1 4403 134 MODULATION OF THE INFLAMMATORY RESPONSE IN POLYCYSTIC OVARY SYNDROME (PCOS)-SEARCHING FOR EPIGENETIC FACTORS. POLYCYSTIC OVARY SYNDROME (PCOS) IS THE MOST COMMON ENDOCRINE DISORDER IN WOMEN OF REPRODUCTIVE AGE. DESPITE ITS INCIDENCE, THE SYNDROME IS POORLY UNDERSTOOD AND REMAINS UNDERDIAGNOSED, AND FEMALE PATIENTS ARE DIAGNOSED WITH A DELAY. THE HETEROGENOUS NATURE OF THIS COMPLEX DISORDER RESULTS FROM THE COMBINED OCCURRENCE OF GENETIC, ENVIRONMENTAL, ENDOCRINE, AND BEHAVIORAL FACTORS. PRIMARY CLINICAL MANIFESTATIONS OF PCOS ARE DERIVED FROM THE EXCESS OF ANDROGENS (ANOVULATION, POLYCYSTIC OVARY MORPHOLOGY, LACK OF OR SCANTY, IRREGULAR MENSTRUAL PERIODS, ACNE AND HIRSUTISM), WHEREAS THE SECONDARY MANIFESTATIONS INCLUDE MULTIPLE METABOLIC, CARDIOVASCULAR, AND PSYCHOLOGICAL DISORDERS. DIETARY AND LIFESTYLE FACTORS PLAY IMPORTANT ROLES IN THE DEVELOPMENT AND COURSE OF PCOS, WHICH SUGGESTS STRONG EPIGENETIC AND ENVIRONMENTAL INFLUENCES. MANY STUDIES HAVE SHOWN A STRONG ASSOCIATION BETWEEN PCOS AND CHRONIC, LOW-GRADE INFLAMMATION BOTH IN THE OVARIAN TISSUE AND THROUGHOUT THE BODY. IN THE VAST MAJORITY OF PCOS PATIENTS, ELEVATED VALUES OF INFLAMMATORY MARKERS OR THEIR GENE MARKERS HAVE BEEN REPORTED. DEVELOPMENT OF THE VICIOUS CYCLE OF THE CHRONIC INFLAMMATORY STATE IN PCOS IS ADDITIONALLY STIMULATED BY HYPERINSULINEMIA AND OBESITY. CHANGES IN DNA METHYLATION, HISTONE ACETYLATION AND NONCODING RNA LEVELS ARE PRESENTED IN THIS REVIEW IN THE CONTEXT OF OXIDATIVE STRESS, REACTIVE OXYGEN SPECIES, AND INFLAMMATORY SIGNALING IN PCOS. EPIGENETIC MODULATION OF ANDROGENIC ACTIVITY IN RESPONSE TO INFLAMMATORY SIGNALING IS ALSO DISCUSSED. 2022 2 3017 30 GENETICS AND EPIGENETICS OF INFLAMMATORY BOWEL DISEASE. THE RELEVANCE OF GENETIC AND EPIGENETIC ALTERATIONS IN THE PATHOGENESIS OF INFLAMMATORY BOWEL DISEASE (IBD) IS STILL POORLY UNDERSTOOD. SO FAR, 240 RISK GENE LOCI HAVE BEEN ASSOCIATED WITH IBD. THEY ARE MAINLY INVOLVED IN REGULATING INNATE AND ADAPTIVE IMMUNITY, AS WELL AS MAINTAINING INTESTINAL EPITHELIAL BARRIER FUNCTION. HOWEVER, THE FUNCTIONAL CONSEQUENCES OF THE IDENTIFIED GENETIC POLYMORPHISMS FOR IBD PATHOGENESIS IN VIVO ARE OFTEN UNKNOWN. EVEN LESS IS KNOWN ABOUT THE ROLE FOR EPIGENETIC MODIFICATIONS IN IBD PATHOGENESIS. THOUGH A NUMBER OF EPIGENETIC EVENTS SEEM TO BE CAUSATIVELY INVOLVED IBD PATHOGENESIS, OUR KNOWLEDGE ABOUT THE FUNCTIONAL RELEVANCE OF THOSE EPIGENETIC MODIFICATIONS IS SCANTY. THIS OPENS UP A BROAD RESEARCH FIELD THAT GENERATES NOVEL INSIGHTS INTO THE PATHOPHYSIOLOGY OF INTESTINAL AND CHRONIC INFLAMMATORY DISEASE. PATTERNS OF DNA METHYLATION AND HISTONE MODIFICATIONS MIGHT SERVE NOT ONLY AS BIOMARKERS OF DISEASE ACTIVITY OR DISEASE COURSE, BUT ALSO AS NEW TARGETS IN THERAPEUTIC INTERVENTIONS IN IBD PATIENTS. 