Search Results (4,886)

Background/Objectives: Dupilumab is an effective long-term treatment for chronic rhinosinusitis with nasal polyps (CRSwNP), but continuous biweekly (Q2W) treatment is associated with high costs, cumulative drug exposure, and treatment burden. Extending injection intervals may reduce these burdens. This real-world study aimed to evaluate the feasibility and clinical outcomes of dupilumab interval extension compared with continued standard Q2W dosing. Methods: In this retrospective single-center study, 35 adults with CRSwNP who had received dupilumab 300 mg Q2W for >12 months underwent a stepwise interval-extension attempt (two-week increments, ≥6 months between steps) and were compared with 30 patients who continued Q2W dosing. Clinical outcomes were assessed every six months using the Sino-Nasal Outcome Test-22 (SNOT-22) and Nasal Polyp Score (NPS). Results: Of the 35 patients, 19 patients (54%) reached a dosing interval of Q4W or longer, and eight patients (23%) maintained a partial extension to Q3W after not tolerating Q4W. The remaining eight patients (23%) returned to Q2W. Thus, 27 patients (77%) stayed on an extended interval beyond the standard Q2W regimen, which was maintained throughout follow-up without reversion to a shorter regimen. SNOT-22 and NPS improved significantly after dupilumab initiation and remained stable throughout follow-up in both groups, with no significant between-group differences in longitudinal outcomes. No patient needed rescue treatments during follow-up. Conclusions: In selected clinically stable patients with CRSwNP, dupilumab interval extension appeared feasible and was associated with maintained disease. Individualized dose tapering, including intermediate intervals such as Q3W, may reduce treatment burden without compromising disease control. Larger prospective studies are needed to define optimal extension protocols and identify predictors of successful interval extension. Full article

Age-related decline in immune system function is characterized by reduced numbers of naïve lymphocytes, the accumulation of senescent cells, impaired function of all immune cell types, and chronic low-grade inflammation (inflammaging). These alterations contribute to increased susceptibility to infections and malignancies, as well as to autoimmunity and other age-associated diseases. This article reviews current evidence on lifestyle interventions that may mitigate immune aging. Lifestyle-related strategies, including regular physical activity, nutritional interventions (e.g., different diets, caloric restriction, and other fasting-related approaches), stress reduction, and vaccination, are discussed as key modulators of immune function and systemic inflammation. Notably, vitamin D supplementation has been shown to reduce the incidence of autoimmune diseases by 22%. In comparison, caloric restriction has led to a decrease in CRP and TNF-α by 40% and 50%, respectively. Emerging complementary approaches, such as mind–body practices and controlled cold exposure, show promise, though current evidence remains limited and inconsistent. Therefore, integrated lifestyle strategies may slow aging-related immune decline and support healthy aging. However, longitudinal trials are required to define the optimal intervention parameters, population-specific thresholds, and the long-term durability of immune rejuvenation. Full article

Background/Objectives Lysyl oxidase-like 2 (LOXL2), a member of the lysyl oxidase family of amine oxidases involved in collagen cross-linking, has emerged as a key mediator of pathological extracellular matrix remodeling and tissue fibrosis. Dysregulated LOXL2 activity has been implicated in various fibrotic diseases; however, its role in fibrosis-driven chronic kidney injury, particularly in the context of calcineurin inhibitor-induced kidney toxicity, remains incompletely defined. Methods To investigate the contribution of LOXL2 inhibitor to cyclosporine A (CsA)-induced nephropathy, a well-established model of progressive tubulointerstitial fibrosis, male CD-1 mice were administered either saline or CsA (15 mg/kg/day, intraperitoneally) for 8 weeks. After 4 weeks of CsA exposure, CsA-treated mice were further divided into two groups and received either vehicle or a LOXL2 inhibitor (10 mg/kg/day, oral gavage) for an additional 4 weeks. Kidney function, albuminuria, histological fibrosis, inflammatory cell infiltration, and profibrotic gene expression were assessed. Results In a murine model of CsA-induced nephropathy, pharmacological inhibition of LOXL2 markedly improved kidney outcomes. LOXL2 inhibition significantly reduced albuminuria and ameliorated kidney dysfunction. In parallel, tubulointerstitial fibrosis was substantially attenuated, accompanied by reduced myofibroblast activation and extracellular matrix accumulation. These protective effects were associated with downregulation of profibrotic and inflammatory mediators and inhibition of TGF-β-related downstream signaling pathways activated by CsA. Conclusions The present preclinical findings suggest that Compound #765-mediated LOXL2 inhibition may offer a potential therapeutic benefit in CsA-induced fibrosis, though further validation is warranted. Full article

