 38(9): 791-801, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31436464

RESUMO

OBJECTIVE: Multimorbidity is a robust predictor of disability in aging adults, but the mechanisms by which multimorbidity is disabling are not clear. Most existing research focuses on disease-specific phenomena, such as diminished lung capacity in chronic obstructive pulmonary disease, which can result in functional limitations. This review takes a different approach by highlighting the potential role of a biological process-inflammation-that is common to many chronic medical conditions and thus, from a medical perspective, relatively disease nonspecific. METHOD: Beginning with a description of inflammation and its measurement, this paper will provide an overview of research on inflammation as a predictor of disease risk in healthy adults and of adverse outcomes (e.g., disability) in those with multimorbidity. RESULTS: The discussion of inflammation is then situated in the context of biopsychosocial influences on health, as inflammation has been shown to be sensitive to a wide range of social and psychological processes that are thought to contribute to healthy aging, including successful adaptation to multimorbidity and reduced risk of disability. CONCLUSIONS: Finally, implications of this broader perspective for interventions to improve outcomes in aging adults with multimorbidity are briefly considered. (PsycINFO Database Record (c) 2019 APA, all rights reserved).


Assuntos
Pessoas com Deficiência/psicologia , Inflamação/fisiopatologia , Multimorbidade/tendências , Adulto , Doença Crônica , Humanos , Inflamação/mortalidade
19.
Clin Interv Aging ; 14: 1277-1283, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31371933

RESUMO

Age-related macular degeneration (AMD) is the leading cause of irreversible blindness among the elderly. Considering the relatively limited effect of therapy on early AMD, it is important to focus on the pathogenesis of AMD, especially early AMD. Ageing is one of the strongest risk factors for AMD, and analysis of the impact of ageing on AMD development is valuable. Among all the ageing hallmarks, increased DNA damage accumulation is regarded as the beginning of cellular senescence and is related to abnormal expression of inflammatory cytokines, which is called the senescence-associated secretory phenotype (SASP). The exact pathway for DNA damage that triggers senescence-associated hallmarks is poorly understood. Recently, mounting evidence has shown that the cGAS/STING pathway is an important DNA sensor related to proinflammatory factor secretion and is associated with another hallmark of ageing, SASP. Thus, we hypothesized that the cGAS/STING pathway is a vital signalling pathway for early AMD development and that inhibition of STING might be a potential therapeutic strategy for AMD cases.


Assuntos
Dano ao DNA/fisiologia , Inflamação/metabolismo , Inflamação/fisiopatologia , Degeneração Macular/metabolismo , Degeneração Macular/fisiopatologia , Idoso , Senescência Celular/genética , Humanos , Degeneração Macular/patologia , Nucleotidiltransferases/metabolismo , Transdução de Sinais
20.
High Blood Press Cardiovasc Prev ; 26(4): 321-329, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31325087

RESUMO

Cardiovascular disease (CVD) remains the leading cause of morbility and mortality worldwide. The identification of common cardiovascular risk factors has led to the development of effective treatments that enabled a significant reduction of the global cardiovascular disease burden. However, a significant proportion of cardiovascular risk remains unexplained by these risk factors leaving many individuals at risk of cardiovascular events despite good control of the risk factors. Recent randomized clinical trials and Mendelian randomization studies have suggested that inflammation explains a significant proportion of the residual cardiovascular risk in subjects with good control of risk factors. An accelerated process of vascular ageing is increasingly recognized as a potential mechanism by which inflammation might increase the risk of CVD. In turn, cellular ageing represents an important source of inflammation within the vascular wall, potentially creating a vicious cycle that might promote progression of atherosclerosis, independently from the individual cardiovascular risk factor burden. In this review, we summarise current evidence suggesting a role for biological ageing in CVD and how inflammation might act as a key mediator of this association.


Assuntos
Envelhecimento/metabolismo , Doenças Cardiovasculares/metabolismo , Mediadores da Inflamação/metabolismo , Inflamação/metabolismo , Telômero/metabolismo , Fatores Etários , Envelhecimento/genética , Envelhecimento/patologia , Animais , Doenças Cardiovasculares/genética , Doenças Cardiovasculares/patologia , Doenças Cardiovasculares/fisiopatologia , Senescência Celular , Humanos , Inflamação/genética , Inflamação/patologia , Inflamação/fisiopatologia , Medição de Risco , Fatores de Risco , Transdução de Sinais , Telômero/genética , Telômero/patologia , Homeostase do Telômero , Encurtamento do Telômero , Fatores de Tempo
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