1 187 129 ACE2 EXPRESSION IS INCREASED IN THE LUNGS OF PATIENTS WITH COMORBIDITIES ASSOCIATED WITH SEVERE COVID-19. THE PANDEMIC CAUSED BY THE SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2 (SARS-COV-2) HAS RESULTED IN SEVERAL THOUSAND DEATHS WORLDWIDE IN JUST A FEW MONTHS. PATIENTS WHO DIED FROM CORONAVIRUS DISEASE 2019 (COVID-19) OFTEN HAD COMORBIDITIES, SUCH AS HYPERTENSION, DIABETES, AND CHRONIC OBSTRUCTIVE LUNG DISEASE. THE ANGIOTENSIN-CONVERTING ENZYME 2 (ACE2) WAS IDENTIFIED AS A CRUCIAL FACTOR THAT FACILITATES SARS-COV2 TO BIND AND ENTER HOST CELLS. TO DATE, NO STUDY HAS ASSESSED THE ACE2 EXPRESSION IN THE LUNGS OF PATIENTS WITH THESE DISEASES. HERE, WE ANALYZED OVER 700 LUNG TRANSCRIPTOME SAMPLES OF PATIENTS WITH COMORBIDITIES ASSOCIATED WITH SEVERE COVID-19 AND FOUND THAT ACE2 WAS HIGHLY EXPRESSED IN THESE PATIENTS, COMPARED TO CONTROL INDIVIDUALS. THIS FINDING SUGGESTS THAT PATIENTS WITH SUCH COMORBIDITIES MAY HAVE HIGHER CHANCES OF DEVELOPING SEVERE COVID-19. WE ALSO FOUND OTHER GENES, SUCH AS RAB1A, THAT CAN BE IMPORTANT FOR SARS-COV-2 INFECTION IN THE LUNG. CORRELATION AND NETWORK ANALYSES REVEALED MANY POTENTIAL REGULATORS OF ACE2 IN THE HUMAN LUNG, INCLUDING GENES RELATED TO HISTONE MODIFICATIONS, SUCH AS HAT1, HDAC2, AND KDM5B. IN FACT, EPIGENETIC MARKS FOUND IN ACE2 LOCUS WERE COMPATIBLE TO WITH THOSE PROMOTED BY KDM5B. OUR SYSTEMS BIOLOGY APPROACH OFFERS A POSSIBLE EXPLANATION FOR INCREASE OF COVID-19 SEVERITY IN PATIENTS WITH CERTAIN COMORBIDITIES. 2020 2 6120 43 THE EPIGENETIC IMPLICATION IN CORONAVIRUS INFECTION AND THERAPY. EPIGENETICS IS A RELATIVELY NEW FIELD OF SCIENCE THAT STUDIES THE GENETIC AND NON-GENETIC ASPECTS RELATED TO HERITABLE PHENOTYPIC CHANGES, FREQUENTLY CAUSED BY ENVIRONMENTAL AND METABOLIC FACTORS. IN THE HOST, THE EPIGENETIC MACHINERY CAN REGULATE GENE EXPRESSION THROUGH A SERIES OF REVERSIBLE EPIGENETIC MODIFICATIONS, SUCH AS HISTONE METHYLATION AND ACETYLATION, DNA/RNA METHYLATION, CHROMATIN REMODELING, AND NON-CODING RNAS. THE CORONAVIRUS DISEASE 19 (COVID-19) IS A HIGHLY TRANSMITTABLE AND PATHOGENIC VIRAL INFECTION. THE SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2 (SARS-COV-2), WHICH EMERGED IN WUHAN, CHINA, AND SPREAD WORLDWIDE, CAUSES IT. COVID-19 SEVERITY AND CONSEQUENCES LARGELY DEPEND ON PATIENT AGE AND HEALTH STATUS. IN THIS REVIEW, WE WILL SUMMARIZE AND COMPARATIVELY ANALYZE HOW VIRUSES REGULATE THE HOST EPIGENOME. MAINLY, WE WILL BE FOCUSING ON HIGHLY PATHOGENIC RESPIRATORY RNA VIRUS INFECTIONS SUCH AS CORONAVIRUSES. IN THIS CONTEXT, EPIGENETIC ALTERATIONS MIGHT PLAY AN ESSENTIAL ROLE IN THE ONSET OF CORONAVIRUS DISEASE COMPLICATIONS. ALTHOUGH MANY THERAPEUTIC APPROACHES ARE UNDER STUDY, MORE RESEARCH IS URGENTLY NEEDED TO IDENTIFY EFFECTIVE VACCINE OR SAFER CHEMOTHERAPEUTIC DRUGS, INCLUDING EPIGENETIC DRUGS, TO COPE WITH THIS VIRAL OUTBREAK AND TO DEVELOP PRE- AND POST-EXPOSURE PROPHYLAXIS AGAINST COVID-19. 2020 3 1207 43 COVID-19 AND CROSSTALK WITH THE HALLMARKS OF AGING. WITHIN THE PAST SEVERAL DECADES, THE EMERGENCE OF NEW VIRAL DISEASES WITH SEVERE HEALTH COMPLICATIONS AND MORTALITY IS EVIDENCE OF AN AGE-DEPENDENT, COMPROMISED BODILY RESPONSE TO ABRUPT STRESS WITH CONCOMITANTLY REDUCED IMMUNITY. THE NEW SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2, SARS-COV-2, CAUSES CORONAVIRUS DISEASE 2019 (COVID-19). IT HAS INCREASED MORBIDITY AND MORTALITY IN PERSONS WITH UNDERLYING CHRONIC DISEASES AND THOSE WITH A COMPROMISED IMMUNE SYSTEM REGARDLESS OF AGE AND IN OLDER ADULTS WHO ARE MORE LIKELY TO HAVE THESE CONDITIONS. WHILE SARS-COV-2 IS HIGHLY VIRULENT, THERE IS VARIABILITY IN THE SEVERITY OF THE DISEASE AND ITS COMPLICATIONS IN HUMANS. SEVERE PNEUMONIA, ACUTE RESPIRATORY DISTRESS SYNDROME, LUNG FIBROSIS, CARDIOVASCULAR EVENTS, ACUTE KIDNEY INJURY, STROKE, HOSPITALIZATION, AND MORTALITY HAVE BEEN REPORTED THAT RESULT FROM PATHOGEN-HOST INTERACTIONS. HALLMARKS OF AGING, INTERACTING WITH ONE ANOTHER, HAVE BEEN PROPOSED TO INFLUENCE HEALTH SPAN IN OLDER ADULTS, POSSIBLY VIA MECHANISMS REGULATING THE IMMUNE SYSTEM. HERE, WE REVIEW THE POTENTIAL ROLES OF THE HALLMARKS OF AGING, COUPLED WITH HOST-CORONAVIRUS INTERACTIONS. OF THESE HALLMARKS, WE FOCUSED ON THOSE THAT DIRECTLY OR INDIRECTLY INTERACT WITH VIRAL INFECTIONS, INCLUDING IMMUNOSENESCENCE, INFLAMMATION AND INFLAMMASOMES, ADAPTIVE IMMUNOSENESCENCE, GENOMIC INSTABILITY, MITOCHONDRIAL DYSFUNCTION, EPIGENETIC ALTERATIONS, TELOMERE ATTRITION, AND IMPAIRED AUTOPHAGY. THESE HALLMARKS LIKELY CONTRIBUTE TO THE INCREASED PATHOPHYSIOLOGICAL RESPONSES TO SARS-COV-2 AMONG OLDER ADULTS AND MAY PLAY ROLES AS AN ADDITIVE RISK OF ACCELERATED BIOLOGICAL AGING EVEN AFTER RECOVERY. WE ALSO BRIEFLY DISCUSS THE ROLE OF ANTIAGING DRUG CANDIDATES THAT REQUIRE PARAMOUNT ATTENTION IN COVID-19 RESEARCH. 