Leaf samples were collected in spring 2018 from a riparian floodplain forest in central Moravia, Czechia, where Ericales plants were absent. The analyzed trees were Alnus glutinosa, Carpinus betulus, Corylus avellana, Quercus petraea and Q. robur. The investigators also mined the GlobalFungi database for published environmental sequences to assess the occurrence of Exobasidium beyond known host plants.

After filtering, the researchers identified 75 Exobasidium amplicon sequence variants from leaves and insect guts, which clustered into 12 phylotypes. Seven grouped with described species that had publicly available DNA barcodes, including E. arescens, E. bisporum, E. camelliae, E. euryae, E. gracile, E. maculosum and E. miyabei. The other five had less than 94% similarity to sequenced species in the National Center for Biotechnology Information database, indicating possible undescribed or as-yet-unsequenced diversity.

This interpretation remains uncertain because many named Exobasidium species still lack public molecular data. Exobasidium communities differed significantly among host tree species in an analysis of similarity based on Jaccard and Morisita-Horn indices with 9,999 permutations. Quercus petraea had the highest measured alpha diversity, with a mean Shannon index of 0.50 and a mean Simpson index of 0.39, while Q. robur had the lowest values, at 0.32 and 0.17, respectively.

Principal component analysis also separated several tree-associated communities. Phylotype 9 accounted for more than 66% of Exobasidium reads on A. glutinosa and 62% on Q. robur, occurred in more than 30% of leaf samples from every analyzed tree and also dominated several caterpillar-gut communities. Overall, the gut datasets did not differ significantly from one another, and their phylotype proportions broadly reflected those in the corresponding tree phyllospheres.

Phylotype 9 was recovered in pure culture from two Tischeria ekebladella caterpillars and from healthy Tilia cordata leaves collected in Slovakia. All three isolates were genetically identical. Phylogenetic analysis placed them as a sister lineage to E. woronichinii and E. rhododendri.

The isolates differed from E. woronichinii by 3.9% of nucleotides in the ITS region and 1.8% in the LSU region, supporting their recognition as Exobasidium phylloplanum. Its name refers to the phylloplane, the leaf surface. The species produces filamentous colonies with fusiform blastoconidia measuring 8.2 ± 3.0 micrometres long and 1.8 ± 0.2 micrometres wide.

Physiological tests found growth from 6 to 25 °C, with optimal growth between 20 and 25 °C. Salinity of 16% or higher prevented growth. The isolates used all 16 tested carbon sources and grew on glucose without fermenting it.

In the GlobalFungi analysis, 17 of 40 examined Exobasidium species or phylotypes appeared in at least one environmental sample. E. phylloplanum was the most frequently detected lineage, occurring in 841 samples from 52 studies, mainly in European forests and in samples from plant shoots and soil. Its records were concentrated in temperate regions, with an absence in the otherwise well-surveyed boreal and Mediterranean areas.

Known parasites E. arescens, E. vaccinii and E. camelliae were also detected in environmental records, while some environmental phylotypes in the E. bisporum and E. miyabei clades occurred more frequently than the available reference sequences. The researchers could not establish that these environmental phylotypes represented the corresponding parasitic species in the sampled regions. They instead proposed that Exobasidium includes a continuum of life histories, ranging from predominantly parasitic species with short saprotrophic phases to lineages with longer environmental phases and possibly predominantly saprotrophic species.

The genome of E. phylloplanum strain CCF 7021 was assembled into five nuclear scaffolds totaling 17.7 megabases. The assembly had an N50 of 5.8 megabases, 95.5% BUSCO completeness and 7,463 annotated proteins. Comparative analyses found broadly similar numbers of carbohydrate-active enzyme genes and genes associated with pathogen–host interactions among E. phylloplanum and other Exobasidium species.

E. phylloplanum was distinguished by an expanded set of type I polyketide synthases, consistent with its production of red-brown gunacin pigments. The comparison did not identify a genomic feature that explained its apparently different lifestyle. A central limitation is that environmental DNA cannot by itself distinguish actively growing cells from dormant or wind-dispersed propagules.

Nevertheless, the non-random association of phylotypes with host trees, their recovery from healthy leaves and their isolation from insect guts support active surface colonization, although they do not prove a complete saprotrophic life cycle. It remains unresolved whether E. phylloplanum has an unrecognized pathogenic stage, a predominantly saprotrophic lifestyle or another form of ecological flexibility; the study establishes neither outcome. Infection experiments would be required to assess its parasitic potential.

