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Background Persons with HIV (PWHIV) on highly active antiretroviral treatments (HAART) may require specialized care based on health and demographic indicators. This study investigated the association of comorbidities, race, weight status, and gastrointestinal (GI) and cardiovascular (CV) symptoms among PWHIV. Methods The Symptom Checklist, Co-Morbidity Questionnaire, and Sociodemographic Questionnaire were used to assess weight status and GI and CV symptoms among 283 PWHIV. Data were analyzed using latent class analysis on John’s Macintosh Project 13 Platform. Results Participants were majority Black (50%), 69% male, and 35% AIDS diagnosed. Ages were 25 to 66. Clusters included least symptomatic status, weight gain, and weight loss by Black and non-Black participants. The non-Black weight gain cluster reported a higher incidence of AIDS (70.6% vs 38.2%), nausea (70.6% vs 17.6%), diarrhea (70.6% vs 26.5%), and shortness of breath (58.8% vs 20.6%) compared to the Black weight gain cluster. The Black weight loss cluster reported a higher incidence of CV symptoms such as chest palpitations (42.2% vs 2.7%), chest pain (44.4% vs 8.1%), and shortness of breath (73.3% vs 35.1%). Moreover, the Black weight loss cluster reported a higher incidence of all GI symptoms with the most prominent being diarrhea (71.1% vs 48.6%) compared to the non-Black weight loss cluster. Conclusions The existing racial disparities in health-related quality of life for PWHIV may be improved through precision health and nutrition modifications. Continued research is needed investigating differential health outcomes among PWHIV on HAART. Clinical Trial Registration Number NCT00222716. Registered 22 September 2005. Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT00222716?term=NCT00222716&draw=2&rank=1

Background: Exclusive breastfeeding practice for 6 months is a critical global public health goal. In 2020, only 44% of infants globally, 31% in Central and West Africa, and 43% in Ghana, were exclusively breastfed for the first 6 months of life. Research Aim: To critically evaluate disparities in exclusive breastfeeding practice for 6 months in Ghana. Methods: The scoping review was guided by Arksey and O’Malley’s (2005) six-stage scoping review process. The online databases of American Psychological Association PsychInfo (APA PsychInfo), Cumulative Index to Nursing and Allied Health Literature (CINAHL), PubMed, and Scopus were searched with keywords inclusive of Ghana, exclusive breastfeeding, breastfeeding, infant feeding, lactation, lactating, and exclusive. Eligibility criteria included full-text, peer-reviewed research articles written in the English language without limitation to specific years. Data were analyzed thematically. Results: Initially, 317 records were identified, and 15 full-text articles were eligible for the scoping review. Four main themes emerged as disparities in exclusive breastfeeding practice in Ghana. The themes were healthcare (prenatal clinic visits, delivery place, exclusive breastfeeding knowledge), personal (maternal age, Human Immunodeficiency Virus status, parity, type of delivery, breast problem), employment (unemployed, formal, or informal sector worker), and sociocultural (ethnicity/region, family support, religious beliefs, cultural practices). Conclusion: Disparities in exclusive breastfeeding in Ghana warrant the collaborative efforts of stakeholders for successful mitigation. Future researchers should explore the role of religion and sociocultural practices to protect, promote, and support 6 months of exclusive breastfeeding in Ghana.

The critical time to continue or stop breastfeeding is during the first month after hospital discharge. Mothers receive lactation and physical support by fathers and others bottle-feeding human or formula milk to their infants.To describe the effect of feeders (mothers, fathers, and others) and different milk feeding on infants' weekly exclusive breastfeeding rates, from birth to 1 month after discharge.This study was a secondary analysis of a descriptive longitudinal study of mothers' (full-term: n = 77; late preterm: n = 39) breastfeeding experience, frequency of feeding, and infant feeding behaviors. Mothers completed a weekly questionnaire of who (mothers, fathers, and others) fed their infants human or formula milk by direct breastfeeding or bottle-feeding.More than 60% of mothers reported fathers and others bottle-fed their infants. Exclusive breastfeeding rates were significantly higher when only mothers fed their infants at week 1 ( P.001), week 3 ( P.05), and week 4 ( P.05). Exclusive breastfeeding rates were negatively affected across time by bottle-feeding any human or formula milk for all feeders. When fathers bottle-fed their infants at week 1, the relative rates of exclusive breastfeeding at week 4 decreased to 52% (OR = 0.103; 95% CI, 0.26-0.404; P.0001).Individuals providing early bottle-feeding adversely affect breastfeeding outcomes. Providers need to address maternal and paternal knowledge gaps about early breastfeeding practice.Further research is needed to explore clinical standard of care for management of infant weight loss, early supplementation, and support of exclusive breastfeeding outcomes.

In the United States, there are racial disparities in 6 months of exclusive breastfeeding. Only, 25.8% of American infants were breastfed for the first 180 days of life, with African American infants least (19.8%) exclusively breastfed in 2018.The meta-ethnography explored the breastfeeding support for African American women in the United States.The online databases of American Psychological Association, PsycINFO, Cumulative Index to Nursing and Allied Health Literature, PubMed, and Scopus were searched with key words, and the search was not limited by the year of publication.The inclusion criteria for the study selection entailed all qualitative studies conducted on breastfeeding support among self-identified African American women in the United States, written in English language, peer reviewed, or dissertation. The initial search produced 905 articles of which 8 met the eligibility criteria.Data extraction and analysis were guided by Noblit and Hare's (1988) meta-ethnography approach. The analysis process was completed by a team of researchers, inclusive of breastfeeding experts.Five overarching themes emerged including trustworthy information; early postpartum support by key influencers; maternal culture; tangible resources, and Black mothers' empowerment.Social support is a major determinant for the initiation and continuation of breastfeeding among African American women in the United States. Future longitudinal studies are warranted to explore the social support of breastfeeding among African American women in the United States.