2020 4 727 38 CAN VITAMINS, AS EPIGENETIC MODIFIERS, ENHANCE IMMUNITY IN COVID-19 PATIENTS WITH NON-COMMUNICABLE DISEASE? PURPOSE OF REVIEW: THE HIGHLY INFECTIOUS TRANSMISSIBLE DISEASE, THE NOVEL SARS-COV-2, CAUSING THE CORONAVIRUS DISEASE (COVID-19), HAS A MEDIAN INCUBATION TIME OF 5 TO 15 DAYS. THE SYMPTOMS VARY FROM PERSON TO PERSON AND MANY ARE "HIDDEN CARRIERS." FEW PEOPLE EXPERIENCE IMMEDIATE REACTION AND EVEN DEATH WITHIN 48 H OF INFECTION. HOWEVER, MANY SHOW MILD TO CHRONIC SYMPTOMS AND RECOVER. NEVERTHELESS, THE DEATH RATE DUE TO COVID-19 TRANSMISSION IS HIGH ESPECIALLY AMONG PATIENTS WITH NON-COMMUNICABLE DISEASES. THE PURPOSE OF THIS REVIEW IS TO PROVIDE EVIDENCE TO CONSIDER VITAMINS AS EPIGENETIC MODIFIERS TO ENHANCE IMMUNITY AND REDUCE INFLAMMATORY RESPONSE IN COVID-19 PATIENTS WITH NON-COMMUNICABLE DISEASES. RECENT FINDINGS: CLINICAL EVIDENCE HAS SUGGESTED THE RISK OF GETTING INFECTED IS HIGH AMONG INDIVIDUALS WITH NON-COMMUNICABLE DISEASES SUCH AS CARDIOVASCULAR DISEASE, TYPE-2 DIABETES, CANCER, ACUTE RESPIRATORY DISTRESS SYNDROME, AND RENAL DISEASE, AS WELL AS THE ELDERLY WITH HIGH MORTALITY RATE AMONG THE COHORT. THE IMPACT IS DUE TO AN ALREADY COMPROMISED IMMUNE SYSTEM OF PATIENTS. EVERY PATIENT HAS A DIFFERENT RESPONSE TO COVID-19, WHICH SHOWS THAT THE ABILITY TO COMBAT THE DEADLY VIRUS VARIES INDIVIDUALLY. THUS, TREATMENT CAN BE PERSONALIZED AND ADJUSTED TO HELP PROTECT AND COMBAT COVID-19 INFECTIONS, ESPECIALLY IN INDIVIDUALS WITH NON-COMMUNICABLE DISEASES. BASED ON CURRENT PUBLISHED SCIENTIFIC AND MEDICAL EVIDENCE, THE SUGGESTIONS MADE IN THIS ARTICLE FOR COMBINATION OF VITAMIN THERAPY AS EPIGENETIC MODIFIERS TO CONTROL THE UNREGULATED INFLAMMATORY AND CYTOKINE MARKER EXPRESSIONS, FURTHER NEEDS TO BE CLINICALLY PROVEN. FUTURE RESEARCH AND CLINICAL TRIALS CAN APPLY THE SUGGESTIONS GIVEN IN THIS ARTICLE TO SUPPORT METABOLIC ACTIVITIES IN PATIENTS AND ENHANCE THE IMMUNE RESPONSE. 2020 5 5135 40 POTENTIAL MECHANISMS FOR LUNG FIBROSIS ASSOCIATED WITH COVID-19 INFECTION. PULMONARY FIBROSIS IS A SEQUELAE OF SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2 (SARS-COV-2) INFECTION THAT CURRENTLY LACKS EFFECTIVE PREVENTATIVE OR THERAPEUTIC MEASURES. POST-VIRAL LUNG FIBROSIS DUE TO SARS-COV-2 HAS BEEN SHOWN TO BE PROGRESSIVE ON SELECTED PATIENTS USING IMAGING STUDIES. PERSISTENT INFILTRATION OF MACROPHAGES AND MONOCYTES, A MAIN FEATURE OF SARS-COV-2 PULMONARY FIBROSIS, AND LONG-LIVED CIRCULATING INFLAMMATORY MONOCYTES MIGHT BE DRIVING FACTORS PROMOTING THE PROFIBROTIC MILIEU IN THE LUNG. THE UPSTREAM SIGNAL(S) THAT REGULATES THE PRESENCE OF THESE IMMUNE CELLS (DESPITE COMPLETE VIRAL CLEARANCE) REMAINS TO BE EXPLORED. CURRENT DATA INDICATE THAT MUCH OF THE STIMULATING SIGNALS ARE LOCALIZED IN THE LUNGS. HOWEVER, AN ONGOING LOW-GRADE SYSTEMIC INFLAMMATION IN LONG CORONAVIRUS DISEASE 2019 (COVID-19) SYMPTOMS SUGGESTS THAT CERTAIN NON-PULMONARY REGULATORS SUCH AS EPIGENETIC CHANGES IN HEMATOPOIETIC STEM CELLS MIGHT BE CRITICAL TO THE CHRONIC INFLAMMATORY RESPONSE. SINCE NEARLY ONE-THIRD OF THE WORLD POPULATION HAVE BEEN INFECTED, A TIMELY UNDERSTANDING OF THE UNDERLYING PATHOGENESIS LEADING TO TISSUE REMODELING IS REQUIRED. HEREIN, WE REVIEW THE POTENTIAL PATHOGENIC MECHANISMS DRIVING LUNG FIBROSIS FOLLOWING SARS-COV-2 INFECTION BASED UPON AVAILABLE STUDIES AND OUR PRELIMINARY FINDINGS (GRAPHICAL ABSTRACT). 2023 6 1711 39 DYSFUNCTIONAL STATE OF T CELLS OR EXHAUSTION DURING CHRONIC VIRAL INFECTIONS AND COVID-19: A REVIEW. CORONAVIRUS DISEASE 2019 (COVID-19) CONTINUOUSLY AFFECTING THE LIVES OF MILLIONS OF PEOPLE. THE VIRUS IS SPREAD THROUGH THE RESPIRATORY ROUTE TO AN UNINFECTED PERSON, CAUSING MILD-TO-MODERATE RESPIRATORY DISEASE-LIKE SYMPTOMS THAT SOMETIMES PROGRESS TO SEVERE FORM AND CAN BE FATAL. WHEN THE HOST IS INFECTED WITH THE VIRUS, BOTH INNATE AND ADAPTIVE IMMUNITY COMES INTO PLAY. THE EFFECTOR T CELLS ACT AS THE MASTER PLAYER OF ADAPTIVE IMMUNE RESPONSE IN ERADICATING THE VIRUS FROM THE SYSTEM. BUT DURING CANCER AND CHRONIC VIRAL INFECTIONS, THE FATE OF AN EFFECTOR T CELL IS ALTERED, AND THE T CELL MAY ENTERS A STATE OF EXHAUSTION, WHICH IS MARKED BY LOSS OF EFFECTOR FUNCTION, DEPLETED PROLIFERATIVE CAPACITY AND CYTOTOXIC EFFECT ACCOMPLISHED BY AN INCREASED EXPRESSION OF NUMEROUS INHIBITORY RECEPTORS SUCH AS PROGRAMMED CELL DEATH PROTEIN 1 (PD-1), LYMPHOCYTE-ACTIVATION PROTEIN 3 (LAG-3), AND CYTOTOXIC T LYMPHOCYTE-ASSOCIATED ANTIGEN 4 (CTLA-4) ON THEIR SURFACE. VARIOUS OTHER TRANSCRIPTIONAL AND EPIGENETIC CHANGES TAKE PLACE INSIDE THE T CELL WHEN IT ENTERS INTO AN EXHAUSTED STATE. LATEST STUDIES POINT TOWARD THE INDUCTION OF AN ABNORMAL IMMUNE RESPONSE SUCH AS LYMPHOPENIA, CYTOKINE STORM, AND T CELL EXHAUSTION DURING SARS-COV-2 (SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2) INFECTION. THIS REVIEW SHEDS LIGHT ON THE DYSFUNCTIONAL STATE OF T CELLS DURING CHRONIC VIRAL INFECTION AND COVID-19. UNDERSTANDING THE CAUSE AND THE EFFECT OF T CELL EXHAUSTION OBSERVED DURING COVID-19 MAY HELP RESOLVE NEW THERAPEUTIC POTENTIALS FOR TREATING CHRONIC INFECTIONS AND OTHER DISEASES. 