Subject of Research: Environmental, cultural and genomic evidence for saprotrophic diversity in the fungal genus Exobasidium

Article Title: The saprotrophic dimension of Exobasidium ( Exobasidiales , Basidiomycota ): evidence for greater diversity and ecological flexibility than previously recognized

Article References: Veselská, T., Ježková, T., Ngubane, N. P., Wennrich, A., Kostovčík, M., Hařovská, D., Šigut, M., Pyszko, P., Bracewell, R., Drozd, P., Begerow, D., & Kolařík, M. (2026). The saprotrophic dimension of Exobasidium (Exobasidiales, Basidiomycota): evidence for greater diversity and ecological flexibility than previously recognized. IMA Fungus, 17, Article e180524. https://doi.org/10.3897/imafungus.17.180524

Image Credits: AI Generated

DOI: 10.3897/imafungus.17.180524

Keywords: Exobasidium, Exobasidium phylloplanum, saprotroph, environmental DNA, ITS2 metabarcoding, phyllosphere, fungal diversity, phylogenomics, caterpillar gut microbiome, Exobasidiales, saprotrophic, dimension

The authors, Guido Caluori and Sebastien Chaigne, ground their case in a striking pattern that recurs across the cardiovascular spectrum. Cellular and tissue remodeling, including cardiac hypertrophy, myocardial stiffening, and impaired diastolic filling, precedes clinical symptoms and diagnosis. Atrial fibrosis and mitochondrial remodeling may develop long before atrial fibrillation appears. Endothelial dysfunction precedes hypertension and atherosclerosis. Even rare conditions such as J-wave syndromes are now considered cardiomyopathies with subtle structural abnormalities that standard imaging cannot detect. Disturbances in protein homeostasis and metabolic adaptation also occur well before clinical manifestations. Sudden cardiac events, in other words, are often the visible end of biological processes that have been running silently for years.

These temporal trajectories differ markedly across pathologies, are not linear, and are modulated by age, sex, lifestyle, and inter-organ interactions. That interindividual variability, the authors argue, calls for a personalized temporal framework for diagnosis and therapy rather than a single, universally applied diagnostic threshold. Current clinical categories illustrate the problem. Heart failure is subdivided into phenotypes with reduced, mildly reduced, and preserved ejection fraction, which share common pathophysiological mechanisms, including neurohormonal modulation, myocardial fibrosis, and inflammation, but differ in their temporal trajectories and therapeutic responses. Similarly, the conventional classification of atrial fibrillation into paroxysmal and persistent forms, later expanded to include long-standing persistent and permanent categories, fails to capture individual risk profiles and the progressive nature of the underlying atrial myopathy. These labels likely represent overlapping but temporally and mechanistically divergent trajectories rather than strict separate entities.

Diagnostic thresholds, the authors contend, anchor disease to the moment of clinical recognition rather than to its biological origin. Hypertension is diagnosed when blood pressure exceeds a fixed numerical value; heart failure is defined once the ejection fraction falls below a critical value. Yet the cardiovascular system may be biologically much older or younger than its chronological age. The coronary endothelium of a 50-year-old patient may exhibit a molecular signature typically observed in older subjects, characterized by the accumulation of senescent cells and impaired nitric oxide signaling. Conversely, an octogenarian with a biologically younger myocardium, marked by preserved mitochondrial function, low systemic inflammation, and maintained protein homeostasis, may remain healthy beyond the expected clinical limits. An ejection fraction measured at a single moment reflects vulnerability and biological age only at the time it is measured, not the trajectory that produced it.

This mismatch between biological and chronological cardiovascular age leads directly to what the authors call the tipping point problem. Biological systems initially buffer stress through compensatory mechanisms, but once a critical threshold is crossed, they shift rapidly and irreversibly toward a pathological state. Disease does not emerge abruptly; it reflects a progressive erosion of adaptive reserve that proceeds toward a tipping point. This framework may explain why clinically stable periods can precede sudden and unexpected decompensation. Drawing on the mathematics of critical transitions in complex systems, the authors note that as a system approaches a critical threshold, critical slowing down and changes in its dynamics, including increased variance and instability, may provide early-warning signals of the transition. Applied to cardiovascular disease trajectories, this approach may help identify subclinical signs of maladaptive capacity before irreversible decompensation, yet these signals remain largely invisible to current diagnostic tools.

The dynamics differ across heart failure phenotypes and directly influence the optimal timing of intervention. Heart failure with reduced ejection fraction often reaches a tipping point marked by irreversible cardiomyocyte loss and fibrosis, whereas heart failure with preserved ejection fraction may progress more gradually through accumulating diastolic dysfunction and microvascular impairment. The mildly reduced phenotype may represent an intermediate and potentially more reversible stage. Determining where patients are positioned along this trajectory is crucial for identifying the window during which intervention can still prevent irreversible decompensation. The authors propose a staged temporal model, beginning with an adaptive, compensated phase characterized by very low fibrosis and preserved electrical and endothelial function, detectable only through subtle changes in BNP, slight elevations in hs-CRP, and minor diastolic dysfunction on echocardiography, and ending with advanced disease marked by refractory heart failure and severe structural damage.

