Biological Research For Nursing

Metabolomics, one of the newest omics, allows for investigation of holistic responses of living systems to myriad biological, behavioral, and environmental factors. Researcher use metabolomics to examine the underlying mechanisms of clinically observed phenotypes. However, these methods are complex, potentially impeding their uptake by scientists. In this scoping review, we summarize literature illustrating nurse scientists’ use of metabolomics. Using electronic search methods, we identified metabolomics investigations conducted by nurse scientists and published in English-language journals between 1990 and November 2019. Of the studies included in the review (N = 30), 9 (30%) listed first and/or senior authors that were nurses. Studies were conducted predominantly in the United States and focused on a wide array of clinical conditions across the life span. The upward trend we note in the use of these methods by nurse scientists over the past 2 decades mirrors a similar trend across scientists of all backgrounds. A broad range of study designs were represented in the literature we reviewed, with the majority involving untargeted metabolomics (n = 16, 53.3%) used to generate hypotheses (n = 13, 76.7%) of potential metabolites and/or metabolic pathways as mechanisms of clinical conditions. Metabolomics methods match well with the unique perspective of nurse researchers, who seek to integrate the experiences of individuals to develop a scientific basis for clinical practice that emphasizes personalized approaches. Although small in number, metabolomics investigations by nurse scientists can serve as the foundation for robust programs of research to answer essential questions for nursing.

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.

The co-occurrence of multiple psychoneurological symptoms, including pain, sleep disturbance, fatigue, depression, anxiety, and cognitive disturbance among adult cancer survivors led us to question which common biological mechanisms are shared among these conditions. Variances in tryptophan (Trp) levels and downstream metabolites of the kynurenine (Kyn) metabolic pathway are known to affect immune response and psychoneurological symptoms. The objective of this systematic review was to help us (a) better understand the role of the Kyn pathway in psychoneurological symptoms among adult cancer survivors and (b) identify common significant biomarkers across psychoneurological symptoms as a guide for future research. Some evidence has shown that decreased Trp levels and increased Kyn, Trp/Kyn ratio, and kynurenic acid/Trp ratio in parallel with immune activation are correlated with some psychoneurological symptoms among people undergoing cancer treatment, although discrepancies exist between studies. Kyn pathway activation could also be associated with psychoneurological symptoms among adult cancer survivors, but further research is needed to confirm its exact etiological role with respect to psychoneurological symptoms.

Traumatic brain injuries (TBIs) are a significant health problem, impacting millions of people every year. Although emerging evidence suggests that the composition of the gut microbiome is altered after TBI, no systematic review has been published on this topic. The objective of the present systematic review is to analyze publications that evaluate the impact of TBI on gut microbiome composition. Research articles were pulled from seven databases. The systematic review was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. In order for publications to be eligible for this review, they had to (1) report on original human- or animal-subjects research, (2) evaluate the impact of TBI on the microbiome, and (3) be written in English and (4) be published in a peer-reviewed journal. Of the seven articles that met these criteria, one involved human participants, while the other six reported on experimental animal studies. All studies found changes in the gut microbiome following TBI, with similar changes in bacterial populations observed across studies. The limitations of these studies included the use of primarily male animals, limitations of 16 S rRNA gene sequencing, and small sample sizes. This review was also limited by the small pool of studies conducted in this area. In summary, changes in bacterial populations of the gut microbiome, specifically increases in proteobacteria and firmicutes, were observed across the studies. By evaluating the changes in the microbiome resulting from TBI, potential therapeutic interventions could be explored.