2022 7 734 34 CANCER HEALTHCARE DISPARITIES AMONG AFRICAN AMERICANS IN THE UNITED STATES. A NEED EXISTS TO EXAMINE RACIAL DISPARITIES IN THE HEALTHCARE ARENA AND THE IMPACT ON PATIENTS WITH CANCER. DESPITE ONGOING EFFORTS TO INCREASE EQUITY IN PRIMARY HEALTHCARE ACCESS, RACIAL AND SOCIOECONOMIC DISPARITIES PERSIST, THUS CONTRIBUTING TO DISPROPORTIONATE TREATMENT OUTCOMES AND SURVIVORSHIP AMONG MINORITY AND LOW-INCOME PATIENTS. SUCH DISPARITIES HAVE BEEN REVEALED IN TREATMENT COHORTS OF PATIENTS WITH MULTIPLE FORMS OF CANCER, INCLUDING BREAST, CERVICAL, OVARIAN, ENDOMETRIAL, PROSTATE, LUNG, COLORECTAL, GASTROINTESTINAL, AND HEPATOCELLULAR, AND HAVE BEEN ATTRIBUTED TO A RANGE OF CO-OCCURRING BEHAVIORAL, SOCIAL DETERMINANTS OF HEALTH, UNDERLYING GENETIC FACTORS, AS WELL AS ACCESS TO EDUCATIONAL OPPORTUNITIES THAT LIMIT THE QUALITY OF INFORMED HEALTHCARE. THESE VARIOUS INTERRELATED FACTORS WIDEN CANCER HEALTHCARE DISPARITIES SYNERGISTICALLY THROUGHOUT UNDERSERVED COMMUNITIES, AND THEIR INFLUENCE HAS BEEN AMPLIFIED BY THE CORONAVIRUS DISEASE 2019 (COVID-19) PANDEMIC. FUNDAMENTALLY, A LACK OF BASIC AND CLINICAL RESEARCH EXISTS THAT FAILS TO ADEQUATELY REFLECT DIVERSITY AND MINORITY INVOLVEMENT IN DRUG DEVELOPMENT. ALTHOUGH OVERCOMING THE OBSTACLES RESPONSIBLE FOR CHRONIC TREATMENT DISPARITIES IS A FORMIDABLE TASK, PROMISING MEANS OF ACHIEVING MORE UNIFORM QUALITY HEALTHCARE ARE BECOMING MORE CLEARLY ELUCIDATED. TO REDUCE DISEASE PROGRESSION, INCREASE OVERALL SURVIVAL, AND IMPROVE THE HEALTH OF VULNERABLE POPULATIONS, IT IS NECESSARY TO IDENTIFY AND FULLY DISCLOSE ENVIRONMENTAL, BIOLOGICAL, AND ANCESTRAL FACTORS THAT IMPACT THE RISK FOR CANCER; HEAL HISTORICAL FRACTURES WITHIN COMMUNITIES; AND INCREASE PARTICIPATION OF RACIAL AND ETHNIC MINORITIES IN SCREENING EFFORTS AND RESEARCH STUDIES. THIS REQUIRES DEVELOPING A SYSTEM OF JUSTICE AND TRUST BASED ON SPECIFIC, SOLUTION-ORIENTED GRASSROOTS COMMUNITY EFFORTS WORKING IN TANDEM WITH MEDICAL AND PHARMACEUTICAL LEADERS. BY FULLY EXPLORING AND PINPOINTING THE UNDERLYING CAUSES OF HEALTHCARE DISPARITIES, IT SHOULD BE POSSIBLE TO DEFINE STRATEGIES AND INTERVENTIONS MOST LIKELY TO TRANSFORM CANCER CARE. THE ULTIMATE GOAL IS UNDERSTANDING INDIVIDUAL, CULTURAL, AND BIOLOGICAL VULNERABILITIES, INCLUDING ENVIRONMENTAL AND EPIGENETIC LIABILITIES, TO OPTIMIZE CANCER PREVENTION, DIAGNOSIS, AND TREATMENT. 2022 8 6407 37 THE SEVERITY OF SARS-COV-2 INFECTION IS DICTATED BY HOST FACTORS? EPIGENETIC PERSPECTIVES. THE EMERGENCE OF COVID-19, CAUSED BY SARS-COV-2 POSES A SIGNIFICANT THREAT TO HUMANS AS IT IS HIGHLY CONTAGIOUS WITH INCREASING MORTALITY. THERE EXISTS A HIGH DEGREE OF HETEROGENEITY IN THE MORTALITY RATES OF COVID-19 ACROSS THE GLOBE. THERE ARE MULTIPLE SPECULATIONS ON THE VARYING DEGREE OF MORTALITY. STILL, ALL THE CLINICAL REPORTS HAVE INDICATED THAT PREEXISTING CHRONIC DISEASES LIKE HYPERTENSION, DIABETES, CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD), KIDNEY DISORDERS, AND CARDIOVASCULAR DISEASES ARE ASSOCIATED WITH THE INCREASED RISK FOR HIGH MORTALITY IN SARS-COV-2 INFECTED PATIENTS. IT IS WORTH NOTING THAT HOST FACTORS, MAINLY EPIGENETIC FACTORS COULD PLAY A SIGNIFICANT ROLE IN DECIDING THE OUTCOME OF COVID-19 DISEASES. OVER THE RECENT YEARS, IT IS EVIDENT THAT CHRONIC DISEASES ARE DEVELOPED DUE TO ALTERED EPIGENOME THAT INCLUDES A SELECTIVE LOSS/GAIN OF DNA AND HISTONE METHYLATION ON THE CHROMATIN OF THE CELLS. SINCE, THERE IS A HIGH POSITIVE CORRELATION BETWEEN CHRONIC DISEASES AND ELEVATED MORTALITY DUE TO SARS-COV-2, IN THIS REVIEW; WE DISCUSS THE OVERALL PICTURE OF THE ABERRANT EPIGENOME MAP IN VARYING CHRONIC AILMENTS AND ITS IMPLICATIONS IN COVID-19 DISEASE SEVERITY AND HIGH MORTALITY. 