Ask about this productRelated genes to: PI15 Blocking Peptide
- Gene:
- PI15 NIH gene
- Name:
- peptidase inhibitor 15
- Previous symbol:
- -
- Synonyms:
- P25TI
- Chromosome:
- 8q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-11
- Date modifiied:
- 2016-10-05
Related products to: PI15 Blocking Peptide
Related articles to: PI15 Blocking Peptide
- Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder. It is characterized by the accumulation of misfolded α-synuclein (α-syn) and progressive loss of dopaminergic neurons in the substantia nigra. Due to the limitations of current therapies, mesenchymal stromal cell (MSC) transplantation has emerged as a promising neuroprotective strategy. This study evaluated the neuroprotective potential of decidua-derived mesenchymal stromal cells (DMSCs) in vitro using a human neuroblastoma cell line (NB69) exposed to the neurotoxin 1-methyl-4-phenylpyridinium (MPP+) as a PD model. The NB69 cells were differentiated into a mature dopaminergic phenotype using dibutyryl cyclic adenosine monophosphate (dbcAMP) and then exposed to MPP+. In proliferative NB69 cells, the effect of DMSCs was masked by their inherent antitumor activity against the neuroblastoma phenotype. Conversely, in the differentiated NB69 model, DMSCs demonstrated a significant protective role against MPP+-induced cytotoxicity. Interestingly, the mechanism by which DMSCs might exert a neuroprotective effect against MPP+ damage in differentiated NB69 cells appears to involve improving mitochondrial function by reducing free radicals. In summary, these findings suggest that DMSCs exert a neuroprotective effect in a dopaminergic-like context and highlight the importance of using differentiated cell models to accurately evaluate cell-based therapies for PD in the striatum. - Source: PubMed
Publication date: 2026/04/28
Coto-Vilcapoma AlmudenaSánchez-Carretero LauraArenas-Gonzalez DanielMolina José AMorán-Jiménez María JoséMerino José JoaquínTorre Paz de laFlores Ana I - Sex differences in mental health are often overlooked, yet gut microbiota-host metabolite interactions may contribute to sexual dimorphism in depression. In a population-based cohort, we investigated sex-specific links among plasma tryptophan metabolites, depressive symptoms (PHQ-9), and the gut microbiome, controlling for smoking, diet, alcohol, and physical activity. Women (N = 419) exhibited higher plasma indole-3-acetic acid (IAA) and picolinic acid (PA) concentrations, but lower trigonelline (TRIG) than men (N = 383). Machine learning models with SHAP explanations revealed that IAA and TRIG were positively associated, whereas PA was negatively associated with depression severity in women, whereas only kynurenic acid (KA) was inversely associated in men. In women, depression severity strongly correlated with methanogenic archaea, including Methanobrevibacter smithii, and microbial methane-production pathways. Methanobrevibacter and specifically M. smithii were negatively linked to genes for tryptophan, PA, and KA biosynthesis, but positively to genes for IAA and nicotinate/nicotinamide metabolism. Most microbial species associated with depression severity in women were predicted to produce IAA. These findings reveal pronounced sex-specific microbiome-metabolite interactions, highlighting potentially distinct microbial mechanisms shaping depression in men and women. - Source: PubMed
Publication date: 2026/05/04
Motger-Albertí AnnaGallardo-Nuell LauraRosell-Díaz MariselStefoglo MihaelaPons JavierGarre-Olmo JosepPérez-Brocal VicenteMoya AndrésPuig JosepRamos RafaelMayneris-Perxachs JordiFernández-Real José Manuel - The aim of the study was to assess the microbial composition of bronchial secretions in chronic obstructive pulmonary disease (COPD), focusing on the impact of the exacerbation patterns on the common components of the respiratory flora and their relationship with inflammatory proteins. A total of 72 clinically stable COPD patients provided sputum and blood samples for 16S rRNA gene amplification and peripheral biomarkers. Beta-diversity analyses of the bronchial microbiome showed significant differences between infrequent and frequent (≥2) exacerbators ( = 0.001). was underrepresented in frequent exacerbators (relative abundance [RA] 0.07 [0.003-0.31] vs. 0.24 [0.06-2.36], = 0.02) while the presence of was increased (7.70 [0.66-11.68] vs. 1.11 [0.37-2.88], = 0.01). Eight common taxa, , , , , , , and , showed significant decreases in their RAs when exacerbations required hospitalization. RAs of and eight common taxa were positively correlated ( < 0.01). Among them, , and showed a negative correlation with blood interleukin-8 (IL-8) ( < 0.01) and an equivalent correlation was found for . Frequent exacerbations cause a decrease in the RA of and have a more extensive impact when hospitalization is required. The RAs of common bronchial bacteria were closely related and some of them were inversely associated with blood IL-8 levels. - Source: PubMed