2018 3 3750 34 INSULIN RESISTANCE IN POLYCYSTIC OVARY SYNDROME ACROSS VARIOUS TISSUES: AN UPDATED REVIEW OF PATHOGENESIS, EVALUATION, AND TREATMENT. POLYCYSTIC OVARY SYNDROME (PCOS) IS A COMMON ENDOCRINE DISORDER CHARACTERIZED BY CHRONIC OVULATION DYSFUNCTION AND OVERABUNDANCE OF ANDROGENS; IT AFFECTS 6-20% OF WOMEN OF REPRODUCTIVE AGE. PCOS INVOLVES VARIOUS PATHOPHYSIOLOGICAL FACTORS, AND AFFECTED WOMEN USUALLY HAVE SIGNIFICANT INSULIN RESISTANCE (IR), WHICH IS A MAJOR CAUSE OF PCOS. IR AND COMPENSATORY HYPERINSULINAEMIA HAVE DIFFERING PATHOGENESES IN VARIOUS TISSUES, AND IR VARIES AMONG DIFFERENT PCOS PHENOTYPES. GENETIC AND EPIGENETIC CHANGES, HYPERANDROGENAEMIA, AND OBESITY AGGRAVATE IR. INSULIN SENSITIZATION DRUGS ARE A NEW TREATMENT MODALITY FOR PCOS. WE SEARCHED PUBMED, GOOGLE SCHOLAR, ELSEVIER, AND UPTODATE DATABASES IN THIS REVIEW, AND FOCUSED ON THE PATHOGENESIS OF IR IN WOMEN WITH PCOS AND THE PATHOPHYSIOLOGY OF IR IN VARIOUS TISSUES. IN ADDITION, THE REVIEW PROVIDES A COMPREHENSIVE OVERVIEW OF THE CURRENT PROGRESS IN THE EFFICACY OF INSULIN SENSITIZATION THERAPY IN THE MANAGEMENT OF PCOS, PROVIDING THE LATEST EVIDENCE FOR THE CLINICAL TREATMENT OF WOMEN WITH PCOS AND IR. 2023 4 5104 21 POLYCYSTIC OVARIAN SYNDROME. WOMEN WITH PCOS PRESENT WITH SIGNS OF CHRONIC ANOVULATION, HYPERANDROGENISM, AND METABOLIC ABNORMALITIES. THE NIH RECENTLY EMBRACED THE ROTTERDAM CRITERIA TO BROADLY IDENTIFY ALL THE PHENOTYPES OF PCOS. WOMEN WITH PCOS ARE OFTEN OBESE WITH INSULIN RESISTANCE AND HENCE HAVE AN INCREASED SUSCEPTIBILITY TO GLUCOSE INTOLERANCE AND TYPE 2 DIABETES. FUTURE RESEARCH SHOULD FOCUS ON THE GENETIC, EPIGENETIC, AND ENVIRONMENTAL DETERMINANTS OF PCOS TO DEVELOP NEW THERAPIES TO ADDRESS THE PREVENTION OF THIS DISORDER AND ITS LONG-TERM COMPLICATIONS. 2015 5 6825 27 [GENETIC AND EPIGENETIC FACTORS OF POLYCYSTIC OVARY SYNDROME]. THE DEVELOPMENT OF POLYCYSTIC OVARY SYNDROME AND ITS EXACT PATHOPHYSIOLOGICAL MECHANISM IS STILL UNCLEAR, BUT ENVIRONMENTAL AND GENETIC FACTORS LIKELY PLAY A ROLE. EXPOSITION TO TERATOGENIC EFFECTS DURING THE PRENATAL DEVELOPMENT CAN LEAD TO CHRONIC DISEASES IN THE POSTNATAL PERIOD. THIS FINDING CONFIRMS THE COMMON FAMILIAL AGGREGATION AS WELL. A LITERATURE SEARCH WAS CONDUCTED UP TO JANUARY 1, 2016 FOR ARTICLES DEALING WITH THE GENETIC OR EPIGENETIC FACTORS OF POLYCYSTIC OVARY SYNDROME. THIS REVIEW WILL DISCUSS THE CURRENT UNDERSTANDING OF THE GENETIC BASIS AND CLINICAL PRESENTATION OF THIS DISEASE. ORV. HETIL., 2016, 157(32), 1275-1281. 