Changes in carbohydrate metabolism are a key feature of aging which also manifest in the epidermis. Furthermore, the synthesis and distribution of epidermal lipids changes with age. Both these parameters cannot be investigated with immunohistochemistry, as neither serves as useful epitope. We developed a multimodal analytical histocytometry approach combining modalities that localize lipids and enzymatic activities with immunofluorescent imaging of the skin to localize changes that are correlated with appearance of senescent cells. The activities of key metabolic enzymes were determined on tissue sections of aged and juvenile skin with a formazan-based assay. Lipids were localized and quantified using FTICR MALDI - mass spectrometric imaging. We correlated those modalities with immunofluorescent imaging and analyzed the intensities of the respective signals at single cell level, using Strataquest tissue cytometry. We analyzed skin from donors of young (< 30 y) versus advanced (> 67 y) ages and we investigated epidermal equivalent models containing labeled UV-damaged or senescent keratinocytes. Enzymatic activities displayed specific patterns across the stratifying epidermis, and had diverging trajectories in aging, with a marked decrease in suprabasal glucose-6-phosphate dehydrogenase (G6PD) activity. G6PD, the rate limiting enzyme of the pentose phosphate pathway was also identified as a rapid response pathway activated upon UV damage in the epidermis.  The lipid molecular imaging identified differentiation- and age-related changes of polar lipids in skin biopsies and epidermal equivalents, and pro-senescent stress dependent reactive aldehydophospholipid species in the basal epidermal layers.  While these methodologies are still in development, it is evident that correlative analytical imaging – with the aid of AI driven histocytometry – will continue to yield novel insights into skin and epidermal biology by localizing previously undetectable parameters within the epidermis in the context of aging.

The World Health Organization (WHO) estimates that noise pollution leads to the loss of 1.6 million healthy life years annually in Western Europe alone, primarily due to night-time noise exposure which disrupts sleep and triggers stress responses. This study investigates the adverse health effects of aircraft noise on the brain-heart-vessel axis, combining cardiovascular and neuropsychiatric approaches. We aim to characterize the functional and biochemical consequences of both short-term and long-term noise exposure utilizing an established mouse model. Behavioural changes in exposed mice, including cognition, anxiety, depression, and social behaviour were assessed alongside cardiovascular parameters such as blood pressure, endothelial function tests, and analyses of oxidative stress and inflammation markers. Short-term noise exposure did not lead to any significant differences in the behaviour of the noise-exposed mice, whereas long-term noise-exposure leads to reduced social interaction and working memory as behavioural markers of depression. Functional cardiovascular parameters point to hypertension and impaired endothelial function in both short-term and long-term noise exposure, as well as oxidative stress and inflammation. These findings underscore previously reported cardiovascular impact of noise exposure while adding the suspected behavioural changes and metabolic markers of the affected brain-heart axis. The observed behavioural changes and cardiovascular impairments emphasize the complex interplay between environmental stressors and health, suggesting that long-term noise exposure can have profound effects on both mental and cardiovascular health. This study provides a comprehensive framework for future research aimed at reducing the adverse effects of noise pollution on the brain-heart-vessel axis.

Small cell lung cancer (SCLC) is the leading cause of cancer-related deaths worldwide and is characterized by rapid growth, early metastasis, and high mortality rates. This study investigated the prognostic potential of leukocyte telomere length (LTL) and paraoxonase 1 (PON1) activity in 60 SCLC patients treated with a cisplatin/etoposide (PE) regimen. Patients were observed at baseline, after 2 cycles, and after 4 cycles of chemotherapy. The primary objective was to evaluate the prognostic potential of these biomarkers for patient survival. LTL was measured from isolated genomic DNA using real-time quantitative polymerase chain reaction (RTq-PCR), while PON1 activity was determined using a spectrophotometric method. A Kaplan-Meier survival analysis was performed with cut-off values below the 25^th percentile for LTL and PON1 activity to determine their prognostic power for overall survival. The analysis revealed that both LTL and PON1 are significant predictors of patient survival, suggesting that patients with levels below the 25^th percentile have a higher risk of death (Log Rank = 3.956, p = 0.047; Log Rank = 3.834, p = 0.050, respectively). Telomeres, the protective caps at the ends of chromosomes, shorten with each cell division and reflect cell aging and genomic stability. Shorter telomere lengths in leukocytes have been associated with a poorer prognosis and lower survival rates in SCLC patients. Similarly, reduced PON1 activity is associated with increased oxidative stress, which contributes to cancer progression and poorer clinical outcomes. Monitoring PON1 activity could help in assessing patient prognosis and adjusting treatment strategies. These findings suggest that LTL and PON1 activity have significant prognostic value in SCLC and serve as useful indicators for identifying high-risk patients and guiding treatment decisions to improve outcomes.