Background/Objectives: Ventilator-associated pneumonia (VAP) remains a major complication in patients requiring prolonged mechanical ventilation. The effect of tracheostomy on VAP risk remains controversial, particularly when differences in duration of mechanical ventilation are considered. This study evaluated the association between tracheostomy, VAP occurrence, and clinical outcomes in mechanically ventilated ICU patients. Methods: We conducted a retrospective matched exposed–unexposed cohort study in a tertiary-care ICU in Mexico City. Patients undergoing tracheostomy were compared with an age- and sex-matched subcohort of intubated patients receiving invasive mechanical ventilation for ≥48 h. VAP incidence was assessed using cumulative incidence, incidence density, and multivariable generalized linear models. Results: A total of 218 patients were included (55 tracheostomized and 163 intubated). VAP incidence density was similar between groups (31.5 vs. 30.3 per 1000 ventilator-days; RR 1.04, 95% CI 0.7–1.7), whereas cumulative incidence was higher among tracheostomized patients (61.8% vs. 22.7%; RR 2.7, 95% CI 1.9–3.9). Broad-spectrum antibiotics, mechanical ventilation ≥ 5 days, chronic pulmonary disease, and ICU stay remained associated with VAP occurrence in an exploratory multivariable model. Gram-negative microorganisms predominated, and antimicrobial resistance was more frequent among tracheostomized patients. Conclusions: Tracheostomy was associated with higher cumulative incidence of VAP, but a similar incidence density compared with endotracheal intubation. The crude association between tracheostomy and VAP disappeared after adjustment for confounding factors, suggesting that prolonged mechanical ventilation and ICU exposure are more important determinants of VAP risk than tracheostomy itself. Full article

The incidence of cancer in young adults has risen worldwide. Women comprise a disproportionate share of young-onset cases, among whom breast cancer predominates. This shift parallels globalization and urbanization, including the wider adoption of Western-pattern diets. Although hereditary syndromes explain a minority of cases, the secular rise underscores the impact of modifiable exposures, particularly diet. Prenatal life, neonatal life, childhood, adolescence, and early adulthood are critical periods during which dietary exposures may shape long-term mammary development. Mammary tissue undergoes rapid proliferation and differentiation during development, creating windows of heightened susceptibility to carcinogenic insults. However, most existing studies emphasize dietary exposures during a single developmental period; the entire span of critical developmental windows plays a formative role in shaping young-onset breast cancer (YoBC) risk, and the mechanisms underlying this life-course shaping remain insufficiently characterized. This review comprehensively synthesizes evidence on how nutrition across sensitive developmental windows shapes the risk of YoBC. We evaluate protective and adverse dietary factors within these stages and examine mechanistic pathways linking early-life nutrition to carcinogenesis, focusing on hormonal regulation, epigenetic programming, chronic inflammation, and the gut microbiome. A structured literature search was conducted in PubMed, Embase, and Web of Science for English-language articles published from 1990 through May 2026, supplemented by hand-searching of relevant reviews and key primary studies. By framing nutrition and breast cancer through a life-course lens, this review provides an integrated foundation for stage-specific prevention strategies and identifies priority directions for future research on early-life dietary determinants of YoBC. Full article

