1  3913 132 LIFESTYLE MODIFICATIONS AND NUTRITIONAL AND THERAPEUTIC INTERVENTIONS IN DELAYING THE PROGRESSION OF CHRONIC KIDNEY DISEASE: A REVIEW. CHRONIC KIDNEY DISEASE (CKD) IS A DEBILITATING PROGRESSIVE ILLNESS THAT AFFECTS MORE THAN 10% OF THE WORLD'S POPULATION. IN THIS LITERATURE REVIEW, WE DISCUSSED THE ROLES OF NUTRITIONAL INTERVENTIONS, LIFESTYLE MODIFICATIONS, HYPERTENSION (HTN) AND DIABETES MELLITUS (DM) CONTROL, AND MEDICATIONS IN DELAYING THE PROGRESSION OF CKD. WALKING, WEIGHT LOSS, LOW-PROTEIN DIET (LPD), ADHERENCE TO THE ALTERNATE MEDITERRANEAN (AMED) DIET, AND ALTERNATIVE HEALTHY EATING INDEX (AHEI)-2010 SLOW THE PROGRESSION OF CKD. HOWEVER, SMOKING AND BINGE ALCOHOL DRINKING INCREASE THE RISK OF CKD PROGRESSION. IN ADDITION, HYPERGLYCEMIA, ALTERED LIPID METABOLISM, LOW-GRADE INFLAMMATION, OVER-ACTIVATION OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS), AND OVERHYDRATION (OH) INCREASE DIABETIC CKD PROGRESSION. THE KIDNEY DISEASE: IMPROVING GLOBAL OUTCOMES (KDIGO) GUIDELINES RECOMMEND BLOOD PRESSURE (BP) CONTROL OF <140/90 MMHG IN PATIENTS WITHOUT ALBUMINURIA AND <130/80 MMHG IN PATIENTS WITH ALBUMINURIA TO PREVENT CKD PROGRESSION. MEDICAL THERAPIES AIM TO TARGET EPIGENETIC ALTERATIONS, FIBROSIS, AND INFLAMMATION. CURRENTLY, RAAS BLOCKADE, SODIUM-GLUCOSE COTRANSPORTER-2 (SGLT2) INHIBITORS, PENTOXIFYLLINE, AND FINERENONE ARE APPROVED FOR MANAGING CKD. IN ADDITION, ACCORDING TO THE COMPLETED STUDY OF DIABETIC NEPHROPATHY WITH ATRASENTAN (SONAR), ATRASENTAN, AN ENDOTHELIN RECEPTOR ANTAGONIST (ERA), DECREASED THE RISK OF RENAL EVENTS IN DIABETIC CKD PATIENTS. HOWEVER, ONGOING TRIALS ARE STUDYING THE ROLE OF OTHER AGENTS IN SLOWING THE PROGRESSION OF CKD.	2023	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           
2  5037  25 PHARMACOGENETICS IN PAIN TREATMENT. PAIN IS AN UNPLEASANT FEELING USUALLY RESULTING FROM TISSUE DAMAGE THAT CAN PERSIST ALONG WEEKS, MONTHS, OR EVEN YEARS AFTER THE INJURY, TURNING INTO PATHOLOGICAL CHRONIC PAIN, THE LEADING CAUSE OF DISABILITY. CURRENTLY, PHARMACOLOGY INTERVENTIONS ARE USUALLY THE FIRST-LINE THERAPY BUT THERE IS A HIGHLY VARIABLE ANALGESIC DRUG RESPONSE. PHARMACOGENETICS (PGX) OFFERS A MEANS TO IDENTIFY GENETIC BIOMARKERS THAT CAN PREDICT INDIVIDUAL ANALGESIC RESPONSE OPENING DOORS TO PRECISION MEDICINE. PGX ANALYZE THE WAY IN WHICH THE PRESENCE OF VARIATIONS IN THE DNA SEQUENCE (SINGLE-NUCLEOTIDE POLYMORPHISMS, SNPS) COULD BE RESPONSIBLE FOR PORTIONS OF THE POPULATION REACHING DIFFERENT LEVELS OF PAIN RELIEF (PHENOTYPE) DUE TO GENE INTERFERENCE IN THE DRUG MECHANISM OF ACTION (PHARMACODYNAMICS) AND/OR ITS CONCENTRATION AT THE PLACE OF ACTION (PHARMACOKINETICS). SNPS IN THE CYTOCHROME P450 ENZYMES GENES (CYP2D6) INFLUENCE METABOLISM OF CODEINE, TRAMADOL, HYDROCODONE, OXYCODONE, AND TRICYCLIC ANTIDEPRESSANTS. BLOOD CONCENTRATIONS OF SOME NSAIDS DEPEND ON CYP2C9 AND/OR CYP2C8 ACTIVITY. ADDITIONAL CANDIDATE GENES ENCODE FOR OPIOID RECEPTORS, TRANSPORTERS, AND OTHER MOLECULES IMPORTANT FOR PHARMACOTHERAPY IN PAIN MANAGEMENT. HOWEVER, PGX STUDIES ARE OFTEN CONTRADICTORY, SLOWING THE UPTAKE OF THIS INFORMATION. THIS IS LIKELY DUE, IN LARGE PART, TO A LACK OF ROBUST EVIDENCE DEMONSTRATING CLINICAL UTILITY AND TO ITS POLYGENIC RESPONSE MODULATED BY OTHER EXOGENOUS OR EPIGENETICS FACTORS. NOVEL THERAPIES, INCLUDING TARGETING OF EPIGENETIC CHANGES AND GENE THERAPY-BASED APPROACHES, BROADEN FUTURE OPTIONS TO IMPROVE UNDERSTANDING OF PAIN AND THE TREATMENT OF PEOPLE WHO SUFFER IT.	2018	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             
