The Impact of EU Political Ambiguity Towards Migrant Crisis on the Mental Health of Migrants

For last couple of years, EU is facing migrant crisis that is challenging its capacity to help and its unity to decide the modes of assistance. Such political context brings additional uncertainty and insecurity into migrants’ lives which causes extreme experiences that are often damaging migrants’ mental health. In humanitarian plans regarding assistance for migrants, mental health is a cross cutting issue. Status of mental health is a result of complex intertwining of genetics, developmental and current life experiences. The experience of migration is a current life event which highly determines migrants’ mental health. Hardships of travel along migration route are worsened by often hostile reception by authorities at borders of countries that are on the way to desired rich EU countries. On migrants’ way to desired safety, there are countries like Slovenia and Hungary which protect their borders with wire. Therefore, migrants are stuck in countries, like Greece and Croatia, which are not their desirable destination. While waiting to get free passage, migrants are exposed to various political rhetoric of politicians of EU countries who hold their destiny in their hands. Migration experience does not make migrants mentally ill but it does make them vulnerable in that respect. Migrants’ vulnerability is highly challenged by ambiguity of political decisions, media coverage influenced by the same policies and concomitant changes in immediate surrounding. It is crucial to make publicly clear that political decisions mean life or death, health or mental disorder to migrants and that therefore they at least carry ethical responsibility.Disclosure of interestThe author has not supplied his/her declaration of competing interest.</jats:sec

A cross-sectional study of the role of epithelial cell injury in kidney transplant outcomes

Background. Expression of acute kidney injury–associated (AKI-associated) transcripts in kidney transplants may reflect recent injury and accumulation of epithelial cells in “failed repair” states. We hypothesized that the phenomenon of failed repair could be associated with deterioration and failure in kidney transplants. Methods. We defined injury-induced transcriptome states in 4,502 kidney transplant biopsies injury-induced gene sets and classifiers previously developed in transplants. Results. In principal component analysis (PCA), PC1 correlated with both acute and chronic kidney injury and related inflammation and PC2 with time posttransplant. Positive PC3 was a dimension that correlated with epithelial remodeling pathways and anticorrelated with inflammation. Both PC1 and PC3 correlated with reduced survival, with PC1 effects strongly increasing over time whereas PC3 effects were independent of time. In this model, we studied the expression of 12 “new” gene sets annotated in single-nucleus RNA-sequencing studies of epithelial cells with failed repair in native kidneys. The new gene sets reflecting epithelial-mesenchymal transition correlated with injury PC1 and PC3, lower estimated glomerular filtration rate, higher donor age, and future failure as strongly as any gene sets previously derived in transplants and were independent of nephron segment of origin and graft rejection. Conclusion. These results suggest 2 dimensions in the kidney transplant response to injury: PC1, AKI-induced changes, failed repair, and inflammation; and PC3, a response involving epithelial remodeling without inflammation. Increasing kidney age amplifies PC1 and PC3. Trial registration. INTERCOMEX (ClinicalTrials.gov NCT01299168); Trifecta-Kidney (ClinicalTrials.gov NCT04239703). Funding. Genome Canada; Natera, Inc.; and Thermo Fisher Scientific

A cross-sectional study of the role of epithelial cell injury in kidney transplant outcomes

BACKGROUND: Expression of acute kidney injury-associated (AKI-associated) transcripts in kidney transplants may reflect recent injury and accumulation of epithelial cells in failed repair states. We hypothesized that the phenomenon of failed repair could be associated with deterioration and failure in kidney transplants. METHODS: We defined injury-induced transcriptome states in 4,502 kidney transplant biopsies injury-induced gene sets and classifiers previously developed in transplants. RESULTS: In principal component analysis (PCA), PC1 correlated with both acute and chronic kidney injury and related inflammation and PC2 with time posttransplant. Positive PC3 was a dimension that correlated with epithelial remodeling pathways and anticorrelated with inflammation. Both PC1 and PC3 correlated with reduced survival, with PC1 effects strongly increasing over time whereas PC3 effects were independent of time. In this model, we studied the expression of 12 new gene sets annotated in single-nucleus RNA-sequencing studies of epithelial cells with failed repair in native kidneys. The new gene sets reflecting epithelial-mesenchymal transition correlated with injury PC1 and PC3, lower estimated glomerular filtration rate, higher donor age, and future failure as strongly as any gene sets previously derived in transplants and were independent of nephron segment of origin and graft rejection. CONCLUSION: These results suggest 2 dimensions in the kidney transplant response to injury: PC1, AKI-induced changes, failed repair, and inflammation; and PC3, a response involving epithelial remodeling without inflammation. Increasing kidney age amplifies PC1 and PC3. TRIAL REGISTRATION: INTERCOMEX (ClinicalTrials.gov NCT01299168); Trifecta-Kidney (ClinicalTrials.gov NCT04239703). FUNDING: Genome Canada; Natera, Inc.; and Thermo Fisher Scientific

Subthreshold rejection activity in many kidney transplants currently classified as having no rejection

Most kidney transplant patients who undergo biopsies are classified as having no rejection based on consensus thresholds. However, we hypothesized that because these patients have normal adaptive immune systems, T cell-mediated rejection (TCMR) and antibody-mediated rejection (ABMR) may exist as subthreshold activity in some transplants currently classified as no rejection. To examine this question, we studied genome-wide microarray results from 5086 kidney transplant biopsies (from 4170 patients). An updated molecular archetypal analysis designated 56% of biopsies as no rejection. Subthreshold molecular TCMR and/or ABMR activity molecular activity was detectable as elevated classifier scores in many biopsies classified as no rejection, with ABMR activity in many TCMR biopsies and TCMR activity in many ABMR biopsies. In biopsies classified as no rejection histologically and molecularly, molecular TCMR classifier scores correlated with increases in histologic TCMR features and molecular injury, lower estimated glomerular filtration rate, and higher risk of graft loss, and molecular ABMR activity correlated with increased glomerulitis and donor-specific antibody. No rejection biopsies with high subthreshold TCMR or ABMR activity had a higher probability of having TCMR or ABMR, respectively, diagnosed in a future biopsy. We conclude that many kidney transplant recipients have unrecognized subthreshold TCMR or ABMR activity, with significant implications for future problems