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The aim of this practice report is to discuss the implementation of a service-learning module developed to support the psychological wellbeing of postgraduate students and older adults in the community, with a view to fostering their connection and tackling loneliness in both populations. The module, 'Self-Identity, Intergenerational and Intercultural Learning' (SIIL), was offered to students enrolled in the Mental Health Studies Master of Science at the Institute of Psychiatry, Psychology & Neuroscience, King's College London. The module included lectures on the scientific underpinnings of wellbeing and ageism positionally within intercultural and intergenerational contexts. Students were introduced to qualitative research with a focus on autoethnography. They engaged with older adults through phone conversations and undertook wellbeing-promoting experiential exercises and self-reflection. The interactions provided students the opportunity to learn at an academic and personal level, while allowing older adults to share their experiences during the COVID-19 pandemic. These lessons learnt will inform future practice. Future directions for further developments of this methodology in other disciplines are also discussed in this practice report.

Purpose: Interdisciplinary approaches to health education are becoming increasingly common. Here, the authors describe an arts-based approach designed by academics and artists to both supplement the study of mental illness and support the individual mental health of undergraduate and postgraduate university students, by raising the visibility of mental illness in an innovative way. Design/methodology/approach: Through workshops, university students were guided in a sensory and physical way to discuss psychological health and vulnerability. This was followed by the creation of physical representations of mental distress through art pieces. Findings: Students were able to design their own art pieces and discuss mental health issues in an open and creative way. Students reported that the arts-based initiative was beneficial to their practice as future professionals and provided a holistic learning experience. At the same time, artists were able to generate powerful images which facilitated further discussions within the faculty. Practical implications: This project provides an innovative model for workshops which could be employed to raise the visibility of common mental health disorders among university students while providing a safe space to discuss and support wellbeing. Additionally, variations could be implemented to enhance the teaching of affective disorders within a university curriculum. Originality/value: This paper presents the results of collaboration between academics and artists, who together generated an innovative way to both support students' mental health and provide an alternative way to supplement experiential learning about common mental health conditions such as anxiety and depression.

Wellbeing concerns increased during the Covid-19 pandemic, with university students being a population deserving special attention. Considering this, and the positive impact that coaching psychology can make in promoting wellbeing and resilience, we designed Time to Thrive (version 2022), a coaching psychology programme for undergraduate students based on an integrative model of cognitive-behavioural solution-focused coaching, positive psychology coaching and principles of neuroscience. This paper presents 1) the coaching psychology model used as a framework to structure the content of the programme. The model, called EMERALD, is based on the following domains for wellbeing and resilience: Emotions, Meaning and Engagement, Relationships, Achievements, Living better and Driving change; and 2) the co-creation approach that we used to design the programme and its upcoming evaluation, and a thematic analysis of semi-structured interviews with students after a pilot run. Voluntary response sampling was used to recruit first-year undergraduate students across the different faculties of the university. Preliminary results (N=6) indicate that the acceptability of Time to Thrive is high among undergraduate students. Participants commented on perceived outcomes from engaging with the programme, topic content, the virtual learning environment resources and materials, interaction with other students, structure and timeline, and recruitment strategies for increasing the visibility of Time to Thrive and reaching students more broadly. By presenting EMERALD and the initial results of this student-centred project, we hope to contribute to the work of other colleagues aiming to develop similar coaching psychology strategies to promote student wellbeing and resilience at universities and other educational settings. [ABSTRACT FROM AUTHOR]

Breast cancer is the leading cause of death among women worldwide, and certain subtypes are highly aggressive and drug resistant. As oxidative stress is linked to the onset and progression of cancer, new alternative therapies, based on plant-derived compounds that activate signaling pathways involved in the maintenance of cellular redox homeostasis, have received increasing interest. Among the bioactive dietary compounds considered for cancer prevention and treatment are flavonoids, such as quercetin, carotenoids, such as lycopene, polyphenols, such as resveratrol and stilbenes, and isothiocyanates, such as sulforaphane. In healthy cells, these bioactive phytochemicals exhibit antioxidant, anti-apoptotic and anti-inflammatory properties through intracellular signaling pathways and epigenetic regulation. Short-chain fatty acids (SCFAs), produced by intestinal microbiota and obtained from the diet, also exhibit anti-inflammatory and anti-proliferative properties related to their redox signaling activity—and are thus key for cell homeostasis. There is evidence supporting an antioxidant role for SCFAs, mainly butyrate, as modulators of Nrf2-Keap1 signaling involving the inhibition of histone deacetylases (HDACs) and/or Nrf2 nuclear translocation. Incorporation of SCFAs in nutritional and pharmacological interventions changes the composition of the the intestinal microbiota, which has been shown to be relevant for cancer prevention and treatment. In this review, we focused on the antioxidant properties of SCFAs and their impact on cancer development and treatment, with special emphasis on breast cancer. [ABSTRACT FROM AUTHOR]