3  6615  25 ULTRAVIOLET-A1 IRRADIATION THERAPY FOR SYSTEMIC LUPUS ERYTHEMATOSUS. SYSTEMIC LUPUS ERYTHEMATOSUS (LUPUS, SLE) IS A CHRONIC AUTOIMMUNE DISEASE CHARACTERIZED BY THE PRODUCTION OF AUTOANTIBODIES, WHICH BIND TO ANTIGENS AND ARE DEPOSITED WITHIN TISSUES TO FIX COMPLEMENT, RESULTING IN WIDESPREAD SYSTEMIC INFLAMMATION. THE STUDIES PRESENTED HEREIN ARE CONSISTENT WITH HYPERPOLARIZED, ADENOSINE TRIPHOSPHATE (ATP)-DEFICIENT MITOCHONDRIA BEING CENTRAL TO THE DISEASE PROCESS. THESE HYPERPOLARIZED MITOCHONDRIA RESIST THE DEPOLARIZATION REQUIRED FOR ACTIVATION-INDUCED APOPTOSIS. THE MITOCHONDRIAL ATP DEFICITS ADD TO THIS RESISTANCE TO APOPTOSIS AND ALSO REDUCE THE MACROPHAGE ENERGY THAT IS NEEDED TO CLEAR APOPTOTIC BODIES. IN BOTH CASES, NECROSIS, THE ALTERNATIVE PATHWAY OF CELL DEATH, RESULTS. INTRACELLULAR CONSTITUENTS SPILL INTO THE BLOOD AND TISSUES, ELICITING INFLAMMATORY RESPONSES DIRECTED AT THEIR REMOVAL. WHAT RESULTS IS "AUTOIMMUNITY." ULTRAVIOLET (UV)-A1 PHOTONS HAVE THE CAPACITY TO REMEDIATE THIS ABERRANCY. EXOGENOUS EXPOSURE TO LOW-DOSE, FULL-BODY, UV-A1 RADIATION GENERATES SINGLET OXYGEN. SINGLET OXYGEN HAS TWO MAJOR PALLIATIVE ACTIONS IN PATIENTS WITH LUPUS AND THE UV-A1 PHOTONS THEMSELVES HAVE SEVERAL MORE. SINGLET OXYGEN DEPOLARIZES THE HYPERPOLARIZED MITOCHONDRION, TRIGGERING NON-ATP-DEPENDENT APOPTOSIS THAT DETERS NECROSIS. NEXT, SINGLET OXYGEN ACTIVATES THE GENE ENCODING HEME OXYGENASE (HO-1), A MAJOR GOVERNOR OF SYSTEMIC HOMEOSTASIS. HO-1 CATALYZES THE DEGRADATION OF THE OXIDANT HEME INTO BILIVERDIN (CONVERTED TO BILIRUBIN), FE, AND CARBON MONOXIDE (CO), THE FIRST THREE OF THESE EXERTING POWERFUL ANTIOXIDANT EFFECTS, AND IN CONJUNCTION WITH A FOURTH, CO, PROTECTING AGAINST INJURY TO THE CORONARY ARTERIES, THE CENTRAL NERVOUS SYSTEM, AND THE LUNGS. THE UV-A1 PHOTONS THEMSELVES DIRECTLY ATTENUATE DISEASE IN LUPUS BY REDUCING B CELL ACTIVITY, PREVENTING THE SUPPRESSION OF CELL-MEDIATED IMMUNITY, SLOWING AN EPIGENETIC PROGRESSION TOWARD SLE, AND AMELIORATING DISCOID AND SUBACUTE CUTANEOUS LUPUS. FINALLY, A COMBINATION OF THESE MECHANISMS REDUCES LEVELS OF ANTICARDIOLIPIN ANTIBODIES AND PROTECTS DURING LUPUS PREGNANCY. CAPPING ALL OF THIS IS THAT UV-A1 IRRADIATION IS AN ESSENTIALLY INNOCUOUS, HIGHLY MANAGEABLE, AND COMFORTABLE THERAPEUTIC AGENCY.	2017	
                                                                                                                                                                                                                                                                                                                                                               
4  6490  17 TRACING SLOW PHENOPTOSIS TO THE PRENATAL STAGE IN SOCIAL VERTEBRATES. VLADIMIR SKULACHEV'S COINING OF THE TERM "PHENOPTOSIS" 25 YEARS AGO (SKULACHEV, V. P., BIOCHEMISTRY (MOSCOW), 62, 1997) HIGHLIGHTED THE THEORETICAL POSSIBILITY THAT AGING IS A PROGRAMMED PROCESS TO SPEED THE EXIT OF INDIVIDUALS POSING SOME DANGER TO THEIR SOCIAL GROUP. WHILE RAPID "ACUTE PHENOPTOSIS" MIGHT OCCUR AT ANY AGE (E.G., TO PREVENT SPREAD OF DEADLY INFECTIONS), "SLOW PHENOPTOSIS" IS GENERALLY CONSIDERED TO OCCUR LATER IN LIFE IN THE FORM OF CHRONIC AGE-RELATED DISORDERS. HOWEVER, RECENT RESEARCH INDICATES THAT RISKS FOR SUCH CHRONIC DISORDERS CAN BE GREATLY RAISED BY EARLY LIFE ADVERSITY, ESPECIALLY DURING THE PRENATAL STAGE. MUCH OF THIS RESEARCH USES INDICATORS OF BIOLOGICAL AGING, THE SPEEDING OR SLOWING OF NATURAL PHYSIOLOGICAL DETERIORATION IN RESPONSE TO ENVIRONMENTAL INPUTS, LEADING TO DIVERGENCE FROM CHRONOLOGICAL AGE. STUDIES USING BIOLOGICAL AGING INDICATORS COMMONLY FIND IT IS ACCELERATED NOT ONLY IN OLDER INDIVIDUALS WITH CHRONIC DISORDERS, BUT ALSO IN VERY YOUNG INDIVIDUALS WITH HEALTH PROBLEMS. THIS REVIEW WILL EXPLAIN HOW ACCELERATED BIOLOGICAL AGING EQUATES TO SLOW PHENOPTOSIS. ITS OCCURRENCE EVEN IN THE PRENATAL STAGE IS THEORETICALLY SUPPORTED BY W. D. HAMILTON'S PROPOSAL THAT OFFSPRINGS DETECTING THEY HAVE DANGEROUS MUTATIONS SHOULD THEN AUTOMATICALLY SPEED THEIR DEMISE, IN ORDER TO IMPROVE THEIR INCLUSIVE FITNESS BY GIVING THEIR PARENTS THE CHANCE TO PRODUCE OTHER FITTER SIBLINGS.	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  
