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Haptic and Thermal Rendering of Astronomical Data: A Multimodal Approach to Inclusive Science Communication
Beatriz Garcia
,Johanna Casado
,Alexis Mancilla
Posted: 10 March 2026
Hierarchical Curriculum Learning for Multi-Document Reasoning in Large Language Models
Yueting Li
,Yuqi Tang
,Ke Wu
,Yun Yang
,Yilin Li
,Yihan Xue
Posted: 10 March 2026
Application of Artificial Intelligence in Analysing Meteorological Data for Health Research: A Rapid Review
Lysanne Veerle Michels
,Lucy Smith
,Suzan Ghannam
,Charles Gadd
,Hajira Dambha-Miller
Posted: 10 March 2026
Exploring the Ethical Challenges of "Go to Court if Not Satisfied" Language in Healthcare Communication
Benjamin Otsen
,Xin Zheng
,Ren Chen
,Shuo Ding
Posted: 10 March 2026
The Kinome-Microbiota Axis in Precision Nutrition as a Target for Restoration and Maintenance of Cellular Flexibility
Vincenzo Sorrenti
,Stefano Fortinguerra
,Lorenzo Mauro
,Alessandro Buriani
Posted: 10 March 2026
On the Correct Way of Choosing a Frame of Reference in Mechanics and Thermodynamics and on Some Consequences
Neven Ninić
,Ivan Tolj
,Damir Sedlar
Posted: 10 March 2026
Sphere-in-Contact Model/Theorem for the Development of New Graphite-based Intercalated Battery Materials
Jonathan Kae
,Constantinos D. Zeinalipour-Yazdi
Posted: 10 March 2026
ChipForm: Automated Constraint-Driven IC Layout Optimization via Reinforcement Learning
Wenxuan Zhang
,Zhimo Han
Posted: 10 March 2026
Ten Years of Congenital Zika Syndrome: From Outbreak to a Decade of Clinical, Therapeutic, and Preventive Advances in a Tropical Disease Context
Fabricio Silva Pessoa
Posted: 10 March 2026
Black Holes as Landauer-Saturating Erasure Channels: Horizon Diagnostics, Area Quantization, and the Measurement Complement
Moses Rahnama
Posted: 10 March 2026
Recovery of Bioactive Compounds from Pomegranate Seeds (Punica granatum granatum L.) Using Microwave and Ultrasound-Assisted Extraction Techniques
Wendy Magaly Arias Balderas
,Elba Ronquillo de Jesús
,Omar Patiño Rodríguez
,Chelsi Amairani Cortes Reyna
,Miguel Angel Aguilar Méndez
Posted: 10 March 2026
Environmental Disclosure of Fuel Station Companies in the Municipality of Mossoró/RN Based on the Corporate Sustainability Index – ISE
Thiago José Lima Rosa
,Jorge Luís de Oliveira Pinto Filho
Posted: 10 March 2026
5-ALA/SFC Mitigates Tau Toxicity via Lowering Oxidative Stress in a Drosophila Model of Tau Toxicity
5-ALA/SFC Mitigates Tau Toxicity via Lowering Oxidative Stress in a Drosophila Model of Tau Toxicity
Arisa Tamura
,Marie Noguchi
,Naoko Nozawa
,Emiko Suzuki
,Kanae Ando
Mitochondrial dysfunctions are believed to contribute to the pathogenesis of tauopathies, a group of neurodegenerative diseases with abnormal accumulation of microtubule-associated protein tau. The combination of 5-aminolevulinic acid (5-ALA) and sodium ferrous citrate (SFC) is known to improve mitochondrial functions. Here, we report that 5-ALA combined with SFC (5-ALA/SFC) improves mitochondrial functions and mitigates neurodegeneration in transgenic Drosophila expressing human tau. We found that tau reduces ATP levels, decreases mitochondrial distribution to neurites, and increases mitochondrial reactive oxygen species (ROS). Expression of oxidative phosphorylation (OXPHOS) genes was upregulated and activities of complexes I and IV were elevated. Feeding 5-ALA/SFC to tau flies lowers oxidative damages without correcting OXPHOS activities or mitochondrial distribution. 5-ALA/SFC treatment suppressed pathological tau phosphorylation and mitigated tau-induced neurodegeneration. Our results suggest that 5-ALA/SFC decreases a neurodegenerative pathway involving tau, mitochondria, and ROS.