Preterm infants are at risk for severe infections due to their immature immune systems. Factors such as early life pain/stress experiences and feeding may influence immune activation and maturation of immune systems. However, the underlying mechanism remains unclear. Fecal calprotectin (FCP) is a noninvasive surrogate biomarker of mucosal inflammation in the gastrointestinal tract and has been used in detecting intestinal inflammation in specific pediatric gastrointestinal disorders.To describe the longitudinal trajectory of FCP levels in preterm infants and investigate the contributing factors that are associated with FCP levels.A longitudinal study design was used.Preterm infants were recruited from 2 neonatal intensive care units (NICU) of a children's medical center in the North-eastern US.Preterm infants were followed during their first 4 weeks of NICU hospitalization. Stool samples were collected twice per week to quantify the FCP levels. Cumulative pain/stress experiences and feeding types were measured daily. A linear mixed-effect model was used to examine the associations between FCP levels and demographic and clinical characteristics, cumulative pain/stress, and feeding over time.Forty-nine preterm infants were included in the study. Infants' FCP levels varied largely with a mean of 268.7±261.3 µg/g and increased over time. Preterm infants experienced an average of 7.5±5.0 acute painful procedures and 15.3±20.8 hours of chronic painful procedures per day during their NICU stay. The mean percentage of mother's own milk increased from the first week (57.1±36.5%) to the fourth week (60.7±38.9%) after birth. Elevated FCP concentration was associated with acute and cumulative (chronic) pain/stress levels, mother's own milk, non-White race, and higher severity of illness score.FCP levels were elevated in preterm infants with wide interindividual and intraindividual variations. Cumulative pain/stress during the NICU hospitalization, feeding, race, and health status may influence FCP concentrations in early life that may be associated with inflammatory gut processes.

Background As genomic science moves beyond government-academic collaborations into routine healthcare operations, nursing’s holistic philosophy and evidence-based practice approach positions nurses as leaders to advance genomics and precision health care in routine patient care. Purpose To examine the status of and identify gaps for U.S. genomic nursing health care policy and precision health clinical practice implementation. Methods We conducted a scoping review and policy priorities analysis to clarify key genomic policy concepts and definitions, and to examine trends and utilization of health care quality benchmarking used in precision health. Findings Genomic nursing health care policy is an emerging area. Educating and training the nursing workforce to achieve full dissemination and integration of precision health into clinical practice remains an ongoing challenge. Use of health care quality measurement principles and federal benchmarking performance evaluation criteria for precision health implementation are not developed. Discussion Nine recommendations were formed with calls to action across nursing practice workforce and education, nursing research, and health care policy arenas. Conclusions To advance genomic nursing health care policy, it is imperative to develop genomic performance measurement tools for clinicians, purchasers, regulators and policymakers and to adequately prepare the nursing workforce.

Background: Disparities in breastfeeding (BF) continue to be a public health challenge, as currently only 42% of infants in the world and 25.6% of infants in the United States are exclusively breastfed for the first 6 months of life. In 2019, the infants least likely to be exclusively breastfed at 6 months are African Americans (AA) (17.2%). Materials and Methods: A scoping review of the literature was undertaken by using Arksey and O'Malley's six-stage framework to determine key themes of AA women's experience BF through an equity lens. Electronic databases of CINAHL and PubMed were searched for peer-reviewed, full-text articles written in the English language within the past 5 years by using the terms BF, AA, Black, sociological, cultural, equity, health, attitude, exposure, initiation, continuation, barriers, and facilitators. Results: Initially, 497 articles were identified, and 26 peer-reviewed articles met the eligibility criteria. Through an equity lens, three main themes emerged, which summarized AA women's BF experience: cultural (family, peers and community support; misconceptions; personal factors), sociological (prejudices, racism, home environment; financial status; sexuality issues; BF role models; employment policies), and health dimensions (family involvement; timely and honest information from staff; baby-friendly hospital initiatives; postnatal follow-up; special supplemental nutrition program for women, infants, and children). Conclusion: For AA women, exclusively BF is beset with diverse cultural, health, and sociological challenges. Multifaceted approaches are needed for successful resolution of BF challenges to bridge the racial gap in BF in the United States. Future studies may explore interventions targeted to modifiable barriers to improve BF outcomes.

Background: Irritable bowel syndrome (IBS) is a chronic gastrointestinal condition predominantly affecting the female sex, and is characterized by brain-gut axis dysregulation. Relevance of hormones along the hypothalamic-pituitary gonadal axis and hypothalamic-pituitary adrenal axis to IBS symptomatology remain unclear, as does the significance of other modulators including brain derived neurotrophic factor (BDNF), leptin, and transforming growth factor βeta 1 (TGF-β1). Methods: Females with IBS were compared with female healthy controls (HC) on age, race, hormonal contraceptive use, body mass index, adrenocorticotropic hormone, cortisol, estradiol, follicular stimulating hormone, luteinizing hormone, progesterone, total cholesterol, Center for Epidemiological Studies Depression Scale (CES-D) and Perceived Stress Scale (PSS). BDNF, leptin, and TGF-β1 were quantified using enzyme-linked immunosorbent assay. Descriptive statistics, non-parametric techniques, and regression analyses were performed. Results: Participants with IBS (n = 12) displayed higher estradiol ( p = .027) than did HC (n = 21). Direction of associations among study variables often differed between groups: BDNF and progesterone in HC (rs = .623) and in IBS (rs = −.723). The relationship between log (CES-D) and log (estradiol) varied by IBS status (interaction term p = 0.019). Discussion: Elevated estradiol in participants with IBS, and differential patterns of biological and psychological indices between groups, encourages further inquiry on the relevance of sex hormones, BDNF, leptin, and TGF-β1 to symptoms of IBS. Future research endeavors should conduct longitudinal quantification of sex hormones with subjective symptom assessment to facilitate insight on the pathophysiology and female sex bias in IBS.

The intestinal microbiota changes throughout pregnancy and influences maternal metabolic adaptations to support fetal growth. Obesity induces alterations to the microbiota that include decreased microbial diversity and shifts in microbial composition, though specific species changes are inconsistent between published studies. In animal models, probiotics and exercise moderate maternal weight gain and partially correct the maternal microbiota. Supplemental Escherichia coli, however, exacerbate maternal obesity during the perinatal period, lending weight to the theory that inflammation-induced gut epithelial barrier leak influences metabolic dysregulation. Although birth weight is not always altered when offspring are exposed to an obesogenic diet during gestation, insulin resistance and lipid metabolism are impacted through adulthood in association with this exposure and can lead to increased body weight in adulthood. Postnatal offspring growth is accelerated in response to maternal overnutrition during lactation. Offspring microbiota, metabolism, and behavior are altered in response to early exposure to high fat and high sucrose diets. Consequences to this exposure include impaired glucose and insulin homeostasis, fatty liver, and neurobehavioral deficits that can be ameliorated by improving the microbial environment. In this mini review, we provide an overview of the use of translational animal models to understand the mechanisms associated with changes to the gastrointestinal microbiota due to maternal obesity and the microbial impact on the metabolic changes of pregnancy.