2016 6 4892 47 OXIDATIVE STRESS AND REPRODUCTIVE FUNCTION: OXIDATIVE STRESS IN POLYCYSTIC OVARY SYNDROME. IN BRIEF: A GENETIC, EPIGENETIC, AND ENVIRONMENTAL ASSOCIATION EXISTS BETWEEN OXIDATIVE STRESS (OS) AND POLYCYSTIC OVARY SYNDROME (PCOS), EXPRESSED IN A MULTIFACETED CLINICAL PROFILE. THIS REVIEW SUMMARIZES AND DISCUSSES THE ROLE OF OS IN THE PATHOGENESIS OF PCOS SYNDROME, FOCUSING ON METABOLIC, REPRODUCTIVE, AND CANCER COMPLICATIONS. ABSTRACT: OXIDATIVE STRESS (OS), AN IMBALANCE BETWEEN OXIDANTS AND ANTIOXIDANTS IN CELLS, IS ONE OF MANY FACTORS PLAYING ESSENTIAL ROLES IN THE PATHOGENESIS OF POLYCYSTIC OVARY SYNDROME (PCOS). PCOS IS DESCRIBED MAINLY AS A DISPROPORTION OF REPRODUCTIVE HORMONES, LEADING TO CHRONIC ANOVULATION AND INFERTILITY IN WOMEN. INTERESTINGLY, OS IN PCOS MAY BE ASSOCIATED WITH MANY DISORDERS AND DISEASES. THIS REVIEW FOCUSES ON CHARACTERISTIC MARKERS OF OS IN PCOS AND THE RELATIONSHIP BETWEEN OS AND PCOS RELATED TO INSULIN RESISTANCE (IR), HYPERANDROGENEMIA, OBESITY, CHRONIC INFLAMMATION, CARDIOVASCULAR DISEASES, AND CANCER. INTERESTINGLY, IN PATIENTS WITH PCOS, AN INCREASE IN OXIDATIVE STATUS AND INSUFFICIENT COMPENSATION OF THE INCREASE IN ANTIOXIDANT STATUS BEFORE ANY CARDIOVASCULAR COMPLICATIONS ARE OBSERVED. MOREOVER, FREE RADICALS PROMOTE CARCINOGENESIS IN PCOS PATIENTS. HOWEVER, DESPITE THESE DATA, IT HAS NOT BEEN ESTABLISHED WHETHER OXYGEN STRESS INFLUENCES PCOS DEVELOPMENT OR A SECONDARY DISORDER RESULTING FROM HYPERGLYCEMIA, IR, AND CARDIOVASCULAR AND CANCER COMPLICATIONS IN WOMEN. 2022 7 2952 23 GENETIC AND EPIGENETIC ETIOLOGY OF INFLAMMATORY BOWEL DISEASE: AN UPDATE. INFLAMMATORY BOWEL DISEASE (IBD) IS A CHRONIC DISEASE WITH PERIODS OF EXACERBATION AND REMISSION OF THE DISEASE. THE ETIOLOGY OF IBD IS NOT FULLY UNDERSTOOD. MANY STUDIES POINT TO THE PRESENCE OF GENETIC, IMMUNOLOGICAL, ENVIRONMENTAL, AND MICROBIOLOGICAL FACTORS AND THE INTERACTIONS BETWEEN THEM IN THE OCCURRENCE OF IBD. THE REVIEW LOOKS AT GENETIC FACTORS IN THE CONTEXT OF BOTH IBD PREDISPOSITION AND PHARMACOGENETICS. 2022 8 4665 23 NEW INSIGHTS AND ADVANCES IN PATHOGENESIS AND TREATMENT OF VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE. VERY EARLY ONSET INFLAMMATORY BOWEL DISEASE (VEO-IBD) IS CHARACTERIZED BY MULTIFACTORIAL CHRONIC RECURRENT INTESTINAL INFLAMMATION. COMPARED WITH ELDERLY PATIENTS, THOSE WITH VEO-IBD HAVE A MORE SERIOUS CONDITION, NOT RESPONSIVE TO CONVENTIONAL TREATMENTS, WITH A POOR PROGNOSIS. RECENT STUDIES FOUND THAT GENETIC AND IMMUNOLOGIC ABNORMALITIES ARE CLOSELY RELATED TO VEO-IBD. INTESTINAL IMMUNE HOMEOSTASIS MONOGENIC DEFECTS (IIHMDS) ARE CHANGED THROUGH VARIOUS MECHANISMS. RECENT STUDIES HAVE ALSO REVEALED THAT ABNORMALITIES IN GENES AND IMMUNE MOLECULAR MECHANISMS ARE CLOSELY RELATED TO VEO-IBD. IIHMDS CHANGE THROUGH VARIOUS MECHANISMS. EPIGENETIC FACTORS CAN MEDIATE THE INTERACTION BETWEEN THE ENVIRONMENT AND GENOME, AND GENETIC FACTORS AND IMMUNE MOLECULES MAY BE INVOLVED IN THE PATHOGENESIS OF THE ENVIRONMENT AND GUT MICROBIOTA. THESE DISCOVERIES WILL PROVIDE NEW DIRECTIONS AND IDEAS FOR THE TREATMENT OF VEO-IBD. 2022 9 3845 17 IS AGING A "RETRO"SPECTIVE EVENT? REACTIVATION OF ENDOGENOUS RETROVIRUSES (ERVS), THE RELICS OF ANCIENT INFECTIONS, HAS BEEN IMPLICATED IN A NUMBER OF DISEASE CONTEXTS. IN THIS ISSUE OF CELL, LIU ET AL. SHOW HOW REACTIVATION OF ERVS IN OLD AGE CAN INDUCE SENESCENCE. THIS AWAKENING OF ERVS IS ASSOCIATED WITH THEIR EPIGENETIC DEREPRESSION AND CONTRIBUTES TO AGE-ASSOCIATED CHRONIC INFLAMMATION. 