Swiss School of Archaeology in Greece
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Infection with Mycobacterium tuberculosis alters the antibody response to HIV-1
No full textCo-infection with Mycobacterium tuberculosis (MTB) differentially modulates untreated HIV-1 infection, with asymptomatic MTB reducing HIV-1 viremia and opportunistic infections and active tuberculosis (TB) accelerating AIDS progression. Here, we investigate antibody (Ab) responses to HIV-1 in people with HIV (PWH) without MTB, with asymptomatic MTB, and with later progression to active TB to elucidate MTB-associated effects on HIV-1 immune control.
Using the Swiss HIV Cohort Study (SHCS), we conducted a retrospective study that included 2,840 PWH with data on MTB status and HIV-1-specific plasma binding-/neutralizing-responses. We evaluated associations between MTB status and binding-/neutralizing-responses while adjusting for key disease and demographic parameters.
Among the included 2,840 PWH, 263 PWH had asymptomatic MTB based on either a positive TST-/IGRA-test at the baseline (time of HIV-1 Ab measurement) or on later progression to active TB. Compared to PWH without MTB infection, PWH with asymptomatic MTB infection showed reduced HIV-1 Ab levels, both for Env binding (e.g., IgG1 BG505 trimer antigen, p = 0.024) and neutralization of a diverse panel of HIV-1 viruses (p = 0.012). Conversely, PWH (n = 32) who later progressed to active TB (>180 days after baseline) demonstrated a significant shift towards IgG3 in their HIV-1 Ab repertoire (p = 0.011), detectable in median 3.8 years (IQR 2.4 - 8.7) before active TB onset.
Our data indicate that asymptomatic MTB infection and active TB exert profound heterologous effects on HIV-1 specific Ab development. These findings advance our understanding of host-pathogen dynamics and may have implications for new diagnostic approaches in predicting future active TB.
Copyright: © 2025 Zeeb et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
The diagnostic value of faecal calprotectin levels in patients with perianal fistula: A systematic review
No full textPerianal fistula (PAF) is a common condition encountered in surgical and gastroenterological practice. Distinguishing between cryptoglandular disease (CGD) and inflammatory bowel disease (IBD)-related perianal disease is critical to ensure appropriate management. Faecal calprotectin (FC) has emerged as a promising non-invasive biomarker for IBD; however, its role in acute perianal disease is not well established. This systematic review aimed to evaluate the diagnostic accuracy of FC in distinguishing IBD-related perianal disease from CGD.
A systematic literature search was conducted in PubMed, Embase and Cochrane databases following PRISMA guidelines. Studies were included if they assessed FC levels in patients with PAF and provided diagnostic accuracy metrics. Data extraction focused on study design, population characteristics, FC cut-off values, sensitivity, specificity and area under the curve (AUC) metrics.
Three studies met the inclusion criteria, all reporting significantly higher FC levels in IBD-related PAF compared to CGD-related fistulas. The proposed FC cut-off values varied, ranging from 110 μg/g to 344 μg/g, with corresponding sensitivities between 52% and 81%, as well as specificities between 77% and 93%. The AUC values indicated moderate to high diagnostic accuracy.
FC shows potential as a diagnostic tool for differentiating IBD-related perianal disease from CGD. A cut-off of 110-150 μg/g appears most suitable for early screening, whereas a higher threshold may be appropriate for confirmatory diagnosis. Further prospective studies with standardized protocols are necessary to refine these thresholds and validate FC as a clinical decision-making tool.
© 2025 Association of Coloproctology of Great Britain and Ireland
Causal Discovery in Multivariate Extremes: A Study of Swiss Hydrological Catchments
No full textABSTRAC
Experiences of healthcare and administrative staff working with asylum seekers in the current polycrisis context: a qualitative study.
No full textHealthcare and administrative staff working with asylum seekers are at risk of burnout, compassion fatigue and vicarious traumatization. Moreover, they face a series of crises, with the refugee crisis in 2015-2016, the Covid-19 pandemic, the war in Ukraine and climate change, complexifying their daily practice and increasing the number of asylum seekers. Despite this alarming context, scarce research has explored the personal experiences of healthcare and administrative staff working with asylum seekers. In response, this qualitative study aimed to explore their work-related experiences, resources and needs in the current polycrisis context in Switzerland.
Participants (N = 24) were part of the front-line care team working with asylum seekers in the Canton of Vaud (Switzerland). The sample included nurses, administrative staff, physicians and psychologists. They participated in semi-structured interviews exploring the personal experiences of their work, difficulties and challenges encountered and their resources and needs. Inductive content analysis was used to organize data and identify themes.
Main findings highlighted a significant emotional burden for staff related to their patients' migratory journey and experiences in the asylum system. Next, participants expressed various challenges associated with their work, such as heavy workload, lack of partners in the healthcare network, communication barriers and the polycrisis context. Further, findings documented that participants' strong intrinsic motivation and personal and institutional resources support them in overcoming these difficulties. Finally, participants made some suggestions for the improvement of their working environment, including promotion of exchange between colleagues, collaboration with partners and hiring additional staff.