Introduction: Prevention of cardiovascular disease and diabetes is a priority in low- and middle-income countries, especially in South Asia where these are leading causes of morbidity and mortality. The metabolic syndrome is a tool to identify cardiometabolic risk, but the validity of the metabolic syndrome as a clinical construct is debated. This study tested the existence of the metabolic syndrome, explored alternative cardiometabolic risk characterisations, and examined genetic and environmental factors in a South Asian population sample. Methods: Data came from the Colombo Twin and Singleton follow-up Study, which recruited twins and singletons in Colombo, Sri Lanka, in 2012–2015 (n = 3476). Latent class analysis tested the clustering of metabolic syndrome indicators (waist circumference, high-density lipoprotein cholesterol, triglycerides, blood pressure, fasting plasma glucose, medications, and diabetes). Regression analyses tested cross-sectional associations between the identified latent cardiometabolic classes and sociodemographic covariates and health behaviours. Structural equation modelling estimated genetic and environmental contributions to cardiometabolic risk profiles. All analyses were stratified by sex (n = 1509 men, n = 1967 women). Results: Three classes were identified in men: 1) "Healthy" (52.3%), 2) "Central obesity, high triglycerides, high fasting plasma glucose" (40.2%), and 3) "Central obesity, high triglycerides, diabetes" (7.6%). Four classes were identified in women: 1) "Healthy" (53.2%), 2) "Very high central obesity, low high-density lipoprotein cholesterol, raised fasting plasma glucose" (32.8%), 3) "Very high central obesity, diabetes" (7.2%) and 4) "Central obesity, hypertension, raised fasting plasma glucose" (6.8%). Older age in men and women, and high socioeconomic status in men, was associated with cardiometabolic risk classes, compared to the "Healthy" classes. In men, individual differences in cardiometabolic class membership were due to environmental effects. In women, genetic differences predicted class membership. Conclusion: The findings did not support the metabolic syndrome construct. Instead, distinct clinical profiles were identified for men and women, suggesting different aetiological pathways. [ABSTRACT FROM AUTHOR]

The additional new mutations designed for manipulating the architecture of heme pocket in recombinant human serum albumin (rHSA)-heme complexes by altering distal amino acids are described. The replacement of polar Arg-186 with Leu or Phe has increased the hydrophobicity of the distal environment, has yielded a complex with reduced [O.sub.2] binding affinity, which is almost the same as that of human red blood cells and therefore better tuned to a role in [O.sub.2] transport.

Background: Previous studies have shown associations between major depression and C-reactive protein (CRP) levels. Few studies have considered the extent to which shared genetic and environmental factors contribute to this association, nor have they considered the relationship outside of European populations. We examined the association between CRP levels and depression and their aetiology in a Sri Lankan population.Methods: Data were collected from 2577 twins and 899 singletons in Colombo, Sri Lanka. Depression symptoms were assessed using the revised Beck Depression Inventory (BDI-II). High-sensitive CRP blood levels were assessed using immunoturbidimetry. Linear regressions were performed to test the association between CRP and depression. The heritability of CRP levels was estimated using Structural Equation Modelling.Results: CRP was significantly associated with BMI (p < 0.01) but not depression (p > 0.05). In males, variance in CRP levels was explained by shared environment (51% 95%CIs: 13-62) and non-shared environment (45% 95%CIs: 36-54). In contrast, in females, CRP variance was explained by genetic (41% 95%CIs: 10-52) and non-shared environment (56% 95%CIs: 47-67). A genetic correlation between CRP and BMI was observed in females only.Limitations: CRP level was based on a single data collection point, longer term data collection would give a more accurate picture of an individual's state of inflammation.Conclusions: The lack of association between depression and CRP strengthens the hypothesis that inflammation might contribute to the development of some, but not all types of depression. CRP levels were moderated by the environment, suggesting interventions aimed at reducing CRP levels and risk for inflammatory conditions, particularly in males. [ABSTRACT FROM AUTHOR]

4-thio D-ribono-1, 4-lactone resulted from D-gulono-1,4-lactone through its 2,3-O-isopropylidene derivative, as part of a facile preparation of enantiomerically pure aldopentono-1,4-thiolactones. The derivatives 5,6-glycol system were oxidized with NaIO4. 2,3,-O-isopropylidene-L-lyxono-1,4-lactone resulted from the characteristic reduction of the subsequently obtained aldehyde function with NaBH3CN.