2023 10 5500 31 REVISITING MIGRAINE: THE EVOLVING PATHOPHYSIOLOGY AND THE EXPANDING MANAGEMENT ARMAMENTARIUM. MIGRAINE AFFECTS ABOUT ONE BILLION PEOPLE WORLDWIDE YEARLY AND IS ONE OF THE MOST COMMON NEUROLOGIC ILLNESSES, WITH A HIGH PREVALENCE AND MORBIDITY, PARTICULARLY AMONG YOUNG ADULTS AND FEMALES. MIGRAINE IS ASSOCIATED WITH MANY COMORBIDITIES, INCLUDING STRESS, SLEEP DIFFICULTIES, AND SUICIDAL IDEATION. MIGRAINE, DESPITE ITS WIDESPREAD OCCURRENCE, IS UNDERDIAGNOSED AND UNDERTREATED. BECAUSE OF THE COMPLICATED AND PRIMARILY UNKNOWN MECHANISMS OF MIGRAINE FORMATION, SEVERAL SOCIAL AND BIOLOGICAL RISK FACTORS, SUCH AS HORMONE IMBALANCES, GENETIC AND EPIGENETIC IMPACTS, AND CARDIOVASCULAR, NEUROLOGICAL, AND AUTOIMMUNE ILLNESSES, HAVE BEEN PROPOSED. THROUGH THE MID-20TH CENTURY DIVERSION OF THE NOW-DEFUNCT VASCULAR THEORY, THE PATHOPHYSIOLOGY OF MIGRAINE HAS DEVELOPED FROM A HISTORICAL STUDY OF THE "HUMOURS" TO A DISTINCT ENTITY AS A NEUROLOGICAL DISORDER. THE RANGE OF THERAPEUTIC TARGETS HAS BROADENED SIGNIFICANTLY, INCREASING THE NUMBER OF SPECIALIZED CLINICAL TRIALS. UNDERSTANDING THE BIOLOGY OF MIGRAINE THROUGH CAREFUL RESEARCH HAS RESULTED IN THE IDENTIFICATION OF MAJOR THERAPEUTIC CLASSES: (I) TRIPTANS, SEROTONIN 5-HT1B/1D RECEPTOR AGONISTS, (II) GEPANTS, CALCITONIN GENE-RELATED PEPTIDE (CGRP) RECEPTOR ANTAGONISTS, (III) DITANS, 5-HT1F RECEPTOR AGONISTS, (IV) CGRP MONOCLONAL ANTIBODIES, AND (V) GLURANTS, MGLU5 MODULATORS, WITH FURTHER TARGETS BEING EXPLORED. THIS REVIEW PROVIDES A COMPREHENSIVE OVERVIEW OF THE MOST RECENT LITERATURE ON EPIDEMIOLOGY AND RISK FACTORS AND EXPOSES KNOWLEDGE GAPS. 2023 11 4973 39 PATHOPHYSIOLOGICAL EFFECTS OF CONTEMPORARY LIFESTYLE ON EVOLUTIONARY-CONSERVED SURVIVAL MECHANISMS IN POLYCYSTIC OVARY SYNDROME. POLYCYSTIC OVARY SYNDROME (PCOS) IS INCREASINGLY BEING CHARACTERIZED AS AN EVOLUTIONARY MISMATCH DISORDER THAT PRESENTS WITH A COMPLEX MIXTURE OF METABOLIC AND ENDOCRINE SYMPTOMS. THE EVOLUTIONARY MODEL PROPOSES THAT PCOS ARISES FROM A COLLECTION OF INHERITED POLYMORPHISMS THAT HAVE BEEN CONSISTENTLY DEMONSTRATED IN A VARIETY OF ETHNIC GROUPS AND RACES. IN UTERO DEVELOPMENTAL PROGRAMMING OF SUSCEPTIBLE GENOMIC VARIANTS ARE THOUGHT TO PREDISPOSE THE OFFSPRING TO DEVELOP PCOS. POSTNATAL EXPOSURE TO LIFESTYLE AND ENVIRONMENTAL RISK FACTORS RESULTS IN EPIGENETIC ACTIVATION OF DEVELOPMENTALLY PROGRAMMED GENES AND DISTURBANCE OF THE HALLMARKS OF HEALTH. THE RESULTING PATHOPHYSIOLOGICAL CHANGES REPRESENT THE CONSEQUENCES OF POOR-QUALITY DIET, SEDENTARY BEHAVIOUR, ENDOCRINE