1  455 162 APPLICATIONS OF YOGA IN ORAL ONCOLOGY: A SYSTEMATIC SCOPING REVIEW. BACKGROUND AND AIMS: YOGA IS WELL-THOUGHT-OUT AS AN ALL-INCLUSIVE APPROACH GLOBALLY AND CAN BE ADMINISTERED IN CLINICAL CARE AS AN INTEGRATIVE OR ALTERNATE APPROACH TO REGULAR TREATMENT. YOGA EXERCISE HAS BEEN DISCLOSED TO INFLUENCE REMISSION FROM CANCER CELLS OVER A LONG PERIOD OF TIME AND ALSO REVERSES EPIGENETIC ALTERATIONS. APPLICATIONS OF YOGA IN THE MANAGEMENT OF ORAL ONCOLOGY PATIENTS ARE SCARCE, HENCE THE NEED FOR A SCOPING REVIEW OF THE LITERATURE. HENCE, THIS STUDY AIMED TO CONDUCT A SCOPING REVIEW OF THE EXISTING EMPIRICAL EVIDENCE ON THE APPLICATIONS OF YOGA IN ORAL ONCOLOGY. METHODS: THE REVIEW METHODOLOGY WAS INFORMED BY JOANNA BRIGG'S INSTITUTE GUIDELINES FOR SYSTEMATIC SCOPING REVIEWS, AND THE REVIEW WAS REPORTED IN ACCORDANCE WITH THE PREFERRED REPORTING ITEMS FOR SYSTEMATIC REVIEWS AND META-ANALYSES EXTENSION FOR SCOPING REVIEWS. TEN DATABASES WERE SEARCHED. THE RECORDS OF ALL THE LITERATURE RETRIEVED FROM THE SEARCH WERE IMPORTED INTO THE RAYYAN SOFTWARE FOR DEDUPLICATION. AFTER THE FULL-TEXT SCREENING, ONLY TWO WERE FOUND ELIGIBLE FOR INCLUSION IN THE SCOPING REVIEW. DATA OBTAINED IN THE INCLUDED LITERATURE WERE EXTRACTED AND SYNTHESIZED. RESULTS: THIS REVIEW FOUND THAT YOGA WAS NOT SIGNIFICANTLY EFFECTIVE IN THE MANAGEMENT OF STRESS AMONG ORAL CANCER PATIENTS (P-VALUES > 0.04). HOWEVER, IT WAS FOUND THAT YOGA SIGNIFICANTLY REDUCED ANXIETY, SALIVA STICKINESS, AND EPISODES OF FALLING ILL (P-VALUES < 0.05) WHILE IT IMPROVED MENTAL WELL-BEING, COGNITIVE FUNCTIONING, EMOTIONAL FUNCTIONING, AND HEAD AND NECK PAIN OF THOSE ORAL CANCER PATIENTS THAT RECEIVED IT (P-VALUES < 0.05). CONCLUSION: AN INTEGRATIVE CARE APPROACH THAT CONSIDERS NONPHARMACEUTICAL TECHNIQUES SUCH AS YOGA COULD HELP TO REDUCE CARE COST WHILE IMPROVING CARE OUTCOMES AND QUALITY OF LIFE OF ORAL CANCER PATIENTS. HENCE, IT IS IMPERATIVE TO CONSIDER YOGA ALONG WITH ITS POTENTIAL BENEFITS, AND WE RECOMMEND GRADUAL INCORPORATION OF YOGA INTO ORAL CANCER CARE.	2023	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              
2 2108  45 EPIGENETIC FACTORS RELATED TO LOW BACK PAIN: A SYSTEMATIC REVIEW OF THE CURRENT LITERATURE. LOW BACK PAIN (LBP) IS ONE OF THE MOST COMMON CAUSES OF PAIN AND DISABILITY. AT PRESENT, TREATMENT AND INTERVENTIONS FOR ACUTE AND CHRONIC LOW BACK PAIN OFTEN FAIL TO PROVIDE SUFFICIENT LEVELS OF PAIN RELIEF, AND FULL FUNCTIONAL RESTORATION CAN BE CHALLENGING. CONSIDERING THE SIGNIFICANT SOCIO-ECONOMIC BURDEN AND RISK-TO-BENEFIT RATIO OF MEDICAL AND SURGICAL INTERVENTION IN LOW BACK PAIN PATIENTS, THE IDENTIFICATION OF RELIABLE BIOMARKERS SUCH AS EPIGENETIC FACTORS ASSOCIATED WITH LOW BACK PAIN COULD BE USEFUL IN CLINICAL PRACTICE. THE AIM OF THIS STUDY WAS TO REVIEW THE AVAILABLE LITERATURE REGARDING THE EPIGENETIC FACTORS ASSOCIATED WITH LOW BACK PAIN. THIS REVIEW WAS CARRIED OUT IN ACCORDANCE WITH PREFERENTIAL REPORTING ITEMS FOR SYSTEMATIC REVIEWS AND META-ANALYSES (PRISMA) GUIDELINES. THE SEARCH WAS CARRIED OUT IN OCTOBER 2022. ONLY PEER-REVIEWED ARTICLES WERE CONSIDERED FOR INCLUSION. FOURTEEN STUDIES WERE INCLUDED AND SHOWED PROMISING RESULTS IN TERMS OF RELIABLE MARKERS. EPIGENETIC MARKERS FOR LBP HAVE THE POTENTIAL TO SIGNIFICANTLY MODIFY DISEASE MANAGEMENT. MOST RECENT EVIDENCE SUGGESTS THAT EPIGENETICS IS A MORE PROMISING FIELD FOR THE IDENTIFICATION OF FACTORS ASSOCIATED WITH LBP, OFFERING A RATIONALE FOR FURTHER INVESTIGATION IN THIS FIELD WITH THE LONG-TERM GOAL OF FINDING EPIGENETIC BIOMARKERS THAT COULD CONSTITUTE BIOLOGICAL TARGETS FOR DISEASE MANAGEMENT AND TREATMENT.	2023	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       
3 2093  42 EPIGENETIC EFFECTS FOLLOWING ACUTE AND CHRONIC EXERCISE IN CARDIOVASCULAR DISEASE: A SYSTEMATIC REVIEW. INTRODUCTION: ACUTE EXERCISE AND EXERCISE TRAINING MAY CONFER EPIGENETIC MODIFICATIONS IN HEALTHY SUBJECTS. EPIGENETIC EFFECTS AFTER EXERCISE HAVE BEEN SHOWED IN PATIENTS WITH CARDIOVASCULAR DISEASE. THE AIM OF THIS SYSTEMATIC REVIEW WAS TO SUMMARIZE THE EVIDENCE FROM AVAILABLE CLINICAL TRIALS THAT STUDY EPIGENETIC ADAPTATIONS AFTER EXERCISE IN PATIENTS WITH CARDIOVASCULAR DISEASE. METHODS: THE SEARCH STRATEGY WAS PERFORMED IN PUBMED AND CENTRAL DATABASES ON ARTICLES PUBLISHED UNTIL SEPTEMBER 2020. STUDIES WITH TITLES AND ABSTRACTS RELEVANT TO EXERCISE EPIGENETIC MODIFICATION APPLIED TO CARDIOVASCULAR PATIENTS WERE FULLY EXAMINED. INCLUSION AND EXCLUSION CRITERIA WERE UTILIZED FOR STUDIES SCREENING. QUALITY ASSESSMENT WITH PEDRO SCALE AND EVALUATION BY TWO INDEPENDENT REVIEWERS WAS PERFORMED. RESULTS: OF THE 1714 ARTICLES RETRIEVED, 88 ARTICLES WERE ASSESSED FOR ELIGIBILITY CRITERIA AND 8 ARTICLES MATCHED OUR SEARCH CRITERIA AND FINALLY INCLUDED IN THE SYSTEMATIC ANALYSIS. THE ACUTE EXERCISE EPIGENETIC (MIRNAS) EFFECTS WERE ASSESSED IN THREE STUDIES AND THE CHRONIC EXERCISE TRAINING EFFECTS (MIRNAS AND DNA METHYLATION) IN SIX STUDIES. THE RESULTS HAVE SHOWN THAT THERE IS POSSIBLY AN ACUTE SIGNIFICANT EXERCISE EFFECT ON EPIGENETIC TARGETS WHICH IS MORE EVIDENT AFTER CHRONIC EXERCISE TRAINING. CONCLUSIONS: BY THE PRESENT SYSTEMATIC REVIEW, WE PROVIDE PRELIMINARY EVIDENCE OF BENEFICIAL EPIGENETIC ADAPTATIONS FOLLOWING ACUTE AND CHRONIC EXERCISE IN PATIENTS WITH CARDIOVASCULAR DISEASE. MORE CONTROLLED STUDIES ARE NEEDED TO CONFIRM SUCH EVIDENCE.	2021	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            