Persons with HIV (PWHIV) on highly active antiretroviral treatments (HAART) may require specialized care based on health and demographic indicators. This study investigated the association of comorbidities, race, weight status, and gastrointestinal (GI) and cardiovascular (CV) symptoms among PWHIV.The Symptom Checklist, Co-Morbidity Questionnaire, and Sociodemographic Questionnaire were used to assess weight status and GI and CV symptoms among 283 PWHIV. Data were analyzed using latent class analysis on John's Macintosh Project 13 Platform.Participants were majority Black (50%), 69% male, and 35% AIDS diagnosed. Ages were 25 to 66. Clusters included least symptomatic status, weight gain, and weight loss by Black and non-Black participants. The non-Black weight gain cluster reported a higher incidence of AIDS (70.6% vs 38.2%), nausea (70.6% vs 17.6%), diarrhea (70.6% vs 26.5%), and shortness of breath (58.8% vs 20.6%) compared to the Black weight gain cluster. The Black weight loss cluster reported a higher incidence of CV symptoms such as chest palpitations (42.2% vs 2.7%), chest pain (44.4% vs 8.1%), and shortness of breath (73.3% vs 35.1%). Moreover, the Black weight loss cluster reported a higher incidence of all GI symptoms with the most prominent being diarrhea (71.1% vs 48.6%) compared to the non-Black weight loss cluster.The existing racial disparities in health-related quality of life for PWHIV may be improved through precision health and nutrition modifications. Continued research is needed investigating differential health outcomes among PWHIV on HAART.NCT00222716. Registered 22 September 2005. Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT00222716?term=NCT00222716draw=2rank=1.

Background Irritable bowel syndrome (IBS) is characterized by abdominal pain, bowel habit alterations, and psychiatric comorbidities. Although pathophysiology remains incompletely understood, prior work demonstrates associations with brain-derived neurotrophic factor (BDNF) and catechol-O-methyltransferase (COMT). The purpose of this study was to quantify BDNF and COMT in plasma and in neuronal-enriched extracellular vesicles (nEVs), assess relationships with psychological symptoms, and gain insight on the brain-gut connection in IBS. Methods Clinical data and biorepository samples from a parent investigation were used, including scores on the Perceived Stress Scale (PSS) and Center for Epidemiological Studies Depression Scale (CES-D). Distinct subpopulations of nEVs were isolated using neural cell adhesion molecule L1CAM; levels of COMT, mature BDNF, and pro-BDNF were quantified in plasma and in nEVs using ELISA. Key results Data from 47 females (28.11 ± 6.85 years) included 18 IBS and 29 healthy control (HC) participants. IBS participants displayed reduced plasma levels of mature BDNF compared with HC (p = 0.024). Levels of COMT plasma and IBS grouping significantly predicted CES-D scores (p = 0.034). Exploratory analyses by IBS subtype and race revealed African American HC display lower levels of COMT EV than Caucasian HC (p = 0.022). Conclusions & inferences Lower levels of mature BDNF in IBS participants, preliminary patterns detected in cargo content of nEVs, and relevance of COMT and IBS status to CES-D scores, offer insight on depressive symptomatology and brain-gut dysregulation in IBS. Lower COMT levels in nEVs of African Americans highlight the relevance of race when conducting such analyses across diverse populations.

Background: Persons living with HIV (PLWHIV) on highly active antiretroviral treatments (HAART) may require specialized care based on health and demographic indicators. This study investigated the association of co-morbidities, race, weight status, gastrointestinal (GI), and cardiovascular symptoms (CV) and among PLWHIV. Methods: The Symptom Checklist, Co-Morbidity, and Sociodemographic Questionnaires were used to assessed weight status, GI, and CV symptoms among 283 PLWHIV. Data were analyzed using Latent Class Analysis on John's Macintosh Project 13 Platform. Results: Participants were majority Black (50%), 69% male, and 35% AIDS diagnosed. Ages were 25 to 66. Clusters included least symptomatic status, weight gain, and weight loss by Black and non-Black participants. The non-Black weight gain cluster reported a higher incidence of AIDS (70.6% vs 38.2%), nausea (70.6% vs 17.6%), diarrhea (70.6% vs 26.5%), and shortness of breath (58.8% vs 20.6%) compared to the Black weight gain cluster. The Black weight loss cluster reported a higher incidence of CV symptoms such as chest palpitations (42.2% vs 2.7%), chest pain (44.4% vs 8.1%), and shortness of breath (73.3% vs 35.1%), and a higher incidence of all GI symptoms with the most prominent being diarrhea (71.1% vs 48.6%) compared to the non-Black weight loss cluster. Conclusions: The existing racial disparities in health-related quality of life for PLWHIV may be improved through precision health and nutrition modifications. Continued research is needed investigating differential health outcomes among PLWHIV on HAART.Clinical Trial Registration Number: NCT00222716

Background: Psychological state, stress level, and gastrointestinal function are intricately related and relevant to symptom exacerbation in patients with irritable bowel syndrome (IBS), but genetic contributors to this brain–gut connection are not fully understood. The purpose of this exploratory study was to compare gene expression in participants with IBS to that of healthy controls (HC) and to examine patterns of expression in participants with IBS by sex and IBS subtype. Method: Participants were recruited to an ongoing protocol at the National Institutes of Health. Differences in demographic and clinical characteristics were assessed using descriptive statistics and Mann–Whitney U tests. Expression levels of 84 genes were evaluated in peripheral whole blood using Custom RT2 Profiler polymerase chain reaction (PCR) Arrays, and data analysis was performed through GeneGlobe Data Analysis Center. Results: Participants with IBS ( n = 27) reported greater levels of perceived stress ( p = .037) and differed in expression values of ±2 for the genes ADIPOR1, ADIPOR2, CNR2, COMT, OXTR, and PPARA compared to HC ( n = 43). Further analyses by sex and IBS subtype revealed differential patterns of gene expression related to the endocannabinoid system, cytokines, stress, and sex steroid hormones. Conclusions: Diverse yet interconnected processes such as metabolism, inflammation, immunity, social behavior, and pain are associated with differences in gene expression between participants with IBS and HC. These findings lend support for genomic associations with the brain–gut connection in patients with IBS and highlight the relevance of sex and IBS subtype in performing such analyses.