DISRUPTING CHEMICALS, STRESS, CIRCADIAN DISRUPTION, AND OTHER LIFESTYLE FACTORS. EMERGING EVIDENCE SUGGESTS THAT LIFESTYLE-INDUCED GASTROINTESTINAL DYSBIOSIS PLAYS A CENTRAL ROLE IN THE PATHOGENESIS OF PCOS. LIFESTYLE AND ENVIRONMENTAL EXPOSURES INITIATE CHANGES THAT RESULT IN DISTURBANCE OF THE GASTROINTESTINAL MICROBIOME (DYSBIOSIS), IMMUNE DYSREGULATION (CHRONIC INFLAMMATION), ALTERED METABOLISM (INSULIN RESISTANCE), ENDOCRINE AND REPRODUCTIVE IMBALANCE (HYPERANDROGENISM), AND CENTRAL NERVOUS SYSTEM DYSFUNCTION (NEUROENDOCRINE AND AUTONOMIC NERVOUS SYSTEM). PCOS CAN BE A PROGRESSIVE METABOLIC CONDITION THAT LEADS TO OBESITY, GESTATIONAL DIABETES, TYPE TWO DIABETES, METABOLIC-ASSOCIATED FATTY LIVER DISEASE, METABOLIC SYNDROME, CARDIOVASCULAR DISEASE, AND CANCER. THIS REVIEW EXPLORES THE MECHANISMS THAT UNDERPIN THE EVOLUTIONARY MISMATCH BETWEEN ANCIENT SURVIVAL PATHWAYS AND CONTEMPORARY LIFESTYLE FACTORS INVOLVED IN THE PATHOGENESIS AND PATHOPHYSIOLOGY OF PCOS. 2023 12 555 26 AXIAL SPONDYLOARTHRITIS: RESHAPE THE FUTURE-FROM THE "2022 GISEA INTERNATIONAL SYMPOSIUM". THE TERM "AXIAL SPONDYLOARTHRITIS" (AXSPA) REFERS TO A GROUP OF CHRONIC RHEUMATIC DISEASES THAT PREDOMINANTLY INVOLVE THE AXIAL SKELETON AND CONSIST OF ANKYLOSING SPONDYLITIS, REACTIVE ARTHRITIS, ARTHRITIS/SPONDYLITIS ASSOCIATED WITH PSORIASIS (PSA) AND ARTHRITIS/SPONDYLITIS ASSOCIATED WITH INFLAMMATORY BOWEL DISEASES (IBD). MOREOVER, PAIN IS AN IMPORTANT AND COMMON SYMPTOM OF AXSPA. IT MAY PROGRESS TO CHRONIC PAIN, A MORE COMPLICATED BIO-PSYCHOSOCIAL PHENOMENA, LEADING TO A SIGNIFICANT WORSENING OF QUALITY OF LIFE. THE DEVELOPMENT OF THE AXSPA INFLAMMATORY PROCESS IS GROUNDED IN THE COMPLEX INTERACTION BETWEEN GENETIC (SUCH AS HLA B27), EPIGENETIC, AND ENVIRONMENTAL FACTORS ASSOCIATED WITH A DYSREGULATED IMMUNE RESPONSE. CONSIDERING THE PIVOTAL CONTRIBUTION OF IL-23 AND IL-17 IN AXSPA INFLAMMATION, THE INHIBITION OF THESE CYTOKINES HAS BEEN EVALUATED AS A POTENTIAL THERAPEUTIC STRATEGY. WITH THIS CONTEXT, HERE WE DISCUSS THE MAIN PATHOGENETIC MECHANISMS, THERAPEUTIC APPROACHES AND THE ROLE OF PAIN IN AXSPA FROM THE 2022 INTERNATIONAL GISEA/OEG SYMPOSIUM. 2022 13 3920 21 LINKING IMMUNITY, EPIGENETICS, AND CANCER IN INFLAMMATORY BOWEL DISEASE. MOST OF WHAT IS KNOWN ABOUT THE PATHOGENESIS OF INFLAMMATORY BOWEL DISEASE (IBD) PERTAINS TO COMPLEX INTERPLAY BETWEEN HOST GENETICS, IMMUNITY, AND ENVIRONMENTAL FACTORS. EPIGENETIC MODIFICATIONS PLAY PIVOTAL ROLES IN INTESTINAL IMMUNITY AND MUCOSAL HOMEOSTASIS AS WELL AS MEDIATING GENE-ENVIRONMENT INTERACTIONS. IN THIS ARTICLE, WE PROVIDE A HISTORICAL ACCOUNT OF EPIGENETIC RESEARCH EITHER DIRECTLY RELATED OR PERTINENT TO THE PATHOGENESIS AND MANAGEMENT OF IBD. WE FURTHER COLLATE EMERGING EVIDENCE SUPPORTING ROLES FOR EPIGENETIC MECHANISMS IN RELEVANT ASPECTS OF IBD BIOLOGY, INCLUDING DEREGULATED IMMUNITY, HOST-PATHOGEN RECOGNITION AND MUCOSAL INTEGRITY. FINALLY, WE HIGHLIGHT KEY EPIGENETIC MECHANISMS THAT LINK CHRONIC INFLAMMATION TO SPECIFIC IBD COMORBIDITIES, INCLUDING COLITIS-ASSOCIATED CANCER AND DISCUSS THEIR POTENTIAL UTILITY AS NOVEL BIOMARKERS OR PHARMACOLOGIC TARGETS IN IBD THERAPY. 