4 2510  42 EPIGENETICS AND POSTSURGICAL PAIN: A SCOPING REVIEW. OBJECTIVE: MULTIPLE FACTORS ARE INVOLVED IN THE PHYSIOLOGY AND VARIABILITY OF POSTSURGICAL PAIN, A GREAT PART OF WHICH CAN BE EXPLAINED BY GENETIC AND ENVIRONMENTAL FACTORS AND THEIR INTERACTION. EPIGENETICS REFERS TO THE MECHANISM BY WHICH THE ENVIRONMENT ALTERS THE STABILITY AND EXPRESSION OF GENES. WE CONDUCTED A SCOPING REVIEW TO EXAMINE THE AVAILABLE EVIDENCE IN BOTH ANIMAL MODELS AND CLINICAL STUDIES ON EPIGENETIC MECHANISMS INVOLVED IN THE REGULATION OF POSTSURGICAL AND CHRONIC POSTSURGICAL PAIN. METHODS: THE ARKSEY AND O'MALLEY FRAMEWORK AND THE PRISMA-SCR (PREFERRED REPORTING ITEMS FOR SYSTEMATIC REVIEW AND META-ANALYSIS, SCOPING REVIEWS EXTENSION) GUIDELINES WERE USED. THE PUBMED, WEB OF SCIENCE, AND GOOGLE SCHOLAR DATABASES WERE SEARCHED, AND THE ORIGINAL ARTICLES CITED IN REVIEWS LOCATED THROUGH THE SEARCH WERE ALSO REVIEWED. ENGLISH-LANGUAGE ARTICLES WITHOUT TIME LIMITS WERE RETRIEVED. ARTICLES WERE SELECTED IF THE ABSTRACT ADDRESSED INFORMATION ON THE EPIGENETIC OR EPIGENOMIC MECHANISMS, HISTONE, OR DNA METHYLATION AND MICRORIBONUCLEIC ACIDS INVOLVED IN POSTSURGICAL AND CHRONIC POSTSURGICAL PAIN IN ANIMAL MODELS AND CLINICAL STUDIES. RESULTS: THE INITIAL SEARCH PROVIDED 174 ARTICLES, AND 95 WERE USED. THE AVAILABLE STUDIES TO DATE, MOSTLY IN ANIMAL MODELS, HAVE SHOWN THAT EPIGENETICS CONTRIBUTES TO THE REGULATION OF GENE EXPRESSION IN THE PATHWAYS INVOLVED IN POSTSURGICAL PAIN AND IN MAINTAINING LONG-TERM PAIN. CONCLUSION: RESEARCH ON POSSIBLE EPIGENETIC MECHANISMS INVOLVED IN POSTSURGICAL PAIN AND CHRONIC POSTSURGICAL PAIN IN HUMANS IS SCARCE. IN VIEW OF THE EVIDENCE AVAILABLE IN ANIMAL MODELS, THERE IS A NEED TO EVALUATE EPIGENETIC PAIN MECHANISMS IN THE CONTEXT OF HUMAN AND CLINICAL STUDIES.	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     
5 6112  52 THE EPIGENETIC CLOCK AS A PREDICTOR OF DISEASE AND MORTALITY RISK: A SYSTEMATIC REVIEW AND META-ANALYSIS. BACKGROUND: AGEING IS ONE OF THE PRINCIPAL RISK FACTORS FOR MANY CHRONIC DISEASES. HOWEVER, THERE IS CONSIDERABLE BETWEEN-PERSON VARIATION IN THE RATE OF AGEING AND INDIVIDUAL DIFFERENCES IN THEIR SUSCEPTIBILITY TO DISEASE AND DEATH. EPIGENETIC MECHANISMS MAY PLAY A ROLE IN HUMAN AGEING, AND DNA METHYLATION AGE BIOMARKERS MAY BE GOOD PREDICTORS OF AGE-RELATED DISEASES AND MORTALITY RISK. THE AIMS OF THIS SYSTEMATIC REVIEW WERE TO IDENTIFY AND SYNTHESISE THE EVIDENCE FOR AN ASSOCIATION BETWEEN PERIPHERALLY MEASURED DNA METHYLATION AGE AND LONGEVITY, AGE-RELATED DISEASE, AND MORTALITY RISK. METHODS: A SYSTEMATIC SEARCH WAS CONDUCTED IN LINE WITH THE PREFERRED REPORTING ITEMS FOR SYSTEMATIC REVIEWS AND META-ANALYSES (PRISMA) GUIDELINES. USING RELEVANT SEARCH TERMS, MEDLINE, EMBASE, COCHRANE CENTRAL REGISTER OF CONTROLLED TRIALS, AND PSYCHINFO DATABASES WERE SEARCHED TO IDENTIFY ARTICLES MEETING THE INCLUSION CRITERIA. STUDIES WERE ASSESSED FOR BIAS USING JOANNA BRIGGS INSTITUTE CRITICAL APPRAISAL CHECKLISTS. DATA WAS EXTRACTED FROM STUDIES MEASURING AGE ACCELERATION AS A PREDICTOR OF AGE-RELATED DISEASES, MORTALITY OR LONGEVITY, AND THE FINDINGS FOR SIMILAR OUTCOMES COMPARED. USING REVIEW MANAGER 5.3 SOFTWARE, TWO META-ANALYSES (ONE PER EPIGENETIC CLOCK) WERE CONDUCTED ON STUDIES MEASURING ALL-CAUSE MORTALITY. RESULTS: TWENTY-THREE RELEVANT ARTICLES WERE IDENTIFIED, INCLUDING A TOTAL OF 41,607 PARTICIPANTS. FOUR STUDIES FOCUSED ON AGEING AND LONGEVITY, 11 ON AGE-RELATED DISEASE (CANCER, CARDIOVASCULAR DISEASE, AND DEMENTIA), AND 11 ON MORTALITY. THERE WAS SOME, ALTHOUGH INCONSISTENT, EVIDENCE FOR AN ASSOCIATION BETWEEN INCREASED DNA METHYLATION AGE AND RISK OF DISEASE. META-ANALYSES INDICATED THAT EACH 5-YEAR INCREASE IN DNA METHYLATION AGE WAS ASSOCIATED AN 8 TO 15% INCREASED RISK OF MORTALITY. CONCLUSION: DUE TO THE SMALL NUMBER OF STUDIES AND HETEROGENEITY IN STUDY DESIGN AND OUTCOMES, THE ASSOCIATION BETWEEN DNA METHYLATION AGE AND AGE-RELATED DISEASE AND LONGEVITY IS INCONCLUSIVE. INCREASED EPIGENETIC AGE WAS ASSOCIATED WITH MORTALITY RISK, BUT POSITIVE PUBLICATION BIAS NEEDS TO BE CONSIDERED. FURTHER RESEARCH IS NEEDED TO DETERMINE THE EXTENT TO WHICH DNA METHYLATION AGE CAN BE USED AS A CLINICAL BIOMARKER.	2019	
                                                                                                                                                                                                                                                                                                                                                                                                                                                