Precision health refers to personalized healthcare based on a person’s unique genetic, genomic, or omic composition within the context of lifestyle, social, economic, cultural and environmental influences to help individuals achieve well-being and optimal health. Precision health utilizes big data sets that combine omics (i.e. genomic sequence, protein, metabolite, and microbiome information) with clinical information and health outcomes to optimize disease diagnosis, treatment and prevention specific to each patient. Successful implementation of precision health requires interprofessional collaboration, community outreach efforts, and coordination of care, a mission that nurses are well-positioned to lead. Despite the surge of interest and attention to precision health, most nurses are not well-versed in precision health or its implications for the nursing profession. Based on a critical analysis of literature and expert opinions, this paper provides an overview of precision health and the importance of engaging the nursing profession for its implementation. Other topics reviewed in this paper include big data and omics, information science, integration of family health history in precision health, and nursing omics research in symptom science. The paper concludes with recommendations for nurse leaders in research, education, clinical practice, nursing administration and policy settings for which to develop strategic plans to implement precision health. Keywords: Nurses, Genomics, Omics, Precision medicine, Precision health

Introduction: Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver disease that accompanies obesity and the metabolic syndrome. Excess fructose consumption can initiate or exacerbate NAFLD in part due to a consequence of impaired hepatic fructose metabolism. Preclinical data emphasized that fructose-induced altered gut microbiome, increased gut permeability, and endotoxemia play an important role in NAFLD, but human studies are sparse. The present study aimed to determine if two weeks of excess fructose consumption significantly alters gut microbiota or permeability in humans. Methods: We performed a pilot double-blind, cross-over, metabolic unit study in 10 subjects with obesity (body mass index [BMI] 30–40 mg/kg/m2). Each arm provided 75 grams of either fructose or glucose added to subjects’ individual diets for 14 days, substituted isocalorically for complex carbohydrates, with a 19-day wash-out period between arms. Total fructose intake provided in the fructose arm of the study totaled a mean of 20.1% of calories. Outcome measures included fecal microbiota distribution, fecal metabolites, intestinal permeability, markers of endotoxemia, and plasma metabolites. Results: Routine blood, uric acid, liver function, and lipid measurements were unaffected by the fructose intervention. The fecal microbiome (including Akkermansia muciniphilia), fecal metabolites, gut permeability, indices of endotoxemia, gut damage or inflammation, and plasma metabolites were essentially unchanged by either intervention. Conclusions: In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD.

Background The mid-career nurse scientist, defined as an associate professor with/without tenure, is often faced with a multitude of challenges and opportunities Purpose This paper shares strategies to assist mid-career scientists as they juggle required career demands and navigate the mid-career phase in pursuit of the rank of full professor. Method A review of the literature was performed on mid-career nurse scientists. Discussion A combination of increased research responsibilities, increased institutional teaching and service demands, and dwindling support can result in a sense of overwhelm and burnout. The mid-career nurse scientist must balance several balls in the air at one time to remain successful. Conclusion Strategies aligned with the Ecological Framework, focus on intrapersonal, interpersonal, institutional, organizational, and public policy domains to provide a wide scope of strategies that target the mid-career scientist and engage the larger nursing community.

Background and AimsNon-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver disease that accompanies obesity and the metabolic syndrome. Excess fructose consumption can initiate or exacerbate NAFLD due in part to a consequence of impaired hepatic fructose metabolism. Pre-clinical data have emphasized that fructose-induced altered gut microbiome, increased gut permeability, and endotoxemia play an important role in NAFLD, but human studies are sparse. The present study aimed to explore the relevance of these pre-clinical studies to observations in humans.MethodsWe performed a classical double-blind metabolic unit study in 10 obese subjects (BMI 30-40 mg/kg/m2) providing 75gms. of either fructose or glucose in their individual diets substituted isocalorically for complex carbohydrates in a cross-over study. Excess fructose intake was provided in the fructose arm of the study and totaled a mean of 22.7% of calories.ResultsRoutine blood, uric acid, liver function and lipid measurements were unaffected by the fructose intervention. The fecal microbiome (including Akkermansia muciniphilia), fecal metabolites, gut permeability, indices of endotoxemia, gut damage or inflammation and plasma metabolites were essentially unchanged by either intervention.ConclusionsAlthough pre-clinical rodent studies have shown that excess fructose causes pronounced changes in the gut microbiome, metabolome, and permeability as well as endotoxemia, this did not occur in obese individuals fed fructose in amounts known to enhance NAFLD. Therapeutic efforts to improve NAFLD through changes in the gut microbiome and gut homeostasis may not be beneficial.

The quantification of metabolites in blood and urine allows nurses to explore new hypotheses about the microbiome. This review summarizes findings from recent studies with a focus on how the state of the science can influence future nursing research initiatives. Metabolomics can advance nursing research by identifying physiologic/pathophysiologic processes underlying patients’ symptoms and can be useful for testing the effects of nursing interventions. To date, metabolomics has been used to study cardiovascular, respiratory, endocrine, autoimmune, and infectious conditions, with research focused on understanding the microbial metabolism of substrates resulting in circulating/excreted biomarkers such as trimethylamine N-oxide. This review provides specific recommendations for the collection of specimens and goals for future studies.