2014 14 1643 28 DOES RHEUMATOID ARTHRITIS REPRESENT AN ADAPTIVE, THRIFTY CONDITION? THE PRESENT ARTICLE PRESENTS EPIDEMIOLOGICAL, AND COMPARATIVE EVIDENCE SUPPORTING THE HYPOTHESIS THAT RHEUMATOID ARTHRITIS (RA) MAY REPRESENT A THRIFTY ADAPTATION SELECTED TO COMPEL ANIMALS TO MINIMIZE VOLUNTARY ENERGY EXPENDITURE. THE AUTOIMMUNE, PATHOPHYSIOLOGICAL MANIFESTATIONS UNDERLYING RA ARE FRAMED HERE AS CONSTITUTING AN EVOLVED, PROTECTIVE MECHANISM THAT WOULD HAVE INFLUENCED ANIMALS TO AVOID EXERTION AND MAINTAIN A SEDENTARY LIFESTYLE IN ORDER TO MINIMIZE METABOLIC OUTPUT AND ULTIMATELY ESCAPE STARVATION. ARTHRITIC PAIN IS CHARACTERIZED HERE AS A DEFENSIVE, INNATE SIGNAL MUCH LIKE FATIGUE, FEVER, NAUSEA AND REFLEXIVE PAIN, AND LIKE THESE, IS SEEN ON A CONTINUUM VARYING BETWEEN IMPERCEPTIBLE ENCUMBRANCE AND DEBILITATING DISABILITY. THE EPIGENETIC RELATIONSHIP BETWEEN ACUTE PSYCHOLOGICAL STRESS AND FLARE-UP OF ARTHRITIC SYMPTOMS IS EXAMINED AND TAKEN TO SUGGEST THAT ARTHRITIS MAY BE A PREDICTIVE, ADAPTIVE RESPONSE TO SEVERE STRESS ALLOWING REDUCTIONS IN METABOLISM TO FOLLOW ADVERSE CONDITIONS OR NUTRITIONAL SCARCITY. THE CLOSE ASSOCIATIONS BETWEEN RHEUMATOID ARTHRITIS AND THE METABOLIC SYNDROME ARE ALSO EXPLORED ALONG WITH POTENTIAL TIES TO THE "THRIFTY GENOTYPE" AND "THRIFTY PHENOTYPE" PHENOMENA. THIS HYPOTHESIS IS EXAMINED IN THE CONTEXTS OF EVOLUTIONARY MEDICINE, PHENOTYPIC PLASTICITY, THE STRESS RESPONSE AND THE BIOENERGETICS OF THRIFT. A BRIEF AND EXPLORATORY REVIEW OF PERTINENT EVIDENCE SUGGESTS THAT RA, ITS SUBCLINICAL MANIFESTATIONS, AND EVEN OTHER FORMS OF ARTHROPATHY MAY POSSIBLY REPRESENT ADAPTATIONS THAT PROMOTED METABOLIC THRIFT DURING OUR EVOLUTIONARY PAST. 2010 15 4670 26 NEW INSIGHTS INTO THE EPIGENETIC REGULATION OF INFLAMMATORY BOWEL DISEASE. INFLAMMATORY BOWEL DISEASE (IBD) IS A CHRONIC INFLAMMATORY DISEASE OF THE COLONIC MUCOSA. ENVIRONMENTAL FACTORS, GENETICS, INTESTINAL MICROBIOTA, AND THE IMMUNE SYSTEM ARE ALL INVOLVED IN THE PATHOPHYSIOLOGY OF IBD. LATELY, ACCUMULATING EVIDENCE HAS SHOWN THAT ABNORMAL EPIGENETIC CHANGES IN DNA METHYLATION, HISTONE MARKERS, AND NON-CODING RNA EXPRESSION GREATLY CONTRIBUTE TO THE DEVELOPMENT OF THE ENTIRE DISEASE. EPIGENETICS REGULATES MANY FUNCTIONS, SUCH AS MAINTAINING THE HOMEOSTASIS OF THE INTESTINAL EPITHELIUM AND REGULATING THE IMMUNE SYSTEM OF THE IMMUNE CELLS. IN THE PRESENT STUDY, WE SYSTEMATICALLY SUMMARIZED THE LATEST ADVANCES IN EPIGENETIC MODIFICATION OF IBD AND HOW EPIGENETICS REVEALS NEW MECHANISMS OF IBD. OUR PRESENT REVIEW PROVIDED NEW INSIGHTS INTO THE PATHOPHYSIOLOGY OF IBD. MOREOVER, EXPLORING THE PATTERNS OF DNA METHYLATION AND HISTONE MODIFICATION THROUGH EPIGENETICS CAN NOT ONLY BE USED AS BIOMARKERS OF IBD BUT ALSO AS A NEW TARGET FOR THERAPEUTIC INTERVENTION IN IBD PATIENTS. 