A worldwidemental health crisis is expected, as millions worldwide fear death and disease while being forced into repeated isolation. Thus, there is a need for new proactive approaches to improve mental resilience and prevent mental health conditions. Since the 1990s, art has emerged as an alternative mental health therapy in the United States and Europe, becoming part of the social care agenda. This article focuses on how visual esthetic experiences can create similar patterns of neuronal activity as those observed when the reward system is activated. The activation of the reward structures could have a stress buffering effect, given the interdependence observed between the reward and stress systems. Therefore, could visual esthetic experiences stimulate mental resilience? And if this were the case, could art-based interventions be offered for mental health in the context of COVID-19 and beyond? [ABSTRACT FROM AUTHOR]

Introduction. Biobanks are a valuable resource for creating advancements in science through cutting-edge omics research. Twin research methods allow us to understand the degree to which genetics and environmental factors contribute to health outcomes. Methods. The Sri Lankan Twin Registry biobank (SLTR-b) was established in 2015 as part of Colombo Twin and Singleton Follow-up Study. Venous blood and urine were collected from twins and comparative sample of singletons for clinical investigations and biobanking. Results. The SLTR-b currently houses 3369 DNA and serum samples. Biobank specimens are linked to longitudinal questionnaire data, clinical investigations, anthropometric measurements, and other data. Discussion. The SLTR-b aims to address gaps in health and genetics research. It will provide opportunities for academic collaborations, local and international, and capacity building of future research leaders in twin and omics research. This paper provides a cohort profile of the SLTR-b and its linked data, and an overview of the strategies used for biobanking. [ABSTRACT FROM AUTHOR]

Inflammation has been identified as one of the main pathophysiological mechanisms underlying neuropsychiatric and neurodegenerative disorders. Despite the role of inflammation in those conditions, there is still a lack of effective anti-inflammatory therapeutic strategies. Omega-3 polyunsaturated fatty acids (n-3 PUFAs) can reduce depressive symptoms and exert anti-inflammatory action putatively by the production of distinct n-3 PUFA-derived metabolites, such as resolvins D (RvD) and E (RvE) series, maresins (MaR) and protectins (PD), which are collectively named specialized pro-resolving mediators (SPMs) and act as strong anti-inflammatory agents. In this review we summarize evidence showing the effects of treatment with those metabolites in pre-clinical models of psychiatric, neurodegenerative and neurological disorders. A total of 25 pre-clinical studies were identified using the PubMed database. Overall, RvD and RvE treatment improved depressive-like behaviors, whereas protectins and maresins ameliorated neurological function. On a cellular level, RvDs increased serotonin levels in a model of depression, and decreased gliosis in neurodegenerative disorders. Protectins prevented neurite and dendrite retraction and apoptosis in models of neurodegeneration, while maresins reduced cell death across all studies. In terms of mechanisms, all SPMs down-regulated pro-inflammatory cytokines. Resolvins activated mTOR and MAP/ERK signaling in models of depression, while resolvins and maresins activated the NF-κB pathway in models of neurodegeneration and neurological disorders. Our review indicates a potential promising approach for tailored therapy with n-3 PUFAs-derived metabolites in the treatment of psychiatric, neurodegenerative, and neurological conditions. [ABSTRACT FROM AUTHOR]

Proximal histidine is introduced into the subdomain IB of human serum albumin (HSA) by site-directed mutagenesis to construct a tailor-made heme pocket that allows a reversible O2 binding to the prosthetic heme group. The structural and mutagenic approach allows the enhancement of O2 binding properties of recombinant HSA (rHSA)-heme complexes and thereby mimics the diverse biological reactivities of natural hemoproteins.