6 2213  52 EPIGENETIC MODIFICATIONS AS OUTCOMES OF EXERCISE INTERVENTIONS RELATED TO SPECIFIC METABOLIC ALTERATIONS: A SYSTEMATIC REVIEW. BACKGROUND: CHRONIC DISEASES ARISE AS A CONSEQUENCE OF AN UNHEALTHY LIFESTYLE PRIMARILY CHARACTERIZED BY PHYSICAL INACTIVITY AND UNBALANCED DIETS. REGULAR PHYSICAL ACTIVITY CAN IMPROVE HEALTH, AND THERE IS CONSISTENT EVIDENCE THAT THESE IMPROVEMENTS MAY BE THE RESULT OF EPIGENETIC MODIFICATIONS. OBJECTIVE: TO IDENTIFY EPIGENETIC MODIFICATIONSAS OUTCOMES OF EXERCISE INTERVENTIONS RELATED TO SPECIFIC METABOLIC ALTERATIONS. METHODS: THE PREFERRED REPORTING ITEMS FOR SYSTEMATIC REVIEWS AND META-ANALYSES PROTOCOLS (PRISMA-P) METHODOLOGY FOR MANUSCRIPT RESEARCH AND PREPARATION WAS FOLLOWED USING PUBMED AND EBSCO DATABASES FOR LITERATURE REVIEW. OUT OF 2,638 ARTICLES IDENTIFIED, ONLY 34 ARTICLES MET THE INCLUSION CRITERIA. RESULTS: THE SECTIONS OF THE REVIEW WERE ORGANIZED BY METABOLIC ALTERATIONS IN WHICH STUDIES WERE GROUPED ACCORDING TO HEALTHY, DISEASED, AND TRAINED INDIVIDUALS. RESISTANCE EXERCISE IN HUMANS INDUCED EPIGENETIC CHANGES IN PATHWAYS ASSOCIATED WITH ENERGY METABOLISM AND INSULIN SENSITIVITY, CONTRIBUTING TO HEALTHY SKELETAL MUSCLE. ENDURANCE EXERCISE ALSO CAUSED MODIFICATIONS IN BIOMARKERS ASSOCIATED TO METABOLIC ALTERATIONS THROUGH CHANGES IN DNA METHYLATION AND THE EXPRESSION OF SPECIFIC MIRNAS. HOWEVER, BOTH RESISTANCE AND ENDURANCE EXERCISE ARE NECESSARY TO OBTAIN A BETTER PHYSIOLOGICAL ADAPTATION AND A COMBINATION OF BOTH SEEMS TO BE NEEDED TO PROPERLY TACKLE THE INCREASING PREVALENCE OF NON-COMMUNICABLE PATHOLOGIES. CONCLUSION: GIVEN THE HETEROGENEITY AND COMPLEXITY OF THE EXISTING LITERATURE, IT IS CURRENTLY NOT POSSIBLE TO PROPOSE A SPECIFIC RECOMMENDATION ABOUT THE TYPE, INTENSITY, OR DURATION OF EXERCISE THAT COULD BE BENEFICIAL FOR DIFFERENT SUBSETS OF THE POPULATION (HEALTHY, DISEASED, AND/OR TRAINED). NEVERTHELESS, THIS REVIEW HIGHLIGHTS THE IMPORTANCE OF EXERCISE FOR HEALTH AND SHOWS THE NEED TO PERFORM MORE RESEARCH IN THIS EMERGING AREA TO IDENTIFY EPIGENETIC BIOMARKERS THAT COULD SERVE AS INDICATORS OF EXERCISE ADAPTATIONS.	2019	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    
7 6127  40 THE EPIGENETIC OVERLAP BETWEEN OBESITY AND MOOD DISORDERS: A SYSTEMATIC REVIEW. (1) BACKGROUND: OBESITY AND MOOD DISORDERS ARE CONSIDERED AS THE MOST PREVALENT MORBIDITIES IN MANY COUNTRIES. WE SUPPOSE THAT EPIGENETIC MECHANISMS MAY INDUCE HIGHER RATES OF OBESITY IN SUBJECTS WHO SUFFER FROM MOOD DISORDERS. IN THIS SYSTEMATIC REVIEW, WE FOCUSED ON THE POTENTIAL ROLES OF DNA METHYLATION ON MOOD DISORDERS AND OBESITY DEVELOPMENT. (2) METHODS: THIS SYSTEMATIC REVIEW WAS CONDUCTED IN ACCORDANCE WITH THE PRISMA STATEMENT AND REGISTERED IN PROSPERO. A SYSTEMATIC SEARCH WAS CONDUCTED IN MEDLINE, SCOPUS, WEB OF SCIENCE, COCHRANE CENTRAL DATABASE, EMBASE, AND CINHAL. WE ALSO CONDUCTED A GREY LITERATURE SEARCH, SUCH AS GOOGLE SCHOLAR. (3) RESULTS: AFTER DEDUPLICATION, WE IDENTIFIED 198 POTENTIALLY RELATED CITATIONS. FINALLY, TEN UNIQUE STUDIES MET OUR INCLUSION CRITERIA. WE HAVE FOUND THREE OVERLAP GENES THAT SHOW SIGNIFICANT DNA METHYLATION CHANGES, BOTH IN OBESITY AND DEPRESSION. PATHWAY ANALYSIS INTERACTION FOR TAPBP, BDNF, AND SORBS2 CONFIRMED THE RELATION OF THESE GENES IN BOTH OBESITY AND MOOD DISORDERS. (4) CONCLUSIONS: WHILE MECHANISMS LINKING BOTH OBESITY AND MOOD DISORDERS TO EPIGENETIC RESPONSE ARE STILL UNKNOWN, WE HAVE ALREADY KNOWN CHRONIC INFLAMMATION INDUCES A NOVEL EPIGENETIC PROGRAM. AS THE RESULTS OF GENE ENRICHMENT, PATHWAYS ANALYSIS SHOWED THAT TAPBP, BDNF, AND SORBS2 LINKED TOGETHER BY INFLAMMATORY PATHWAYS. HYPERMETHYLATION IN THESE GENES MIGHT PLAY A CRUCIAL RULE IN THE CO-OCCURRENCE OF OBESITY AND MOOD DISORDERS.	2020	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   
8 6524  44 TRANSCRIPTIONAL AND EPIGENETIC RESPONSE TO SEDENTARY BEHAVIOR AND PHYSICAL ACTIVITY IN CHILDREN AND ADOLESCENTS: A SYSTEMATIC REVIEW. BACKGROUND: THE LINKS OF SEDENTARY BEHAVIOR AND PHYSICAL ACTIVITY WITH HEALTH OUTCOMES IN CHILDREN AND ADOLESCENTS IS WELL KNOWN. HOWEVER, THE MOLECULAR MECHANISMS INVOLVED ARE POORLY UNDERSTOOD. WE AIMED TO SYNTHESIZE THE CURRENT KNOWLEDGE OF THE ASSOCIATION OF SEDENTARY BEHAVIOR AND PHYSICAL ACTIVITY (ACUTE AND CHRONIC EFFECTS) WITH GENE EXPRESSION AND EPIGENETIC MODIFICATIONS IN CHILDREN AND ADOLESCENTS. METHODS: PUBMED, WEB OF SCIENCE, AND SCOPUS DATABASES WERE SYSTEMATICALLY SEARCHED UNTIL APRIL 2022. A TOTAL OF 15 ARTICLES WERE ELIGIBLE FOR THIS REVIEW. THE RISK OF BIAS ASSESSMENT WAS PERFORMED USING THE JOANNA BRIGGS INSTITUTE CRITICAL APPRAISAL TOOL FOR SYSTEMATIC REVIEWS AND/OR A MODIFIED VERSION OF THE DOWNS AND BLACK CHECKLIST. RESULTS: THIRTEEN STUDIES USED CANDIDATE GENE APPROACH, WHILE ONLY 2 STUDIES PERFORMED HIGH-THROUGHPUT ANALYSES. THE CANDIDATE GENES SIGNIFICANTLY LINKED TO SEDENTARY BEHAVIOR OR PHYSICAL ACTIVITY WERE: FOXP3, HSD11B2, IL-10, TNF-ALPHA, ADRB2, VEGF, HSP70, SOX, AND GPX. NON-CODING RIBONUCLEIC ACIDS (RNAS) REGULATED BY