2021 9 6878 34 [REGIONAL EXPERIENCE OF A COMPREHENSIVE DYNAMIC ASSESSMENT OF THE ADOLESCENTS' HEALTH STATUS WITH POST-COVID-19 SYNDROME DURING AFTERCARE IN A SANATORIUM]. OBJECTIVE: TO DETERMINE THE CHARACTERISTICS OF SANATORIUM-RESORT THERAPY IMPACT ON CHILDREN WITH POST-COVID-19 SYNDROME OF VARIOUS SEVERITY, AS WELL AS TO REVEAL ASSOCIATION OF ITS SEVERITY WITH FAMILY HISTORY DATA AND GENETIC POLYMORPHISMS OF ALPHA-1-ANTITRYPSIN-SERPIN-1 COMPLEX. MATERIAL AND METHODS: THIS 2-WEEK RETROSPECTIVE COHORT STUDY INVOLVED 42 ADOLESCENTS AFTER NEW CORONAVIRUS INFECTION (COVID-19). THE FIRST GROUP INCLUDED 28 (67%) PATIENTS (MEAN AGE 13.1+/-0.8 YEARS) AFTER MILD COVID-19 (WITHOUT CONFIRMED CORONAVIRUS PNEUMONIA), THE SECOND GROUP - 14 (33%) PATIENTS (MEAN AGE 14.5+/-0.1.2 YEARS) AFTER MODERATE OR SEVERE DISEASE (WITH CONFIRMED CORONAVIRUS PNEUMONIA). A COMPLEX OF PROCEDURES, ACCORDING TO THE APPROVED STANDARD, WAS PRESCRIBED FOR ALL PATIENTS ADMITTED AFTER OUTPATIENT AND HOSPITAL TREATMENT TO THE PULMONOLOGY DEPARTMENT OF THE STATE CHILDREN'S SANATORIUM IN ORDER TO AFTERCARE. THE CERTAIN FOLLOW-UP PARAMETERS WERE EVALUATED: SYMPTOMS SEVERITY, LIFE QUALITY, RESPIRATORY FUNCTION AND RESPIRATORY GASES, AS WELL AS FAMILY MEDICAL HISTORY AND ALPHA-1-ANTITRYPSIN-SERPIN-1 COMPLEX. RESULTS: PATIENTS AFTER MODERATE AND SEVERE COVID-19 HAD INITIALLY LOWER AND LESS DYNAMIC GROWTH OF INTEGRAL LIFE QUALITY INDEX, MORE TORPID FOLLOW-UP RATES OF SPIROMETRY, PULSE OXIMETRY AND EXHALED GASES. ADDITIONALLY, THE HIGHER INCIDENCE DEGREE OF ADVERSE FAMILY MEDICAL HISTORY ASSOCIATED WITH RESPIRATORY ILLNESSES WAS ESTABLISHED IN THE GROUP AFTER NEW CORONAVIRUS INFECTION. MOREOVER, RELATIVELY MORE DEFICIENT ALPHA-1-ANTITRYPSIN AND MORE FREQUENT HETEROZYGOUS POLYMORPHISM TYPE OF SERPIN-1 WERE FOUND IN THE GROUP AFTER SEVERE NEW CORONAVIRUS INFECTION. CONCLUSION: THE REVEALED COMPLEX OF EPIGENETIC AND GENETIC FACTORS MAY INDICATE VARIOUS RISK AND DEVELOPMENT PHENOTYPES OF BOTH ACUTE AND CHRONIC RESPIRATORY DISEASES. 2023 10 1209 50 COVID-19: A REVIEW ON SARS-COV-2 ORIGIN, EPIDEMIOLOGY, VIROLOGY, CLINICAL MANIFESTATIONS AND COMPLICATIONS WITH SPECIAL EMPHASIS ON ADVERSE OUTCOME IN BHOPAL GAS TRAGEDY SURVIVOR. AFTER THE GLOBAL OUTBREAK OF CORONAVIRUSES CAUSED DISEASES SUCH AS MIDDLE EAST RESPIRATORY SYNDROME (MERS) AND SEVERE ACUTE RESPIRATORY SYNDROME (SARS), AN OUTBREAK DUE TO THESE VIRUSES OCCURRED IN DECEMBER, 2019 IN WUHAN, HUBEI PROVINCE, CHINA AND LED TO A WORLDWIDE SPREAD. CORONAVIRUS 2019 DISEASE (COVID-19) HAS EMERGED AS A SERIOUS GLOBAL HEALTH EMERGENCY AND SPREAD FROM A PERSON TO ANOTHER WHO HAS THE VIRUS. BUT THE SCOPE OF AN INTERMEDIATE HOST IS NOT KNOWN. POPULATION AT HIGHER RISK INCLUDES INDIVIDUALS IN HIGHER AGE GROUP (>60 YEARS) OR WITH COMORBIDITIES SUCH AS DIABETES, HYPERTENSION, CARDIOVASCULAR DISEASE AND WEAKER IMMUNE SYSTEM. MANY UNKNOWN AND UNDERESTIMATE RISK FACTORS COULD BE RESPONSIBLE FOR ADVERSE OUTCOMES IN COVID-19. THESE RISK FACTORS SHOULD BE APPROPRIATELY IDENTIFIED, ADDRESSED AND NECESSARY ACTIONS SHOULD BE TAKEN TO MITIGATE THE EFFECT OF COVID-19 PANDEMIC. BHOPAL GAS TRAGEDY WAS ONE OF THE WORLD'S WORST INDUSTRIAL CHEMICAL LEAK DISASTER. THE SURVIVORS OF THIS INCIDENT STILL SUFFER FROM THE VARIOUS COMPLICATIONS SUCH AS INCREASED RATE OF CANCERS, CHRONIC ILLNESS LIKE TUBERCULOSIS, RESPIRATORY DISEASES, BIRTH DEFECTS, NERVE INJURY, GROWTH RETARDATIONS, GYNECOLOGICAL ILLNESS AND MANY MORE. THE SURVIVORS OF BHOPAL GAS TRAGEDY ARE AT HIGHER RISK OF DEVELOPING COVID-19 RELATED ADVERSE OUTCOME. ONE OF THE POSSIBLE EXPLANATIONS CAN BE LONG TERM EFFECT OF METHYL ISOCYANATE (MIC). MIC EXPOSURE CAN LEAD TO POSSIBLE TOXIC EFFECT ON GENETIC, EPIGENETIC AND NON-GENETIC FACTORS. IN THIS REVIEW, WE AIM TO ESTABLISH THE SCIENTIFIC BASIS FOR ADVERSE OUTCOME IN COVID-19 PATIENTS WHO ARE ALSO VICTIMS OF BHOPAL GAS TRAGEDY. 2021 11 74 38 A MULTIDISCIPLINARY APPROACH AND CURRENT PERSPECTIVE OF NONALCOHOLIC FATTY LIVER DISEASE: A SYSTEMATIC REVIEW. IN RECENT TIMES, NONALCOHOLIC FATTY LIVER DISEASE (NAFLD) HAS BEEN CONSIDERED ONE OF THE MAJOR CAUSES OF LIVER DISEASE ACROSS THE WORLD. NAFLD IS DEFINED AS THE DEPOSITION OF TRIGLYCERIDES IN THE LIVER AND IS ASSOCIATED WITH OBESITY AND METABOLIC SYNDROME. HYPERINSULINEMIA, INSULIN RESISTANCE (IR), FATTY LIVER, HEPATOCYTE INJURY, UNBALANCED PROINFLAMMATORY CYTOKINES, MITOCHONDRIAL DYSFUNCTION, OXIDATIVE STRESS, LIVER INFLAMMATION, AND FIBROSIS ARE THE MAIN PATHOGENESIS IN NAFLD. RECENT STUDIES SUGGEST THAT THE ACTION OF INTESTINAL MICROBIOTA THROUGH CHRONIC INFLAMMATION, INCREASED INTESTINAL PERMEABILITY, AND ENERGY UPTAKE PLAYS A VITAL ROLE IN NAFLD. MOREOVER, POLYCYSTIC OVARIAN SYNDROME ALSO CAUSES NAFLD DEVELOPMENT THROUGH IR. AGE, GENDER, RACE, ETHNICITY, SLEEP, DIET, SEDENTARY LIFESTYLE, AND GENETIC AND EPIGENETIC PATHWAYS ARE SOME CONTRIBUTING FACTORS OF NAFLD THAT CAN EXACERBATE THE RISK OF LIVER CIRRHOSIS AND HEPATOCELLULAR CARCINOMA (HCC) AND EVENTUALLY LEAD TO DEATH. NAFLD HAS VARIOUS PRESENTATIONS, INCLUDING FATIGUE, UNEXPLAINED WEIGHT LOSS, BLOATING, UPPER ABDOMINAL PAIN, DECREASED APPETITE, HEADACHE, ANXIETY, POOR SLEEP, INCREASED THIRST, PALPITATION, AND A FEELING OF WARMTH. SOME STUDIES HAVE SHOWN THAT NAFLD WITH SEVERE