Healthcare and administrative staff working with asylum seekers are exposed to multiple challenges and emotional difficulties linked to their patients' experiences. Findings suggest the need to address the well-being of this population by developing measures to enhance support for them at individual and structural levels, particularly within the current polycrisis context
The Expertise of the Amateur: The Salon des Medecins and the Exercise of Power on the Margins of the Art World
No full textLa recherche sur les « amateurs de carrière » met au jour l’histoire d’une simili-professionnalité artistique. À travers le cas emblématique du Salon des médecins, notre étude propose d’interroger la notion d’expertise appliquée au travail artistique amateur. La légitimité du médecin-artiste se fonde, en effet, au xxe siècle sur l’autodéclaration d’une expertise anatomique qui, dans le prolongement d’une concurrence entre professionnels de la médecine et de l’art, envisage l’extension des missions sociales du corps médical en terrain artistique. Les exemples des travaux exposés par les docteurs Eugène Briau et Charles Villandre permettent, dès lors, d’entrevoir la mise en œuvre de cette expertise, qui procède d’un pouvoir légal sur les corps « vils » des vivants et des morts. À travers le cas des médecins-artistes, il s’agit ainsi de s’interroger sur les moyens et, surtout, sur la pratique d’une expertise à la périphérie amateur des mondes de l’art, expertise qui tend à faire du travail créateur un exercice du pouvoir
Evolving Landscape of Thrombotic Microangiopathy in Kidney Transplant Recipients in the post C5 inhibitor Era
No full textA comprehensive analysis was performed on all consecutive biopsy-proven Thrombotic Microangiopathy (TMA) complicating kidney transplantation in the post C5 inhibitor era (from 2009) to identify pathological profiles, determine causes and establish risk factor associated with death-censored graft survival, in two French center. Pathological criteria were assessed according to the TMA Banff Working Group, followed by an unbiased analysis to identify distinct subgroups. 119 cases were identified, 8(6.7%) primary TMA, and 23(19.3%) antibody-mediated rejection. In 98 cases (82.4%), more than one potential trigger was involved. Latent class analysis identified two groups: acute TMA pattern (n= 79(66.4%)) enriched for fibrin thrombi in glomerular capillaries and arterioles and mesangiolysis, and chronic active TMA pattern (n= 40 (33.6%)) enriched for collapsed capillaries. Both had similar presentation, were not indicative of specific causes but had different outcome. In multivariate analysis, grade 3 hypertension, low hemoglobin levels, proteinuria, baseline serum creatinine and the value of a Banff-based chronicity index (ct + ci + 2xcg +cv) were associated with poorer death-censored graft survival, while fibrin thrombi in glomerular capillaries were associated with a better outcome. KT-TMA is a severe condition in which the pathological pattern may reflect the disease stage, rather than the often intricate underlying mechanism.
Copyright © 2025. Published by Elsevier Inc
Pilot Testing a Peer-Led Self-Management Program for Women After Breast Cancer.
No full textDifferent approaches exist to support self-management in breast cancer (BC) survivors. The aim of this project was to cocreate a new version of an existing peer-led program to meet the needs of BC survivors in Switzerland. In a pilot study, the preliminary efficacy in terms of self-management skills and symptom burden and the feasibility of implementing it in two Swiss university hospitals was assessed.
A prospective nonequivalent pretest-posttest control group design with two consecutive cohorts of women with early-stage BC who had completed primary treatment was applied. BC survivors (peers) led the 7-week course of weekly small-group sessions of 2.5 to 3 hours. The primary outcome was change in self-management skills; secondary outcomes included change in self-efficacy, symptom burden, and health literacy. Between-group changes were assessed using the Mann-Whitney U or X² test, individual changes using the Reliable Change Index. Feasibility was assessed using qualitative methods.
Of the 95 BC survivors screened for inclusion criteria, 68 were eligible, 18 agreed to participate in the control group and 20 in the intervention group. No significant differences were found between the groups for any of the outcomes. Individual changes in self-management skills were noted in both groups. Several issues related to course delivery and feasibility were identified.
The current form of the program did not fully meet the needs of BC survivors, and implementation into the clinical care pathway appeared to be challenging. The program may benefit from providing the possibility of spontaneous interaction and discussion and considering elements of e-health interventions
Maternal exposure to high-fat diet induces long-term mitochondrial alterations in the offspring heart.
No full textHeart disease is a leading cause of death worldwide, with its prevalence exacerbated by inadequate nutritional intake. Particularly concerning is the elevated risk induced by imbalanced nutrition during development, which can impact lifelong heart health. Recent research has underscored mitochondrial dysregulation as a pivotal mechanism driving the enduring consequences of nutritional excess. Building upon previous findings wherein a maternal high-fat diet (HFD) led to cardiac hypertrophy and fibrosis, our current study aimed to evaluate the impact of such a challenge on myocardial mitochondrial function.
