ASSY., PUMP, PERISTALTIC SR10/50
- Known as:
- ASSY., PUMP, PERISTALTIC SR10/50
- Catalog number:
- rvdia03600000016
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Diasource
- Gene target:
- ASSY. PUMP PERISTALTIC SR10/50
Related genes to: ASSY., PUMP, PERISTALTIC SR10/50
- Gene:
- MMP7 NIH gene
- Name:
- matrix metallopeptidase 7
- Previous symbol:
- MPSL1
- Synonyms:
- PUMP-1
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-15
- Date modifiied:
- 2015-08-25
Related products to: ASSY., PUMP, PERISTALTIC SR10/50
0.5 mm 2-pump Connecting Tube0.9 mm 2-pump Connecting Tube1-pump Control Cable, AC-21101-pump Control Cable, AC-21201000UL TRAY ASSY 1ml 60 WELL2-pump Control Cable, AC-21102-pump Control Cable, AC-212023 kDa subunit of V-ATPase,Atp6f,Atp6v0b,Mouse,Mus musculus,Vacuolar proton pump 21 kDa proteolipid subunit,V-ATPase 21 kDa proteolipid subunit,V-type proton ATPase 21 kDa proteolipid subunit32 kDa accessory protein,ATP6D,ATP6V0D1,Bos taurus,Bovine,P39,Vacuolar proton pump subunit d 1,V-ATPase 40 kDa accessory protein,V-ATPase AC39 subunit,V-ATPase subunit d 1,VPATPD,V-type proton ATPase32 kDa accessory protein,ATP6D,ATP6V0D1,Homo sapiens,Human,p39,Vacuolar proton pump subunit d 1,V-ATPase 40 kDa accessory protein,V-ATPase AC39 subunit,V-ATPase subunit d 1,VPATPD,V-type proton ATPaseAC-2110 Perista Pump 1-ch, 110VAC-2110 Perista Pump 1-ch, 230VAC-2110 Perista Pump 2-ch, 110VAC-2110 Perista Pump 2-ch, 230VAC-2120 Perista Pump, 110V Related articles to: ASSY., PUMP, PERISTALTIC SR10/50
- The etiology and underlying mechanisms of acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) remain poorly understood. Although several animal models have been developed to study AE-IPF, a systematic evaluation and comparison of these models has not yet been reported. In the present study, PF was induced in mice by a single intratracheal administration of bleomycin (BLM). On day 14 after the initial BLM challenge, AE-PF in mice was induced by intratracheal re-challenge with replication-deficient adenoviral vectors (ADV), lipopolysaccharide (LPS) or a second dose of BLM. Micro-chest computed tomography (CT) was performed on day 20, and blood, bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected after sacrifice on day 21. Compared with mice receiving a single dose of BLM alone, all three AE-PF groups exhibited significant body weight loss and increased mortality (with the highest mortality in the LPS group), as well as more extensive lung injury on CT. Histopathological scores for inflammation and fibrosis, hydroxyproline content and expression levels of fibrotic markers (fibronectin, collagen I, α-smooth muscle actin and MMP7) were significantly elevated in the AE-PF groups. Inflammatory cytokines (IL-6, IL-1β and TNF-α) were markedly increased in both serum and BALF. Furthermore, the AE-PF models showed downregulation of alveolar epithelial cell markers (E-cadherin and pro-surfactant protein C) and a significant increase in apoptotic activity. Notably, fibrosis progression was more severe in the ADV and two-dose BLM groups than in the LPS group. Taken together, these findings indicate that all three triggers can induce AE-PF through enhanced apoptosis, inflammation and fibrosis. These results support the use of day 14 re-challenge as a standardized model for AE-PF. Among the three models, the ADV-induced AE-PF model may serve as a particularly suitable platform for investigating the pathogenesis of acute exacerbations in idiopathic pulmonary fibrosis. - Source: PubMed
Publication date: 2026/07/24