CORONAVIRUS DISEASE 2019 (COVID-19) HAS POOR OUTCOMES. THE GOLD STANDARD FOR NAFLD DIAGNOSIS IS LIVER BIOPSY. OTHER DIAGNOSTIC TOOLS ARE IMAGING TESTS, SERUM BIOMARKERS, MICROBIOTA MARKERS, AND TESTS FOR EXTRAHEPATIC COMPLICATIONS. THERE ARE NO SPECIFIC TREATMENTS FOR NAFLD. THEREFORE, THE MAIN CONCERN FOR NAFLD IS TREATING THE COMORBID CONDITIONS SUCH AS ANTI-DIABETIC AGENTS FOR TYPE 2 DIABETES MELLITUS, STATINS TO REDUCE HCC PROGRESSION, ANTIOXIDANTS TO PREVENT HEPATOCELLULAR DAMAGE, AND BARIATRIC SURGERY FOR PATIENTS WITH A BMI OF >40 KG/M(2) AND >35 KG/M(2) WITH COMORBIDITIES. LIFESTYLE AND DIETARY CHANGES ARE CONSIDERED PREVENTIVE STRATEGIES AGAINST NAFLD ADVANCEMENT. INADEQUATE TREATMENT OF NAFLD FURTHER LEADS TO CARDIAC CONSEQUENCES, SLEEP APNEA, CHRONIC KIDNEY DISEASE, AND INFLAMMATORY BOWEL DISEASE. IN THIS SYSTEMATIC REVIEW, WE HAVE BRIEFLY DISCUSSED THE RISK FACTORS, PATHOGENESIS, CLINICAL FEATURES, AND NUMEROUS CONSEQUENCES OF NAFLD. WE HAVE ALSO REVIEWED VARIOUS GUIDELINES FOR NAFLD DIAGNOSIS ALONG WITH EXISTING THERAPEUTIC STRATEGIES FOR THE MANAGEMENT AND PREVENTION OF THE DISEASE. 2022 12 4739 38 NOVEL GENE-SPECIFIC TRANSLATION MECHANISM OF DYSREGULATED, CHRONIC INFLAMMATION REVEALS PROMISING, MULTIFACETED COVID-19 THERAPEUTICS. HYPERINFLAMMATION AND LYMPHOPENIA PROVOKED BY SARS-COV-2-ACTIVATED MACROPHAGES CONTRIBUTE TO THE HIGH MORTALITY OF CORONAVIRUS DISEASE 2019 (COVID-19) PATIENTS. THUS, DEFINING HOST PATHWAYS ABERRANTLY ACTIVATED IN PATIENT MACROPHAGES IS CRITICAL FOR DEVELOPING EFFECTIVE THERAPEUTICS. WE DISCOVERED THAT G9A, A HISTONE METHYLTRANSFERASE THAT IS OVEREXPRESSED IN COVID-19 PATIENTS WITH HIGH VIRAL LOAD, ACTIVATES TRANSLATION OF SPECIFIC GENES THAT INDUCE HYPERINFLAMMATION AND IMPAIRMENT OF T CELL FUNCTION OR LYMPHOPENIA. THIS NONCANONICAL, PRO-TRANSLATION ACTIVITY OF G9A CONTRASTS WITH ITS CANONICAL EPIGENETIC FUNCTION. IN ENDOTOXIN-TOLERANT (ET) MACROPHAGES THAT MIMIC CONDITIONS WHICH RENDER PATIENTS WITH PRE-EXISTING CHRONIC INFLAMMATORY DISEASES VULNERABLE TO SEVERE SYMPTOMS, OUR CHEMOPROTEOMIC APPROACH WITH A BIOTINYLATED INHIBITOR OF G9A IDENTIFIED MULTIPLE G9A-ASSOCIATED TRANSLATION REGULATORY PATHWAYS THAT WERE UPREGULATED BY SARS-COV-2 INFECTION. FURTHER, QUANTITATIVE TRANSLATOME ANALYSIS OF ET MACROPHAGES TREATED PROGRESSIVELY WITH THE G9A INHIBITOR PROFILED G9A-TRANSLATED PROTEINS THAT UNITE THE NETWORKS ASSOCIATED WITH VIRAL REPLICATION AND THE SARS-COV-2-INDUCED HOST RESPONSE IN SEVERE PATIENTS. ACCORDINGLY, INHIBITION OF G9A-ASSOCIATED PATHWAYS PRODUCED MULTIFACETED, SYSTEMATIC EFFECTS, NAMELY, RESTORATION OF T CELL FUNCTION, MITIGATION OF HYPERINFLAMMATION, AND SUPPRESSION OF VIRAL REPLICATION. IMPORTANTLY, AS A HOST-DIRECTED MECHANISM, THIS G9A-TARGETED, COMBINED THERAPEUTICS IS REFRACTORY TO EMERGING ANTIVIRAL-RESISTANT MUTANTS OF SARS-COV-2, OR ANY VIRUS, THAT HIJACKS HOST RESPONSES. 2020 13 1208 37 COVID-19 INFECTION AND RESPONSE TO VACCINATION IN CHRONIC KIDNEY DISEASE AND RENAL TRANSPLANTATION: A BRIEF PRESENTATION. CHRONIC KIDNEY DISEASE (CKD) IS ASSOCIATED WITH PHENOTYPIC AND FUNCTIONAL CHANGES IN THE IMMUNE SYSTEM, FOLLOWED BY DETRIMENTAL CLINICAL CONSEQUENCES, SUCH AS SEVERE INFECTIONS AND DEFECTIVE RESPONSE TO VACCINATION. TWO YEARS OF THE PANDEMIC, DUE TO SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2 (SARS-COV-2), HAVE UNDOUBTEDLY CHANGED THE WORLD; HOWEVER, ALL EFFORTS TO CONFRONT INFECTION AND PROVIDE NEW GENERATION VACCINES TREMENDOUSLY IMPROVED OUR UNDERSTANDING OF THE MECHANISMS OF THE IMMUNE RESPONSE AGAINST INFECTIONS AND AFTER VACCINATION. HUMORAL AND CELLULAR RESPONSES TO VACCINES, INCLUDING MRNA VACCINES, ARE APPARENTLY AFFECTED IN CKD PATIENTS, AS ELIMINATION OF RECENT THYMIC EMIGRANT AND NAIVE LYMPHOCYTES AND REGULATORY T-CELLS, TOGETHER WITH CONTRACTION OF T-CELL REPERTOIRE AND HOMEOSTATIC PROLIFERATION RATE, WHICH CHARACTERIZED CKD PATIENTS ARE RESPONSIBLE FOR IMPAIRED IMMUNE ACTIVATION. SUCCESSFUL RENAL TRANSPLANTATION WILL RESTORE SOME OF THESE CHANGES, ALTHOUGH SEVERAL EPIGENETIC CHANGES ARE IRREVERSIBLE AND EVEN ACCELERATED BY THE INDUCTION OF IMMUNOSUPPRESSION. RESPONSE TO VACCINATION IS DEFINITELY IMPAIRED AMONG BOTH CKD AND RT PATIENTS. IN THE PRESENT REVIEW, WE ANALYZED THE DIFFERENCES IN IMMUNE RESPONSE AFTER VACCINATION BETWEEN THESE PATIENTS AND HEALTHY INDIVIDUALS AND DEPICTED SPECIFIC PARAMETERS, SUCH AS ALTERATIONS IN THE IMMUNE SYSTEM, PREDISPOSING TO THIS DEFICIENT RESPONSE. 