User evaluation of a mobile education application for the management of metabolic syndrome among cancer survivors.

OBJECTIVE: This study aimed to develop a smartphone education application for managing metabolic syndrome among cancer survivors and obtain user evaluation based on quantitative and qualitative data. METHODS: Ten cancer survivors and 10 oncology nurse specialists responded to a structured usability evaluation tool (Mobile Application Rating Scale: MARS). Quantitative data analysis was performed through descriptive statistics using SPSS version 25.0. We conducted semi-structured interviews of the cancer survivors and oncology nurse specialists. Qualitative data of interview responses were coded as the app's strengths and weaknesses, information, motivation, and behavioral change. RESULTS: The overall usability evaluation score of the app was 3.66 ± 0.39 for cancer survivors and 3.79 ± 0.20 for oncology nurse specialists. Both cancer survivors and oncology nurse specialists scored the area of functionality as the highest and engagement as the lowest. Additionally, the qualitative usability evaluation suggested that the app should be visually improved by including figures and tables to enhance readability and providing videos and more specific guidelines to directly elicit behavioral change. CONCLUSIONS: Metabolic syndrome in cancer survivors can be effectively managed by using the educational application developed in this study by improving the shortcomings of the app for cancer survivors.

Neuroimmune signatures in chronic low back pain subtypes.

We recently showed that patients with different chronic pain conditions (such as chronic low back pain, fibromyalgia, migraine and Gulf War illness) demonstrated elevated brain and/or spinal cord levels of the glial marker 18-kDa translocator protein (TSPO), which suggests that neuroinflammation might be a pervasive phenomenon observable across multiple aetiologically heterogeneous pain disorders. Interestingly, the spatial distribution of this neuroinflammatory signal appears to exhibit a degree of disease specificity (e.g. with respect to the involvement of the primary somatosensory cortex), suggesting that different pain conditions may exhibit distinct 'neuroinflammatory signatures'. To explore this hypothesis further, we tested whether neuroinflammatory signal can characterize putative aetiological subtypes of chronic low back pain patients based on clinical presentation. Specifically, we explored neuroinflammation in patients whose chronic low back pain either did or did not radiate to the leg (i.e. 'radicular' versus 'axial' back pain). Fifty-four patients with chronic low back pain, 26 with axial back pain [43.7 ± 16.6 years old (mean ± SD)] and 28 with radicular back pain (48.3 ± 13.2 years old), underwent PET/MRI with 11C-PBR28, a second-generation radioligand for TSPO. 11C-PBR28 signal was quantified using standardized uptake values ratio (validated against volume of distribution ratio; n = 23). Functional MRI data were collected simultaneously to the 11C-PBR28 data (i) to functionally localize the primary somatosensory cortex back and leg subregions; and (ii) to perform functional connectivity analyses (in order to investigate possible neurophysiological correlations of the neuroinflammatory signal). PET and functional MRI measures were compared across groups, cross-correlated with one another and with the severity of 'fibromyalgianess' (i.e. the degree of pain centralization, or 'nociplastic pain'). Furthermore, statistical mediation models were used to explore possible causal relationships between these three variables. For the primary somatosensory cortex representation of back/leg, 11C-PBR28 PET signal and functional connectivity to the thalamus were: (i) higher in radicular compared to axial back pain patients; (ii) positively correlated with each other; (iii) positively correlated with fibromyalgianess scores, across groups; and finally (iv) fibromyalgianess mediated the association between 11C-PBR28 PET signal and primary somatosensory cortex-thalamus connectivity across groups. Our findings support the existence of 'neuroinflammatory signatures' that are accompanied by neurophysiological changes and correlate with clinical presentation (in particular, with the degree of nociplastic pain) in chronic pain patients. These signatures may contribute to the subtyping of distinct pain syndromes and also provide information about interindividual variability in neuroimmune brain signals, within diagnostic groups, that could eventually serve as targets for mechanism-based precision medicine approaches.

Striatal hypofunction as a neural correlate of mood alterations in chronic pain patients.