Background/Objectives: Foot and ankle presentations during Hajj occur in a dense mass-gathering environment where prolonged walking, heat exposure, crowding, variable footwear, and limited self-care can interact with chronic disease and wound vulnerability. Previous Hajj studies have described foot injuries and diabetes-related complications, but less is known about whether simple high-risk foot documentation flags identify presentation records with higher care-pathway intensity. The primary objective was to estimate the presentation-level burden of core high-risk foot profiles among pilgrims presenting with foot and ankle conditions during Hajj 2025. Secondary objectives were to evaluate associations with a surgery-coded care-intensity indicator, hospital referral, and component heterogeneity. Methods: This observational presentation-level analysis included 3957 foot and ankle presentation records. The unit of analysis was the presentation/case record, not a unique individual pilgrim. A core high-risk foot profile was defined as diabetes, neuropathy, diabetic foot ulcer, foot ulcer, complications of open wound, or osteomyelitis. The primary outcome was a surgery-coded care-intensity indicator, defined solely from treatment documentation containing “Surgery” and interpreted as a care-pathway proxy rather than confirmed operating-room surgery. Logistic regression estimated crude and adjusted odds ratios (ORs); exploratory risk-category analyses assessed heterogeneity within the composite profile. Results: Core high-risk foot profiles were identified in 1793/3957 presentations (45.3%). The primary outcome occurred in 239/1793 high-risk presentations (13.3%) and 201/2164 non-high-risk presentations (9.3%), an absolute difference of 4.0 percentage points. The crude OR was 1.50 (95% CI 1.23–1.83; p < 0.001). The association persisted in the primary adjusted model (adjusted OR 1.47; 95% CI 1.20–1.79; p < 0.001) and in the extended clinical sensitivity model (adjusted OR 1.47; 95% CI 1.20–1.80; p < 0.001). Care pathways and secondary outcomes are summarized was also more frequent in high-risk presentations (12.2% vs. 9.8%; crude OR 1.28; 95% CI 1.05–1.57; p = 0.017). Exploratory category analysis showed that chronic-risk-only presentations had a primary outcome rate similar to non-high-risk presentations (9.0% vs. 9.3%), whereas ulcer/wound/deep-infection presentations had a higher rate (17.3%; crude OR 2.04; 95% CI 1.63–2.55; p < 0.001). Model discrimination was modest (C-statistics 0.55–0.64). Conclusions: Core high-risk foot flags were common among Hajj foot and ankle presentation records and were associated with surgery-coded care-intensity and referral documentation. However, the composite was clinically heterogeneous, the outcome was not a validated surgery endpoint, and the models were not prediction tools. These findings support cautious use of high-risk foot flags as operational prompts for assessment and pathway planning rather than as standalone clinical risk estimates. Full article

Eating behavior and eating habits are shaped from the earliest stages of life through interactions among biological, familial, social, and environmental factors. The aim of this narrative review is to integrate evidence on the early-life determinants of eating behavior and their influence on dietary intake from infancy to adolescence. A narrative review was conducted with a structured search approach prioritized on longitudinal studies, intervention trials, and policy evaluations when available, and using cross-sectional evidence mainly to describe patterns and sociodemographic factors. Synthesizing the current evidence, our framework proposes that breastfeeding, responsive complementary feeding, and self-regulatory parenting are associated with higher responsiveness to internal hunger, satiety cues, and preference for nutrient-dense foods. Conversely, coercive practices, early exposure to highly palatable foods, and the influence of food marketing are linked to dominant hedonic responses and impulsive consumption patterns. Furthermore, family environments characterized by stress or food insecurity, together with high access to low-nutrient foods, may increase vulnerability to poor eating habits and emotional eating during adolescence. Overall, the evidence highlights the need for preventive interventions that integrate parenting support, school food education, digital marketing regulation policies, and the promotion of healthy food environments across multiple sectors. Understanding the biological, psychological, and social factors linking early determinants to dietary intake and eating behaviors across development is essential for promoting a balanced relationship with food and preventing chronic diseases from an early age. Full article

Health impact assessments of ambient particulate matter remain far less developed in sub-Saharan African cities, despite fine particulate matter (PM_2.5) being a significant contributor to premature mortality globally. This study quantified the public health burdens of adult mortality associated with long-term PM_2.5 exposure in Addis Ababa, Ethiopia, under different counterfactual air quality scenarios. Hourly PM_2.5 data were collected across nine monitoring stations from 2022 to 2023. AirQ+ tool was utilized to estimate attributable natural-cause and cardiovascular disease (CVD) mortality among adults aged ≥ 30 years. Spatial analysis showed mean concentrations ranging from 15 µg/m³ to 33 µg/m³, with an overall mean of 26.74 µg/m³, exceeding the WHO annual guideline by more than fivefold. Seasonal peaks occurred from June to August and diurnal maxima at 7:00 AM. In 2022, attributable natural-cause deaths ranged from 1489 (6.16%) at the less stringent WHO Interim Target 3 (15 µg/m³) to 3169 (13.11%) at the WHO Air Quality Guidelines (5 µg/m³). In 2023, the range was 1544 (6.40%) to 3218 (13.33%). For specific chronic endpoints, PM_2.5 concentration level was responsible for between 509 and 1071 CVD deaths in 2022, and between 535 and 1126 CVD deaths in 2023 across the counterfactual scenario. These results highlight the substantial health burden posed by ambient PM₂.₅ in Addis Ababa and emphasize the urgent need for targeted interventions. Full article