5  5336  21 QUANTIFICATION OF THE PACE OF BIOLOGICAL AGING IN HUMANS THROUGH A BLOOD TEST, THE DUNEDINPOAM DNA METHYLATION ALGORITHM. BIOLOGICAL AGING IS THE GRADUAL, PROGRESSIVE DECLINE IN SYSTEM INTEGRITY THAT OCCURS WITH ADVANCING CHRONOLOGICAL AGE, CAUSING MORBIDITY AND DISABILITY. MEASUREMENTS OF THE PACE OF AGING ARE NEEDED AS SURROGATE ENDPOINTS IN TRIALS OF THERAPIES DESIGNED TO PREVENT DISEASE BY SLOWING BIOLOGICAL AGING. WE REPORT A BLOOD-DNA-METHYLATION MEASURE THAT IS SENSITIVE TO VARIATION IN PACE OF BIOLOGICAL AGING AMONG INDIVIDUALS BORN THE SAME YEAR. WE FIRST MODELED CHANGE-OVER-TIME IN 18 BIOMARKERS TRACKING ORGAN-SYSTEM INTEGRITY ACROSS 12 YEARS OF FOLLOW-UP IN N = 954 MEMBERS OF THE DUNEDIN STUDY BORN IN 1972-1973. RATES OF CHANGE IN EACH BIOMARKER OVER AGES 26-38 YEARS WERE COMPOSITED TO FORM A MEASURE OF AGING-RELATED DECLINE, TERMED PACE-OF-AGING. ELASTIC-NET REGRESSION WAS USED TO DEVELOP A DNA-METHYLATION PREDICTOR OF PACE-OF-AGING, CALLED DUNEDINPOAM FOR DUNEDIN(P)ACE(O)F(A)GING(M)ETHYLATION. VALIDATION ANALYSIS IN COHORT STUDIES AND THE CALERIE TRIAL PROVIDE PROOF-OF-PRINCIPLE FOR DUNEDINPOAM AS A SINGLE-TIME-POINT MEASURE OF A PERSON'S PACE OF BIOLOGICAL AGING.	2020	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     
6  5024  16 PERSONALIZED EPIGENETIC MANAGEMENT OF DIABETES. THE NOVEL GENOME-WIDE ASSAYS OF EPIGENETIC MARKS HAVE RESULTED IN A GREATER UNDERSTANDING OF HOW GENETICS AND THE ENVIRONMENT INTERACT IN THE DEVELOPMENT AND INHERITANCE OF DIABETES. CHRONIC HYPERGLYCEMIA INDUCES EPIGENETIC CHANGES IN MULTIPLE ORGANS, CONTRIBUTING TO DIABETIC COMPLICATIONS. SPECIFIC EPIGENETIC-MODIFYING COMPOUNDS HAVE BEEN DEVELOPED TO ERASE THESE MODIFICATIONS, POSSIBLY SLOWING DOWN THE ONSET OF DIABETES-RELATED COMPLICATIONS. THE CURRENT REVIEW IS AN UPDATE OF THE PREVIOUSLY PUBLISHED PAPER, DESCRIBING THE MOST RECENT ADVANCES IN THE EPIGENETICS OF DIABETES.	2017	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         
7  6872  23 [POLYPHENOLS AS PROMISING BIOACTIVE COMPOUNDS]. POLYPHENOLS ARE DIVERSE AND WIDESPREAD BIOACTIVE PLANT-BASED COMPOUNDS. THESE COMPOUNDS ARE FOUND IN VARIOUS FOODS SUCH AS BERRIES, FRUITS, VEGETABLES, CEREALS, NUTS, COFFEE, CACAO, SPICES, SEEDS. THEY ARE DIVIDED INTO PHENOLIC ACIDS, STILBENES, FLAVONOIDS, LIGNANS DEPENDING ON THEIR MOLECULAR STRUCTURE. THEY ATTRACT THE ATTENTION OF RESEARCHERS DUE TO WIDE RANGE OF BIOLOGICAL EFFECTS ON HUMAN BODY. THE PURPOSE OF THIS WORK WAS TO ANALYZE MODERN SCIENTIFIC PUBLICATIONS ON THE BIOLOGICAL EFFECTS OF POLYPHENOLS. MATERIAL AND METHODS. THE REVIEW IS BASED ON PUBLICATIONS PRESENTED IN THE PUBMED, GOOGLE SCHOLAR, RESEARCHGATE, ELSEVIER, ELIBRARY, CYBERLENINKA DATABASES USING "POLYPHENOLS", "FLAVONOIDS", "RESVERATROL", "QUERCETIN", "CATECHINS" AS KEY WORDS. PREFERENCE WAS GIVEN TO ORIGINAL RESEARCHES OVER THE PAST 10 YEARS PUBLISHED IN REFEREED JOURNALS. RESULTS. OXIDATIVE STRESS, CHRONIC INFLAMMATION, MICROBIOME DISORDERS, INSULIN RESISTANCE, EXCESSIVE PROTEIN GLYCATION, AND GENOTOXIC EFFECTS ARE AT THE HEART OF THE PATHOGENESIS OF MANY DISEASES, INCLUDING THOSE ASSOCIATED WITH AGE. A LARGE AMOUNT OF MATERIAL HAS BEEN ACCUMULATED ON THE ANTIOXIDANT, ANTICARCINOGENIC, EPIGENETIC, METABOLIC, GEROPROTECTIVE, ANTI-INFLAMMATORY AND ANTIVIRAL EFFECTS OF POLYPHENOLS. THIS GIVES REASONS TO CONSIDER POLYPHENOLS AS VERY PROMISING MICRONUTRIENTS, WHICH INCLUSION IN THE DIET CAN REDUCE THE RISK OF DEVELOPING CARDIOVASCULAR, ONCOLOGICAL, NEURODEGENERATIVE DISEASES, DIABETES MELLITUS, OBESITY, METABOLIC SYNDROME, PREMATURE AGING, THAT IS, THE MAIN CAUSES OF DEATH, A DECREASE IN THE DURATION AND QUALITY OF LIFE OF A MODERN PERSON. CONCLUSION. EXPANDING THE RANGE OF PRODUCTS ENRICHED WITH POLYPHENOLS WITH THEIR HIGH BIOAVAILABILITY IS A PROMISING AREA OF SCIENTIFIC RESEARCH AND DEVELOPMENT OF PRODUCTION IN ORDER TO PREVENT SOCIALLY SIGNIFICANT AGE-ASSOCIATED DISEASES.	2023	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          