BACKGROUND: Chronic pain and mood disorders share common neuroanatomical substrates involving disruption of the reward system. Although increase in negative affect (NA) and decrease in positive affect (PA) are well-known factors complicating the clinical presentation of chronic pain patients, our understanding of the mechanisms underlying the interaction between pain and PA/NA remains limited. Here, we used a validated task probing behavioral and neural responses to monetary rewards and losses in conjunction with functional magnetic resonance imaging (fMRI) to test the hypothesis that dysfunction of the striatum, a key mesolimbic structure involved in the encoding of motivational salience, relates to mood alterations comorbid with chronic pain. METHODS: Twenty-eight chronic musculoskeletal pain patients (chronic low back pain, n=15; fibromyalgia, n=13) and 18 healthy controls underwent fMRI while performing the Monetary Incentive Delay (MID) task. Behavioral and neural responses were compared across groups and correlated against measures of depression (Beck Depression Inventory) and hedonic capacity (Snaith-Hamilton Pleasure Scale). RESULTS: Compared to controls, patients demonstrated higher anhedonia and depression scores, and a dampening of striatal activation and incentive-related behavioral facilitation (reduction in reaction times) during reward and loss trials of the MID task (ps â€‹< â€‹0.05). In all participants, lower activation of the right striatum during reward trials was correlated with lower incentive-related behavioral facilitation and higher anhedonia scores (ps â€‹< â€‹0.05). Finally, among patients, lower bilateral striatal activation during loss trials was correlated with higher depression scores (ps â€‹< â€‹0.05). CONCLUSIONS: In chronic pain, PA reduction and NA increase are accompanied by striatal hypofunction as measured by the MID task.

Oncology nurses' knowledge and awareness on metabolic syndrome in cancer survivors and the perceived barriers to the provision of related care: A mixed-method study.

OBJECTIVE: To identify oncology nurses' level of knowledge and awareness of metabolic syndrome (MetS) in cancer survivors and the perceived barriers to the provision of MetS-related care. METHODS: In this mixed-method study, 196 participants responded to a structured modified questionnaire that included items pertaining to MetS-related knowledge and awareness. Concurrently, 24 semi-structured interviews were conducted. A qualitative survey and quantitative interview were conducted between October 2018 and December 2018. RESULTS: While oncology nurses had a high level of knowledge of MetS in terms of its individual components, they failed to accurately differentiate MetS cases from non-MetS ones. Further, they showed a high level of awareness of MetS-related care for cancer survivors but did not apply their knowledge in clinical settings. In the qualitative survey, the nurses cited various factors pertaining to their perceived barriers to the provision of MetS-related care, including the fact that cancer survivors are distinguished by the specificity of the subject and inpatient environmental constraints. CONCLUSIONS: Oncology nurses had a high level of knowledge of MetS but failed to accurately identify MetS cases. Thus, their level of knowledge should be improved, and strategies are needed to overcome the perceived barriers to the provision of MetS-related care.

Assessing Information Needs Regarding Metabolic Syndrome Among Gynecological Cancer Survivors: A Concurrent Mixed Method.

BACKGROUND: Cancer survivors have an increased risk of non-cancer-related deaths, particularly metabolic syndrome (MetS). OBJECTIVE: We aimed to assess knowledge deficits regarding metabolism-related diseases among gynecological cancer survivors and the preferred source of health information. METHODS: Using a mixed methods approach, 70 participants responded to a structured modified version of the MetS questionnaire. We conducted 28 semistructured interviews of gynecological cancer survivors with MetS. Responses were independently coded by 2 researchers, including MetS knowledge, behaviors for self-management, and preferred learning methods. RESULTS: Metabolic syndrome was diagnosed in 17% of the participants. More than 50% of the participants wanted to learn about MetS and requested a consultation with healthcare providers, 70% reported that they had heard of MetS, and 61.4% reported that they had MetS-related knowledge (correct answer rate by MetS-related component, ~50%). The level of MetS-related knowledge was poor in both the quantitative and qualitative data. Most of the participants defined MetS-related self-management health behaviors as regular eating and exercise in their own words. Participants mostly wanted exercise management (29% of the participants), followed by dietary life management (27.4%), stress management (17.4%), weight management (13.7%), definition and diagnostic methods of MetS (9.1%), and smoking and drinking management (3.3%). Participants wished to use a handbook in small groups or receive counseling by healthcare providers. CONCLUSION: We observed poor awareness and knowledge level and the need for information regarding MetS among gynecological cancer survivors. IMPLICATIONS FOR PRACTICE: An educational handbook or counseling could effectively improve self-management of health-related behaviors.