Cardiovascular–kidney–metabolic (CKM) syndrome is a systemic, interdependent disorder arising from the convergence of metabolic dysfunction, chronic kidney disease, and cardiovascular pathology. Anchored in the Developmental Origins of Health and Disease (DOHaD) framework, this review advances a “parallel hit” model, primarily based on evidence from experimental animal studies, particularly rodent models, posited that early-life environmental insults concurrently program structural and functional vulnerabilities in both renal and central nervous system hubs. These early perturbations prime susceptibility long before clinical manifestations emerge. CKM progression is conceptualized as a two-stage trajectory, with an initial phase of parallel programming affecting kidney and brain development, followed by a transition to maladaptive bidirectional crosstalk. In the later phase, heightened efferent sympathetic outflow and aberrant afferent renal signaling—potentiated by uremic toxin accumulation, neuroinflammation, and blood–brain barrier disruption—drive a self-perpetuating cycle that accelerates cardiorenal and metabolic injury. Key integrative mechanisms, including oxidative stress, chronic low-grade inflammation, mitochondrial dysfunction, and gut microbiota dysbiosis, serve as convergent pathways linking early-life exposures to adult CKM phenotypes. These pathways not only sustain disease progression but also represent actionable therapeutic targets. Importantly, this framework underscores the translational potential of early-life “reprogramming” strategies. Interventions such as precision nutrition, antioxidant supplementation, microbiota-directed therapies (including prebiotics, probiotics, and postbiotics), and mechanism-based pharmacotherapies may mitigate or reverse maladaptive programming. However, much of the current mechanistic evidence remains preclinical, and further human studies are needed to validate these pathways and therapeutic approaches. Collectively, this dual-hub paradigm reframes CKM syndrome as a life-course continuum rather than a late-stage comorbidity cluster, emphasizing the necessity of early, mechanism-driven interventions to stabilize the brain–kidney axis and improve long-term cardiovascular–kidney–metabolic outcomes. Full article

Lung adenocarcinoma (LUAD) remains the leading cause of mortality worldwide, while asthma is the most prevalent chronic disease affecting individuals of all ages. The shared airway involvement in these global health concerns results in exposure to common risk factors, suggesting a potential overlap in their genetic background. Given the roles oxidative stress and chronic inflammation play in both LUAD and asthma, we aimed to investigate similarities in their molecular mechanisms and to explore whether these shared transcriptomic signatures may prove useful for potential drug repurposing hypotheses by analyzing relevant transcriptomic datasets. This analysis identified a set of genes and co-expression interactions shared between asthma and LUAD, suggesting potential common molecular mechanisms underlying both diseases. Specifically, DNAJC3, APOBEC3G, and PRDX4 were highlighted as potential common molecular mediators underlying both diseases, offering correlative evidence for shared pathways. These genes may represent key molecular links connecting the pathogenic processes of asthma and LUAD. The transcriptomic profiles of asthma and lung cancer datasets reveal common molecular interactions, suggesting potential shared biological mechanisms between the two diseases. These findings provide a computational framework that may guide future studies investigating therapeutic associations and possible drug–gene relationships in lung adenocarcinoma and asthma. Full article