SEDENTARY BEHAVIOR OR PHYSICAL ACTIVITY WERE: MIRNA-222, MIRNA-146(A), MIRNA-16, MIRNA-126, MIR-320(A), AND LONG NON-CODING RNA MALAT1. THESE MOLECULES ARE INVOLVED IN INFLAMMATION, IMMUNE FUNCTION, ANGIOGENIC PROCESS, AND CARDIOVASCULAR DISEASE. TRANSCRIPTOMICS ANALYSES DETECTED THOUSANDS OF GENES THAT WERE ALTERED FOLLOWING AN ACUTE BOUT OF PHYSICAL ACTIVITY AND ARE LINKED TO GENE PATHWAYS RELATED TO IMMUNE FUNCTION, APOPTOSIS, AND METABOLIC DISEASES. CONCLUSION: THE EVIDENCE FOUND TO DATE IS RATHER LIMITED. MULTIDISCIPLINARY STUDIES ARE ESSENTIAL TO CHARACTERIZE THE MOLECULAR MECHANISMS IN RESPONSE TO SEDENTARY BEHAVIOR AND PHYSICAL ACTIVITY IN THE PEDIATRIC POPULATION. LARGER COHORTS AND RANDOMIZED CONTROLLED TRIALS, IN COMBINATION WITH MULTI-OMICS ANALYSES, MAY PROVIDE THE NECESSARY DATA TO BRING THE FIELD FORWARD. SYSTEMATIC REVIEW REGISTRATION: [WWW.CLINICALTRIALS.GOV], IDENTIFIER [CRD42021235431].	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          
9 1045  36 CLINICAL CORRELATION AMONG MALE INFERTILITY AND OVERALL MALE HEALTH: A SYSTEMATIC REVIEW OF THE LITERATURE. PURPOSE: ONGOING EVIDENCE HAS SUGGESTED THE ROLE OF MALE FACTOR INFERTILITY AS A POTENTIAL PREDICTOR OF MORTALITY AND GENERAL HEALTH STATUS. THE AIM OF THE PRESENT REVIEW IS TO UPDATE THE CURRENT KNOWLEDGE BASE REGARDING THE ASSOCIATION BETWEEN MALE FACTOR INFERTILITY AND GENERAL HEALTH THROUGH A CRITICAL REVIEW OF THE LITERATURE. MATERIALS AND METHODS: A SYSTEMATIC REVIEW OF THE LITERATURE WAS CARRIED OUT FROM INCEPTION TO NOVEMBER 2019 IN ORDER TO EVALUATE SIGNIFICANT ASSOCIATIONS BETWEEN MALE INFERTILITY AND ADVERSE HEALTH OUTCOMES SUCH AS CARDIOVASCULAR, ONCOLOGIC, METABOLIC AND AUTOIMMUNE DISEASES AS WELL AS OVERALL MORTALITY. RESULTS: IN ALL, 27 STUDIES MET INCLUSION CRITERIA AND WERE CRITICALLY EXAMINED. FIVE STUDIES EXAMINED MALE INFERTILITY AND CARDIOVASCULAR DISEASE RISK, 11 EXAMINED ONCOLOGIC RISK (E.G., OVERALL CANCER RISK, TESTIS AND PROSTATE CANCER), 8 EXAMINED AGGREGATE CHRONIC MEDICAL DISEASES AND 5 INFERTILITY RELATED TO INCIDENCE OF MORTALITY, FOR A TOTAL OF 599,807 MEN DIAGNOSED WITH ANY MALE FACTOR INFERTILITY COVERING A PERIOD FROM 1916 TO 2016. CONCLUSIONS: A MAN'S FERTILITY AND OVERALL HEALTH APPEAR TO BE INTERCONNECTED. THEREFORE, A DIAGNOSIS OF MALE INFERTILITY MAY ALLOW A WINDOW INTO FUTURE COMORBIDITY AND/OR MORTALITY WHICH MAY HELP GUIDE CLINICAL DECISIONS AND COUNSELING. SEVERAL POSSIBLE ETIOLOGIES SUCH AS GENETIC, EPIGENETIC, DEVELOPMENTAL, AND LIFESTYLE-BASED FACTORS NEED TO BE FURTHER EVALUATED IN ORDER TO ESTABLISH THE UNDERLYING MECHANISMS BETWEEN MALE INFERTILITY AND HEALTH.	2020	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         
10  367  32 AMPLIFIED PAIN SYNDROMES IN CHILDREN: TREATMENT AND NEW INSIGHTS INTO DISEASE PATHOGENESIS. PURPOSE OF REVIEW: ALTHOUGH MANY DIAGNOSTIC TERMS ARE USED FOR PEDIATRIC CHRONIC PAIN, EVIDENCE SUGGESTS A COMMON THREAD OF SIGNAL AMPLIFICATION, LEADING TO THE UNIFYING TERM 'AMPLIFIED PAIN SYNDROMES'. ONGOING RESEARCH PROVIDES NEW INSIGHTS INTO BIOPSYCHOSOCIAL CONTRIBUTORS AND TREATMENTS FOR PEDIATRIC AMPLIFIED PAIN SYNDROMES. RECENT FINDINGS: BASIC SCIENCE INDICATES A COMPLEX INTERPLAY OF GENETIC, EPIGENETIC, NEUROCHEMICAL, ENDOCRINE, AND INFLAMMATORY CONTRIBUTORS, ALONG WITH ENVIRONMENTAL AND PSYCHOLOGICAL FACTORS. ALTHOUGH MEDICATIONS AND INTERVENTIONS REMAIN COMMON APPROACHES TO CHILDREN WITH CHRONIC PAIN, THEIR EVIDENCE IS LIMITED. PRELIMINARY EVIDENCE EXISTS FOR MINDFULNESS-BASED THERAPIES, YOGA, AND OTHER COMPLEMENTARY/ALTERNATIVE MEDICINE APPROACHES. THE STRONGEST EVIDENCE IS FOR EXERCISE-BASED AND COGNITIVE-BEHAVIORAL TREATMENTS, IN PARTICULAR, WHEN COMBINED IN A MULTIDISCIPLINARY FORMAT. INTENSIVE APPROACHES (PAIN REHABILITATION) HAVE THE POTENTIAL TO EFFECTIVELY AND EFFICIENTLY TREAT THOSE MOST DISABLED BY AMPLIFIED PAIN SYNDROMES, AND LEAD TO SUSTAINED IMPROVEMENT IN PAIN, FUNCTIONING, AND MEDICAL UTILIZATION. SUMMARY: ALTHOUGH UNDERSTANDING OF THE MECHANISMS UNDERLYING PEDIATRIC AMPLIFIED PAIN SYNDROMES EVOLVES, STANDARD OF CARE IS MULTIDISCIPLINARY EMPHASIZING EXERCISE THERAPY, COGNITIVE-BEHAVIORAL TREATMENT, AND SELF-REGULATION. TREATMENT SHOULD TARGET FULL RETURN TO PHYSICAL FUNCTION, WHICH LEADS TO SUBSEQUENT IMPROVEMENT OR RESOLUTION OF PAIN. MULTIDISCIPLINARY CARE CAN BE COORDINATED BY A RHEUMATOLOGIST OR OTHER PHYSICIAN WITH APPROPRIATE REFERRALS, OR THROUGH A MULTIDISCIPLINARY TEAM.	2014	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      