Mitochondrial dysfunctions are believed to contribute to the pathogenesis of tauopathies, a group of neurodegenerative diseases with abnormal accumulation of microtubule-associated protein tau. The combination of 5-aminolevulinic acid (5-ALA) and sodium ferrous citrate (SFC) is known to improve mitochondrial functions. Here, we report that 5-ALA combined with SFC (5-ALA/SFC) improves mitochondrial functions and mitigates neurodegeneration in transgenic Drosophila expressing human tau. We found that tau reduces ATP levels, decreases mitochondrial distribution to neurites, and increases mitochondrial reactive oxygen species (ROS). Expression of oxidative phosphorylation (OXPHOS) genes was upregulated and activities of complexes I and IV were elevated. Feeding 5-ALA/SFC to tau flies lowers oxidative damages without correcting OXPHOS activities or mitochondrial distribution. 5-ALA/SFC treatment suppressed pathological tau phosphorylation and mitigated tau-induced neurodegeneration. Our results suggest that 5-ALA/SFC decreases a neurodegenerative pathway involving tau, mitochondria, and ROS.
Posted: 10 March 2026
Ahmed Negida
,Moaz Elsayed Aboelmagd
,Belal Mohamed Hamed
,Yousef Hawas
,Aya Dziri
,Yasmin Negida
,Brian D. Berman
,Matthew J. Barrett
Background: Parkinson’s disease (PD) is clinically heterogeneous, yet the genetic architecture underlying this heterogeneity remains incompletely understood. We examined the genetic correlates of four complementary PD subtyping frameworks: clinical motor subtype (tremor-dominant [TD] vs. postural instability/gait difficulty [PIGD]), alpha-synuclein seed amplification assay status (SAA+ vs. SAA−), pathological subtype (brain-first vs. body-first, based on REM sleep behavior disorder), and data-driven subtype (diffuse malignant [DM] vs. mild-motor predominant [MMP] vs. intermediate [IM]). Methods: We analyzed 1,597 PD patients from the Parkinson’s Progression Markers Initiative (PPMI) with genetic testing for seven PD-associated genes (LRRK2, GBA, SNCA, PRKN, PINK1, PARK7, VPS35), including specific variant resolution (LRRK2 G2019S, R1441G/C/H; GBA N409S, severe variants; SNCA A53T), and APOE genotyping (ε2/ε3/ε4 alleles). Genetic variant frequencies were compared across subtypes using chi-square or Fisher’s exact tests with Benjamini–Hochberg false discovery rate (FDR) correction. Effect sizes were quantified using Cramér’s V. Multivariable logistic regression (statsmodels) estimated adjusted odds ratios with Wald-based 95% confidence intervals. Results: Among 1,390 genotyped PD patients, LRRK2 carriers constituted 13.7% (190/1,390; 170 G2019S, 18 R1441G/C/H), GBA 8.6% (119/1,390; 96 N409S, 23 severe), and SNCA 2.0% (28/1,390; all A53T). APOE ε4 carriers comprised 23.4% (323/1,380). SAA-negative patients were markedly enriched for LRRK2 variants (37.1% vs. 10.2%, P = 3.7 × 10⁻¹⁹, q < 0.001, V = 0.25), driven by G2019S (28.5% vs. 9.6%, P = 4.9 × 10⁻¹¹, q < 0.001) and R1441G/C/H (7.9% vs. 0.5%, P = 2.7 × 10⁻¹², q < 0.001). Body-first PD was enriched for GBA carriers (12.3% vs. 6.7%, P = 0.004, q = 0.021) and depleted for LRRK2 (7.9% vs. 15.0%, P = 0.002, q = 0.013). The DM subtype carried the highest GBA frequency (14.0% vs. MMP 5.9%, P < 0.001, q = 0.003). After FDR correction, 10 of 48 univariate tests remained significant. Clinical subtypes (TD vs. PIGD) showed only nominal LRRK2 differences that did not survive FDR correction. APOE genotype did not differ across any framework. Conclusions: PD subtypes defined by alpha-synuclein pathology (SAA), pathological onset pattern (brain-first/body-first), and data-driven classification (DM/MMP/IM) show distinct genetic profiles that survive multiple comparison correction. LRRK2 variants strongly associate with SAA-negativity (V = 0.25); GBA variants associate with the severe body-first onset and the diffuse malignant subtype.