8  4783  25 NUTRIGENOMICS IN PARKINSON'S DISEASE: DIVERSITY OF MODULATORY ACTIONS OF POLYPHENOLS ON EPIGENETIC EFFECTS INDUCED BY TOXINS. ALTHOUGH THE PATHOGENESIS OF PARKINSON'S DISEASE (PD) IS NOT COMPLETELY UNDERSTOOD, THERE IS A CONSENSUS THAT IT CAN BE CAUSED BY MULTIFACTORIAL MECHANISMS INVOLVING GENETIC SUSCEPTIBILITY, EPIGENETIC MODIFICATIONS INDUCED BY TOXINS AND MITOCHONDRIAL DYSFUNCTION. IN THE PAST 20 YEARS, GREAT EFFORTS HAVE BEEN MADE IN ORDER TO CLARIFY MOLECULAR MECHANISMS THAT ARE RISK FACTORS FOR THIS DISEASE, AS WELL AS TO IDENTIFY BIOACTIVE AGENTS FOR PREVENTION AND SLOWING DOWN OF ITS PROGRESSION. NUTRACEUTICAL PRODUCTS HAVE RECEIVED SUBSTANTIAL INTEREST DUE TO THEIR NUTRITIONAL, SAFE AND THERAPEUTIC EFFECTS ON SEVERAL CHRONIC DISEASES. THE AIM OF THIS REVIEW WAS TO GATHER THE MAIN EVIDENCE OF THE EPIGENETIC MECHANISMS INVOLVED IN THE NEUROPROTECTIVE EFFECTS OF PHENOLIC COMPOUNDS CURRENTLY UNDER INVESTIGATION FOR THE TREATMENT OF TOXIN-INDUCED PD. THESE STUDIES CONFIRM THAT THE NEUROPROTECTIVE ACTIONS OF POLYPHENOLS INVOLVE COMPLEX EPIGENETIC MODULATIONS, DEMONSTRATING THAT THE INTAKE OF THESE NATURAL COMPOUNDS CAN BE A PROMISING, LOW-COST, PHARMACOGENOMIC STRATEGY AGAINST THE DEVELOPMENT OF PD.	2023	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         
9  6480  22 TOWARDS PRECISION MEDICINE IN GENERALIZED ANXIETY DISORDER: REVIEW OF GENETICS AND PHARMACO(EPI)GENETICS. GENERALIZED ANXIETY DISORDER (GAD) IS A PREVALENT AND CHRONIC MENTAL DISORDER THAT ELICITS WIDESPREAD FUNCTIONAL IMPAIRMENT. GIVEN THE HIGH DEGREE OF NON-RESPONSE/PARTIAL RESPONSE AMONG PATIENTS WITH GAD TO AVAILABLE PHARMACOLOGICAL TREATMENTS, THERE IS A STRONG NEED FOR NOVEL APPROACHES THAT CAN OPTIMIZE OUTCOMES, AND LEAD TO MEDICATIONS THAT ARE SAFER AND MORE EFFECTIVE. ALTHOUGH INVESTIGATIONS HAVE IDENTIFIED INTERESTING TARGETS PREDICTING TREATMENT RESPONSE THROUGH PHARMACOGENETICS (PGX), PHARMACO-EPIGENETICS, AND NEUROIMAGING METHODS, THESE STUDIES ARE OFTEN SOLITARY, NOT REPLICATED, AND CARRY SEVERAL LIMITATIONS. THIS REVIEW PROVIDES AN OVERVIEW OF THE CURRENT STATUS OF GAD GENETICS AND PGX AND PRESENTS POTENTIAL STRATEGIES TO IMPROVE TREATMENT RESPONSE BY COMBINING BETTER PHENOTYPING WITH PGX AND IMPROVED ANALYTICAL METHODS. THESE STRATEGIES CARRY THE DUAL BENEFIT OF DELIVERING DATA ON BIOMARKERS OF TREATMENT RESPONSE AS WELL AS POINTING TO DISEASE MECHANISMS THROUGH THE BIOLOGY OF THE MARKERS ASSOCIATED WITH RESPONSE. OVERALL, THESE EFFORTS CAN SERVE TO IDENTIFY CLINICAL, GENETIC, AND EPIGENETIC FACTORS THAT CAN BE INCORPORATED INTO A PHARMACO(EPI)GENETIC TEST THAT MAY ULTIMATELY IMPROVE TREATMENT RESPONSE AND REDUCE THE SOCIOECONOMIC BURDEN OF GAD.	2019	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         
10  5154  24 PRAKRITI-BASED MEDICINE: A STEP TOWARDS PERSONALIZED MEDICINE. THE CONCEPT OF PERSONALIZED MEDICINE HAS BEEN AROUND FOR AS LONG AS PEOPLE HAVE BEEN PRACTICING MEDICINE. FROM CHARAKA TO HIPPOCRATES, ALL HAVE PRACTICED THE PERSONALIZED APPROACH FOR TREATING A DISEASE. IN THE 21(ST) CENTURY, PERSONALIZED MEDICINE IS ALL ABOUT DNA. WHEREAS THE SINGLE NUCLEOTIDE POLYMORPHISM (SNP) AND EPIGENETIC FACTORS INFLUENCE DRUG RESPONSE AND FORM THE BASIS OF PERSONALIZED MEDICINE, THE TRIDOSHA THEORY FORMS THE BASIS OF PRAKRITI-BASED MEDICINE. IT IS WELL ESTABLISHED BY NOW THAT WESTERN ALLOPATHIC MEDICINE IS EXCELLENT IN HANDLING ACUTE MEDICAL CRISES, WHEREAS AYURVEDA HAS SUCCESSFULLY DEMONSTRATED AN ABILITY TO MANAGE CHRONIC DISORDERS THAT WESTERN MEDICINE HAS BEEN UNABLE TO CURE. WITH EFFECTIVE INTEGRATION OF 'OMICS' PRAKRITI-BASED MEDICINE CAN PLAY A VITAL ROLE IN THIS CHANGING SCENARIO OF GLOBAL HEALTH WISDOM AS AYURVEDA OFFERS ITS MODALITIES BY WAY OF AHARA (DIET), VIHARA (LIFESTYLE), AND AUSHADHI (MEDICATION), WHICH ARE THE THREE PILLARS OF PRAKRITI-BASED MEDICINE MAKING IT A HOLISTIC SCIENCE. PRAKRITI-BASED MEDICINE AND OTHER TRADITIONAL MEDICINE SYSTEMS HAVE THE POTENTIAL TO OFFER REMEDIES TO THE CHALLENGING HEALTH ISSUES LIKE ADVERSE DRUG REACTIONS, DRUG WITHDRAWALS, AND ECONOMIC DISPARITIES AMONG FEW. AN INTEGRATIVE GLOBAL APPROACH COULD DO WONDERS TO HEALTH SCIENCES BENEFITING A BROAD SPECTRUM OF PATIENTS.	2011	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              