2022 14 4165 41 MEDICAL SCHOOL HOTLINE: IMMUNOEPIGENETIC-MICROBIOME AXIS: IMPLICATIONS FOR HEALTH DISPARITIES RESEARCH IN NATIVE HAWAIIANS AND PACIFIC ISLANDERS. NATIVE HAWAIIAN AND PACIFIC ISLANDER (NHPI) POPULATIONS SUFFER FROM DISPROPORTIONATELY HIGHER RATES OF CHRONIC CONDITIONS, SUCH AS TYPE 2 DIABETES, THAT ARISES FROM METABOLIC DYSFUNCTION AND ARE OFTEN ASSOCIATED WITH OBESITY AND INFLAMMATION. IN ADDITION, THE GLOBAL CORONAVIRUS DISEASE 2019 PANDEMIC HAS FURTHER COMPOUNDED THE EFFECT OF HEALTH INEQUITIES OBSERVED IN INDIGENOUS POPULATIONS, INCLUDING NHPI COMMUNITIES. REVERSIBLE LIFESTYLE HABITS, SUCH AS DIET, MAY EITHER BE PROTECTIVE OF OR CONTRIBUTE TO THE INCREASING PREVALENCE OF HEALTH INEQUITIES IN THESE POPULATIONS VIA THE IMMUNOEPIGENETIC-MICROBIOME AXIS. THIS AXIS OFFERS INSIGHT INTO THE CONNECTION BETWEEN DIET, EPIGENETICS, THE MICROBIOME COMPOSITION, IMMUNE FUNCTION, AND RESPONSE TO VIRAL INFECTION. EPIGENETIC MECHANISMS THAT REGULATE INFLAMMATORY STATES ASSOCIATED WITH METABOLIC DISEASES, INCLUDING DIABETES, ARE IMPACTED BY DIET. FURTHERMORE, DIET MAY MODULATE THE GUT MICROBIOME BY INFLUENCING MICROBIAL DIVERSITY AND RICHNESS; DYSBIOSIS OF THE MICROBIOME IS ASSOCIATED WITH CHRONIC DISEASE. A HIGH FIBER DIET FACILITATES A FAVORABLE MICROBIOME COMPOSITION AND IN TURN INCREASES PRODUCTION OF INTERMEDIATE METABOLITES NAMED SHORT-CHAIN FATTY ACIDS (SCFAS) THAT ACT ON METABOLIC AND IMMUNE PATHWAYS. IN CONTRAST, LOW FIBER DIETS TYPICALLY ASSOCIATED WITH A WESTERNIZED LIFESTYLE DECREASES THE ABUNDANCE OF MICROBIAL DERIVED SCFAS. THIS DECREASED ABUNDANCE IS CHARACTERISTIC OF METABOLIC SYNDROMES AND ACTIVATION OF CHRONIC INFLAMMATORY STATES, HAVING LARGER IMPLICATIONS IN DISEASE PATHOGENESIS OF BOTH COMMUNICABLE AND NON-COMMUNICABLE DISEASES. NATIVE HAWAIIANS AND PACIFIC ISLANDERS THAT ONCE THRIVED ON HEALTHY TRADITIONAL DIETS MAY BE MORE SENSITIVE THAN NON-INDIGENOUS PEOPLES TO THE METABOLIC PERTURBATION OF WESTERNIZED DIETS THAT IMPINGE ON THE IMMUNOEPIGENETIC-GUT MICROBIOME AXIS. RECENT STUDIES CONDUCTED IN THE MAUNAKEA LAB AT THE UNIVERSITY OF HAWAI'I AT MANOA JOHN A. BURNS SCHOOL OF MEDICINE HAVE HELPED ELUCIDATE THE CONNECTIONS BETWEEN DIET, MICROBIOME COMPOSITION, METABOLIC SYNDROME, AND EPIGENETIC REGULATION OF IMMUNE FUNCTION TO BETTER UNDERSTAND DISEASE PATHOGENESIS. POTENTIALLY, THIS RESEARCH COULD POINT TO WAYS TO PREVENT PRE-DISEASE CONDITIONS THROUGH NOVEL BIOMARKER DISCOVERY USING COMMUNITY-BASED APPROACHES. 2021 15 5224 36 PRIORITIZED RESEARCH FOR THE PREVENTION, TREATMENT, AND REVERSAL OF CHRONIC DISEASE: RECOMMENDATIONS FROM THE LIFESTYLE MEDICINE RESEARCH SUMMIT. DECLINING LIFE EXPECTANCY AND INCREASING ALL-CAUSE MORTALITY IN THE UNITED STATES HAVE BEEN ASSOCIATED WITH UNHEALTHY BEHAVIORS, SOCIOECOLOGICAL FACTORS, AND PREVENTABLE DISEASE. A GROWING BODY OF BASIC SCIENCE, CLINICAL RESEARCH, AND POPULATION HEALTH EVIDENCE POINTS TO THE BENEFITS OF HEALTHY BEHAVIORS, ENVIRONMENTS AND POLICIES TO MAINTAIN HEALTH AND PREVENT, TREAT, AND REVERSE THE ROOT CAUSES OF COMMON CHRONIC DISEASES. SIMILARLY, INNOVATIONS IN RESEARCH METHODOLOGIES, STANDARDS OF EVIDENCE, EMERGENCE OF UNIQUE STUDY COHORTS, AND BREAKTHROUGHS IN DATA ANALYTICS AND MODELING CREATE NEW POSSIBILITIES FOR PRODUCING BIOMEDICAL KNOWLEDGE AND CLINICAL TRANSLATION. TO UNDERSTAND THESE ADVANCES AND INFORM FUTURE DIRECTIONS RESEARCH, THE LIFESTYLE MEDICINE RESEARCH SUMMIT WAS CONVENED AT THE UNIVERSITY OF PITTSBURGH ON DECEMBER 4-5, 2019. THE SUMMIT'S GOAL WAS TO REVIEW CURRENT STATUS AND DEFINE RESEARCH PRIORITIES IN THE SIX CORE AREAS OF LIFESTYLE MEDICINE: PLANT-PREDOMINANT NUTRITION, PHYSICAL ACTIVITY, SLEEP, STRESS, ADDICTIVE BEHAVIORS, AND POSITIVE PSYCHOLOGY/SOCIAL CONNECTION. FORTY INVITED SUBJECT MATTER EXPERTS (1) REVIEWED EXISTING KNOWLEDGE AND GAPS RELATING LIFESTYLE BEHAVIORS TO COMMON CHRONIC DISEASES, SUCH AS CARDIOVASCULAR DISEASE, DIABETES, MANY CANCERS, INFLAMMATORY- AND IMMUNE-RELATED DISORDERS AND OTHER CONDITIONS; AND (2) DISCUSSED THE POTENTIAL FOR APPLYING CUTTING-EDGE MOLECULAR, CELLULAR, EPIGENETIC AND EMERGING SCIENCE KNOWLEDGE AND COMPUTATIONAL METHODOLOGIES, RESEARCH DESIGNS, AND STUDY COHORTS TO ACCELERATE CLINICAL APPLICATIONS ACROSS ALL SIX DOMAINS OF LIFESTYLE MEDICINE. NOTABLY, FEDERAL HEALTH AGENCIES, SUCH AS THE DEPARTMENT OF DEFENSE AND VETERANS ADMINISTRATION HAVE BEGUN TO ADOPT "WHOLE-PERSON HEALTH AND PERFORMANCE" MODELS THAT ADDRESS THESE LIFESTYLE AND ENVIRONMENTAL ROOT CAUSES OF CHRONIC DISEASE AND ASSOCIATED MORBIDITY, MORTALITY, AND COST. RECOMMENDATIONS STRONGLY SUPPORT LEVERAGING EMERGING RESEARCH METHODOLOGIES, SYSTEMS BIOLOGY, AND COMPUTATIONAL MODELING IN ORDER TO ACCELERATE EFFECTIVE CLINICAL AND POPULATION SOLUTIONS TO IMPROVE HEALTH AND REDUCE SOCIETAL COSTS. NEW AND ALTERNATIVE HIERARCHIES OF EVIDENCE ARE ALSO BE NEEDED IN ORDER TO ASSESS THE QUALITY OF EVIDENCE AND DEVELOP EVIDENCE-BASED GUIDELINES ON LIFESTYLE MEDICINE. CHILDREN AND UNDERSERVED POPULATIONS WERE IDENTIFIED AS PRIORITIZED GROUPS TO STUDY. THE COVID-19 PANDEMIC, WHICH DISPROPORTIONATELY IMPACTS PEOPLE WITH CHRONIC DISEASES THAT ARE AMENABLE TO EFFECTIVE LIFESTYLE MEDICINE INTERVENTIONS, MAKES THE SUMMIT'S FINDINGS AND RECOMMENDATIONS FOR FUTURE RESEARCH PARTICULARLY TIMELY AND RELEVANT. 