Background: Actinic keratosis (AK) is a common premalignant skin disorder associated with chronic ultraviolet exposure and a recognized risk of progression to cutaneous squamous cell carcinoma. Tirbanibulin 1% ointment is an effective short-course field therapy for AK, but its efficacy in hyperkeratotic lesions (Olsen grade II–III) may be limited by reduced drug penetration through a thickened stratum corneum. Keratolytic pretreatment may represent a plausible strategy to improve topical drug delivery in these more challenging lesions. Methods: This retrospective chart review included consecutive adults with Olsen grade II–III AK treated in routine clinical practice with either a bland emollient lead-in followed by tirbanibulin (Group A) or salicylic acid 30% ointment pre-treatment (Decapan, Sanitpharma; Milan, Italy) followed by tirbanibulin (Group B). No study-driven procedures or additional visits were implemented. The 14-day bland emollient lead-in used in Group A was part of the routine clinical management applied during the relevant treatment period and was not introduced or retrospectively constructed for the purposes of the present comparative analysis. Outcomes were extracted from de-identified medical records and photographic documentation obtained as part of standard care. For the purposes of analysis, post-treatment evaluations were grouped into predefined windows of 3–6 weeks (T1), 10–14 weeks (T2), and 22–30 weeks (T3), corresponding approximately to 1, 3, and 6 months after treatment initiation. The primary efficacy endpoints were the Actinic Keratosis Area and Severity Index (AKASI) and Total Lesion Count (TLC). Secondary endpoints included quality of life assessed by the Dermatology Life Quality Index (DLQI). Results: Both treatment regimens were associated with clinically meaningful improvements in AK severity. At T3, mean AKASI was significantly lower in Group B than in Group A (0.86 ± 0.38 vs. 1.35 ± 0.27; p < 0.001), corresponding to reductions from baseline of 60.6% and 36.9%, respectively. Similarly, mean TLC at T3 was significantly lower in Group B than in Group A (4.80 ± 1.5 vs. 6.35 ± 1.6; p < 0.001), corresponding to reductions from baseline of 46.7% and 27.0%, respectively. Quality-of-life outcomes also favored the sequential approach, with lower DLQI scores at T3 in Group B compared with Group A (2.9 ± 1.6 vs. 3.8 ± 1.9; p = 0.006). Both treatments were generally well tolerated. Although the incidence of local skin reactions (LSRs) was similar between groups, Group B showed lower retrospectively documented composite LSR scores and lower patient-reported discomfort (p < 0.001) and lower patient-reported discomfort (p < 0.001). Conclusions: Sequential keratolytic pretreatment followed by tirbanibulin was associated with greater reductions in disease burden and with lower severity of treatment-related local reactions in this retrospective cohort (Olsen grade II–III). This retrospective study suggests that keratolytic pretreatment may represent a useful adjunctive strategy in hyperkeratotic AK treated with tirbanibulin. Prospective randomized studies are warranted to confirm these findings and to define standardized treatment protocols. Full article

Wearable healthcare technologies are transforming the healthcare landscape by enabling remote, real-time health data collection, supporting early diagnosis, personalizing treatment plans, and reducing healthcare costs and medical burdens. Central to these advancements are wearable sensors, which continuously capture physiological data such as heart rate, temperature, activity levels, and biomarker concentrations. However, the large volume and complexity of this data demand effective processing to extract meaningful medical insights. Artificial intelligence (AI) and machine learning (ML) have significantly enhanced the capabilities of wearable sensors by enabling advanced data analysis, pattern recognition, and predictive modeling. AI-enhanced wearable sensors can detect early signs of health issues, such as heart attacks, chronic diseases, and mental health conditions like stress, often before clinical symptoms become apparent. This review examines the integration of AI/ML models with wearable sensors across physical activity recognition, stress assessment, cardiovascular monitoring, personal exposure monitoring, and sweat biomarker detection. Unlike prior application-centered reviews, we emphasize methodological and translational evaluation by comparing task formulations, sensing modalities, dataset scale, validation protocols, performance metrics, and deployment constraints across domains. We further discuss advanced architectures, multimodal fusion, explainable AI, edge deployment, privacy and regulatory considerations, and the translational gap between research prototypes and clinically deployable wearable AI systems. Full article