11  4808  29 OBESITY MANAGEMENT: AT THE FOREFRONT AGAINST DISEASE STIGMA AND THERAPEUTIC INERTIA. OBESITY IS A COMPLEX CHRONIC RELAPSING DISEASE, RESULTING FROM THE INTERACTION BETWEEN MULTIPLE ENVIRONMENTAL, GENETIC AND EPIGENETIC CAUSES, AND SUPPORTED BY CHANGES IN THE NEUROENDOCRINE MECHANISMS REGULATING ENERGY BALANCE AND BODY WEIGHT. ADIPOSE TISSUE DYSFUNCTION CONTRIBUTES TO OBESITY-RELATED COMPLICATIONS. HOWEVER, THE PREVALENT NARRATIVE ABOUT THE CAUSES AND MECHANISMS OF OBESITY REMAINS A MUCH MORE SIMPLISTIC ONE, BASED ON THE FALSE ASSUMPTION THAT INDIVIDUALS CAN FULLY CONTROL THEIR BODY WEIGHT THROUGH APPROPRIATE BEHAVIOURAL CHOICES. ACCORDING TO THIS NARRATIVE, OBESITY IS SIMPLY REVERSIBLE "PERSUADING" THE PATIENT TO FOLLOW HEALTHIER AND MORE VIRTUOUS INDIVIDUAL BEHAVIOURS (MORAL JUDGEMENT). THIS PERSISTENT NARRATIVE FORMS THE DEEP ROOT OF THE STIGMATISATION OF PEOPLE WITH OBESITY AT THE INDIVIDUAL LEVEL AND CREATES A CLEAR DISCREPANCY ON HOW OBESITY PREVENTION AND CURE ARE DESIGNED IN COMPARISON WITH THE CASE OF OTHER NON-COMMUNICABLE CHRONIC DISEASES (CLINICAL STIGMA). THE PROMOTION OF SYSTEMIC PREVENTIVE MEASURES AGAINST OBESITY IS NOT SUPPORTED AT A POLITICAL AND SOCIAL LEVEL BY THE PERSISTENCE OF A NARRATIVE OF OBESITY AS THE SIMPLE CONSEQUENCE OF INDIVIDUAL FAILURES AND LACK OF WILLPOWER. THE SIMPLISTIC NARRATIVE OF OBESITY AS A SELF-IMPOSED CONDITION WITH AN EASY WAY-OUT ("EAT LESS AND MOVE MORE") CREATES A CLEAR DISCREPANCY ON HOW OBESITY IS MANAGED BY HEALTH CARE SYSTEMS IN COMPARISON WITH OTHER NCDS. THE OVER-ESTIMATION OF THE EFFICACY OF THERAPEUTIC INTERVENTION SOLELY BASED ON PATIENTS EDUCATION AND LIFESTYLE MODIFICATION IS RESPONSIBLE OF THERAPEUTIC INERTIA IN HEALTH CARE PROFESSIONALS AND IN CLINICAL GUIDELINES, LIMITING OR DELAYING THE ADOPTION OF MORE EFFECTIVE THERAPEUTIC STRATEGIES, LIKE ANTI-OBESITY MEDICATIONS AND BARIATRIC SURGERY. IN CONCLUSION, THE PERSISTENCE OF A NARRATIVE DESCRIBING OBESITY AS A SELF-INDUCED EASILY REVERSIBLE CONDITION HAS PROFOUND CONSEQUENCES ON HOW OBESITY PREVENTION AND MANAGEMENT ARE BUILD, INCLUDING THE DESIGN AND IMPLEMENTATION OF OBESITY MANAGEMENT GUIDELINES AND A TENDENCY TO THERAPEUTIC INERTIA.LEVEL OF EVIDENCE: NO LEVEL OF EVIDENCE.	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                 
12  6439  25 THERAPEUTIC ANTIBODIES: CURRENT STATE AND FUTURE TRENDS--IS A PARADIGM CHANGE COMING SOON? ANTIBODY-BASED THERAPEUTICS CURRENTLY ENJOY UNPRECEDENTED SUCCESS, GROWTH IN RESEARCH AND REVENUES, AND RECOGNITION OF THEIR POTENTIAL. IT APPEARS THAT THE PROMISE OF THE "MAGIC BULLET" HAS LARGELY BEEN REALIZED. THERE ARE CURRENTLY 22 MONOCLONAL ANTIBODIES (MABS) APPROVED BY THE UNITED STATES FOOD AND DRUG ADMINISTRATION (FDA) FOR CLINICAL USE AND HUNDREDS ARE IN CLINICAL TRIALS FOR TREATMENT OF VARIOUS DISEASES INCLUDING CANCERS, IMMUNE DISORDERS, AND INFECTIONS. THE REVENUES FROM THE TOP FIVE THERAPEUTIC ANTIBODIES (RITUXAN, REMICADE, HERCEPTIN, HUMIRA, AND AVASTIN) NEARLY DOUBLED FROM $6.4 BILLION IN 2004 TO $11.7 BILLION IN 2006. DURING THE LAST SEVERAL YEARS MAJOR PHARMACEUTICAL COMPANIES RACED TO ACQUIRE ANTIBODY COMPANIES, WITH A RECENT EXAMPLE OF MEDIMMUNE BEING PURCHASED FOR $15.6 BILLION BY ASTRAZENECA. THESE THERAPEUTIC AND BUSINESS SUCCESSES REFLECT THE MAJOR ADVANCES IN ANTIBODY ENGINEERING WHICH HAVE RESULTED IN THE GENERATION OF SAFE, SPECIFIC, HIGH-AFFINITY, AND NON-IMMUNOGENIC ANTIBODIES DURING THE LAST THREE DECADES. CURRENTLY, SECOND AND THIRD GENERATIONS OF ANTIBODIES ARE UNDER DEVELOPMENT, MOSTLY TO IMPROVE ALREADY EXISTING ANTIBODY SPECIFICITIES. HOWEVER, ALTHOUGH THE REFINEMENT OF ALREADY KNOWN METHODOLOGIES IS CERTAINLY OF GREAT IMPORTANCE FOR POTENTIAL CLINICAL USE, THERE ARE NO CONCEPTUALLY NEW DEVELOPMENTS IN THE LAST DECADE COMPARABLE, FOR EXAMPLE, TO THE DEVELOPMENT OF ANTIBODY LIBRARIES, PHAGE DISPLAY, DOMAIN ANTIBODIES (DABS), AND ANTIBODY HUMANIZATION TO NAME A FEW. A FUNDAMENTAL QUESTION IS THEN WHETHER THERE WILL BE ANOTHER CHANGE IN THE PARADIGM OF RESEARCH AS HAPPENED 1-2 DECADES AGO OR THE CURRENT TREND OF GRADUAL IMPROVEMENT OF ALREADY DEVELOPED METHODOLOGIES AND THERAPEUTIC ANTIBODIES WILL CONTINUE. ALTHOUGH ANY PREDICTION COULD