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- Safety Data Sheet
Catalog #: Product Name: 100-1603 Anti-Mouse CD4 Antibody, Clone GK1.5, FITC Catalog #: 100-1603 Product Name: Anti-Mouse CD4 Antibody, Clone GK1.5, FITC - ReferenceS. E. Fernandes et al. (Sep 2025) Nature Communications 16
Evolutionary loss of an antibiotic efflux pump increases Pseudomonas aeruginosa quorum sensing mediated virulence in vivo
Antibiotic resistance is a threat to human health, yet recent work highlights how loss of resistance may drive pathogenesis in some bacteria. In two recent studies, we found that β-lactam antibiotics and nutrient stresses faced during infection selected for genetic inactivation of the Pseudomonas aeruginosa antibiotic efflux pump mexEFoprN . Unexpectedly, efflux pump mutations increased P. aeruginosa virulence during infection; however, neither the prevalence of mexEFoprN inactivating mutations in real human infections, nor the mechanisms driving increased virulence of efflux pump mutants are known. We hypothesized that human infection would select for virulence enhancing mutations. Using genome sequencing of clinical isolates, we show that mexEFoprN efflux pump inactivating mutations are enriched in P. aeruginosa isolates from cystic fibrosis infections relative to isolates from acute respiratory infections. Combining RNA-seq, metabolomics, genetic approaches, and infection models we show that efflux pump mutants have elevated quorum sensing driven expression of elastase and rhamnolipids which increase P. aeruginosa virulence during acute and chronic infections. Restoration of the efflux pump in a representative respiratory isolate and the notorious cystic fibrosis Liverpool epidemic strain reduced their virulence. These findings suggest that mutations inactivating antibiotic resistance mechanisms could lead to greater patient mortality and morbidity. Subject terms: Antimicrobial resistance, Pathogens, Bacteriology, Molecular evolutionCatalog #: Product Name: 05001 PneumaCult™-ALI Medium 05040 PneumaCult™-Ex Plus Medium Catalog #: 05001 Product Name: PneumaCult™-ALI Medium Catalog #: 05040 Product Name: PneumaCult™-Ex Plus Medium ReferenceM. E. Cooke et al. (Oct 2025) Biofabrication 17 4Tailoring agarose fluid gels for use in suspension bath bioprinting and culture of spheroid-based bioinks
Suspension bath bioprinting, whereby bioinks are extruded into a yield stress bath with rapid recovery from shearing, has enabled the printing of low viscosity bioinks into constructs with high geometric complexity. Previous studies have often relied upon external stabilisation of the suspension bath (e.g. collagen) in order to culture soft materials without loss of printed structure. Here, we report a systematic investigation of suspension bath properties that support the printing, fusion, and culture of spheroid-based bioinks without added stabilisation. Specifically, agarose fluid gels of varied polymer concentrations and dilutions were produced and characterised morphologically and rheologically. Juvenile bovine chondrocytes or mesenchymal stromal cells (MSCs) were formed into spheroids of ∼150 µ m in diameter and investigated within agarose suspension baths either for their fusion in hanging drop cultures or as jammed bioinks. MSC spheroids were also printed when mixed with hydrogel microparticles to demonstrate additional versatility to the approach. Suspension baths of lower polymer concentrations and increased dilution enabled faster spheroid fusion; however, the most heavily diluted suspension bath was unable to maintain print fidelity. Other formulations supported the printing, fusion, and culture of spheroid-based inks, either as simple lines or more complex patterns. These findings help to inform the design of suspension baths for bioprinting and culture.Catalog #: Product Name: 34411 ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢400 Catalog #: 34411 Product Name: ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢400 Safety Data SheetCatalog #: Product Name: 100-1602 Anti-Mouse CD4 Antibody, Clone GK1.5, APC Catalog #: 100-1602 Product Name: Anti-Mouse CD4 Antibody, Clone GK1.5, APC ReferenceZ. Li et al. (Sep 2025) Journal of Asthma and Allergy 18 4Inhibition of LOXL2 Suppresses Nasal Mucosal Inflammation and Remodeling in Allergic Rhinitis