The middle phases of this model are where the therapeutic opportunity lies. In the pre-pathology phase, fibrosis and inflammation initiate, endothelial dysfunction develops, and metabolic remodeling begins, with detectable signals including elevated galectin-3, subtle ECG changes, altered heart rate variability, and early diastolic filling abnormalities. This is the opportunity for targeted prevention and risk stratification using biomarkers and imaging. At the tipping point itself, compensatory mechanisms fail, and the balance between phenotypes shifts, often signaled by paroxysmal atrial fibrillation, acute decompensated heart failure, or a first myocardial infarction. Once decompensation occurs, reversibility is limited and the focus shifts to symptom control, risk reduction, and device or ablative strategies. The insidious phase, the authors emphasize, represents a key but systematically underexplored therapeutic window, when intervention may be most effective but where detection is limited.

To make this framework operational, the authors argue that current cardiovascular research remains largely reductionist and linear. Systems biology has transformed the field through multi-omics integration, spatial transcriptomics, single-cell sequencing, and computational physiology, but these advances remain incomplete without explicit integration of time. Most experimental models rely on young male animals and fail to recapitulate human biological aging and cumulative environmental exposures such as smoking, diet, inactivity, and obesity. The authors point to cumulative electrophysiological remodeling that develops over years, reflecting a gradual disruption of ion-channel homeostasis, mechano-electrical coupling, and repolarization reserve that grows with biological aging and environment. This progressive remodeling is associated with QT interval prolongation and increased repolarization heterogeneity on the ECG, reflecting a growing ionic imbalance and destabilization of spatial and regional electrophysiological control systems. Because most atrial fibrillation and heart failure models are induced in young animals, which lack the age-related calcium dysregulation, oxidative stress, fibrosis, and reduced repolarization reserve that underlie arrhythmogenesis in humans, such models poorly recapitulate transient arrhythmogenic events, including early and delayed afterdepolarizations at the cellular level.

The authors propose integrating biological age as a mechanistic dimension of disease rather than treating it as a simple time-based variable. Biological age should reflect molecular damage, immune remodeling, mitochondrial dysfunction, and ion-channel alterations. Epigenetic clocks such as GrimAge and PhenoAge enable estimation of biological age independently of chronological age. Integrating these measures into digital twin frameworks would allow reconstruction of disease trajectories and quantification of the velocity of aging over time, distinguishing adaptive, pre-pathological, unstable, and decompensated states and capturing transitions rather than static categories. Structural remodeling, electrophysiological instability, inflammatory signaling, and metabolic aging likely interact synergistically to reduce cardiovascular adaptive capacity over time. The authors also note that the term four-dimensional has previously been used in cardiovascular chronobiology to describe the circadian regulation of cardiac physiology across hourly-to-daily timescales; here, however, the fourth dimension captures the longitudinal trajectory of disease development and biological aging over years, a distinct temporal scale and conceptual framework.

The most speculative section of the article confronts the question of biological time inversion. Partial in vivo reprogramming through transient Yamanaka factor expression has been shown to reset epigenetic landscapes while preserving cellular identity, restoring chromatin accessibility and regenerative capacity in aged tissues. Naked mole rats may reach an age of 40 years with remarkably limited cardiovascular aging. Heterochronic parabiosis models indicate that exposure to a young systemic milieu can reverse cardiac hypertrophy and improve myocardial function in aged mice, although the identity and reproducibility of circulating rejuvenating factors remain controversial, particularly for candidates such as GDF11. Partial reprogramming has also restored vision in aged mice, supporting the concept of persistent epigenetic plasticity in adult mammalian tissues. These findings challenge the classical view of aging as a strictly linear and irreversible trajectory, suggesting instead a dynamic continuum of modifiable biological states. The authors caution, however, that the magnitude, durability, and safety of such effects remain highly context-dependent, with unresolved risks including tumorigenicity, loss of cellular identity, and long-term genomic instability. In the cardiovascular system, where remodeling emerges from tightly integrated mechanical, metabolic, and inflammatory signaling, such plasticity appears partial and temporally constrained. Biological time modulation, they conclude, should be viewed not as a true reversal of aging, but as a constrained reprogramming of cardiovascular trajectories within a broader four-dimensional disease continuum.