PROVE INCORRECT, IT APPEARS THAT CONCEPTUALLY NEW METHODOLOGIES ARE NEEDED TO OVERCOME THE FUNDAMENTAL PROBLEMS OF DRUG (ANTIBODY) RESISTANCE DUE TO GENETIC OR/AND EPIGENETIC ALTERATIONS IN CANCER AND CHRONIC INFECTIONS, AS WELL AS PROBLEMS RELATED TO ACCESS TO TARGETS AND COMPLEXITY OF BIOLOGICAL SYSTEMS. IF NEW METHODOLOGIES ARE NOT DEVELOPED, IT IS LIKELY THAT GRADUAL SATURATION WILL OCCUR IN THE PIPELINE OF CONCEPTUALLY NEW ANTIBODY THERAPEUTICS. IN THIS SCENARIO WE WILL WITNESS AN INCREASE IN COMBINATION OF TARGETS AND ANTIBODIES, AND FURTHER ATTEMPTS TO PERSONALIZE TARGETED TREATMENTS BY USING APPROPRIATE BIOMARKERS AS WELL AS TO DEVELOP NOVEL SCAFFOLDS WITH PROPERTIES THAT ARE SUPERIOR TO THOSE OF THE ANTIBODIES NOW IN CLINICAL USE.	2009	

13    96  18 A PRIMER ON METABOLIC MEMORY: WHY EXISTING DIABESITY TREATMENTS FAIL. DESPITE MASSIVE GOVERNMENT AND PRIVATE SECTOR INVESTMENTS INTO PREVENTION OF CARDIOVASCULAR DISEASE, DIABETES MELLITUS AND OBESITY, EFFORTS HAVE LARGELY FAILED, AND THE BURDEN OF COST REMAINS IN THE TREATMENT OF DOWNSTREAM MORBIDITY AND MORTALITY, WITH OVERALL STAGNATING OUTCOMES. A NEW PARADIGM SHIFT IN THE APPROACH TO THESE PATIENTS MAY EXPLAIN WHY EXISTING TREATMENT STRATEGIES FAIL, AND OFFER NEW TREATMENT TARGETS. THIS REVIEW AIMS TO PROVIDE A CLINICIAN-CENTRED PRIMER ON METABOLIC MEMORY, DEFINED AS THE SUM OF IRREVERSIBLE GENETIC, EPIGENETIC, CELLULAR AND TISSUE-LEVEL ALTERATIONS THAT OCCUR WITH LONG-TIME EXPOSURE TO METABOLIC DERANGEMENTS.	2021	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            
14  4871  22 OUR GENES ARE NOT OUR DESTINY: INCORPORATING MOLECULAR MEDICINE INTO CLINICAL PRACTICE. IN MANY DEVELOPED NATIONS, THE STATE OF PUBLICLY ADMINISTERED HEALTH CARE IS INCREASINGLY PRECARIOUS AS A RESULT OF ESCALATING NUMBERS OF CHRONICALLY ILL PATIENTS, INADEQUATE MEDICAL PERSONNEL AND HOSPITAL FACILITIES, AS WELL AS SPARSE FUNDING FOR ONGOING UPGRADES TO STATE-OF-THE-ART DIAGNOSTIC AND THERAPEUTIC TECHNOLOGY - AN INCREASED EMPHASIS ON AETIOLOGY-CENTRED MEDICINE SHOULD BE CONSIDERED IN ORDER TO ACHIEVE IMPROVED HEALTH FOR PATIENTS AND POPULATIONS. MEDICAL PRACTICE PATTERNS WHICH ARE DESIGNED TO PROVIDE QUICK AND EFFECTIVE AMELIORATION OF SIGNS AND SYMPTOMS ARE FREQUENTLY NOT AN ENDURING SOLUTION TO MANY HEALTH AFFLICTIONS AND CHRONIC DISEASE STATES. RECENT SCIENTIFIC DISCOVERY HAS RENDERED THE DRUG-ORIENTED ALGORITHMIC PARADIGM COMMONLY FOUND IN CONTEMPORARY EVIDENCE-BASED MEDICINE TO BE A REDUCTIONIST APPROACH TO CLINICAL PRACTICE. UNFOLDING EVIDENCE APPEARS TO SUPPORT A GENETIC PREDISPOSITION MODEL OF HEALTH AND ILLNESS RATHER THAN A FATALISTIC PREDESTINATION CONSTRUCT - MODIFIABLE EPIGENETIC AND ENVIRONMENTAL FACTORS HAVE ENORMOUS POTENTIAL TO INFLUENCE CLINICAL OUTCOMES. BY UNDERSTANDING AND APPLYING FUNDAMENTAL CLINICAL PRINCIPLES RELATING TO THE EMERGING FIELDS OF MOLECULAR MEDICINE, NUTRIGENOMICS AND HUMAN EXPOSURE ASSESSMENT, DOCTORS WILL BE EMPOWERED TO ADDRESS CAUSALITY OF AFFLICTION WHEN POSSIBLE AND ACHIEVE SUSTAINED REPRIEVE FOR MANY SUFFERING PATIENTS.	2008	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               
15  5218  26 PREVENTION OF HEPATOCELLULAR CARCINOMA. PREVENTION IS THE ONLY REALISTIC APPROACH FOR REDUCING MORTALITY RATES ASSOCIATED WITH HEPATOCELLULAR CARCINOMA (HCC) WORLDWIDE. VACCINATION AGAINST HEPATITIS B AND SCREENING OF BLOOD DONATIONS ARE EFFECTIVE MEASURES OF PRIMARY PREVENTION. SCREENING OF BLOOD DONATIONS HAS LED TO A SUBSTANTIAL REDUCTION IN VIRAL HEPATITIS TRANSMISSION AMONG THE GENERAL POPULATION, AND IN TAIWAN VACCINATION AGAINST HEPATITIS B CAUSED A SIGNIFICANT REDUCTION IN HCC INCIDENCE AMONG INFANTS. PRIMARY PREVENTION ALSO INCLUDES APPROACHES THAT ALTER EPIGENETIC AND GENETIC CHANGES IN HEPATOCYTES, KNOWN TO INCREASE SUSCEPTIBILITY TO HCC, AS WELL AS TREATMENTS SLOWING PROGRESSION TO CIRRHOSIS. THE ONLY EVIDENCE THAT CHEMOPREVENTION REDUCES HCC RISK IS A MULTICENTER RANDOMIZED PROSPECTIVE STUDY IN ASIAN PATIENTS WITH ADVANCED HEPATITIS B WHO RECEIVED THE ORAL NUCLEOSIDE ANALOGUE