From optical communications to quantum computing: Photonics is a key technology for the future. To strengthen the connection between research and industry, partners from both sectors, together with researchers from the Paul Scherrer Institute PSI, have founded the Swiss PIC Technology Transfer Center. The festive inauguration took place on Nov. 24, 2025, at the Park Innovaare site, with the opening of a manufacturing centre for the integration of light-based microchips.

Pelvic organ prolapse (POP), a condition whose development is shaped by both genetic and clinical risk factors, significantly impairs women’s quality of life, yet genetic insights into non-European populations and comprehensive risk models that integrate genetic and clinical data remain insufficiently explored. To address this gap, the first polygenic risk score (PRS) for POP in the Chinese population was constructed, leveraging 20 disease-associated genetic variants derived from the largest available genome-wide association study (GWAS) on POP. The research analyzed two cohorts: a discovery cohort comprising 576 POP cases and 623 controls, and a validation cohort with 264 cases and 200 controls. Results confirmed that the POP case group had a significantly higher PRS than the control group; notably, women in the top 10% of PRS values (highest genetic risk) had an odds ratio of 2.6 for developing POP compared to those in the bottom 10% (lowest genetic risk). A high PRS was also found to correlate significantly with POP occurrence in specific subgroups: women over 50 years old and those with one or no childbirths. Additionally, an integrated prediction model combining PRS with clinical risk factors demonstrated better predictive accuracy than existing PRS-only models. This combined risk assessment tool proves robust for POP risk prediction and stratification, providing valuable guidance for personalized preventive measures and treatment strategies in future clinical practice.

Psoriasis, a chronic inflammatory skin disease, relies heavily on abnormal angiogenesis for its pathogenesis, and AlkB homolog 5 (ALKBH5)—an N⁶-methyladenosine (m⁶A) demethylase with known roles in regulating angiogenesis in cardiovascular and eye diseases—has emerged as a key player in this process. In imiquimod (IMQ)-induced psoriasis mouse models, ALKBH5 was found to be upregulated in skin lesions compared to control groups, with co-localization with cluster of differentiation 31 (CD31), an endothelial cell marker linked to angiogenesis. ALKBH5-deficient (ALKBH5-KO) mice showed reduced IMQ-induced psoriatic dermatitis, with histological improvements including thinner epidermis, less hyperkeratosis, fewer dermal capillaries, and decreased inflammatory cell infiltration. These mice also exhibited alleviated angiogenesis in psoriatic lesions, mediated by downregulation of the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway. In vitro, human umbilical vein endothelial cells (HUVECs) treated with IL-17A— a cytokine critical to psoriasis pathogenesis—showed significant upregulation of ALKBH5, which further promoted the expression of angiogenesis-related cytokines and endothelial cell proliferation. ALKBH5 knockdown in HUVECs suppressed cell proliferation and angiogenesis, while overexpression had the opposite effect, with both processes regulated via the AKT-mTOR pathway. Collectively, these findings highlight ALKBH5’s pivotal role in psoriatic dermatitis and angiogenesis, identifying it as a potential therapeutic target for psoriasis.

Effective axon regeneration is critical for restoring nerve function in patients with axon injury-related neurological diseases, yet adult mammals show limited regenerative capacity in central axonal branches of dorsal root ganglion (DRG) neurons compared to their peripheral counterparts. To explore molecular drivers of this difference, rat sciatic nerve or dorsal root axotomy was performed to examine the expression of dysbindin domain containing 2 (DBNDD2) in DRGs after regenerative peripheral or non-regenerative central axon injury. Results revealed DBNDD2 is down-regulated in DRGs post-peripheral injury but up-regulated after central injury. Additionally, DBNDD2 expression varies between neonatal and adult rat DRGs, increasing gradually with development. Functional tests via DBNDD2 knockdown demonstrated that silencing this gene promotes neurite outgrowth in both neonatal and adult DRG neurons and stimulates robust axon regeneration in adult rats following sciatic nerve crush injury. Bioinformatic analysis further identified that transcription factor estrogen receptor 1 (ESR1) interacts with DBNDD2, exhibits a similar expression trend post-axon injury, and may target DBNDD2. These findings suggest that reduced DBNDD2 levels after peripheral injury and low neonatal DBNDD2 abundance contribute to axon regeneration, highlighting DBNDD2 manipulation as a promising therapeutic strategy for improving recovery after axon damage.