The implications for precision cardiology are considerable. Emerging approaches based on biomarkers and wearable or implantable devices will increasingly enable real-time monitoring of individual disease trajectories for earlier detection of warning signals before irreversible remodeling occurs. A central challenge is to identify the therapeutically actionable window during which pathological remodeling remains reversible in order to limit disease progression. The next paradigm shift in cardiovascular research, the authors argue, will be fundamentally conceptual, requiring integration of the principles of personalized medicine and a move from static, symptom-driven definitions of disease toward dynamic, trajectory-based frameworks grounded in systems biology. The focus will shift from detecting electromechanical and structural abnormalities to unveiling early signs of instability across different levels of biological organization. Without integrating biological time as a fourth dimension, cardiovascular biology remains fundamentally incomplete, and progress toward improved patient outcomes will continue to be constrained by the lack of more integrative and translational research frameworks.

Whether the four-dimensional framework will reshape clinical practice remains to be seen. But the core insight is difficult to dismiss: cardiovascular diseases rarely begin at symptom onset, and when heart failure, atrial fibrillation, or coronary disease becomes clinically apparent, the underlying biology has often been active for years. The observed pathology reflects the final stage of a prolonged silent process. Recognizing that the individual cardiovascular system may be biologically older or younger than its chronological age represents a mechanistic determinant with implications for prevention and clinical intervention. Redefining heart failure phenotypes and atrial fibrillation categories through a temporal and biological age framework transforms them from diagnostic labels into dynamic disease states. This shift allows interventions to be timed to an individual’s progression toward phenotype-specific tipping points, rather than to symptom onset. It also suggests that causality in cardiovascular disease should be understood in direct relation to biological trajectories and their evolution over time, rather than solely by the timing of events. For a field long organized around thresholds crossed at single moments, that reframing may prove the most consequential idea of all.

Subject of Research: Time as an indispensable causal dimension in cardiovascular diseases: toward a four-dimensional biology

Article Title: Time as an indispensable causal dimension in cardiovascular diseases: toward a four-dimensional biology

Article References: Caluori, G., & Chaigne, S. (2026). Time as an indispensable causal dimension in cardiovascular diseases: toward a four-dimensional biology. Frontiers in Cardiovascular Medicine, 13, Article 1952188. https://doi.org/10.3389/fcvm.2026.1952188

Image Credits: AI Generated

DOI: 10.3389/fcvm.2026.1952188

Keywords: Time, indispensable, causal, dimension, cardiovascular, diseases, toward, four-dimensional, biology, scientific research

The study focused on Australia and New Zealand, contexts that the authors note are underrepresented in a literature dominated by American data. Participants included 21 people with a Christian background and lived experience of an eating disorder, and 16 eating disorder healthcare providers, with six individuals belonging to both groups. Recruitment proceeded through media announcements, professional organisations and personal contacts. All participants first completed an initial survey, from which 31 were purposively selected to ensure demographic diversity and invited into semi-structured interviews averaging 73 minutes in length. The transcripts were then subjected to thematic analysis, a qualitative method that identifies recurring patterns of meaning across accounts rather than testing predetermined hypotheses. The result is not a measure of how often faith matters in eating disorders, but a rich map of how, when and why it does, and why clinicians so often avoid the topic altogether.

Three major themes emerged from the analysis, and the first was labelled by the researchers with an evocative phrase: relevance, or ‘an elephant in the room’. For many, though not all, participants, religion and spirituality were deeply intertwined with personal identity, worldview, and the risk and recovery dynamics of their eating disorder. Some patients described faith as a source of guilt or perfectionism that fed disordered eating; others described it as a wellspring of hope, meaning and unconditional worth that sustained them through treatment. The study’s central contention is that when clinicians overlook this dimension entirely, they may miss opportunities to personalise care and may even create miscommunication, for example by dismissing values that a patient regards as central to who they are. Importantly, the authors are careful to note that not every participant considered religion relevant to their illness or care, a nuance that guards against any suggestion that faith should be imposed on treatment conversations.

The second theme, reservations, captured under the phrase ‘wearing gloves’, describes the barriers that keep religion and spirituality out of clinical dialogue. These barriers operated at multiple levels. Patients and providers alike reported uncertainty about whether such topics were appropriate to raise at all, and if so, how to raise them without crossing professional or personal boundaries. Some clinicians worried about lacking the training or language to discuss faith competently, or feared that raising religion might be experienced as proselytising. Systemic factors compounded the hesitation: time-pressured consultations, treatment frameworks that do not include spiritual assessment, and institutional cultures that treat faith as private rather than clinical territory. The metaphor of wearing gloves captures a defensive posture, a handling of a sensitive subject at arm’s length that protects the clinician but may leave the patient’s actual struggles unexplored.