2020 16 2474 49 EPIGENETIC UNDERPINNINGS OF INFLAMMATION: CONNECTING THE DOTS BETWEEN PULMONARY DISEASES, LUNG CANCER AND COVID-19. INFLAMMATION IS AN ESSENTIAL COMPONENT OF SEVERAL RESPIRATORY DISEASES, SUCH AS CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD), ASTHMA AND ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS). IT IS CENTRAL TO LUNG CANCER, THE LEADING CANCER IN TERMS OF ASSOCIATED MORTALITY THAT HAS AFFECTED MILLIONS OF INDIVIDUALS WORLDWIDE. INFLAMMATION AND PULMONARY MANIFESTATIONS ARE ALSO THE MAJOR CAUSES OF COVID-19 RELATED DEATHS. ACUTE HYPERINFLAMMATION PLAYS AN IMPORTANT ROLE IN THE COVID-19 DISEASE PROGRESSION AND SEVERITY, AND DEVELOPMENT OF PROTECTIVE IMMUNITY AGAINST THE VIRUS IS GREATLY SOUGHT. FURTHER, THE SEVERITY OF COVID-19 IS GREATLY ENHANCED IN LUNG CANCER PATIENTS, PROBABLY DUE TO THE GENES SUCH AS ACE2, TMPRSS2, PAI-1 AND FURIN THAT ARE COMMONLY INVOLVED IN CANCER PROGRESSION AS WELL AS SAR-COV-2 INFECTION. THE IMPORTANCE OF INFLAMMATION IN PULMONARY MANIFESTATIONS, CANCER AND COVID-19 CALLS FOR A CLOSER LOOK AT THE UNDERLYING PROCESSES, PARTICULARLY THE ASSOCIATED INCREASE IN IL-6 AND OTHER CYTOKINES, THE DYSREGULATION OF IMMUNE CELLS AND THE COAGULATION PATHWAY. TOWARDS THIS END, SEVERAL REPORTS HAVE IDENTIFIED EPIGENETIC REGULATION OF INFLAMMATION AT DIFFERENT LEVELS. EXPRESSION OF SEVERAL KEY INFLAMMATION-RELATED CYTOKINES, CHEMOKINES AND OTHER GENES IS AFFECTED BY METHYLATION AND ACETYLATION WHILE NON-CODING RNAS, INCLUDING MICRORNAS AS WELL AS LONG NON-CODING RNAS, ALSO AFFECT THE OVERALL INFLAMMATORY RESPONSES. SELECT MIRNAS CAN REGULATE INFLAMMATION IN COVID-19 INFECTION, LUNG CANCER AS WELL AS OTHER INFLAMMATORY LUNG DISEASES, AND CAN SERVE AS EPIGENETIC LINKS THAT CAN BE THERAPEUTICALLY TARGETED. FURTHERMORE, EPIGENETIC CHANGES ALSO MEDIATE THE ENVIRONMENTAL FACTORS-INDUCED INFLAMMATION. THEREFORE, A BETTER UNDERSTANDING OF EPIGENETIC REGULATION OF INFLAMMATION CAN POTENTIALLY HELP DEVELOP NOVEL STRATEGIES TO PREVENT, DIAGNOSE AND TREAT CHRONIC PULMONARY DISEASES, LUNG CANCER AND COVID-19. 2022 17 264 26 ADVANCING ASTHMA CARE: THE GLASS IS ONLY HALF FULL! OVER THE PAST 20 YEARS, THERE HAS BEEN A CONCERTED EFFORT IN THE UNITED STATES TO REDUCE MORBIDITY RELATED TO CHRONIC DISEASE, INCLUDING ASTHMA. ATTENTION WAS INITIALLY DIRECTED TOWARD ASTHMA IN RESPONSE TO THE RECOGNITION THAT ASTHMA MORTALITY WAS INCREASING AND THAT THE BURDEN OF DISEASE WAS SIGNIFICANT. THESE EFFORTS TO ADDRESS ASTHMA MORTALITY LED TO MANY NEW INITIATIVES TO DEVELOP CLINICAL PRACTICE GUIDELINES, IMPLEMENT THE ASTHMA GUIDELINES INTO CLINICAL PRACTICE, CONDUCT RESEARCH TO FILL THE GAPS IN THE GUIDELINES, AND CONTINUOUSLY REVISE THE ASTHMA GUIDELINES AS MORE INFORMATION BECAME AVAILABLE. AN ASSESSMENT OF OUR PROGRESS SHOWS SIGNIFICANT ACCOMPLISHMENTS IN RELATION TO REDUCING ASTHMA MORTALITY AND HOSPITALIZATIONS. CONSEQUENTLY, WE ARE NOW AT A CROSSROADS IN ASTHMA CARE. ALTHOUGH WE HAVE RECOGNIZED SOME REMARKABLE ACCOMPLISHMENTS IN REDUCING ASTHMA MORTALITY AND MORBIDITY, THE AVAILABILITY OF NEW TOOLS TO MONITOR DISEASE ACTIVITY, INCLUDING BIOMARKERS AND EPIGENETIC MARKERS, ALONG WITH INFORMATION TECHNOLOGY SYSTEMS TO MONITOR ASTHMA CONTROL HOLD SOME PROMISE IN IDENTIFYING GAPS IN DISEASE MANAGEMENT. THESE ADVANCES SHOULD PROMPT THE EVOLUTION OF NEW STRATEGIES AND NEW TREATMENTS TO FURTHER REDUCE DISEASE BURDEN. IT NOW BECOMES IMPERATIVE TO CONTINUE A FOCUS ON WAYS TO FURTHER REDUCE THE BURDEN OF ASTHMA AND PREVENT ITS ONSET. 2011 18 5025 33 PERSONALIZED MANAGEMENT OF CARDIOVASCULAR DISORDERS. PERSONALIZED MANAGEMENT OF CARDIOVASCULAR DISORDERS (CVD), ALSO REFERRED TO AS PERSONALIZED OR PRECISION CARDIOLOGY IN ACCORDANCE WITH GENERAL PRINCIPLES OF PERSONALIZED MEDICINE, IS SELECTION OF THE BEST TREATMENT FOR AN INDIVIDUAL PATIENT. IT INVOLVES THE INTEGRATION OF VARIOUS "OMICS" TECHNOLOGIES SUCH AS GENOMICS AND PROTEOMICS AS WELL AS OTHER NEW TECHNOLOGIES SUCH AS NANOBIOTECHNOLOGY. MOLECULAR DIAGNOSTICS AND BIOMARKERS ARE IMPORTANT FOR LINKING DIAGNOSIS WITH THERAPY AND MONITORING THERAPY. BECAUSE CVD INVOLVE PERTURBATIONS OF LARGE COMPLEX BIOLOGICAL NETWORKS, A SYSTEMS BIOLOGY APPROACH TO CVD RISK STRATIFICATION MAY BE USED FOR IMPROVING RISK-ESTIMATING ALGORITHMS, AND MODELING OF PERSONALIZED BENEFIT OF TREATMENT MAY BE HELPFUL FOR GUIDING THE CHOICE OF INTERVENTION. BIOINFORMATICS TOOLS ARE HELPFUL IN