Purpose: To examine a) whether there are significant differences in the severity of symptoms of fatigue, sleep disturbance, or depression between patients with rectal cancer who develop co-occurring symptoms and those with no symptoms before and at the end of chemotherapy and radiation therapy (CRT); b) differences in gut microbial diversity between those with co-occurring symptoms and those with no symptoms; and c) whether before-treatment diversity measurements and taxa abundances can predict co-occurrence of symptoms. Methods: Stool samples and symptom ratings were collected from 31 patients with rectal cancer prior to and at the end of (24–28 treatments) CRT. Descriptive statistics were computed and the Mann-Whitney U test was performed for symptoms. Gut microbiome data were analyzed using R’s vegan package software. Results: Participants with co-occurring symptoms reported greater severity of fatigue at the end of CRT than those with no symptoms. Bacteroides and Blautia2 abundances differed between participants with co-occurring symptoms and those with no symptoms. Our random forest classification (unsupervised learning algorithm) predicted participants who developed co-occurring symptoms with 74% accuracy, using specific phylum, family, and genera abundances as predictors. Conclusion: Our preliminary results point to an association between the gut microbiota and co-occurring symptoms in rectal cancer patients and serves as a first step in potential identification of a microbiota-based classifier.

Objectives. The objectives of this proof of concept study were to (a) examine the temporal changes in fatigue and diversity of the gut microbiome over the course of chemoradiotherapy (CRT) in adults with rectal cancers; (b) investigate whether there are differences in diversity of the gut microbiome between fatigued and nonfatigued participants at the middle and at the end of CRT; and (c) investigate whether there are differences in the relative abundance of fecal microbiota at the phylum and genus levels between fatigued and nonfatigued participants at the middle and at the end of CRT. Methods. Stool samples and symptom ratings were collected prior to the inception of CRT, at the middle (after 12–16 treatments) and at the end (after 24–28 treatments) of the CRT. Descriptive statistics and Mann–Whitney U test were computed for fatigue. Gut microbiome data were analyzed using the QIIME2 software. Results. Participants (N = 29) ranged in age from 37 to 80 years. The median fatigue score significantly changed at the end of CRT (median = 23.0) compared with the median score before the initiation of CRT for the total sample (median = 17.0; p≤0.05). At the middle of CRT, the alpha diversity (abundance of Operational Taxonomic Units) was lower for fatigued participants (149.30 ± 53.1) than for nonfatigued participants (189.15 ± 44.18, t(23) = 2.08, p≤0.05). A similar trend was observed for the Shannon and Faith diversity indexes at the middle of CRT. However, at the end of CRT, there were no significant differences for any alpha diversity indexes between fatigued and nonfatigued participants. Proteobacteria, Firmicutes, and Bacteroidetes were the dominant phyla for fatigued participants, and Escherichia, Bacteroides, Faecalibacterium, and Oscillospira were the most abundant genera for fatigued participants. Conclusion. CRT-associated perturbation of the gut microbiome composition may contribute to fatigue.

Visceral pain is one of the most common pain conditions and among the top causes of disability worldwide. Visceral pain may be associated with a specific pathology such as gastroenteritis, inflammatory conditions; however, most chronic visceral pain does not have an identifiable pathophysiological origin that is known. The characterization of visceral pain in terms of location, intensity, and severity of symptoms for phenotyping and investigation of underlying mechanisms is of upmost important to better understand not only the underlying mechanisms but ultimately the treatment for this chronic debilitating painful symptom. The following chapter will review the state-of-the-science on the genomics of visceral pain and comorbid symptoms (stress and sleep disturbance) and review methods of phenotyping visceral pain and the multi-omic methods for measurement. Additional focus will include current challenges and areas of future discovery.

Hepatitis C virus (HCV) infection induces interferon (IFN)-stimulated genes (ISGs) and downstream innate immune responses. This study investigated whether baseline and on-treatment differences in these responses predict response versus virological breakthrough during therapy with direct-acting antivirals (DAAs). Thirteen HCV genotype 1b-infected patients who had previously failed a course of pegylated IFN/ribavirin were retreated with asunaprevir/daclatasvir for 24 weeks. After pretreatment biopsy, patients were randomized to undergo a second biopsy at week 2 or 4 on therapy. Microarray and NanoString analyses were performed on paired liver biopsies and analyzed using linear mixed models. As biomarkers for peripheral IFN responses, peripheral blood natural killer cells were assessed for phosphorylated signal transducer and activator of transcription 1 (pSTAT1) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) expression and degranulation. Nine of 13 (69%) patients achieved sustained virological response at 12 weeks off therapy (SVR12), and 4 experienced virological breakthroughs between weeks 4 and 12. Patients who achieved SVR12 displayed higher ISG expression levels in baseline liver biopsies and a higher frequency of pSTAT1 and TRAIL-expressing, degranulating natural killer cells in baseline blood samples than those who experienced virological breakthrough. Comparing gene expression levels from baseline and on-therapy biopsies, 408 genes (±1.2-fold, P < 0.01) were differentially expressed. Genes down-regulated on treatment were predominantly ISGs. Down-regulation of ISGs was rapid and correlated with HCV RNA suppression. Conclusion: An enhanced IFN signature is observed at baseline in liver and blood of patients who achieve SVR12 compared to those who experience a virological breakthrough; the findings suggest that innate immunity may contribute to clearance of HCV during DAA therapy by preventing the emergence of resistance-associated substitutions that lead to viral breakthrough during DAA therapy.

Background Sex and subtype differences within patients with irritable bowel syndrome (IBS) complicate the understanding of disorder pathogenesis and hinder the design of efficacious, therapeutic interventions. Objectives The aims of this study were to harness the power of shotgun proteomic analysis, identify circulating proteins that differentiate African American female patients with IBS from healthy controls (HC), and gain biological insight on symptomatology. Methods Serum proteome analysis was performed upon a cohort of overweight, African American female participants with constipation predominant IBS symptoms (n = 5) and HC (n = 5), matched on age, sex, years of education, body mass index, and 11 physiological markers. Tandem mass tags for multiplexed proteomic analysis were performed, incorporating reverse-phase liquid chromatography and liquid chromatography-tandem mass spectrometry. Results Participants with IBS did not differ from HC in demographics, clinical characteristics, or initial proteomic analysis. Nested case control analysis of six samples (IBS: n = 3, HC: n = 3), hierarchically clustered into two main groups, with 12 out of 1,317 proteins significantly different in levels of expression: TGFβ1, PF4V1, PF4, APP, MMP9, PPBP, CTGF, SRGN, THBS1, WRN, LTBP1 (Isoform 3), and IGLV5-48. Top associations of identified proteins in DAVID and STRING resources (upregulated in HC vs. IBS) involve platelet alpha granule lumen, platelet activation/degranulation, extracellular region, and secretion by cell. Discussion Differentially expressed proteins between participants with IBS and HC involving platelet-related associations prompt inquiry as to differences in serotonergic signaling, inflammatory or immunomodulatory mechanisms underlying IBS symptomatology. Although preliminary and requiring validation in larger cohorts, these findings bear relevance to understanding pathogenic processes of IBS and biological effects of the disorder.