Publication date: 2026/04/10
Monsó EduardCasadevall CarmeQuero SaraPascual-Guàrdia SergiEnríquez-Rodríguez César JésseMillares LauraMontón ConcepciónFaner RosaCapilla SilviaSeijo Luis MiguelCastro-Acosta AdyAlvarez-Martínez CarlosSibila OriolPeces-Barba GermánCosio Borja GAgustí AlvarGea Joaquim - Diffusing capacity for carbon monoxide (DLCO) reflects pulmonary gas exchange efficiency, but its measurement and interpretation remain challenging due to physiological and technical variability. Quantitative computed tomography (CT) provides structural insights that may help address these limitations. This study investigated associations among demographic factors, spirometric values, DLCO, and CT-derived metrics in patients with various lung conditions. Additionally, we developed predictive models for DLCO. We analyzed mean lung density (MLD), percentile index 15 (PI15), percentages of low and high attenuation areas (LAA% and HAA%), emphysema size heterogeneity (D-slope), airway wall thickness (AWTPi10), and pulmonary vascular indices. Network analysis and random forest regression were employed to identify determinants and predictors of DLCO. DLCO correlated positively with weight and whole lung volume, and negatively with age, MLD variation, HAA%, and D-slope. DLCO/alveolar volume was positively associated with weight, body mass index, and lung density metrics (PI15), and negatively with LAA% and D-slope. CT-derived metrics exhibited distinct correlation patterns compared to spirometric measurements. The random forest model predicted DLCO with correlation coefficient of 0.82, an RMSE of 3.04 mL/min/mmHg, and an R of 0.58, indicating considerable predictive performance. Integrating quantitative CT metrics improves the understanding of DLCO. Imaging-based models may enhance diagnostic precision and support personalized management strategies for pulmonary diseases. - Source: PubMed
Publication date: 2026/04/28
Chung Sung JunKang JiyeonKim Deok HeeKang Hyung KooSong PamelaLee Sung SoonKim Ki HwanKim YoulimMoon Ji-YongKoo Hyeon-Kyoung - The Clinical High Risk (CHR) state for psychosis is consistently associated with widespread cortical thinning. However, the underlying mechanisms driving this neuroanatomical phenotype remain poorly understood. Here, we integrated the ENIGMA CHR Working Group's large pooled dataset (N = 1782 CHR, N = 1333 healthy controls) with an open-source PET molecular atlas to identify, for the first time, potential neurochemical drivers of cortical thinning associated with psychosis risk, transition, and its core symptoms. Using multilinear model analysis, we show that local chemoarchitecture significantly explains CT differences associated with CHR case-control status, the severity of negative symptoms, and future psychosis transition after excluding medication confounds. PET-based maps of dopamine, GABA, glutamate, serotonin, and norepinephrine consistently emerged as the strongest predictors of lower CT in CHR and psychosis transition (total dominance range: 62-69% and 58-87%, respectively), with contributions of monoamine systems being especially sensitive to medication exposure (8-23% change in dominance range). Negative symptom-associated cortical thinning was best explained by PET-based maps of dopamine, histamine, serotonin and opioid systems (total dominance range: 60-81%), with contributions of histamine being sensitive to medication exposure (9-19% change in dominance range). Combined, these results uniquely identify specific neurochemical systems - particularly monoaminergic, glutamatergic, and GABAergic pathways - as key molecular mechanisms associated with cortical thinning in people at high risk of developing psychosis. - Source: PubMed
Publication date: 2026/04/04
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