Background: Glucocorticoid resistance—reduced function of the glucocorticoid receptor (GR)—is seen in many depressed patients. It is argued that this resistance to glucocorticoids leads to failure of normal feedback regulation on the immune system. High levels of pro-inflammatory cytokines result. Purpose: We sought to identify evidence supporting or refuting a link between glucocorticoid resistance and immune dysregulation in depression and to summarize retrieved evidence in aggregate form. Methods: We systematically reviewed and meta-analyzed studies that examined cytokine levels in depressed patients compared with controls and that also reported a measure of glucocorticoid resistance. These measures included plasma cortisol, the dexamethasone suppression test (DST), GR expression levels, and the results of in vitro assays of GR function. We conducted four separate meta-analyses to test for moderating effects of glucocorticoid resistance on cytokine production in depression. Results: After sub-grouping 32 studies by the ratio of cortisol levels in patients compared with controls, we observed a trend for increasing glucocorticoid resistance (i.e., the most hypercortisolemic patients) to be associated with increased production of interleukin (IL)-6 [ d = 0.94; 95% CI (0.29, 1.59)] and tumour necrosis factor (TNF)-α [ d = 0.46; 95% CI (0.12, 0.79)]. We stratified nine studies that reported DST results by relative glucocorticoid resistance between patients and controls, identifying a trend for higher glucocorticoid resistance in patients, compared with controls, to be associated with higher cytokine production in patients (170 patients and 187 controls). This was particularly evident when studies were sub-grouped by source of cytokine—plasma (d = 1.04; 95% CI, 0.57–1.50) versus in vitro (d = 0.24; 95% CI, −0.20 to 0.67). Stratifying the four studies (147 patients and 118 controls) that used in vitro assays of GR function or GR expression to quantify glucocorticoid resistance revealed variable contributions to cytokine production in patients compared with controls (overall effect size: d = 1.35; 95% CI 0.53–2.18). Combining our analyses of studies that reported DST results with those that used in vitro assays of GR function or GR expression to quantify glucocorticoid resistance (302 patients and 277 controls), we noted that although depressed patients produced more cytokines than controls (d = 1.02; 95% CI, 0.55–1.49), there was no evident positive correlation between glucocorticoid resistance and inflammation. Conclusions: Our work provides some support for a model conceptualizing glucocorticoid resistance as a requisite for increased inflammation in depression. The limited number of studies identified highlights the need for purpose-designed investigations that directly examine the relationship between glucocorticoid resistance and cytokine production in depression. [ABSTRACT FROM AUTHOR]

Background: In humans, interferon-α treatment for chronic viral hepatitis is a well-recognized clinical model for inflammation-induced depression, but the molecular mechanisms underlying these effects are not clear. Following peripheral administration in rodents, interferon-α induces signal transducer and activator of transcription-1 (STAT1) within the hippocampus and disrupts hippocampal neurogenesis. Methods: We used the human hippocampal progenitor cell line HPC0A07/03C to evaluate the effects of 2 concentrations of interferon-α, similar to those observed in human serum during its therapeutic use (500 pg/mL and 5000 pg/mL), on neurogenesis and apoptosis. Results: Both concentrations of interferon-α decreased hippocampal neurogenesis, with the high concentration also increasing apoptosis. Moreover, interferon-α increased the expression of interferon-stimulated gene 15 (ISG15), ubiquitin-specific peptidase 18 (USP18), and interleukin-6 (IL-6) via activation of STAT1. Like interferon-α, co-treatment with a combination of ISG15, USP18, and IL-6 was able to reduce neurogenesis and enhance apoptosis via further downstream activation of STAT1. Further experiments showed that ISG15 and USP18 mediated the interferon-α-induced reduction in neurogenesis (potentially through upregulation of the ISGylation-related proteins UBA7, UBE2L6, and HERC5), while IL-6 mediated the interferon-α-induced increase in apoptosis (potentially through downregulation of aquaporin 4). Using transcriptomic analyses, we showed that interferon-α regulated pathways involved in oxidative stress and immune response (e.g., Nuclear Factor erythroid-derived 2)-like 2 [Nrf2] and interferon regulatory factor [IRF] signaling pathway), neuronal formation (e.g., CAMP response element-binding protein [CREB] signaling), and cell death regulation (e.g., tumor protein(p)53 signaling). Conclusions: We identify novel molecular mechanisms mediating the effects of interferon-α on the human hippocampus potentially involved in inflammation-induced neuropsychiatric symptoms. [ABSTRACT FROM AUTHOR]

Repeated lipopolysaccharide exposure is often used in longitudinal preclinical models of depression. However, the potential phenotypic differences from acute depression-mimicking effects are rarely described. This study compared chronic lipopolysaccharide administration of doses previously used in depression research to a new mode of escalating dose injections. Adult male BALB/c mice ( n=8/group) were injected intraperitoneally with either a single 0.83 mg/kg dose, a repeated 0.1 mg/kg lipopolysaccharide dose or a dose which escalated weekly from 0.33 to 0.83 mg/kg lipopolysaccharide for six weeks. The escalating lipopolysaccharide group demonstrated most features of sickness behaviour such as weight loss and reduction in food intake every week, whilst this effect was not sustained in other groups. Moreover, only in the escalating lipopolysaccharide group did most peripheral plasma cytokines levels, measured using Luminex multiplex technology, such as interleukin-6, tumour necrosis factor α and interleukin-2 remain over three-fold elevated on the sixth week. In addition, exposure to escalating doses led to a reduction of neuroblast maturation in the dentate gyrus relevant for depression neurobiology. Therefore, this mode of injections might be useful in the studies attempting to replicate neurobiological aspects of the chronic inflammatory state observed in mood disorders. [ABSTRACT FROM AUTHOR]