Background: Hospitalized adults with chronic kidney disease (CKD) experience high morbidity and mortality. Acute inpatient events frequently occur in combination, yet most studies evaluate individual conditions in isolation. Acute hemodynamic and vascular stressors may represent interacting physiological stressors that define heterogeneous patterns of inpatient risk. Methods: Acute hemodynamic stressors (sepsis, shock, acute decompensated heart failure, and mechanical ventilation) and vascular stressors (acute myocardial infarction, major bleeding, stroke, pulmonary embolism, and deep vein thrombosis) were identified using ICD-10-CM and ICD-10-PCS codes. Stressor burden was defined as the number of stressors (0, 1, 2, or ≥3). Hospitalizations were categorized into mutually exclusive domains: none, hemodynamic only, vascular only, or both. Survey-weighted multivariable regression models examined associations with mortality, acute kidney injury (AKI), length of stay (LOS), and hospital charges. Prespecified sensitivity analyses excluded inter-hospital transfers, and interaction analyses assessed modification by age. Results: Among 1,062,813 CKD hospitalizations, 66.1% experienced at least one acute stressor. Increasing stressor burden demonstrated a marked dose–response relationship with mortality, with adjusted odds ratios of 2.15 (95% CI: 2.08–2.23), 7.36 (95% CI: 7.09–7.64), and 31.65 (95% CI: 30.40–32.95) for 1, 2, and ≥3 stressors, respectively. Increasing stressor burden was also associated with higher odds of AKI, longer LOS, and greater hospital charges. Significant dose–response relationships were observed for all outcomes (all P-trend < 0.001). Isolated hemodynamic stressors were associated with greater mortality risk than isolated vascular stressors (aOR: 4.97 vs. 2.15), while hospitalizations experiencing both domains had the greatest risk (aOR: 13.10, 95% CI: 12.52–13.71). These findings were robust in sensitivity analyses excluding inter-hospital transfers. The relative increase in mortality associated with higher stressor burden was greater among patients younger than 65 years than among older adults (P for interaction <0.001). Conclusions: Acute hemodynamic and vascular stressors define heterogeneous patterns of inpatient risk among hospitalized adults with CKD. Both cumulative stressor burden and stressor domain are strongly associated with mortality, AKI, and resource utilization, with robust dose–response relationships that highlight acute physiological stress as an important determinant of inpatient outcomes in CKD. Full article

Mycoplasma synoviae (MS) poses a continuous threat to the poultry industry in Mainland China, yet a comprehensive nationwide assessment remains lacking. This systematic review and meta-analysis quantified the pooled prevalence of MS and evaluated key epidemiological characteristics and sources of heterogeneity. Peer-reviewed studies were retrieved from multiple databases, and random-effects models were utilized to estimate and compare pooled seroprevalence and molecular detection prevalence. The results revealed a heavy MS infection burden characterized by a distinct diagnostic disparity: a high serological prevalence co-existed with a moderate molecular detection prevalence, reflecting widespread past exposure, chronic carrying, or vaccination. Geographically, the Northwest region exhibited the highest seroprevalence (61.8%), though inter-regional differences were not statistically significant (p = 0.152). Among production types, breeder flocks maintained a relatively high pooled prevalence of 69.6% (95% CI: 40.5–92.0%), although differences among production types were not statistically significant. Subgroup analysis demonstrated a statistically significant difference among age groups; however, the available data did not support definitive conclusions regarding age-specific risk patterns. Breeder flocks exhibited a relatively higher pooled prevalence than layers and broilers, suggesting a potential epidemiological role that warrants further investigation. In conclusion, MS appears to be widely distributed in chickens in mainland China. Differences between the serological and molecular detection results highlight the complexity of interpreting MS prevalence estimates. Given the substantial heterogeneity among studies, the findings should be interpreted cautiously. Future studies incorporating standardized surveillance and detailed vaccination histories are needed to better understand MS epidemiology and support evidence-based control strategies. Full article

This study focused on the spatial and temporal changes in photosynthetic pigment concentrations in the leaves of Ginkgo biloba and their integration into a new bioindicator index, the Pigment Integrity-to-Dust Ratio (PIDR), to assess urban air pollution stress on trees in Budapest, Hungary. High levels of chlorophyll and carotenoids in early summer indicated greater pigment integrity at the moderate-traffic site, whereas there were clear indications of reductions in the high-traffic area. The control site represented a low-traffic, pollution-free baseline. Chlorophyll concentrations dropped in the traffic-exposed leaves, and there were increased levels in the formation of pheophytin. It is thought that these reductions were caused by city stress. Responses of pigments were also variable at the moderate site, perhaps due to some form of recovery or adjustment in the study’s time frame. The observed negative relationships between selected pollutants and PIDR suggested that pollutant exposure was associated with pigment degradation and foliar dust deposition, although these associations should be interpreted as exploratory. The Air Pollution Tolerance Index (APTI) was significantly different between the pollution-exposed sites and the control, reflecting physiological tolerance in chronically exposed trees rather than directly measuring pigment damage. Therefore, the APTI and PIDR provide complementary information. Overall, the PIDR appears to be a promising exploratory bioindicator of physiological stress response, based on pigment concentration changes and dust deposition. Full article