Objective We report a method using functional-molecular databases and network modelling to identify hypothetical mRNA–miRNA interaction networks regulating intestinal epithelial barrier function. The model forms a data-analysis component of our cell culture experiments, which produce RNA expression data from Nanostring Technologies nCounter® system. The epithelial tight-junction (TJ) and actin cytoskeleton interact as molecular components of the intestinal epithelial barrier. Upstream regulation of TJ-cytoskeleton interaction is effected by the Rac/Rock/Rho signaling pathway and other associated pathways which may be activated or suppressed by extracellular signaling from growth factors, hormones, and immune receptors. Pathway activations affect epithelial homeostasis, contributing to degradation of the epithelial barrier associated with osmotic dysregulation, inflammation, and tumor development. The complexity underlying miRNA–mRNA interaction networks represents a roadblock for prediction and validation of competing-endogenous RNA network function. Results We developed a network model to identify hypothetical co-regulatory motifs in a miRNA–mRNA interaction network related to epithelial function. A mRNA–miRNA interaction list was generated using KEGG and miRWalk2.0 databases. R-code was developed to quantify and visualize inherent network structures. We identified a sub-network with a high number of shared, targeting miRNAs, of genes associated with cellular proliferation and cancer, including c-MYC and Cyclin D. Electronic supplementary material The online version of this article (10.1186/s13104-018-3126-y) contains supplementary material, which is available to authorized users.

A recent American Heart Association report shows that 34% of US adults ≥20 years of age have hypertension representing ≈86 million adults.1 A substantial increase in the prevalence of hypertension has occurred globally.2 The projected number of individuals with systolic blood pressure of ≥140 mm Hg has doubled from 442 million in 1990 to 874 million in 2015. Hypertension is one of the most prevalent risk factors for cardiovascular disease (CVD).1 Results of the recently concluded SPRINT (Systolic Blood Pressure Intervention Trial) funded by the National Heart, Lung, and Blood Institute showed that among older adults with hypertension but without diabetes mellitus, lowering systolic blood pressure to a target goal of 120 mm Hg, compared with the standard goal of 140 mm Hg, resulted in significantly lower rates of fatal and nonfatal cardiovascular events and death from any cause.3 Some groups such as blacks who display both disproportionately earlier onset and higher prevalence of hypertension have increased risk of blood pressure (BP)–related cardiovascular and renal disease complications compared with non-Hispanic whites. Despite intensive attempts to influence lifestyle changes, nutritional counseling, and intensive antihypertensive drug treatment strategies, ≈14% of all hypertension patients seem to be resistant to antihypertensive interventions.1 Resistant hypertension is defined as BP above goal (>140/90 mm Hg) on ≥3 BP-lowering medications or needing ≥4 medications prescribed at optimal dose to control BP to goal. Thus, both increased prevalence and inability to achieve BP goals in a large patient population with hypertension are creating a tremendous healthcare burden. In addition, no novel antihypertensive drugs have been added to our formulary since 1995, when the first angiotensin receptor antagonist was approved in the United States. The recent attempts to use percutaneous renal artery sympathetic denervation, as a novel means to control hypertension, have been largely unsuccessful to date.4 …

Background Stress has demonstrated effects on inflammation though underlying cell-cell communication mechanisms remain unclear. We hypothesize that circulating RNAs and extracellular vesicles (EVs) in patients with chronic stress contain signals with functional roles in cell repair. Methods Blood transcriptome from patients with Irritable Bowel Syndrome versus controls were compared to identify signaling pathways and effectors. Plasma EVs were isolated (size-exclusion chromatography) and characterized for effectors' presence (immunogold labelling-electron microscopy). Based on transcriptome pathways and EV-labelling, lysozyme's effects on cell migration were tested in human colon epithelial CRL-1790 cells and compared to the effects of CXCL12, a migration inducer (wound assay). The effect of lysozyme on immune-linked mRNA and protein levels in cells which survived following serum starvation and scratch wound were investigated (NanoString). Results Blood transcriptomes revealed pyridoxal 5’phosphate salvage, pyrimidine ribonucleotides salvage pathways, atherosclerosis, and cell movement signaling with membrane CD9 and extracellular lysozyme as effectors. Plasma EVs showed labelling with CD9, mucins, and lysozyme. This is the first identification of lysozyme on plasma EVs. In CRL-1790 cells, lysozyme induced migration and repaired scratch wound as well as CXCL12. Immune mRNA and protein expressions were altered in cells which survived following serum starvation and scratch wound, with or without lysozyme in serum-free media post-wounding: CD9, IL8, IL6 mRNAs and CD9, NT5E, PD-L1 proteins. Conclusions Repair and inflammatory signals are identified in plasma EVs and circulating RNAs in chronic stress. Registered clinicaltrials.gov #NCT00824941 General significance This study highlights the role of circulating RNAs and EVs in stress., Highlights • Inflammatory pathways are predicted by blood transcriptome. • Plasma EVs from patients and controls show labelling with lysozyme, CD9, and mucins. • Lysozyme induces cell migration in response to wound in vitro. • Lysozyme alters immune-linked mRNA and protein cellular levels in response to wound. • Circulating RNAs and EVs contain signals with roles in cell migration and repair.

Vulnerable preterm infants experience repeated and prolonged pain/stress stimulation during a critical period in their development while in the neonatal intensive care unit (NICU). The contribution of cumulative pain/stressors to altered neurodevelopment remains unclear. The study purpose was to investigate the impact of early life painful/stressful experiences on neurobehavioral outcomes of preterm infants in the NICU.A prospective exploratory study was conducted with fifty preterm infants (28 0/7-32 6/7weeks gestational age) recruited at birth and followed for four weeks. Cumulative pain/stressors (NICU Infant Stressor Scale) were measured daily and neurodevelopmental outcomes (NICU Network Neurobehavioral Scale) were examined at 36-37weeks post-menstrual age. Data analyses were conducted on the distribution of pain/stressors experienced over time and the linkages among pain/stressors and neurobehavioral outcomes.Preterm infants experienced a high degree of pain/stressors in the NICU, both in numbers of daily acute events (22.97±2.30 procedures) and cumulative times of chronic/stressful exposure (42.59±15.02h). Both acute and chronic pain/stress experienced during early life significantly contributed to the neurobehavioral outcomes, particularly in stress/abstinence (p0.05) and habituation responses (p0.01), meanwhile, direct breastfeeding and skin-to-skin holding were also significantly associated with habituation (p0.01-0.05).Understanding mechanisms by which early life experience alters neurodevelopment will assist clinicians in developing targeted neuroprotective strategies and individualized interventions to improve infant developmental outcomes.

