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INTRODUCTION The number of people in Aotearoa New Zealand who identify as Pasifika as their ethnicity is increasing, with ~8% in 2021 (Stats NZ, 2018b). According to Arini et al [...], Many Pasifika students in Aotearoa New Zealand face challenges in their tertiary education. Their academic stress may potentially affect their wellbeing. Using a cross-sectional approach, we aimed to explore the proportion of Pasifika students with insomnia symptoms in the Department of Anatomy at the University of Otago, and whether their academic stress and sleep hygiene were associated with their insomnia symptoms. A brief (10-15 min) online survey was sent to 101 Pasifika science students at second- and third-year undergraduate levels in our department. Data from 57 Pasifika students (21.1 + 1.6 years old; 28.1% Samoan, 26.3% Tongan, 24.6% Fijian) were assessed. The proportions of Pasifika students with no, mild, moderate, and severe insomnia symptoms were 15.8%, 35.1%, 31.6%, and 7% respectively. Insomnia symptoms correlated with higher levels of stresses related to students' academic self-perceptions. Insomnia symptom severity also correlated with sleep hygiene, especially: going to and getting out of bed at irregular times, staying in bed longer than necessary, consuming alcohol/tobacco/caffeine close to bedtime, going to bed feeling distressed, sleeping in an uncomfortable bed, and worrying while in bed. Sleep hygiene mediated the relationship between perceived academic stress and insomnia symptom severity. Pasifika science students in Aotearoa New Zealand may be at elevated risk of having insomnia symptoms due to academic stress. Sleep hygiene education may potentially help improve their wellbeing. Keywords: Acad emic stress, Pasifika students, insomnia symptoms, sleep hygiene, ethnic minority

Q: How did you come to your focus on gynaecology and obstetrics? A: My initial vocation was to specialize in paediatrics, but I decided to focus on gynaecology and obstetrics [...]

Introduction We are experiencing unprecedented growth in the amount of biological and medical information collected from human populations. Large prospective cohorts, such as the UK Biobank (1), the All of [...], Technological advances in rapid data acquisition have transformed medical biology into a data mining field, where new data sets are routinely dissected and analyzed by statistical models of ever- increasing complexity. Many hypotheses can be generated and tested within a single large data set, and even small effects can be statistically discriminated from a sea of noise. On the other hand, the development of therapeutic interventions moves at a much slower pace. They are determined from carefully randomized and well-controlled experiments with explicitly stated outcomes as the principal mechanism by which a single hypothesis is tested. In this paradigm, only a small fraction of interventions can be tested, and an even smaller fraction are ultimately deemed therapeutically successful. In this Review, we propose strategies to leverage large- cohort data to inform the selection of targets and the design of randomized trials of novel therapeutics. Ultimately, the incorporation of big data and experimental medicine approaches should aim to reduce the failure rate of clinical trials as well as expedite and lower the cost of drug development.