11 1517  38 DNA METHYLATION AS A MEDIATOR OF ASSOCIATIONS BETWEEN THE ENVIRONMENT AND CHRONIC DISEASES: A SCOPING REVIEW ON APPLICATION OF MEDIATION ANALYSIS. DNA METHYLATION (DNAM) IS ONE OF THE MOST STUDIED EPIGENETIC MODIFICATIONS. DNAM HAS EMERGED AS A KEY BIOLOGICAL MECHANISM AND BIOMARKERS TO TEST ASSOCIATIONS BETWEEN ENVIRONMENTAL EXPOSURE AND OUTCOMES IN EPIDEMIOLOGICAL STUDIES. ALTHOUGH PREVIOUS STUDIES HAVE FOCUSED ON ASSOCIATIONS BETWEEN DNAM AND EITHER EXPOSURE/OUTCOMES, IT IS USEFUL TO TEST FOR MEDIATION OF THE ASSOCIATION BETWEEN EXPOSURE AND OUTCOME BY DNAM. THE PURPOSE OF THIS SCOPING REVIEW IS TO INTRODUCE THE METHODOLOGICAL ESSENCE OF STATISTICAL MEDIATION ANALYSIS AND TO EXAMINE EMERGING EPIDEMIOLOGICAL RESEARCH APPLYING MEDIATION ANALYSES. WE CONDUCTED THIS SCOPING REVIEW FOR PUBLISHED PEER-REVIEWED JOURNALS ON THIS TOPIC USING ONLINE DATABASES (PUBMED, SCOPUS, COCHRANE, AND CINAHL) ENDING IN DECEMBER 2020. WE EXTRACTED A TOTAL OF 219 ARTICLES BY INITIAL SCREENING. AFTER REVIEWING TITLES, ABSTRACTS, AND FULL TEXTS, A TOTAL OF 69 ARTICLES WERE ELIGIBLE FOR THIS REVIEW. THE BREAKDOWN OF STUDIES ASSIGNED TO EACH CATEGORY WAS 13 FOR SMOKING (18.8%), 8 FOR DIETARY INTAKE AND FAMINE (11.6%), 6 FOR OTHER LIFESTYLE FACTORS (8.7%), 8 FOR CLINICAL ENDPOINTS (11.6%), 22 FOR ENVIRONMENTAL CHEMICAL EXPOSURES (31.9%), 2 FOR SOCIOECONOMIC STATUS (SES) (2.9%), AND 10 FOR GENETIC FACTORS AND RACE (14.5%). IN THIS REVIEW, WE PROVIDE AN EXPOSURE-WIDE SUMMARY FOR THE MEDIATION ANALYSIS USING DNAM LEVELS. HOWEVER, WE FOUND HETEROGENOUS METHODS AND INTERPRETATIONS IN MEDIATION ANALYSIS WITH TYPICAL ISSUES SUCH AS DIFFERENT CELL COMPOSITIONS AND TISSUE-SPECIFICITY. FURTHER ACCUMULATION OF EVIDENCE WITH DIVERSE EXPOSURES, POPULATIONS AND WITH RIGOROUS METHODOLOGY WILL BE EXPECTED TO PROVIDE FURTHER INSIGHT IN THE ROLE OF DNAM IN DISEASE SUSCEPTIBILITY.	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      
12 4865  34 ORO-FACIAL PAIN AND TEMPOROMANDIBULAR DISORDERS CLASSIFICATION SYSTEMS: A CRITICAL APPRAISAL AND FUTURE DIRECTIONS. IT IS A DIFFICULT UNDERTAKING TO DESIGN A CLASSIFICATION SYSTEM FOR ANY DISEASE ENTITY, LET ALONE FOR ORO-FACIAL PAIN (OFP) AND MORE SPECIFICALLY FOR TEMPOROMANDIBULAR DISORDERS (TMD). A FURTHER COMPLICATION OF THIS TASK IS THAT BOTH PHYSICAL AND PSYCHOSOCIAL VARIABLES MUST BE INCLUDED. TO AUGMENT THIS PROCESS, A TWO-STEP SYSTEMATIC REVIEW, ADHERING TO PRISMA GUIDELINES, OF THE CLASSIFICATION SYSTEMS PUBLISHED DURING THE LAST 20 YEARS FOR OFP AND TMD WAS PERFORMED. THE FIRST SEARCH STEP IDENTIFIED 190 POTENTIAL CITATIONS WHICH ULTIMATELY RESULTED IN ONLY 17 ARTICLES BEING INCLUDED FOR IN-DEPTH ANALYSIS AND REVIEW. THE SECOND STEP RESULTED IN ONLY 5 ARTICLES BEING SELECTED FOR INCLUSION IN THIS REVIEW. FIVE ADDITIONAL ARTICLES AND FOUR CLASSIFICATION GUIDELINES/CRITERIA WERE ALSO INCLUDED DUE TO EXPANSION OF THE SEARCH CRITERIA. THUS, IN TOTAL, 14 DOCUMENTS COMPRISING ARTICLES AND GUIDELINES/CRITERIA (8 PROPOSALS OF CLASSIFICATION SYSTEMS FOR OFP; 6 FOR TMD) WERE SELECTED FOR INCLUSION IN THE SYSTEMATIC REVIEW. FOR EACH, A DISCUSSION AS TO THEIR ADVANTAGES, STRENGTHS AND LIMITATIONS WAS PROVIDED. SUGGESTIONS REGARDING THE FUTURE DIRECTION FOR IMPROVING THE CLASSIFICATION PROCESS WITH THE USE OF ONTOLOGICAL PRINCIPLES RATHER THAN TAXONOMY ARE DISCUSSED. FURTHERMORE, THE POTENTIAL FOR EXPANDING THE SCOPE OF AXES INCLUDED IN EXISTING CLASSIFICATION SYSTEMS, TO INCLUDE GENETIC, EPIGENETIC AND NEUROBIOLOGICAL VARIABLES, IS EXPLORED. IT IS THEREFORE RECOMMENDED THAT FUTURE CLASSIFICATION SYSTEM PROPOSALS BE BASED ON COMBINED APPROACHES AIMING TO PROVIDE ARCHETYPAL TREATMENT-ORIENTED CLASSIFICATIONS.	2018	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           
13 6159  43 THE GENETICS AND EPIGENETICS OF FATIGUE. FATIGUE IS A COMMON SYMPTOM AND INCLUDES BOTH PHYSICAL AND MENTAL COMPONENTS. IT CAN BE ASSOCIATED WITH A VARIETY OF DIFFERENT SYNDROMES AND DISEASES, BUT IN MANY CASES IS NOT ASSOCIATED WITH OTHER COMORBID CONDITIONS. MOST HUMANS HAVE EXPERIENCED ACUTE FATIGUE IN RELATION TO DIFFERENT STRESSORS. ACUTE FATIGUE TYPICALLY DECREASES AS THE EFFECT OF THE TRIGGERING FACTOR IS REDUCED AND A NORMAL HOMEOSTATIC BALANCE IS RESTORED. FATIGUE THAT PERSISTS FOR 6 MONTHS OR MORE IS TERMED CHRONIC FATIGUE. CHRONIC FATIGUE (CF) IN COMBINATION WITH A MINIMUM OF 4 OF 8 SYMPTOMS AND THE ABSENCE OF DISEASES THAT COULD EXPLAIN THESE SYMPTOMS, CONSTITUTE THE CASE DEFINITION FOR CHRONIC FATIGUE SYNDROME. IN SPITE OF ITS PREVALENCE, THE BIOLOGY OF FATIGUE IS RELATIVELY POORLY UNDERSTOOD AND BIOLOGICAL MARKERS HAVE NOT YET BEEN IDENTIFIED. THIS LITERATURE SEARCH WAS PERFORMED IN PUBMED TO IDENTIFY RESEARCH ON THE GENETICS AND EPIGENETICS OF FATIGUE. PUBLICATIONS WERE INCLUDED IF FATIGUE WAS A MAJOR TOPIC AND THE TOPIC WAS COMBINED WITH GENETIC AND/OR EPIGENETIC MEASUREMENTS IN ADULT HUMANS. A TOTAL OF 40 PUBLICATIONS WERE IDENTIFIED. ALTHOUGH ALTERED FUNCTIONING IN THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS, THE SEROTONERGIC SYSTEM, AND ASSOCIATIONS WITH INFECTIOUS AGENTS HAVE BEEN IDENTIFIED, THE SEARCH FOR GENETIC OR EPIGENETIC MARKERS OF FATIGUE, EITHER IN THE CONTEXT OF CF OR CHRONIC FATIGUE SYNDROME (CFS) HAS BEEN RELATIVELY UNPRODUCTIVE OR, IN THE CASE OF EPIGENETICS, NONEXISTENT. ALTHOUGH SEVERAL STUDIES, BOTH HYPOTHESIS-TESTING AND HYPOTHESIS-GENERATING, HAVE BEEN PERFORMED TO SEARCH FOR BIOMARKERS, THEY HAVE MOSTLY BEEN UNDERPOWERED, RESTRICTED BY THE HETEROGENEITY OF THE PHENOTYPE, OR LIMITED BY AN UNSYSTEMATIC STUDY DESIGN. TO BE ABLE TO CONFIRM THE HYPOTHESIS THAT RISK FOR, OR LEVELS OF, FATIGUE ARE INFLUENCED BY THE GENETIC OR EPIGENETIC BACKGROUND OF AN INDIVIDUAL, STUDIES NEED TO BE BASED ON LARGER SAMPLE SIZES WITH A MORE CLEARLY DEFINED PHENOTYPE. STUDIES NEED TO FOCUS NOT ONLY ON THE INFLUENCE OF A SINGLE ASPECT SUCH AS SINGLE NUCLEOTIDE POLYMORPHISMS (SNPS) OR DIFFERENTIAL GENE EXPRESSION ON DISEASE RISK OR STATE, BUT ALSO ON THE SYSTEMS BIOLOGY BEHIND THE DISEASE IN COMBINATION WITH INFORMATION ON ENVIRONMENTAL INFLUENCES AND VALIDATION OF FINDINGS IN FUNCTIONAL STUDIES.	