Background Catastrophizing is a cognitive process characterized by a propensity to concentrate on and magnify the value of an actual or anticipated painful stimulus and negatively assesses one’s ability to cope. Catastrophizing is an important predictor of pain-related outcomes. A cornerstone symptom of irritable bowel syndrome (IBS) is abdominal pain or discomfort. Also individuals with IBS have been reported to have a tendency to catastrophize. In a sample of individuals who suffer from IBS, we hypothesized that those individuals who catastrophize (catastrophizers) would have worse outcomes as compared to those who do not catastrophize (non-catastrophizers). Methods One hundred and one adults with IBS (79% female, mean age 42 years, 97% Caucasian) were recruited from outpatient clinics and data were collected through self-report measures. Catastrophizing was measured with the catastrophizing subscale of the Coping Strategies Questionnaire, illness representations were measured with The Revised Illness Perception Questionnaire (IPQ-R), psychological distress was measured with the Brief Symptom Inventory 18 (BSI-18), and health-related quality of life was measured using the Irritable Bowel Syndrome-Quality of Life (IBS-QOL) measure. Descriptive statistics, correlations, and multiple linear regression analyses were completed to describe participants, the associations of the variables of interest, and the unique relationship between psychosocial variables and HRQOL. Results Overall, participants reported poor HRQOL (M = 63.32, range 0–100). Catastrophizers differed significantly on IBS-QOL from non-catastrophizers (M = 48.98 vs. non-catastrophizers M = 78.53; p

Stress is known to perturb the microbiome and exacerbate irritable bowel syndrome (IBS) associated symptoms. Characterizing structural and functional changes in the microbiome is necessary to understand how alterations affect the biomolecular environment of the gut in IBS. Repeated water avoidance (WA) stress was used to induce IBS-like symptoms in rats. The colon-mucosa associated microbiome was characterized in 13 stressed and control animals by 16S sequencing. In silico analysis of the functional domains of microbial communities was done by inferring metagenomic profiles from 16S data. Microbial communities and functional profiles were compared between conditions. WA animals exhibited higher α-diversity and moderate divergence in community structure (β-diversity) compared with controls. Specific clades and taxa were consistently and significantly modified in the WA animals. The WA microbiome was particularly enriched in Proteobacteria and depleted in several beneficial taxa. A decreased capacity in metabolic domains, including energy- and lipid-metabolism, and an increased capacity for fatty acid and sulfur metabolism was inferred for the WA microbiome. The stressed condition favored the proliferation of a greater diversity of microbes that appear to be functionally similar, resulting in a functionally poorer microbiome with implications for epithelial health. Taxa, with known beneficial effects, were found to be depleted, which supports their relevance as therapeutic agents to restore microbial health. Microbial sulfur metabolism may form a key component of visceral nerve sensitization pathways and is therefore of interest as a target metabolic domain in microbial ecological restoration.

Abdominal pain is a chronic condition experienced by approximately 20% of individuals in the United States. The purpose of the study was to assess the validity of the Gastrointestinal Pain Pointer as a measure of abdominal pain intensity. A prospective longitudinal time-series study design was utilized. The sample included 93 outpatients (58.1% female). Participants met Rome III criteria for irritable bowel syndrome (n = 32) or were healthy controls (n = 61). The Gastrointestinal Pain Pointer, a new electronic pain assessment tool, was used to assess self-reported abdominal pain intensity among participants before and after ingestion of an intestinal permeability test solution across 11 time points over a 5-hour time period. The results were compared with the Short-Form McGill Pain Questionnaire. The Gastrointestinal Pain Pointer was found to be valid in the assessment of abdominal pain intensity. The tool is a novel and valid measure of abdominal pain intensity that enhances the ability for clinicians to better quantify, in real time, patient-related pain outcomes for both clinical care and research.

Objectives To evaluate the effect of early breastfeeding cessation on incidence of diarrhea in a cohort of U.S. infants. Design, sample, and measurements A secondary data analysis was conducted using data from 2,340 mother-infant dyads participating in the Infant Feeding Practices Study II. We examined associations between duration of feeding type (e.g., exclusive breastfeeding [EBF], any breastfeeding [BF], formula feeding) and incidence of diarrhea before one year. Results The sample included mother-infant dyads that were 86.2% White, 3% Black, and 5% Hispanic. Interruption of EBF before 3 months was significantly associated with higher odds of having diarrhea at 6 months (OR = 1.80, p value ≤ 0.01) and between 6 and 12 months (OR = 1.45, p ≤ .01). Breastfeeding interruption before 6 months was associated with higher odds of having diarrhea at 6 months (OR = 3.19, p ≤ .01). Formula feeding for ≥3 months was associated with higher odds of diarrhea between 6 and 12 months. Conclusions Exclusive breastfeeding for 3 months accompanied by any breastfeeding for 6 months provided the most protective effect against diarrhea. Public health interventions should address disparities in breastfeeding practices and provide support across clinical, workplace and community settings. Research should include more diverse population groups.

The mechanisms underlying the transition from acute to chronic pain remain unclear. Here, we sought to characterize the transcriptome associated with chronic low back pain as well as the transcriptome of the transition from acute to chronic low back pain. For the analysis, we compared the whole blood transcriptome of: (a) patients at the onset of low back pain who no longer had pain within 6 weeks after onset (acute) with patients who developed chronic low back pain at 6 months (chronic T5); and, (b) patients at the onset of low back pain (chronic T1) who developed chronic pain at 6 months with healthy pain-free (normal) controls. The majority of differentially expressed genes were protein coding. We illustrate a unique chronic low back pain transcriptome characterized by significant enrichment for known pain genes, extracellular matrix genes, and genes from the extended major histocompatibility complex (MHC) genomic locus. The transcriptome of the transition from acute to chronic low back pain was characterized by significant upregulation of antigen presentation pathway (MHC class I and II) genes and downregulation of mitochondrial genes associated with oxidative phosphorylation, suggesting a unique genomic signature of vulnerability to low back pain chronicity.