Tissue remodeling is a key feature of allergic rhinitis (AR), but its underlying molecular mechanisms remain unclear. Lysyl oxidase-like 2 (LOXL2), a regulator of tissue remodeling, has not been studied in AR. Proteomic analysis was performed on nasal mucosal tissues from 8 AR patients and 8 healthy controls (HCs) to identify differentially expressed proteins (DEPs). The top three upregulated DEPs and their association with tissue remodeling markers were validated by immunofluorescence, Western blot, and RT-qPCR in an independent cohort of 30 AR patients and 30 HCs. In vitro, human nasal epithelial cells (HNECs) were treated with IL-4, and the effects of candidate protein inhibitors on remodeling were assessed. An AR mouse model was used to evaluate the impact of these inhibitors on nasal inflammation and remodeling. Proteomic analysis revealed a disease-specific protein expression profile in the nasal mucosa of AR patients, with the top three upregulated proteins being LOXL2, TGF-β1, and TIRAP. Tissue validation showed that LOXL2 was significantly upregulated in the nasal mucosa of AR patients compared to HCs and was significantly correlated with EMT markers (TGF-β1, α-SMA, and E-cadherin). In vitro, IL-4 stimulation significantly upregulated LOXL2, TGF-β1, and α-SMA, while downregulating E-cadherin in a dose-dependent manner in human nasal epithelial cells. These effects were reversed by inhibition of LOXL2. Further investigations demonstrated that LOXL2 promotes tissue remodeling through activation of the TGF-β1/Smad signaling pathway. In the AR mouse model, LOXL2 inhibitors significantly reduced nasal mucosal inflammation and tissue remodeling. Our proteomic analysis suggests that LOXL2 may be involved in the pathological remodeling processes of AR, potentially through modulation of the TGF-β1/Smad signaling pathway. These findings provide preliminary evidence that LOXL2 could serve as a candidate biomarker and a possible therapeutic target in AR, warranting further investigation.Catalog #: Product Name: 05040 PneumaCult™-Ex Plus Medium Catalog #: 05040 Product Name: PneumaCult™-Ex Plus Medium Safety Data SheetCatalog #: Product Name: 100-1601 Anti-Mouse CD4 Antibody, Clone GK1.5 Catalog #: 100-1601 Product Name: Anti-Mouse CD4 Antibody, Clone GK1.5 ReferenceS. Trushin et al. (Sep 2025) eBioMedicine 120 4Therapeutic assessment of a novel mitochondrial complex I inhibitor in in vitro and in vivo models of Alzheimer's disease
Despite recent approval of monoclonal antibodies that reduce amyloid (Aβ) accumulation, the development of disease-modifying strategies targeting the underlying mechanisms of Alzheimer's disease (AD) is urgently needed. We demonstrate that mitochondrial complex I (mtCI) represents a druggable target, where its weak inhibition activates neuroprotective signalling, benefiting AD mouse models with Aβ and p-Tau pathologies. Rational design and structure‒activity relationship studies yielded mtCI inhibitors profiled in a drug discovery funnel designed to address safety, selectivity, and efficacy. The lead compound C458 is highly protective against Aβ toxicity, has favourable pharmacokinetics, and minimal off-target effects. C458 exhibited excellent brain penetrance, activating neuroprotective pathways with a single dose. Preclinical studies in APP/PS1 mice were conducted using functional tests, metabolic assessment, in vivo 31 P-NMR spectroscopy, blood cytokine panels, ex vivo electrophysiology, and Western blotting. Chronic oral administration improved long-term potentiation, reduced oxidative stress and inflammation, and enhanced mitochondrial biogenesis, antioxidant signalling, and cellular energetics. Efficacy against Aβ and p-Tau was confirmed in human organoids. These studies provide further evidence that the restoration of mitochondrial function in response to mild energetic stress represents a promising disease-modifying strategy for AD. This research was supported by grants from NIH AG 5549-06, NS1 07265, AG 062135, UG3/UH3 NS 113776, and ADDF 291204 (all to ET); U19 AG069701 (to TK); the Alzheimer’s Association Research Fellowship grant 23AARF-1027342 (to TKON).Catalog #: Product Name: 08570 STEMdiff™ Cerebral Organoid Kit Catalog #: 08570 Product Name: STEMdiff™ Cerebral Organoid Kit Safety Data SheetCatalog #: Product Name: 100-1600 Anti-Human CD80 (B7-1) Antibody, Clone 2D10.4, APC Catalog #: 100-1600 Product Name: Anti-Human CD80 (B7-1) Antibody, Clone 2D10.4, APC ReferenceA. Chakraborty et al. (Aug 2025) International Journal of Molecular Sciences 26 17Cholesterol Regulates Airway Epithelial Cell Differentiation by Inhibiting p53 Nuclear Translocation