Female rats were fed a chow diet or HFD during gestation and lactation. The hearts of male offspring were analyzed at adulthood. Mitochondrial DNA abundance was evaluated by quantitative polymerase chain reaction. Proteins involved in mitochondrial biogenesis, fusion, fission, damage to the electron transport chain, metabolism, cell death, proliferation, and inflammation were measured by western blot. Mitochondrial clearance was evaluated by the measurement of mitophagy markers on isolated mitochondria. Lipids were visualized by histologic approaches.
We detected decreased cardiac mitochondrial fission factor and mitochondrial adenosine triphosphate synthase beta subunit and increased Parkin, pro-tumor necrosis factor alpha, and pro-interleukin 1 beta protein levels associated with decreased microtubule-associated protein 1A/1B light chain 3B levels in cardiac mitochondrial fraction, with a tendency for increased Oil Red O staining in the adult hearts of male offspring exposed to HFD.
Maternal exposure to HFD enhanced mitochondrial damage and impaired fission and clearance in offspring hearts at adulthood. These alterations were associated with altered expression of proteins involved in the mitochondrial electron transport chain coupled with a propensity for increased fatty acid accumulation and elevated proinflammatory markers
Phosphoenolpyruvate carboxykinase 1-mediated cataplerosis is required to maintain mitochondrial fitness and to avoid kidney disease progression
No full textMetabolic alterations are recognized as key features of kidney injury, but their causal role in kidney repair remains debatable. Here, we investigate the role of phosphoenolpyruvate carboxykinase 1 (PCK1), an enzyme involved in gluconeogenesis and cataplerosis (removal of tricarboxylic acid (TCA) cycle intermediates from the mitochondrial matrix) in kidney disease progression.
We used mice with kidney tubular cell-specific deletion or overexpression of the PCK1 enzyme, and different models of kidney injury such as ischemia-reperfusion injury or cis-platin-induced nephropathy. Furthermore, we measured metabolites in kidney biopsy tissue from patients with stage 3b/4 chronic kidney disease (CKD).
Using flux analysis, we confirm that cataplerosis and the TCA cycle are blocked by PCK1 deficiency. This results in injured mitochondria leading to inflammation, tubular injury and impaired tubular cell repair. Inversely, maintaining PCK1 function in different models of kidney injury preserves kidney structure, improves TCA cycle metabolite clearance and increase ATP production. In kidney biopsies from different patient cohorts, we confirm the correlation between PCK1 loss, mitochondrial injury and a failed tubular cell repair phenotype. Furthermore, in CKD, accumulation of TCA cycle metabolites is consistent with disrupted cataplerosis.
Overall, we demonstrate that PCK1 loss in kidney tubular cells leads to decreased respiration and the accumulation of TCA cycle metabolites. Maintenance of cataplerosis is an important factor of tubular physiology and repair, with PCK1 serving as a causal and potential therapeutic target in this process. PCK1 restoration enhances mitochondrial health, limiting progression to inflammation and fibrosis.
Copyright © 2025 International Society of Nephrology. All rights reserved
Multiomics unravels the complexity of male obesity: a prospective observational study
No full textObesity is associated with varying degrees of metabolic dysfunction. In this study, we aimed to discover markers of the severity of metabolic impairment in men with obesity via a multiomics approach.
Thirty-two morbidly men with obesity who were candidates for Roux-en-Y gastric bypass (RYGB) surgery were prospectively followed. Nine healthy adults served as controls. Deep phenotyping, including targeted metabolomics, transcriptomics, and brain magnetic resonance imaging (MRI), was performed.
Testosterone emerged as a key contributor to phenotypic variability via principal component analysis and was therefore used to further categorize obese patients as having or not having hypogonadotropic hypogonadism (HH). Despite having comparable body mass indices, obese individuals with HH presented with worse metabolic defects than obese individuals without HH, including higher insulin resistance, as well as MRI signs of hypothalamic inflammation and a specific blood transcriptomics signature. The upregulated genes were involved mainly in inflammation, mitochondrial function, and protein translation. Integration of gene expression and clinical data revealed high FGF21 and low cortisol levels as the top markers correlated with the transcriptomic signature of metabolic risk. Following RYGB-induced substantial weight loss, testosterone levels markedly increased in both obese individuals with and without HH, challenging the current definition of hypogonadism. A longitudinal study in a subset of men with obesity following bariatric surgery revealed a unique FGF21 trajectory with a sharp peak at one month post-RYGB that correlated with metabolic and reproductive improvements.
Combining clinical, biochemical, and molecular markers allows adequate stratification of metabolic risk in men with obesity and provides novel tools for personalized care.
© 2025. The Author(s)