2022 16 2556 22 EPIGENETICS IN RHEUMATOID ARTHRITIS. EPIGENETICS IS A STEADILY GROWING RESEARCH AREA. IN MANY HUMAN DISEASES, ESPECIALLY IN CANCERS, BUT ALSO IN AUTOIMMUNE DISEASES, EPIGENETIC ABERRATIONS HAVE BEEN FOUND. RHEUMATOID ARTHRITIS IS AN AUTOIMMUNE DISEASE CHARACTERIZED BY CHRONIC INFLAMMATION AND DESTRUCTION OF SYNOVIAL JOINTS. EVEN THOUGH THE ETIOLOGY IS NOT YET FULLY UNDERSTOOD, RHEUMATOID ARTHRITIS IS GENERALLY CONSIDERED TO BE CAUSED BY A COMBINATION OF GENETIC PREDISPOSITION, DEREGULATED IMMUNOMODULATION, AND ENVIRONMENTAL INFLUENCES. TO GAIN A BETTER UNDERSTANDING OF THIS DISEASE, RESEARCHERS HAVE BECOME INTERESTED IN STUDYING EPIGENETIC CHANGES IN RHEUMATOID ARTHRITIS. HERE, WE WANT TO REVIEW THE CURRENT KNOWLEDGE ON EPIGENETICS IN RHEUMATOID ARTHRITIS. 2010 17 5809 20 STRAWBERRY AND HUMAN HEALTH: EFFECTS BEYOND ANTIOXIDANT ACTIVITY. THE USEFULNESS OF A DIET RICH IN VEGETABLES AND FRUITS ON HUMAN HEALTH HAS BEEN WIDELY RECOGNIZED: A HIGH INTAKE OF ANTIOXIDANT AND BIOACTIVE COMPOUNDS MAY IN FACT PLAY A CRUCIAL ROLE IN THE PREVENTION OF SEVERAL DISEASES, SUCH AS CANCER, CARDIOVASCULAR, NEURODEGENERATIVE, AND OTHER CHRONIC PATHOLOGIES. THE STRAWBERRY (FRAGARIA X ANANASSA DUCH.) POSSESSES A REMARKABLE NUTRITIONAL COMPOSITION IN TERMS OF MICRONUTRIENTS, SUCH AS MINERALS, VITAMIN C, AND FOLATES, AND NON-NUTRIENT ELEMENTS, SUCH AS PHENOLIC COMPOUNDS, THAT ARE ESSENTIAL FOR HUMAN HEALTH. ALTHOUGH STRAWBERRY PHENOLICS ARE KNOWN MAINLY FOR THEIR ANTI-INFLAMMATORY AND ANTIOXIDANT ACTIONS, RECENT STUDIES HAVE DEMONSTRATED THAT THEIR BIOLOGICAL ACTIVITIES ALSO SPREAD TO OTHER PATHWAYS INVOLVED IN CELLULAR METABOLISM AND CELLULAR SURVIVAL. THIS PAPER HAS THE MAIN OBJECTIVE OF REVIEWING CURRENT INFORMATION ABOUT THE POTENTIAL MECHANISMS INVOLVED IN THE EFFECTS ELICITED BY STRAWBERRY POLYPHENOLS ON HUMAN HEALTH, DEVOTING SPECIAL ATTENTION TO THE LATEST FINDINGS. 2014 18 2610 33 EPIGENETICS: A POTENTIAL MECHANISM INVOLVED IN THE PATHOGENESIS OF VARIOUS ADVERSE CONSEQUENCES OF OBSTRUCTIVE SLEEP APNEA. EPIGENETICS IS DEFINED AS THE HERITABLE PHENOTYPIC CHANGES WHICH DO NOT INVOLVE ALTERATIONS IN THE DNA SEQUENCE, INCLUDING HISTONE MODIFICATIONS, NON-CODING RNAS, AND DNA METHYLATION. RECENTLY, MUCH ATTENTION HAS BEEN PAID TO THE ROLE OF HYPOXIA-MEDIATED EPIGENETIC REGULATION IN CANCER, PULMONARY HYPERTENSION, ADAPTATION TO HIGH ALTITUDE, AND CARDIORENAL DISEASE. IN CONTRAST TO SUSTAINED HYPOXIA, CHRONIC INTERMITTENT HYPOXIA WITH RE-OXYGENATION (IHR) PLAYS A MAJOR ROLE IN THE PATHOGENESIS OF VARIOUS ADVERSE CONSEQUENCES OF OBSTRUCTIVE