ANALYZING AND INTEGRATING LARGE AMOUNTS OF DATA FROM VARIOUS SOURCES. PERSONALIZED THERAPY IS CONSIDERED DURING DRUG DEVELOPMENT, INCLUDING METHODS OF TARGETED DRUG DELIVERY AND CLINICAL TRIALS. INDIVIDUALIZED RECOMMENDATIONS CONSIDER MULTIPLE FACTORS - GENETIC AS WELL AS EPIGENETIC - FOR PATIENTS' RISK OF HEART DISEASE. EXAMPLES OF PERSONALIZED TREATMENT ARE THOSE OF CHRONIC MYOCARDIAL ISCHEMIA, HEART FAILURE, AND HYPERTENSION. SIMILAR APPROACHES CAN BE USED FOR THE MANAGEMENT OF ATRIAL FIBRILLATION AND HYPERCHOLESTEROLEMIA, AS WELL AS THE USE OF ANTICOAGULANTS. PERSONALIZED MANAGEMENT INCLUDES PHARMACOTHERAPY, SURGERY, LIFESTYLE MODIFICATIONS, AND COMBINATIONS THEREOF. FURTHER PROGRESS IN UNDERSTANDING THE PATHOMECHANISM OF COMPLEX CARDIOVASCULAR DISEASES AND IDENTIFICATION OF CAUSATIVE FACTORS AT THE INDIVIDUAL PATIENT LEVEL WILL PROVIDE OPPORTUNITIES FOR THE DEVELOPMENT OF PERSONALIZED CARDIOLOGY. APPLICATION OF PRINCIPLES OF PERSONALIZED MEDICINE WILL IMPROVE THE CARE OF THE PATIENTS WITH CVD. 2017 19 3547 45 IMMUNOMODULATORY ROLE OF NUTRIENTS: HOW CAN PULMONARY DYSFUNCTIONS IMPROVE? NUTRITION IS AN IMPORTANT TOOL THAT CAN BE USED TO MODULATE THE IMMUNE RESPONSE DURING INFECTIOUS DISEASES. IN ADDITION, THROUGH DIET, IMPORTANT SUBSTRATES ARE ACQUIRED FOR THE BIOSYNTHESIS OF REGULATORY MOLECULES IN THE IMMUNE RESPONSE, INFLUENCING THE PROGRESSION AND TREATMENT OF CHRONIC LUNG DISEASES, SUCH AS ASTHMA AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD). IN THIS WAY, NUTRITION CAN PROMOTE LUNG HEALTH STATUS. A RANGE OF NUTRIENTS, SUCH AS VITAMINS (A, C, D, AND E), MINERALS (ZINC, SELENIUM, IRON, AND MAGNESIUM), FLAVONOIDS AND FATTY ACIDS, PLAY IMPORTANT ROLES IN REDUCING THE RISK OF PULMONARY CHRONIC DISEASES AND VIRAL INFECTIONS. THROUGH THEIR ANTIOXIDANT AND ANTI-INFLAMMATORY EFFECTS, NUTRIENTS ARE ASSOCIATED WITH BETTER LUNG FUNCTION AND A LOWER RISK OF COMPLICATIONS SINCE THEY CAN DECREASE THE HARMFUL EFFECTS FROM THE IMMUNE SYSTEM DURING THE INFLAMMATORY RESPONSE. IN ADDITION, BIOACTIVE COMPOUNDS CAN EVEN CONTRIBUTE TO EPIGENETIC CHANGES, INCLUDING HISTONE DEACETYLASE (HDAC) MODIFICATIONS THAT INHIBIT THE TRANSCRIPTION OF PROINFLAMMATORY CYTOKINES, WHICH CAN CONTRIBUTE TO THE MAINTENANCE OF HOMEOSTASIS IN THE CONTEXT OF INFECTIONS AND CHRONIC INFLAMMATORY DISEASES. THESE NUTRIENTS ALSO PLAY AN IMPORTANT ROLE IN ACTIVATING IMMUNE RESPONSES AGAINST PATHOGENS, WHICH CAN HELP THE IMMUNE SYSTEM DURING INFECTIONS. HERE, WE PROVIDE AN UPDATED OVERVIEW OF THE ROLES PLAYED BY DIETARY FACTORS AND HOW THEY CAN AFFECT RESPIRATORY HEALTH. THEREFORE, WE WILL SHOW THE ANTI-INFLAMMATORY ROLE OF FLAVONOIDS, FATTY ACIDS, VITAMINS AND MICROBIOTA, IMPORTANT FOR THE CONTROL OF CHRONIC INFLAMMATORY DISEASES AND ALLERGIES, IN ADDITION TO THE ANTIVIRAL ROLE OF VITAMINS, FLAVONOIDS, AND MINERALS DURING PULMONARY VIRAL INFECTIONS, ADDRESSING THE MECHANISMS INVOLVED IN EACH FUNCTION. THESE MECHANISMS ARE INTERESTING IN THE DISCUSSION OF PERSPECTIVES ASSOCIATED WITH SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2 (SARS-COV-2) INFECTION AND ITS PULMONARY COMPLICATIONS SINCE PATIENTS WITH SEVERE DISEASE HAVE VITAMINS DEFICIENCY, ESPECIALLY VITAMIN D. IN ADDITION, RESEARCHES WITH THE USE OF FLAVONOIDS HAVE BEEN SHOWN TO DECREASE VIRAL REPLICATION IN VITRO. THIS WAY, A FULL UNDERSTANDING OF DIETARY INFLUENCES CAN IMPROVE THE LUNG HEALTH OF PATIENTS. 2021 20 5702 30 SINGLE-CELL GENOMICS FOR INVESTIGATING PATHOGENESIS OF INFLAMMATORY DISEASES. RECENT TECHNICAL ADVANCES HAVE ENABLED UNBIASED TRANSCRIPTOMIC AND EPIGENETIC ANALYSIS OF EACH CELL, KNOWN AS "SINGLE-CELL ANALYSIS". SINGLE-CELL ANALYSIS HAS A VARIETY OF TECHNICAL APPROACHES TO INVESTIGATE THE STATE OF EACH CELL, INCLUDING MRNA LEVELS (TRANSCRIPTOME), THE IMMUNE REPERTOIRE (IMMUNE REPERTOIRE ANALYSIS), CELL SURFACE PROTEINS (SURFACE PROTEOME ANALYSIS), CHROMATIN ACCESSIBILITY (EPIGENOME), AND ACCORDANCE WITH GENOME VARIANTS (EQTLS; EXPRESSION QUANTITATIVE TRAIT LOCI). AS AN EFFECTIVE TOOL FOR INVESTIGATING ROBUST IMMUNE RESPONSES IN CORONAVIRUS DISEASE 2019 (COVID-19), MANY RESEARCHERS PERFORMED SINGLE-CELL ANALYSIS TO CAPTURE THE DIVERSE, UNBIASED IMMUNE CELL ACTIVATION AND DIFFERENTIATION. DESPITE CHALLENGES ELUCIDATING THE COMPLICATED IMMUNE MICROENVIRONMENTS OF CHRONIC INFLAMMATORY DISEASES USING EXISTING EXPERIMENTAL METHODS, IT IS NOW POSSIBLE TO CAPTURE THE SIMULTANEOUS IMMUNE FEATURES OF DIFFERENT CELL TYPES ACROSS INFLAMED TISSUES USING VARIOUS SINGLE-CELL TOOLS. IN THIS REVIEW, WE INTRODUCE PATIENT-BASED AND EXPERIMENTAL MOUSE MODEL RESEARCH UTILIZING SINGLE-CELL ANALYSES IN THE FIELD OF CHRONIC INFLAMMATORY DISEASES, AS WELL AS MULTI-ORGAN ATLAS TARGETING IMMUNE CELLS. 2023