Brain glial activation in fibromyalgia - A multi-site positron emission tomography investigation.

Fibromyalgia (FM) is a poorly understood chronic condition characterized by widespread musculoskeletal pain, fatigue, and cognitive difficulties. While mounting evidence suggests a role for neuroinflammation, no study has directly provided evidence of brain glial activation in FM. In this study, we conducted a Positron Emission Tomography (PET) study using [11C]PBR28, which binds to the translocator protein (TSPO), a protein upregulated in activated microglia and astrocytes. To enhance statistical power and generalizability, we combined datasets collected independently at two separate institutions (Massachusetts General Hospital [MGH] and Karolinska Institutet [KI]). In an attempt to disentangle the contributions of different glial cell types to FM, a smaller sample was scanned at KI with [11C]-L-deprenyl-D2 PET, thought to primarily reflect astrocytic (but not microglial) signal. Thirty-one FM patients and 27 healthy controls (HC) were examined using [11C]PBR28 PET. 11 FM patients and 11 HC were scanned using [11C]-L-deprenyl-D2 PET. Standardized uptake values normalized by occipital cortex signal (SUVR) and distribution volume (VT) were computed from the [11C]PBR28 data. [11C]-L-deprenyl-D2 was quantified using λ k3. PET imaging metrics were compared across groups, and when differing across groups, against clinical variables. Compared to HC, FM patients demonstrated widespread cortical elevations, and no decreases, in [11C]PBR28 VT and SUVR, most pronounced in the medial and lateral walls of the frontal and parietal lobes. No regions showed significant group differences in [11C]-L-deprenyl-D2 signal, including those demonstrating elevated [11C]PBR28 signal in patients (p's ≥ 0.53, uncorrected). The elevations in [11C]PBR28 VT and SUVR were correlated both spatially (i.e., were observed in overlapping regions) and, in several areas, also in terms of magnitude. In exploratory, uncorrected analyses, higher subjective ratings of fatigue in FM patients were associated with higher [11C]PBR28 SUVR in the anterior and posterior middle cingulate cortices (p's < 0.03). SUVR was not significantly associated with any other clinical variable. Our work provides the first in vivo evidence supporting a role for glial activation in FM pathophysiology. Given that the elevations in [11C]PBR28 signal were not also accompanied by increased [11C]-L-deprenyl-D2 signal, our data suggests that microglia, but not astrocytes, may be driving the TSPO elevation in these regions. Although [11C]-L-deprenyl-D2 signal was not found to be increased in FM patients, larger studies are needed to further assess the role of possible astrocytic contributions in FM. Overall, our data support glial modulation as a potential therapeutic strategy for FM.

Symptom Clusters and Quality of Life According to the Survivorship Stage in Ovarian Cancer Survivors.

This cross-sectional study evaluated a convenience sample comprising 182 ovarian cancer survivors to identify symptom clusters according to the cancer survivorship stage and to determine their effects on quality of life using the European Organization for Research and Treatment of Cancer Quality of Life-C30 and -OV28 questionnaires. Factor and multiple regression analyses were performed to identify symptom clusters according to the cancer survivorship stage and the symptom clusters that affected the quality of life in each cancer survivorship stage, respectively. Participants in the acute, extended, and permanent survival stages accounted for 33%, 36.3%, and 30.7% of subjects, respectively. Overall, the most common symptom cluster was fatigue-diarrhea, and the symptom clusters affecting the quality of life differed according to the cancer survivorship stage. Thus, to improve the quality of life of ovarian cancer survivors, the main symptom clusters of each cancer survivorship stage must be identified, and management strategies for the related symptoms must be designed.