Background: Parkinson’s disease (PD) is clinically heterogeneous, yet the genetic architecture underlying this heterogeneity remains incompletely understood. We examined the genetic correlates of four complementary PD subtyping frameworks: clinical motor subtype (tremor-dominant [TD] vs. postural instability/gait difficulty [PIGD]), alpha-synuclein seed amplification assay status (SAA+ vs. SAA−), pathological subtype (brain-first vs. body-first, based on REM sleep behavior disorder), and data-driven subtype (diffuse malignant [DM] vs. mild-motor predominant [MMP] vs. intermediate [IM]). Methods: We analyzed 1,597 PD patients from the Parkinson’s Progression Markers Initiative (PPMI) with genetic testing for seven PD-associated genes (LRRK2, GBA, SNCA, PRKN, PINK1, PARK7, VPS35), including specific variant resolution (LRRK2 G2019S, R1441G/C/H; GBA N409S, severe variants; SNCA A53T), and APOE genotyping (ε2/ε3/ε4 alleles). Genetic variant frequencies were compared across subtypes using chi-square or Fisher’s exact tests with Benjamini–Hochberg false discovery rate (FDR) correction. Effect sizes were quantified using Cramér’s V. Multivariable logistic regression (statsmodels) estimated adjusted odds ratios with Wald-based 95% confidence intervals. Results: Among 1,390 genotyped PD patients, LRRK2 carriers constituted 13.7% (190/1,390; 170 G2019S, 18 R1441G/C/H), GBA 8.6% (119/1,390; 96 N409S, 23 severe), and SNCA 2.0% (28/1,390; all A53T). APOE ε4 carriers comprised 23.4% (323/1,380). SAA-negative patients were markedly enriched for LRRK2 variants (37.1% vs. 10.2%, P = 3.7 × 10⁻¹⁹, q < 0.001, V = 0.25), driven by G2019S (28.5% vs. 9.6%, P = 4.9 × 10⁻¹¹, q < 0.001) and R1441G/C/H (7.9% vs. 0.5%, P = 2.7 × 10⁻¹², q < 0.001). Body-first PD was enriched for GBA carriers (12.3% vs. 6.7%, P = 0.004, q = 0.021) and depleted for LRRK2 (7.9% vs. 15.0%, P = 0.002, q = 0.013). The DM subtype carried the highest GBA frequency (14.0% vs. MMP 5.9%, P < 0.001, q = 0.003). After FDR correction, 10 of 48 univariate tests remained significant. Clinical subtypes (TD vs. PIGD) showed only nominal LRRK2 differences that did not survive FDR correction. APOE genotype did not differ across any framework. Conclusions: PD subtypes defined by alpha-synuclein pathology (SAA), pathological onset pattern (brain-first/body-first), and data-driven classification (DM/MMP/IM) show distinct genetic profiles that survive multiple comparison correction. LRRK2 variants strongly associate with SAA-negativity (V = 0.25); GBA variants associate with the severe body-first onset and the diffuse malignant subtype.
Posted: 10 March 2026
MetaThink: Empowering Large Reasoning Models with Adaptive Self-Correction at Inference Time
Jiarui Qi
,Haoyu Bian
Posted: 10 March 2026
Entendiendo los Biosimilares: Una Perspectiva Farmacológica para el Médico Clínico - Understanding Biosimilars: A Pharmacological Perspective for Clinical Physicians
Gustavo Lorenzo Moretta
,Rosana Claudia Chaud Covarrubias
Posted: 10 March 2026
Preoperative HALP Score as a Marker of Tumor Aggressiveness and Survival in Surgically Treated Soft Tissue Sarcoma: A Retrospective Cohort Study
Hüseyin Pülat
,Oğuzhan Söyler
,Ünal Öner
,Deniz Öztaşan
,Cüneyt Akyüz
,Cemil Yuksel
Posted: 10 March 2026
Antimicrobial Resistance in Pseudomonas aeruginosa and the Emerging Role of Phage Therapy
Rediet Guta Mideksa
,Alazar Amare Amdiyee
,Alemayehu Godana Birhanu
Posted: 10 March 2026
Is Insulin Resistance a Potential Pathophysiological Mechanism Underlying the Association Between Bladder Cancer and Its Known Risk Factors?
Giovanni Tarantino
,Vincenzo Citro
,Ciro Imbimbo
,Felice Crocetto
Posted: 10 March 2026
A Governance Framework for Urban AI in Climate-Resilient Housing and Infrastructure Prioritization
Reyhaneh Ahmadi
,Kaveh Ghamisi
Posted: 10 March 2026
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