SLEEP APNEA (OSA), RESEMBLING ISCHEMIA RE-PERFUSION INJURY. NEVERTHELESS, THE ROLE OF EPIGENETICS IN THE PATHOGENESIS OF OSA IS CURRENTLY UNDEREXPLORED. THIS REVIEW PROPOSES THAT EPIGENETIC PROCESSES ARE INVOLVED IN THE DEVELOPMENT OF VARIOUS ADVERSE CONSEQUENCES OF OSA BY INFLUENCING ADAPTIVE POTENTIAL AND PHENOTYPIC VARIABILITY UNDER CONDITIONS OF CHRONIC IHR. IMPROVED UNDERSTANDING OF THE INTERACTION BETWEEN GENETIC AND ENVIRONMENTAL FACTORS THROUGH EPIGENETIC REGULATIONS HOLDS GREAT VALUE TO GIVE DEEPER INSIGHT INTO THE MECHANISMS UNDERLYING IHR-RELATED LOW-GRADE INFLAMMATION, OXIDATIVE STRESS, AND SYMPATHETIC HYPERACTIVITY, AND CLARIFY THEIR IMPLICATIONS FOR BIOMEDICAL RESEARCH. 2019 19 2569 27 EPIGENETICS OF ANKYLOSING SPONDYLITIS: RECENT DEVELOPMENTS. ANKYLOSING SPONDYLITIS (AS) IS A CHRONIC INFLAMMATORY AUTOIMMUNE DISEASE WHICH MAINLY AFFECTS THE SPINE, SACROILIAC JOINT AND PERIPHERAL JOINTS. TO DATE, THE EXACT CAUSES AND PATHOGENESIS OF AS STILL REMAIN UNKNOWN. IT IS CONSIDERED THAT THE PATHOGENESIS OF AS IS ASSOCIATED WITH GENETIC, INFECTION, ENVIRONMENT, IMMUNITY AND OTHER FACTORS. AMONG THEM, THE ROLE OF GENETIC FACTORS IN THE PATHOGENESIS OF AS HAS BEEN STUDIED MOST DEEPLY. HOWEVER, OVER THE PAST FEW YEARS, THE FUNCTION OF ENVIRONMENTAL PREDISPOSITION AND EPIGENETIC MODIFICATION IN THE PATHOGENESIS OF AS HAS RECEIVED EXTENSIVE ATTENTION. THIS PAPER SUMMARIZES THE RECENT PROGRESS IN THE EPIGENETICS OF AS, INCLUDING ABNORMAL EPIGENETIC MODIFICATIONS AT AS-ASSOCIATED GENOMIC LOCI, SUCH AS DNA METHYLATION, HISTONE MODIFICATION, MICRORNA, AND SO ON. IN SUMMARY, THE FINDINGS OF THIS REVIEW ATTEMPT TO EXPLAIN THE ROLE OF EPIGENETIC MODIFICATION IN THE OCCURRENCE AND DEVELOPMENT OF AS. NEVERTHELESS, THERE ARE STILL UNKNOWN AND COMPLICATED ASPECTS WORTH EXPLORING TO DEEPEN OUR UNDERSTANDING OF THE PATHOGENESIS OF AS. 2021 20 3173 19 GUT MICROBIOTA-MICRORNA INTERACTIONS IN ANKYLOSING SPONDYLITIS. ANKYLOSING SPONDYLITIS (AS) IS A CHRONIC AUTOIMMUNE INFLAMMATORY DISABILITY THAT IS PART OF THE RHEUMATIC DISEASE GROUP OF SPONDYLOARTHROPATHIES. AS COMMONLY INFLUENCES THE JOINTS OF THE AXIAL SKELETON. THE CONTRIBUTIONS TO AS PATHOGENESIS OF GENETIC SUSCEPTIBILITY (PARTICULARLY HLA-B27 AND ERAP-1) AND EPIGENETIC MODIFICATIONS, LIKE NON-CODING RNAS, AS WELL AS ENVIRONMENTAL FACTORS, HAVE BEEN INVESTIGATED OVER THE LAST FEW YEARS. BUT THE FUNDAMENTAL ETIOLOGY OF AS REMAINS ELUSIVE TO DATE. THE EVIDENCE SUMMARIZED HERE INDICATES THAT IN THE IMMUNOPATHOGENESIS OF AS, MICRORNAS AND THE GUT MICROBIOME PERFORM CRITICAL FUNCTIONS. WE DISCUSS SIGNIFICANT ADVANCES IN THE IMMUNOLOGICAL MECHANISMS UNDERLYING AS AND ADDRESS POTENTIAL CROSS-TALK BETWEEN THE GUT MICROBIOME AND HOST MICRORNAS. THIS CRITICAL INTERACTION IMPLICATES A CO-EVOLUTIONARY SYMBIOTIC LINK BETWEEN HOST IMMUNITY AND THE GUT MICROBIOME. 2021