Cholesterol is an essential plasma membrane component, and altered cholesterol metabolism has been linked to cholesterol accumulation in the airways of COPD and cystic fibrosis patients. However, its role in airway epithelial differentiation is not well understood. Tandem mass spectrometry-based proteomic analysis of differentiating primary human bronchial epithelial cells (phBECs) revealed an overall inhibition of the cholesterol biosynthesis pathway. We hypothesized that excess cholesterol impairs the differentiation of phBECs into a fully functional bronchial epithelium. PhBECs were differentiated in the presence of 80 µM cholesterol for 21 days, the main airway cell type populations monitored using qRT-PCR and immunofluorescent stainings, and epithelial barrier integrity was analyzed via transepithelial electrical resistance measurements. Chronic cholesterol exposure led to a significant increase in CC10 + secretory cells at the expense of ciliated cells. Pathway enrichment analysis suggested the tumor protein p53 as a master regulator of genes during normal differentiation of phBECs. Chronic cholesterol exposure drastically impaired the nuclear translocation of p53. Our findings suggest that this inhibition underlies the cholesterol-induced expansion of CC10 + secretory cell populations at the expense of ciliated cells. In conclusion, we identify cholesterol as an important regulator of normal bronchial epithelial cell differentiation through inhibition of p53 nuclear translocation.Catalog #: Product Name: 05001 PneumaCult™-ALI Medium 05040 PneumaCult™-Ex Plus Medium Catalog #: 05001 Product Name: PneumaCult™-ALI Medium Catalog #: 05040 Product Name: PneumaCult™-Ex Plus Medium Safety Data SheetCatalog #: Product Name: 100-1599 Anti-Human CD80 (B7-1) Antibody, Clone 2D10.4, PE Catalog #: 100-1599 Product Name: Anti-Human CD80 (B7-1) Antibody, Clone 2D10.4, PE ReferenceT. Nosaka et al. (Aug 2025) Cancers 17 17Clinical Significance of CD90(+) Circulating Tumor Cells as Dynamic Biomarkers in Unresectable Hepatocellular Carcinoma Treated with Atezolizumab/Bevacizumab and Lenvatinib
Atezolizumab plus bevacizumab and lenvatinib are standard treatments for unresectable hepatocellular carcinoma; however, tumor markers such as alpha-fetoprotein and des-gamma-carboxy prothrombin have a limited ability to reflect treatment responses. Circulating tumor cells are non-invasive biomarkers associated with cancer stemness and treatment resistance. We assessed circulating tumor cell subsets expressing cancer stem cell markers (CD90, epithelial cell adhesion molecule, CD133, vimentin) using multiparametric flow cytometry at early and maximal response phases in patients receiving atezolizumab plus bevacizumab or lenvatinib. Early decreases in CD90-positive circulating tumor cells after therapy initiation were associated with tumor shrinkage and longer progression-free survival in both groups, as well as prolonged overall survival in the atezolizumab plus bevacizumab group. At maximal response, changes in CD90-positive circulating tumor cells reflected tumor burden more accurately than alpha-fetoprotein or des-gamma-carboxy prothrombin. These findings highlight the potential of CD90-positive circulating tumor cells to become dynamic biomarkers in systemic therapy for unresectable hepatocellular carcinoma.Catalog #: Product Name: 15122 RosetteSepâ„¢ Human CD45 Depletion Cocktail Catalog #: 15122 Product Name: RosetteSepâ„¢ Human CD45 Depletion Cocktail ReferenceW. Yang et al. (Aug 2025) Cancers 17 17A Polyomavirus-Positive Merkel Cell Carcinoma Mouse Model Supports a Unified Origin for Somatic and Germ Cell Cancers
Cancer research has long focused on mutations in normal body cells, but this approach has not produced major breakthroughs for most cancers. Our study explores a different concept that some aggressive cancers may actually arise from early reproductive cells called primordial germ cells, which normally develop into eggs and sperm. We created a new experimental model showing how a virus can transform human primordial germ cell-like cells into virus-positive Merkel cell carcinoma, a rare but deadly skin cancer. This model shows that cancers can emerge through changes in developmental states rather than relying solely on genetic mutations. By linking cancer development to early germ cells, our findings suggest a unifying explanation for both germ cell cancers and body cancers. This new perspective may guide more effective approaches to study, diagnose, and treat cancer by focusing on early human development rather than only DNA mutations and later developmental stages.Catalog #: Product Name: 05872 ¸é±ð³¢±ð³§¸éâ„¢ Catalog #: 05872 Product Name: ¸é±ð³¢±ð³§¸éâ„¢ Items 277 to 288 of 13914 total
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