The third theme, responses, described as ‘working with’ faith, documented the occasions when religion and spirituality did find their way into care. Participants described experiences in which clinicians explored a patient’s religious and spiritual struggles and supports, and in some cases integrated explicitly Christian resources into treatment. These could include conversations about guilt, forgiveness and body image framed within a patient’s own theological commitments, engagement with faith communities as recovery supports, or collaboration with chaplains and spiritually integrated psychotherapists. Accounts of such integration were mixed, with participants reporting both helpful and unhelpful experiences, but the study suggests that when done respectfully and at the patient’s initiative, attention to faith could strengthen therapeutic alliance and address suffering that standard protocols did not reach.

The technical backdrop to these findings is a growing body of evidence that the authors situate their work within. Emerging research indicates that many patients would like healthcare providers to enquire about their religious and spiritual beliefs, and that spiritually integrated psychotherapies may be as effective as traditional therapies for a range of mental health conditions. Eating disorder care currently leans heavily on structured modalities such as cognitive behavioural therapy and dialectical behaviour therapy, which are powerful but not universally effective, and which rarely include formal space for spiritual concerns. The study’s abbreviations list, spanning anorexia nervosa, bulimia nervosa, binge eating disorder, avoidant restrictive food intake disorder and other specified feeding or eating disorders, underscores the diagnostic breadth across which this gap may matter. The authors argue that for a subset of patients, faith is not an optional extra but a load-bearing structure of the self, and that treatment which ignores it is, by definition, less individualised than it could be.

On the strength of their findings, the researchers propose a clinical framework designed to support healthcare providers in considering religion and spirituality, and in some cases incorporating Christian resources, in eating disorder care. While the published version details the framework’s steps, its logic follows directly from the three themes: first, establish relevance by asking open, non-presumptive questions about whether faith matters to the patient; second, address reservations by normalising the conversation, clarifying consent and boundaries, and acknowledging the clinician’s own uncertainty; and third, where appropriate, work with the patient’s faith, drawing on their own religious supports and, where requested and suitable, Christian resources. The framework is explicitly patient-led, distinguishing respectful exploration from religious imposition, and it is intended to be usable by general practitioners, psychologists, dietitians and other members of multidisciplinary eating disorder teams rather than only by chaplains or specialist pastoral carers.

The study’s limitations and scope deserve emphasis. It examined Christian religion and spirituality specifically, in Australian and New Zealand settings, and its 31 interviewees were recruited partly through personal and professional networks, so the findings are exploratory rather than representative. Qualitative thematic analysis illuminates mechanisms and meanings, not prevalence, and the authors do not claim that faith is relevant to most patients with eating disorders. Nor do they claim that religious involvement is uniformly protective; the accounts collected include ways in which religious contexts can heighten struggle, for instance through perfectionism, shame or unhelpful teachings about the body. What the study does establish is that for a meaningful subset of patients, the intersection is clinically significant in both directions, and that the current silence around it is a choice of the system rather than a reflection of patients’ lived reality.

The broader significance of the work lies in its challenge to whole-person care. Eating disorders devastate health through medical, psychological and social pathways, and treatment guidelines increasingly call for individualised, multidisciplinary approaches. This study adds a dimension to that agenda: if identity, meaning and worldview shape both illness and recovery, then a healthcare system that never asks about them is operating with an incomplete map. The authors suggest that acknowledging and exploring individual religious and spiritual perspectives may enhance care for some patients, and their framework offers a concrete starting point for clinicians who have lacked both permission and method. As eating disorder services grapple with demand that outstrips capacity and outcomes that remain stubbornly poor, the study’s message is that some of the missing leverage may lie in conversations that medicine has been too cautious to begin, conducted with the gloves off, at the patient’s own pace, and on the patient’s own terms.

Subject of Research: The role of Christian religion and spirituality in eating disorder healthcare

Article Title: A missing dimension? Christian religion, spirituality and eating disorder healthcare: a qualitative study

Article References: Thomas, H., O’Callaghan, C., Best, M., Bräutigam, M., Kimber, T., Wade, T., & Sturman, N. (2026). A missing dimension? Christian religion, spirituality and eating disorder healthcare: a qualitative study. Journal of Eating Disorders. https://doi.org/10.1186/s40337-026-01770-z

Image Credits: AI Generated

DOI: 10.1186/s40337-026-01770-z

Keywords: eating disorders, Christianity, religion, spirituality, qualitative research, whole-person care, spiritually integrated psychotherapy, anorexia nervosa, healthcare providers, patient-centred care, missing, dimension