The aim of this study was to investigate the effect of environmental enrichment (EE) on neurotrophin expression in an animal model of Parkinson’s disease (PD). PD was induced via intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Male mice (N = 42) were randomly divided into 3 groups: control, MPTP + standard condition (SC), and MPTP + EE. The groups were raised separately for 28 days. On Day 21 they received 1 injection (20 mg/kg MPTP or saline for MPTP and control groups, respectively) every 2 hr for a total of 4 injections. Animals were sacrificed 7 days after the final injection and their brains were immediately removed. Neurotrophins and messenger ribonucleic acid (mRNA) expression levels were measured. The BCL-2/Bax ratio significantly increased in the MPTP + EE compared to the MPTP + SC group. Nerve growth factor (NGF) mRNA level was upregulated (but not significantly) in the MPTP + EE compared to the MPTP + SC group. Tyrosine hydroxylase (TH) expression significantly increased in the MPTP + EE compared to the MPTP + SC group. Finally, expressions of proNGF and p75 neurotrophin receptor (p75^NTR) were significantly downregulated in the MPTP + EE compared to the MPTP + SC group. Results confirm that EE has neuroprotective effects on dopaminergic neurons via suppression of activation of the p75^NTR-mediated signaling pathway through the binding of proNGF and p75^NTR. Findings suggest that use of EE as a therapeutic intervention would promote healthy aging by facilitating recovery following brain injury and preventing neurodegenerative diseases.

The pathobiology of cancer-related fatigue (CRF) remains elusive, hindering the development of targeted treatments. Radiation therapy (RT), a common treatment for men with prostate cancer, induces cell damage through the generation of free radicals and oxidative stress. We hypothesized that disruption in cellular responses to this surge of nonphysiological oxidative stress might contribute to CRF in men with prostate cancer treated with RT. We evaluated the potential role of three cell damage pathways (apoptosis, autophagy, necrosis) and oxidative stress in CRF in men with prostate cancer receiving RT. Fatigue was measured by the Functional Assessment of Cancer Therapy-Fatigue (FACT-F) questionnaire. Gene expression was measured in whole blood using RT² profiler™ PCR arrays. Data were collected at two time points: either baseline or Day 1 of treatment (T1) and completion of treatment (T2). Participants were grouped into either the fatigued or nonfatigued phenotype at T2 using the recommended FACT-F cut-off score for clinical significance. We observed significant upregulation of seven genes related to three cell damage pathways in the fatigued group from T1 to T2 and no significant changes in the nonfatigued group. We also observed significant downregulation of two genes related to oxidative stress in the fatigued group compared to the nonfatigued group at T2. These collective results provide preliminary evidence that cell damage might be upregulated in the CRF phenotype. Validation of these findings using a larger and more diverse sample is warranted.

While weight gain is common following migration to a new country and Mexican Americans have a disparate prevalence of overweight and obesity. In particular, Mexican American women have one of the world’s highest rates of Metabolic Syndrome (MetS), characterized by abdominal obesity, insulin resistance, hypertension, and dyslipidemia, all of which increase the risk for atherosclerotic cardiovascular disease (CVD). Although the etiology of this dilemma is not well understood, using the framework of allostatic load (AL), we posit that exposure to multiple physiologic, psychosocial and environmental stressors over the course of the lifespan may contribute to an increased risk of MetS among indigenous Mexican immigrant women. Two such frequently overlooked stressors are: 1) a history of childhood growth stunting (CGS) and 2) dietary changes post migration that result in decreased diversity of the gut microbiome (dysbiosis). To date, little is known about how migration experiences differentially affect the relationship between CGS and MetS in adulthood. The purpose of this theoretical article is to present a proposed model of how early life stressors (ELS), specifically CGS, may interact with insalubrious aspects of the immigration experience to promote an increased risk for MetS among indigenous Mexican immigrant women. This model may be used in a bi-national effort to guide intervention efforts to decrease CGS in Mexico and to prevent, monitor or delay the components of MetS post migration in the US.

Big data-driven omics research has led to a steep rise in investigations involving two of the most functional omes, the metabolome and microbiome. The former is touted as the closest to the phenotype, and the latter is implicated in general well-being and a plethora of human diseases. Although some research publications have integrated the concepts of the two domains, most focus their analyses on evidence solely originating from one or the other. With a growing interest in connecting the microbiome and metabolome in the context of disease, researchers must also appreciate the disconnect between the two domains. In the present review, drawing examples from the current literature, tools, and resources, I discuss the connections between the microbiome and metabolome and highlight challenges and opportunities in linking them together for the basic, translational, clinical, and nursing research communities.