Both genetic and environmental factors are suggested to influence overweight and obesity risks. Although individual loci and genes have been frequently shown to be associated with body mass index (BMI), the overall interaction of these genes and their role in BMI remains underexplored. Data were collected in 90 healthy, predominately Caucasian participants (51% female) with a mean age of 26.00 ± 9.02 years. Whole blood samples were assayed by Affymetrix GeneChip Human Genome U133 Plus 2.0 Array. We integrated and analyzed the clinical and microarray gene expression data from those individuals to understand various systematic gene expression patterns underlying BMI. Conventional differential expression analysis identified seven genes RBM20, SEPT12, AX748233, SLC30A3, WTIP, CASP10, and OR12D3 associated with BMI. Weight gene co-expression network analysis among 4,647 expressed genes identified two gene modules associated with BMI. These two modules, with different extents of gene connectivity, are enriched for catabolic and muscle system processes respectively, and tend to be regulated by zinc finger transcription factors. A total of 246 hub genes were converted to non-hub genes, and 286 non-hub genes were converted to hub genes between normal and overweight individuals, revealing the network dynamics underlying BMI. A total of 28 three-way gene interactions were identified, suggesting the existence of high-order gene expression patterns underlying BMI. Our study demonstrated a variety of systematic gene expression patterns associated with BMI and thus provided novel understanding regarding the genetic factors for overweight and obesity risks on system levels.

The Complete Blood Count with Differential hematological assay is a mainstay diagnostic for point-of-care clinical diagnoses for a spectrum of diseases including infection, inflammation, anemia, and leukemia, and CBC-D profiles are under investigation as early prognostic biomarkers for leukemias and other diseases. Chronic abdominal pain (CAP) and irritable bowel syndrome (IBS) are prevalent gastrointestinal disorders in the United States, with obesity among the most common comorbidities. Often, IBS-like gastrointestinal (GI) symptoms persist after resolution of known inflammation and/or enteropathogenic infection, and current literature contains significant discussion of the extent to which IBS is within the biological spectrum of inflammatory disease. Obesity is also associated with generalized signatures of inflammation and may confound accurate diagnoses. We performed ANOVA, multiple means comparisons, statistical analyses of CBC data from our "Brain-Gut Natural History" (BGNH) clinical cohort, with additional ELISA assays for lipopolysaccharide binding protein (LBP), IL-10, cortisol, and ACTH, signatures of immune-inflammatory response and Hypothalamic-Pituitary-Adrenal (HPA) axis activity, respectively. BGNH cohort includes healthy and overweight individuals diagnosed with IBS diarrhea-(IBS-D) and constipation-predominant (IBS-C) subtypes. We identified several potentially significant markers for IBS-D and IBS-C, notably IL-10, mean platelet volume (MPV), with LBP and monocyte percent also showing some statistical significance. Weight also showed significant results for overweight vs. normal weight, regardless of IBS subtype, particularly for Cortisol. CBC-D predictive profiles for IBS subtype and weight were identified using discriminant functions analysis and show that predictivity of marker profiles have poor performance relative to their normal weight subsets. Further refinement of this analysis will be performed utilizing increased sample size, additional molecular profiles, and enhanced statistical analysis.

Colonic epithelial health is implicated in a host of gastrointestinal (GI) diseases and disorders. Lysozyme is suspected to play a role in the ability of the epithelium to recover from injury (Abey et al., in press; Gallo, 2012; Rubio, 2014) [1] , [2] , [3] . Disrupted repair mechanisms may lead to delayed or ineffective recovery and disruptions to epithelial biology resulting in GI symptoms and altered barrier function (Peterson and Artis, 2014) [4] . The effect of lysozyme on the transcriptomic and proteomic profile of healthy colonic epithelial cells was investigated. Epithelial cells in culture were scratch wounded and treated with lysozyme. mRNA and protein profiles were simultaneously quantified in the same sample using a digital counting technology. Gene and protein expressions altered by the presence or absence of lysozyme are described in this article. Extensive statistical and bioinformatic analysis, and interpretation of the results can be found in “Lysozyme association with circulating RNA, extracellular vesicles, and chronic stress” (Abey et al., in press) [1] .

Nutrition is a factor involved in inflammation and a modulator of risk toward some cancers, and the complexity of linkages between dietary components and epigenetics mechanisms (e.g., DNA methylation, histone modification, chromatin remodeling) may affect the inflammation phenotype and the development of cancer. An increasing number of studies support the role of diet in cancer development, prevention, and treatment. Although current knowledge regarding nutria-epigenetics is expanding, more work is needed, and nurse scientists have the potential to significantly contribute to the expansion of this knowledge.

Objective To explore the association of hypothalamic–pituitary–adrenal activity with ovarian functioning in women with and without chronic abdominal pain (CAP). Design and Setting A secondary data analysis was performed with data from female participants in a natural history protocol at the National Institutes of Health. Participants A total of 36 women (age range = 19–39 years, mean = 27.11 years) were included in the study. Methods This pilot study was conducted with a subset of participants enrolled in a natural history protocol conducted in the Hatfield Clinical Research Center at the National Institutes of Health. The parent study included participants with and without CAP who provided a 5-hour urine sample for determination of cortisol levels and serum samples for determination of circulating levels of cortisol, luteinizing hormone, and follicle-stimulating hormone. CAP was defined as presence or absence of chronic pain for at least 6 months and was determined via self-report. Results Anti-Mullerian hormone (AMH) concentrations declined significantly with age as expected. When AMH levels were dichotomized as normal or abnormal (defined as higher or lower than age-specific normative ranges, respectively), there were significant associations between abnormal AMH levels and CAP and urine cortisol levels. Participants with CAP or low urine cortisol levels were significantly more likely to have abnormal AMH levels. Conclusion Results suggest that chronic abdominal pain and hypothalamic–pituitary–adrenal dysregulation may be associated with abnormal AMH levels.