2010	
                                                                                                                                                                                                                                                                                                                                                                                                                                                         
14  456  41 APPLYING A LIFE COURSE BIOLOGICAL AGE FRAMEWORK TO IMPROVING THE CARE OF INDIVIDUALS WITH ADULT CANCERS: REVIEW AND RESEARCH RECOMMENDATIONS. IMPORTANCE: THE PRACTICE OF ONCOLOGY WILL INCREASINGLY INVOLVE THE CARE OF A GROWING POPULATION OF INDIVIDUALS WITH MIDLIFE AND LATE-LIFE CANCERS. MANAGING CANCER IN THESE INDIVIDUALS IS COMPLEX, BASED ON DIFFERENCES IN BIOLOGICAL AGE AT DIAGNOSIS. BIOLOGICAL AGE IS A MEASURE OF ACCUMULATED LIFE COURSE DAMAGE TO BIOLOGICAL SYSTEMS, LOSS OF RESERVE, AND VULNERABILITY TO FUNCTIONAL DETERIORATION AND DEATH. BIOLOGICAL AGE IS IMPORTANT BECAUSE IT AFFECTS THE ABILITY TO MANAGE THE RIGORS OF CANCER THERAPY, SURVIVORS' FUNCTION, AND CANCER PROGRESSION. HOWEVER, BIOLOGICAL AGE IS NOT ALWAYS CLINICALLY APPARENT. THIS REVIEW PRESENTS A CONCEPTUAL FRAMEWORK OF LIFE COURSE BIOLOGICAL AGING, SUMMARIZES CANDIDATE MEASURES, AND DESCRIBES A RESEARCH AGENDA TO FACILITATE CLINICAL TRANSLATION TO ONCOLOGY PRACTICE. OBSERVATIONS: MIDLIFE AND LATE-LIFE CANCERS ARE CHRONIC DISEASES THAT MAY ARISE FROM CUMULATIVE PATTERNS OF BIOLOGICAL AGING OCCURRING OVER THE LIFE COURSE. BEFORE DIAGNOSIS, EACH NEW PATIENT WAS ON A DISTINCT COURSE OF BIOLOGICAL AGING RELATED TO PAST EXPOSURES, LIFE EXPERIENCES, GENETICS, AND NONCANCER CHRONIC DISEASE. CANCER AND ITS TREATMENTS MAY ALSO BE ASSOCIATED WITH BIOLOGICAL AGING. SEVERAL MEASURES OF BIOLOGICAL AGE, INCLUDING P16INK4A, EPIGENETIC AGE, TELOMERE LENGTH, AND INFLAMMATORY AND BODY COMPOSITION MARKERS, HAVE BEEN USED IN ONCOLOGY RESEARCH. ONE OR MORE OF THESE MEASURES MAY BE USEFUL IN CANCER CARE, EITHER ALONE OR IN COMBINATION WITH CLINICAL HISTORY AND GERIATRIC ASSESSMENTS. HOWEVER, FURTHER RESEARCH WILL BE NEEDED BEFORE BIOLOGICAL AGE ASSESSMENT CAN BE RECOMMENDED IN ROUTINE PRACTICE, INCLUDING DETERMINATION OF SITUATIONS IN WHICH KNOWLEDGE ABOUT BIOLOGICAL AGE WOULD CHANGE TREATMENT, ASCERTAINING WHETHER TREATMENT EFFECTS ON BIOLOGICAL AGING ARE SHORT-LIVED OR PERSISTENT, AND TESTING INTERVENTIONS TO MODIFY BIOLOGICAL AGE, DECREASE TREATMENT TOXIC EFFECTS, AND MAINTAIN FUNCTIONAL ABILITIES. CONCLUSIONS AND RELEVANCE: UNDERSTANDING DIFFERENCES IN BIOLOGICAL AGING COULD ULTIMATELY ALLOW CLINICIANS TO BETTER PERSONALIZE TREATMENT AND SUPPORTIVE CARE, DEVELOP TAILORED SURVIVORSHIP CARE PLANS, AND PRESCRIBE PREVENTIVE OR AMELIORATIVE THERAPIES AND BEHAVIORS INFORMED BY AGING MECHANISMS.	2021	
                                                                                                                                                                                                                                                                                                                                                                                                                     
15 6316  39 THE RELEVANCE OF DNA METHYLATION AND HISTONE MODIFICATION IN PERIODONTITIS: A SCOPING REVIEW. BACKGROUND: PERIODONTITIS IS A CHRONIC INFLAMMATORY DISEASE INVOLVING AN INTERPLAY BETWEEN BACTERIA, INFLAMMATION, HOST RESPONSE GENES, AND ENVIRONMENTAL FACTORS. THE MANIFESTATION OF EPIGENETIC FACTORS DURING PERIODONTITIS PATHOGENESIS AND PERIODONTAL INFLAMMATION IS STILL NOT WELL UNDERSTOOD, WITH LIMITED REVIEWS ON HISTONE MODIFICATION WITH PERIODONTITIS MANAGEMENT. THIS SCOPING REVIEW AIMS TO EVALUATE CURRENT EVIDENCE OF GLOBAL AND SPECIFIC DNA METHYLATION AND HISTONE MODIFICATION IN PERIODONTITIS AND DISCUSS THE GAPS AND IMPLICATIONS FOR FUTURE RESEARCH AND CLINICAL PRACTICE. METHODS: A SCOPING LITERATURE SEARCH OF THREE ELECTRONIC DATABASES WAS PERFORMED IN SCOPUS, MEDLINE (PUBMED) AND EMBASE. AS EPIGENETICS IN PERIODONTITIS IS AN EMERGING RESEARCH FIELD, A SCOPING REVIEW WAS CONDUCTED TO IDENTIFY THE EXTENT OF STUDIES AVAILABLE AND DESCRIBE THE OVERALL CONTEXT AND APPLICABILITY OF THESE RESULTS. RESULTS: OVERALL, 30 STUDIES WERE EVALUATED, AND THE FINDINGS CONFIRMED THAT EPIGENETIC CHANGES IN PERIODONTITIS COMPRISE SPECIFIC MODIFICATIONS TO DNA METHYLATION PATTERNS AND HISTONE PROTEINS MODIFICATION, WHICH CAN EITHER DAMPEN OR PROMOTE THE INFLAMMATORY RESPONSE TO BACTERIAL CHALLENGE. CONCLUSIONS: THE PLASTICITY OF EPIGENETIC MODIFICATIONS HAS IMPLICATIONS FOR THE FUTURE DEVELOPMENT OF TARGETED EPI-DRUGS AND DIAGNOSTIC TOOLS IN PERIODONTITIS. SUCH ADVANCES COULD BE INVALUABLE FOR THE EARLY DETECTION AND MONITORING OF SUSCEPTIBLE INDIVIDUALS.	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      