Ye XuZhang MingruiLiu MengyingZhu HuihuiYe XiaolingJiang ChengLi QiHuang XinmeiCao Mengshu - BackgroundVascular risk factors contribute substantially to late-life cognitive impairment and interact with neurodegenerative processes underlying dementia. Blood-brain barrier (BBB) dysfunction has emerged as a key mechanism linking vascular pathology to cognitive decline; however, circulating biomarkers reflecting BBB remodeling remain incompletely characterized.ObjectiveTo explore the association between circulating markers of BBB remodeling, amyloid-β (Aβ) and longitudinal cognitive decline in individuals with vascular risk factors.MethodsIn this prospective cohort study, 101 individuals (mean age 71 ± 5 years; 59.4% women) with long-standing hypertension and/or type 2 diabetes mellitus underwent serial assessment of serum BBB-related biomarkers (matrix metalloproteinases [MMPs], TIMP-1 and soluble tumor necrosis factor-like weak inducer of apoptosis [sTWEAK]), Aβ, brain MRI, and standardized cognitive testing (Mini-Mental State Examination and Addenbrooke's Cognitive Examination Version V) over a mean follow-up of 24 ± 4.9 months. Cognitive decline was defined as a clinically meaningful reduction in global cognitive scores.ResultsTwelve participants (11.9%) developed cognitive decline. Higher serum MMP-7 levels at 12 months were independently associated with subsequent cognitive decline after adjustment for age, sex and baseline cognition (adjusted OR 2.13; 95% CI 1.09-4.13; p = 0.026). Baseline levels of Aβ, MMP-9, and sTWEAK were associated with lower cognitive performance.ConclusionsElevated circulating MMP-7 at 12 months was associated with cognitive decline suggesting a potential role for BBB remodeling in vascular contributions to cognitive impairment. These findings should be considered exploratory and require validation in larger studies. - Source: PubMed
Publication date: 2026/08/04
López-Dequidt IriaLeira YagoCinza-Sanjurjo SergioRey-Aldana DanielJiménez IsabelCampos FranciscoSobrino TomásCastillo JoséRodríguez-Yáñez Manuel - Chronic obstructive pulmonary disease (COPD) increases cardiovascular disease risk. Coronary artery calcification (CAC) predicts cardiovascular events and mortality in COPD. We hypothesized that plasma proteins linked to pulmonary phenotypes mediate CAC burden. - Source: PubMed
Publication date: 2026/08/07
Abbasi AsgharAhmad KhadijePratte Katherine AMoore JeffDeMeo Dawn LManubolu Venkat SKinninger AprilTiller Nicholas BBowler Russell PBudoff MathewCasaburi RichardRossiter Harry B - Transient receptor potential ankyrin 1 (TRPA1) is a cation channel originally identified in lung fibroblasts and extensively studied in sensory neurons, where it is associated with pain and neurogenic inflammation. We and others have recently shown that TRPA1 is also expressed in lung epithelial cells and that its expression is regulated by the cytokine environment. In the present study, we used next-generation sequencing to analyse the role of TRPA1 and the effects of its inhibition on human A549 lung epithelial cell phenotype under inflammatory conditions. Two different TRPA1 inhibitors (HC-030031 and A-967079) were used and found to alter the expression of 968 genes: 576 genes were downregulated, and 392 upregulated. Ingenuity Pathway Analysis (IPA) predicted that TRPA1 inhibitors significantly suppress the activity of pulmonary fibrosis idiopathic signalling and wound healing pathways. In these pathways, altered genes included matrix metalloproteinases (MMPs), growth factors, collagens and transcription factors. The major profibrotic mediators MMP-12 and MMP-7 were among the most strongly inhibited genes by TRPA1 inhibitors. STRING network analysis suggests that TRPA1 regulates fibrosis-related genes through FOS gene and AP-1 transcription factor. These findings together with previous data propose TRPA1 as a factor and therapeutic target in fibrotic lung diseases, which are associated with poor survival and critical need for novel disease-modifying therapies. - Source: PubMed
Halonen LeeviLuostarinen SamuValjus IdaVistbacka JuliaPemmari AnttiMoilanen Eeva - While direct-acting antiviral (DAA) therapies effectively cure most chronic hepatitis C virus (HCV) infections, patients with pre-existing cirrhosis remain at risk for disease progression. Cellular senescence and immune dysregulation drive persistent liver injury post-clearance, but reliable biomarkers and therapeutic targets remain scarce. - Source: PubMed
Publication date: 2026/08/03
Yao YuepingZhou MinYan ZhihanSu TingtingFang HuijingYang XiujuanGuo Xiaoye