LAMIVUDINE. CIRCUMSTANTIAL EVIDENCE SUGGESTS THAT HCC RISK IS ALSO REDUCED IN PATIENTS WITH CHRONIC HEPATITIS C WHO HAVE HAD A SUSTAINED VIROLOGICAL RESPONSE TO INTERFERON THERAPY. HCC IS NOT SUBSTANTIALLY REDUCED IN PATIENTS WITH HEPATITIS B TREATED WITH INTERFERON AND PATIENTS WITH HEPATITIS C WHO DID NOT RESPOND TO INTERFERON. SECONDARY PREVENTION, THAT IS, PREVENTION OF TUMOR RECURRENCE AFTER HEPATIC RESECTION OR LOCAL ABLATIVE THERAPIES, HAS BEEN PURSUED WITH DIFFERENT APPROACHES. RETINOIDS, HEPATIC EMBOLIZATION WITH (131)I LIPIODOL, AND ADOPTIVE ADJUVANT IMMUNOTHERAPY HAVE YIELDED ENCOURAGING RESULTS. OTHER APPROACHES, INCLUDING THOSE BASED ON INTERFERON ALFA OR BETA, PROVIDED INCONCLUSIVE EVIDENCE FOR SECONDARY PROPHYLAXIS OF HCC, MAINLY BECAUSE OF THE POOR METHODOLOGIES AND SCIENTIFIC BACKGROUND OF THE STUDIES. DIETARY INTERVENTIONS AND ANTIAFLATOXIN AGENTS MIGHT HELP TO PREVENT HCC IN SUSCEPTIBLE INDIVIDUALS, BUT THE REAL EFFICACY OF THESE APPROACHES IS FAR FROM BEING DEMONSTRATED.	2005	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            
16  6738  25 WHAT'S YOUR CUP OF TEA? THE ROLE OF HERBAL COMPOUNDS IN THE MANAGEMENT OF MULTIPLE SCLEROSIS. MULTIPLE SCLEROSIS (MS) IS A CHRONIC, INFLAMMATORY, NEURODEGENERATIVE DISEASE THAT IS CHARACTERIZED BY A COMPLEX ETIOLOGY. EFFORTS TOWARDS THE MANAGEMENT OF MS HAVE LONG BEEN DIRECTED TOWARDS SYMPTOMATIC RELIEF, AS WELL AS THE USE OF IMMUNE-MODULATORY, DISEASE MODIFYING THERAPIES; HOWEVER, INCONSISTENT TREATMENT RESPONSES STILL PREVAIL, INCREASING THE RISK FOR DISEASE PROGRESSION. WHILE A GREAT DEAL OF RESEARCH ATTEMPTED TO UNRAVEL THE COMPLEXITY OF TREATMENT RESPONSES IN LIGHT OF EPIGENETIC VARIABILITY, PARALLEL EFFORTS IN THE DIRECTION OF ALTERNATIVE MEDICINE MAY BE AS PARAMOUNT. HERBAL COMPOUNDS HAVE LONG BEEN REGARDED AS SAFE AND VERSATILE OPTIONS FOR AIDING IN VARIOUS DISORDERS, INCLUDING NEURODEGENERATIVE CONDITIONS LIKE MS. NUMEROUS STUDIES HAVE TAKEN INTEREST IN A MYRIAD OF HERBAL PLANTS FOR THEIR POTENTIAL BENEFIT IN ALLEVIATING SOME OF THE MOST COMMON MS SYMPTOMS SUCH AS SPASTICITY AND FATIGUE, DELAYING THE PROGRESSION OF THE DISEASE, AS WELL AS INFLUENCING THE OVERALL QUALITY OF LIFE FOR MS PATIENTS. THIS REVIEW AIMS TO PROVIDE A COMPREHENSIVE OVERVIEW OF RECENT CLINICAL STUDIES EXAMINING THE EFFECTS OF VARIOUS HERBAL PLANTS ON DIFFERENT ASPECTS OF MS, IN AN ATTEMPT TO SHED LIGHT ON AN IMPORTANT TOOL FOR AIDING IN THE MANAGEMENT OF THIS COMPLEX AND MULTIFACTORIAL DISEASE.	2023	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          
17  4809  30 OBESITY PREVENTION. ONCE CONSIDERED A PROBLEM ONLY IN HIGH-INCOME COUNTRIES (HICS), OBESITY HAS BECOME A MAJOR CONTRIBUTOR TO THE GLOBAL DISEASE BURDEN (FINUCANE AND OTHERS 2011; MISRA AND KHURANA 2008). EXCESS ADIPOSITY, PARTICULARLY AROUND THE VISCERAL ABDOMINAL REGION, IS AN IMPORTANT RISK FACTOR FOR MORBIDITY AND MORTALITY FROM TYPE 2 DIABETES, CARDIOVASCULAR DISEASES, AND SOME CANCERS (DANAEI AND OTHERS 2009; WHITLOCK AND OTHERS 2009; WHO 2009). ALTHOUGH SOME STUDIES HAVE SUGGESTED LOWER MORTALITY AMONG OVERWEIGHT OR OBESE PERSONS THAN AMONG HEALTHY-WEIGHT PERSONS (CARNETHON AND OTHERS 2012), THIS OUTCOME HAS NOT BEEN OBSERVED IN STUDIES THAT PROPERLY ACCOUNT FOR THE CONFOUNDING EFFECTS OF SMOKING, PREEXISTING CHRONIC CONDITIONS, AND OTHER BIASES (GLOBAL BMI MORTALITY COLLABORATION 2016; TOBIAS, PAN, AND HU 2014). THE COSTS OF OBESITY AND COMORBID CONDITIONS ARE STAGGERING AS MEASURED BY BOTH HEALTH CARE EXPENDITURES AND QUALITY OF LIFE, UNDERSCORING THE IMPORTANCE OF IMPLEMENTING OBESITY PREVENTION STRATEGIES AND TREATMENT STRATEGIES ON A GLOBAL SCALE. THE CHANGES NEEDED TO REVERSE GLOBAL TRENDS IN OBESITY WILL LIKELY REQUIRE NUMEROUS INTERVENTIONS AND POLICY RECOMMENDATIONS THAT TARGET DIET, LIFESTYLE, ACCESS TO CARE, AND ENVIRONMENTAL RISK FACTORS. IN THIS CHAPTER, WE SUMMARIZE THE GLOBAL BURDEN OF OBESITY AND THE IMPACT OF A SPECTRUM OF OBESITY RISK FACTORS, RANGING FROM SOCIOPOLITICAL AND ECONOMIC FORCES THAT ARE LARGELY BEYOND AN INDIVIDUAL'S CONTROL TO MODIFIABLE LIFESTYLE FACTORS, AND DISCUSS GENETIC AND EPIGENETIC RISKS. WE ALSO REVIEW THE EFFECTIVENESS OF POPULATION-BASED INTERVENTIONS AND POLICIES FOR PREVENTING OBESITY, SOME INDIVIDUAL-LEVEL TREATMENT OPTIONS ACROSS VARIOUS PLATFORMS, AND THE COST-EFFECTIVENESS OF SELECT INTERVENTIONS.	2017	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         