Introduction Endothelial progenitor cells (EPCs), a vasoreparative cell type that is derived from bone marrow hematopoietic stem cells, contributes to neovascularization and re-endothelialization (Krankel et al. 2012). Diabetic patients experience [...], The aim of our work was to test whether thymosin beta 4 protected endothelial progenitor cells against apoptosis induced by advanced glycation endproducts and investigate the underlying mechanism. Treatment with thymosin beta 4 or transfection with microRNA-34a inhibitor enhanced cell viability, reduced apoptosis, abated oxidative stress, and attenuated mitochondrial dysfunction in endothelial progenitor cells exposed to advanced glycation endproducts. Incubation with advanced glycation endproducts led to increased levels of microRNA-34a, which was attenuated by treatment with thymosin beta 4. Transfection with microRNA-34a reversed the beneficial effect of thymosin beta 4 against injuries induced by advanced glycation endproducts. The microRNA-34a could directly bind to the 3&apos;UTRs of the mRNA of B-cell lymphoma 2, and thymosin beta 4 treatment upregulated B-cell lymphoma 2 expression in endothelial progenitor cells exposed to advanced glycation endproducts. More importantly, knockdown of B-cell lymphoma 2 abolished the protection of thymosin beta 4 and microRNA-34a inhibitor against advanced glycation endproducts. In conclusion, inhibition of microRNA-34a mediated protection of thymosin beta 4 in endothelial progenitor cells against advanced glycation endproducts by targeting B-cell lymphoma 2, which was helpful for understanding the therapeutic potential of thymosin beta 4 for diabetic patients. Key words: endothelial progenitor cells, advanced glycation endproducts, thymosin beta 4, microRNA-34a, bcl-2. Nos travaux avaient pour but d&apos;evaluer si la thymosine beta 4 permet de proteger les cellules souches endotheliales contre l&apos;apoptose provoquee par les produits finaux de glycation avancee, ainsi que d&apos;etudier les modes d&apos;action sous-jacents. L&apos;administration de thymosine beta 4 ou la transfection avec un inhibiteur du microRNA-34a entrainait une augmentation de la vitalite des cellules, une diminution de l&apos;apoptose, ainsi qu&apos;une attenuation du stress oxydatif et du dysfonctionnement mitochondrial dans les cellules souches endotheliales exposees aux produits finaux de glycation avancee. L&apos;incubation avec des produits finaux de glycation avancee a mene a une augmentation des taux de microRNA-34a, laquelle etait attenuee par l&apos;administration de thymosine beta 4. La transfection avec le microRNA-34a antagonisait les bienfaits de la thymosine beta 4 contre les lesions engendrees par les produits finaux de glycation avancee. Le microRNA-34a pouvait se lier directement a la region 3&apos;-UTR de l&apos;ARNm de bcl-2 (pour << B-cell lymphoma 2 >>), et l&apos;administration de thymosine beta 4 entrainait une regulation a la hausse de l&apos;expression de bcl-2 dans les cellules souches endotheliales exposees aux produits finaux de glycation avancee. Ce qui est plus important, la repression (<< knockdown >>) de bcl-2 reduisait a neant la protection de la thymosine beta 4 et de l&apos;inhibiteur du microRNA-34a contre les produits finaux de glycation avancee. En conclusion, l&apos;inhibition du microRNA-34a participait a la mediation de la protection de la thymosine beta 4 contre les produits finaux de glycation avancee dans les cellules souches endotheliales en ciblant bcl-2, ce qui etait utile pour comprendre le potentiel therapeutique de la thymosine beta 4 pour les patients atteints de diabete. [Traduit par la Redaction] Mots-cles : cellules souches endotheliales, produits finaux de glycation avancee, thymosine beta 4, microRNA-34a, bcl-2.

EPHA2 expression defines T cell exclusion Although antibodies that block immune checkpoints have revolutionized the management of some tumors with tumor-infiltrating lymphocytes (TILs), most cancer patients still fail to respond [...], Pancreatic ductal adenocarcinoma is projected to become the second-leading cause of cancer-related death and is largely resistant to immunotherapies. The tumor microenvironment, largely composed of heterogeneous myeloid cells, creates a physical, metabolic, and immunosuppressive barrier that prevents T cells from infiltrating cancer beds. In this issue of the JCI, Markosyan and colleagues have reported a tumor-intrinsic mechanism that excludes T cells from the vicinity of tumor cells. They showed that a receptor tyrosine kinase, ephrin-A receptor 2 (EPHA2), regulates prostaglandin endoperoxide synthase 2 (PTGS2) (encodes COX-2) expression in a TGF-[beta] signaling-dependent manner. Genetic ablation of Epha2 or Ptgs2 in preclinical models or pharmacological inhibition of COX-2 elicited the transformation of this immunosuppressive microenvironment into a T cell-permissive milieu. Consequent T cell relocation rendered this immunoresistant malignancy responsive to combinations of checkpoint blockers and CD40 agonists. Because the association between T cell infiltration and the EPHA2/TGF-[beta]/COX-2 axis is supported by independent clinical data, these results provide a rationale for ensuing clinical trials aimed at incorporating pancreatic cancer into the range of immunotherapy- responsive tumors.