16  247  36 ADULTHOOD ASTHMA AS A CONSEQUENCE OF CHILDHOOD ADVERSITY: A SYSTEMATIC REVIEW OF EPIGENETICALLY AFFECTED GENES. THERE IS AN ACCUMULATING DATA THAT SHOWS RELATION BETWEEN CHILDHOOD ADVERSITY AND VULNERABILITY TO CHRONIC DISEASES AS WELL AS EPIGENETIC INFLUENCES THAT IN TURN GIVE RISE TO THESE DISEASES. ASTHMA IS ONE OF THE CHRONIC DISEASES THAT IS INFLUENCED FROM GENETIC REGULATION OF THE INFLAMMATORY BIOMOLECULES AND THEREFORE THE HYPOTHESIS IN THIS RESEARCH WAS CHILDHOOD ADVERSITY MIGHT HAVE CAUSED EPIGENETIC DIFFERENTIATION IN THE ASTHMA-RELATED GENES IN THE POPULATION WHO HAD CHILDHOOD TRAUMA. TO TEST THIS HYPOTHESIS, THE LITERATURE WAS SYSTEMATICALLY REVIEWED TO EXTRACT EPIGENETICALLY MODIFIED GENE DATA OF THE ADULTS WHO HAD CHILDHOOD ADVERSITY, AND AFFECTED GENES WERE FURTHER EVALUATED FOR THEIR ASSOCIATION WITH ASTHMA. PRISMA GUIDELINES WERE ADOPTED AND PUBMED AND GOOGLE SCHOLAR WERE INCLUDED IN THE SEARCHED DATABASES, TO EVALUATE EPIGENETIC MODIFICATIONS IN ASTHMA-RELATED GENES OF PHYSICALLY, EMOTIONALLY OR SEXUALLY ABUSED CHILDREN. AFTER RETRIEVING A TOTAL OF 5245 ARTICLES, 36 OF THEM WERE INCLUDED IN THE STUDY. SEVERAL GENES AND PATHWAYS THAT MAY CONTRIBUTE TO PATHOGENESIS OF ASTHMA DEVELOPMENT, INCREASED INFLAMMATION, OR RESPONSE TO ASTHMA TREATMENT WERE FOUND EPIGENETICALLY AFFECTED BY CHILDHOOD TRAUMAS. CHILDHOOD ADVERSITY, CAUSING EPIGENETIC CHANGES IN DNA, MAY LEAD TO ASTHMA DEVELOPMENT OR INFLUENCE THE COURSE OF THE DISEASE AND THEREFORE SHOULD BE TAKEN INTO ACCOUNT FOR THE PROLONGED HEALTH CONSEQUENCES.	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          
17 4926  43 PARKINSON'S DISEASE AND SARS-COV-2 INFECTION: PARTICULARITIES OF MOLECULAR AND CELLULAR MECHANISMS REGARDING PATHOGENESIS AND TREATMENT. ACCUMULATING DATA SUGGEST THAT CHRONIC NEUROINFLAMMATION-MEDIATED NEURODEGENERATION IS A SIGNIFICANT CONTRIBUTING FACTOR FOR PROGRESSIVE NEURONAL AND GLIAL CELL DEATH IN AGE-RELATED NEURODEGENERATIVE PATHOLOGY. FURTHERMORE, IT COULD BE ENCOUNTERED AS LONG-TERM CONSEQUENCES IN SOME VIRAL INFECTIONS, INCLUDING POST-COVID-19 PARKINSONISM-RELATED CHRONIC SEQUELAE. THE CURRENT SYSTEMATIC REVIEW IS FOCUSED ON A RECENT QUESTION AROUSED DURING THE PANDEMIC'S SUCCESSIVE WAVES: ARE THERE POST-SARS-COV-2 IMMUNE-MEDIATED REACTIONS RESPONSIBLE FOR PROMOTING NEURODEGENERATION? DOES THE HOST'S DYSREGULATED IMMUNE COUNTER-OFFENSIVE CONTRIBUTE TO THE PATHOGENESIS OF NEURODEGENERATIVE DISEASES, EMERGING AS PARKINSON'S DISEASE, IN A COMPLEX INTERRELATION BETWEEN GENETIC AND EPIGENETIC RISK FACTORS? A SYNTHETIC AND SYSTEMATIC LITERATURE REVIEW WAS ACCOMPLISHED BASED ON THE "PREFERRED REPORTING ITEMS FOR SYSTEMATIC PRINCIPLES REVIEWS AND META-ANALYSES" (PRISMA) METHODOLOGY, INCLUDING REGISTRATION ON THE SPECIFIC ONLINE PLATFORM: INTERNATIONAL PROSPECTIVE REGISTER OF SYSTEMATIC REVIEWS-PROSPERO, NO. 312183. INITIALLY, 1894 ARTICLES WERE DETECTED. AFTER FULFILLING THE FIVE STEPS OF THE SELECTION METHODOLOGY, 104 PAPERS WERE SELECTED FOR THIS SYNTHETIC REVIEW. DOCUMENTATION WAS ENHANCED WITH A SUPPLEMENTARY 47 BIBLIOGRAPHIC RESOURCES IDENTIFIED IN THE LITERATURE WITHIN A NON-STANDARDIZED SEARCH CONNECTED TO THE SUBJECT. AS A FINAL STEP OF THE PRISMA METHOD, WE HAVE FULFILLED A POPULATION-INTERVENTION-COMPARISON-OUTCOME-TIME (PICOT)/POPULATION-INTERVENTION-COMPARISON-OUTCOME-STUDY TYPE (PICOS)-BASED METANALYSIS OF CLINICAL TRIALS IDENTIFIED AS CONNECTED TO OUR SEARCH, TARGETING THE OUTCOMES OF REHABILITATIVE KINESITHERAPEUTIC INTERVENTIONS COMPARED TO CLINICAL APPROACHES LACKING SUCH KIND OF TREATMENT. ACCORDINGLY, WE IDENTIFIED 10 CLINICAL TRIALS RELATED TO OUR ARTICLE. THE MULTI/INTERDISCIPLINARY CONVENTIONAL THERAPY OF PARKINSON'S DISEASE AND NON-CONVENTIONAL MULTITARGET APPROACH TO AN INTEGRATIVE TREATMENT WAS BRIEFLY ANALYZED. THIS ARTICLE SYNTHESIZES THE CURRENT FINDINGS ON THE PATHOGENIC INTERFERENCE BETWEEN THE DYSREGULATED COMPLEX MECHANISMS INVOLVED IN AGING, NEUROINFLAMMATION, AND NEURODEGENERATION, FOCUSING ON PARKINSON'S DISEASE AND THE ACUTE AND CHRONIC REPERCUSSIONS OF COVID-19. TIME WILL TELL WHETHER COVID-19 NEUROINFLAMMATORY EVENTS COULD TRIGGER LONG-TERM NEURODEGENERATIVE EFFECTS AND CONTRIBUTE TO THE WORSENING AND/OR EXPLOSION OF NEW CASES OF PD. THE EXTENT OF THE INTERRELATED NEUROPATHOGENIC PHENOMENON REMAINS OBSCURE, SO FURTHER CLINICAL OBSERVATIONS AND PROSPECTIVE LONGITUDINAL COHORT STUDIES ARE NEEDED.	2022	