18  4777  23 NUTRACEUTICALS AND NETWORK PHARMACOLOGY APPROACH FOR ACUTE KIDNEY INJURY: A REVIEW FROM THE DRUG DISCOVERY ASPECT. ACUTE KIDNEY INJURY (AKI) HAS BECOME A GLOBAL HEALTH ISSUE, WITH APPROXIMATELY 12 MILLION REPORTS YEARLY, RESULTING IN A PERSISTENT INCREASE IN MORBIDITY AND MORTALITY RATES. AKI PATHOPHYSIOLOGY IS MULTIFACTORIAL INVOLVING OXIDATIVE STRESS, MITOCHONDRIAL DYSFUNCTION, EPIGENETIC MODIFICATIONS, INFLAMMATION, AND EVENTUALLY, CELL DEATH. HENCE, THERAPIES ABLE TO TARGET MULTIPLE PATHOMECHANISMS CAN AID IN AKI MANAGEMENT. TO CHANGE THE DRUG DISCOVERY FRAMEWORK FROM "ONE DRUG, ONE TARGET" TO "MULTICOMPONENT, MULTITARGET," NETWORK PHARMACOLOGY IS EVOLVING AS A NEXT-GENERATION RESEARCH APPROACH. RESEARCHERS HAVE USED THE NETWORK PHARMACOLOGY APPROACH TO PREDICT THE ROLE OF NUTRACEUTICALS AGAINST DIFFERENT AILMENTS INCLUDING AKI. NUTRACEUTICALS (HERBAL PRODUCTS, ISOLATED NUTRIENTS, AND DIETARY SUPPLEMENTS) BELONG TO THE PIONEERING CATEGORY OF NATURAL PRODUCTS AND HAVE SHOWN PROTECTIVE ACTION AGAINST AKI. NUTRACEUTICALS HAVE RECENTLY DRAWN ATTENTION BECAUSE OF THEIR ABILITY TO PROVIDE PHYSIOLOGICAL BENEFITS WITH LESS TOXIC EFFECTS. THIS REVIEW EMPHASIZES THE NUTRACEUTICALS THAT EXHIBITED RENOPROTECTION AGAINST AKI AND CAN BE USED EITHER AS MONOTHERAPY OR ADJUVANT WITH CONVENTIONAL THERAPIES TO BOOST THEIR EFFECTIVENESS AND LESSEN THE ADVERSE EFFECTS. ADDITIONALLY, THE STUDY SHEDS LIGHT ON THE APPLICATION OF NETWORK PHARMACOLOGY AS A COST-EFFECTIVE AND TIME-SAVING APPROACH FOR THE THERAPEUTIC TARGET PREDICTION OF NUTRACEUTICALS AGAINST AKI.	2023	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                
19  6153  19 THE FUNCTION OF THE METALS IN REGULATING EPIGENETICS DURING PARKINSON'S DISEASE. PARKINSON'S MEANS PARKINSON'S DISEASE, A CHRONIC DEGENERATIVE DISEASE OF CENTRAL NERVOUS SYSTEM. THE MAIN AREA WHICH IS AFFECTED BY THIS DISEASE IS MOTOR SYSTEM. SINCE IT FIRSTLY FOUNDED BY JAMES PARKINSON IN HIS 1817 PUBLICATION, NOWADAYS, PEOPLE STILL HAVE LOTS OF QUESTIONS ABOUT THIS DISEASE. THIS REVIEW MAINLY SUMMARIZES THE EPIGENETICS OF PARKINSON'S. DNA METHYLATION IS ONE OF THE EPIGENETIC MECHANISMS OF PARKINSON'S. DURING THE DEVELOPMENT OF DISEASE, GLOBAL HYPOMETHYLATION, AND HYPERMETHYLATION HAPPEN IN DIFFERENT AREAS OF PATIENTS. ANOTHER EPIGENETIC MECHANISM IS HISTONE MODIFICATION. PEOPLE BELIEVE THAT SOME METALS CAN INDUCE PARKINSON'S DISEASE BY MODULATING EPIGENETIC MECHANISMS. THIS REVIEW SUMMARIZES THE RELATIONSHIPS BETWEEN DIFFERENT METALS AND PARKINSON'S DISEASE. HOWEVER, THE SPECIFIC ROLES OF MOST METALS IN EPIGENETICS ARE STILL UNKNOWN, WHICH NEED FURTHER RESEARCH.	2020	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              
20  1836  19 EFFECTS OF NUTRIENT AND BIOACTIVE FOOD COMPONENTS ON ALZHEIMER'S DISEASE AND EPIGENETIC. ALZHEIMER'S DISEASE (AD) IS THE MOST COMMON FORM OF DEMENTIA IN THE ELDERLY AND IS A CHRONIC NEURODEGENERATIVE DISEASE THAT IS BECOMING WIDESPREAD. FOR THIS REASON, IN RECENT YEARS FACTORS AFFECTING THE DEVELOPMENT, PROGRESSION AND COGNITIVE FUNCTION OF THE AD HAVE BEEN EMPHASIZED. NUTRIENTS AND OTHER BIOACTIVE NUTRIENTS ARE AMONG THE FACTORS THAT ARE EFFECTIVE IN AD. IN PARTICULAR, VITAMINS A, C AND E, VITAMINS B(1), B(6) AND B(12), FOLATE, MAGNESIUM, CHOLINE, INOSITOL, ANTHOCYANINS, ISOFLAVONES ETC. NUTRIENTS AND BIOACTIVE NUTRIENTS ARE KNOWN TO BE EFFECTIVE IN THE DEVELOPMENT OF AD. NUTRIENTS AND NUTRIENT COMPONENTS MAY ALSO HAVE AN EPIGENETIC EFFECT ON AD. AT THE SAME TIME, NUTRIENTS AND BIOACTIVE FOOD COMPONENTS SLOW DOWN THE PROGRESSION OF THE DISEASE. FOR THIS REASON, THE EFFECT OF NUTRIENTS AND FOOD COMPONENTS ON AD WAS EXAMINED IN THIS REVIEW.	2019