18 2715  33 EXERCISE-INDUCED BIOCHEMICAL CHANGES AND THEIR POTENTIAL INFLUENCE ON CANCER: A SCIENTIFIC REVIEW. AIM: TO REVIEW AND DISCUSS THE AVAILABLE INTERNATIONAL LITERATURE REGARDING THE INDIRECT AND DIRECT BIOCHEMICAL MECHANISMS THAT OCCUR AFTER EXERCISE, WHICH COULD POSITIVELY, OR NEGATIVELY, INFLUENCE ONCOGENIC PATHWAYS. METHODS: THE PUBMED, MEDLINE, EMBASE AND COCHRANE LIBRARIES WERE SEARCHED FOR PAPERS UP TO JULY 2016 ADDRESSING BIOCHEMICAL CHANGES AFTER EXERCISE WITH A PARTICULAR REFERENCE TO CANCER. THE THREE AUTHORS INDEPENDENTLY ASSESSED THEIR APPROPRIATENESS FOR INCLUSION IN THIS REVIEW BASED ON THEIR SCIENTIFIC QUALITY AND RELEVANCE. RESULTS: 168 PAPERS WERE SELECTED AND CATEGORISED INTO INDIRECT AND DIRECT BIOCHEMICAL PATHWAYS. THE INDIRECT EFFECTS INCLUDED CHANGES IN VITAMIN D, WEIGHT REDUCTION, SUNLIGHT EXPOSURE AND IMPROVED MOOD. THE DIRECT EFFECTS INCLUDED INSULIN-LIKE GROWTH FACTOR, EPIGENETIC EFFECTS ON GENE EXPRESSION AND DNA REPAIR, VASOACTIVE INTESTINAL PEPTIDE, OXIDATIVE STRESS AND ANTIOXIDANT PATHWAYS, HEAT SHOCK PROTEINS, TESTOSTERONE, IRISIN, IMMUNITY, CHRONIC INFLAMMATION AND PROSTAGLANDINS, ENERGY METABOLISM AND INSULIN RESISTANCE. SUMMARY: EXERCISE IS ONE OF SEVERAL LIFESTYLE FACTORS KNOWN TO LOWER THE RISK OF DEVELOPING CANCER AND IS ASSOCIATED WITH LOWER RELAPSE RATES AND BETTER SURVIVAL. THIS REVIEW HIGHLIGHTS THE NUMEROUS BIOCHEMICAL PROCESSES, WHICH EXPLAIN THESE POTENTIAL ANTICANCER BENEFITS.	2017	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 
19  844  37 CHILDHOOD ALLERGY DISEASE, EARLY DIAGNOSIS, AND THE POTENTIAL OF SALIVARY PROTEIN BIOMARKERS. ALLERGIC DISEASE HAS RISEN TO EPIDEMIC PROPORTIONS SINCE THE LAST DECADE AND IS AMONG THE MOST COMMON NONCOMMUNICABLE, CHRONIC DISEASES IN CHILDREN AND ADOLESCENTS WORLDWIDE. ALLERGIC DISEASE USUALLY OCCURS IN EARLY LIFE; THUS, EARLY BIOMARKERS OF ALLERGIC SUSCEPTIBILITY ARE REQUIRED FOR PREVENTIVE MEASURES TO HIGH-RISK INFANTS WHICH ENABLE EARLY INTERVENTIONS TO DECREASE ALLERGIC SEVERITY. HOWEVER, TO DATE, THERE IS NO RELIABLE GENERAL OR SPECIFIC ALLERGY PHENOTYPE DETECTION METHOD THAT IS EASY AND NONINVASIVE FOR CHILDREN. MOST REPORTED ALLERGIC PHENOTYPE DETECTION METHODS ARE INVASIVE, SUCH AS THE SKIN PRICK TEST (SPT), ORAL FOOD CHALLENGE (OFC), AND BLOOD TEST, AND MANY INVOLVE NOT READILY ACCESSIBLE BIOLOGICAL SAMPLES, SUCH AS CORD BLOOD (CB), MATERNAL BLOOD, OR NEWBORN VERNIX. SALIVA IS A BIOLOGICAL SAMPLE THAT HAS GREAT POTENTIAL AS A BIOMARKER MEASUREMENT AS IT CONSISTS OF AN ABUNDANCE OF BIOMARKERS, SUCH AS GENETIC MATERIAL AND PROTEINS. IT IS EASILY ACCESSIBLE, NONINVASIVE, COLLECTED VIA A PAINLESS PROCEDURE, AND AN EASY BEDSIDE SCREENING FOR REAL-TIME MEASUREMENT OF THE ONGOING HUMAN PHYSIOLOGICAL SYSTEM. ALL THESE ADVANTAGES EMPHASISE SALIVA AS A VERY PROMISING DIAGNOSTIC CANDIDATE FOR THE DETECTION AND MONITORING OF DISEASE BIOMARKERS, ESPECIALLY IN CHILDREN. FURTHERMORE, PROTEIN BIOMARKERS HAVE THE ADVANTAGES AS MODIFIABLE INFLUENCING FACTORS RATHER THAN GENETIC AND EPIGENETIC FACTORS THAT ARE MOSTLY NONMODIFIABLE FACTORS FOR ALLERGIC DISEASE SUSCEPTIBILITY IN CHILDHOOD. SALIVA HAS GREAT POTENTIAL TO REPLACE SERUM AS A BIOLOGICAL FLUID BIOMARKER IN DIAGNOSING CLINICAL ALLERGY. HOWEVER, TO DATE, SALIVA IS NOT CONSIDERED AS AN ESTABLISHED MEDICALLY ACCEPTABLE BIOMARKER. THIS REVIEW CONSIDERS WHETHER THE SALIVA COULD BE SUITABLE BIOLOGICAL SAMPLES FOR EARLY DETECTION OF ALLERGIC RISK. SUCH TOOLS MAY BE USED AS JUSTIFICATION FOR TARGETED INTERVENTIONS IN EARLY CHILDHOOD FOR DISEASE PREVENTION AND ASSISTING IN REDUCING MORBIDITY AND MORTALITY CAUSED BY CHILDHOOD ALLERGY.	2021	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      
20 1736  34 EARLY DETECTION AND PREVENTION OF SCHIZOPHRENIC PSYCHOSIS-A REVIEW. PSYCHOTIC DISORDERS OFTEN RUN A CHRONIC COURSE AND ARE ASSOCIATED WITH A CONSIDERABLE EMOTIONAL AND SOCIAL IMPACT FOR PATIENTS AND THEIR RELATIVES. THEREFORE, EARLY RECOGNITION, COMBINED WITH THE POSSIBILITY OF PREVENTIVE INTERVENTION, IS URGENTLY WARRANTED SINCE THE DURATION OF UNTREATED PSYCHOSIS (DUP) SIGNIFICANTLY DETERMINES THE FURTHER COURSE OF THE DISEASE. IN ADDITION TO ESTABLISHED DIAGNOSTIC TOOLS, NEUROBIOLOGICAL FACTORS IN THE DEVELOPMENT OF SCHIZOPHRENIC PSYCHOSES ARE INCREASINGLY BEING INVESTIGATED. IT IS SHOWN THAT NUMEROUS MOLECULAR ALTERATIONS ALREADY EXIST BEFORE THE CLINICAL ONSET OF THE DISEASE. AS SCHIZOPHRENIC PSYCHOSES ARE NOT ELICITED BY A SINGLE MUTATION IN THE DEOXYRIBONUCLEIC ACID (DNA) SEQUENCE, EPIGENETICS LIKELY CONSTITUTE THE MISSING LINK BETWEEN ENVIRONMENTAL INFLUENCES AND DISEASE DEVELOPMENT AND COULD POTENTIALLY SERVE AS A BIOMARKER. THE RESULTS FROM TRANSCRIPTOMIC AND PROTEOMIC STUDIES POINT TO A DYSREGULATED IMMUNE SYSTEM, LIKELY EVOKED BY EPIGENETIC ALTERATIONS. DESPITE THE INCREASING KNOWLEDGE OF THE NEUROBIOLOGICAL MECHANISMS INVOLVED IN THE DEVELOPMENT OF PSYCHOTIC DISORDERS, FURTHER RESEARCH EFFORTS WITH LARGE POPULATION-BASED STUDY DESIGNS ARE NEEDED TO IDENTIFY SUITABLE BIOMARKERS. IN CONCLUSION, A COMBINATION OF BLOOD EXAMINATIONS, FUNCTIONAL IMAGING TECHNIQUES, ELECTROENCEPHALOGRAPHY (EEG) INVESTIGATIONS AND POLYGENIC RISK SCORES SHOULD BE CONSIDERED AS THE BASIS FOR PREDICTING HOW SUBJECTS WILL TRANSITION INTO MANIFEST PSYCHOSIS.	2021