Chimpanzee TNF_alpha ELISPOT antibody pair
- Known as:
- Chimpanzee TNF_alpha ELISPOT (anti-) pair
- Catalog number:
- CT632-10
- Product Quantity:
- 10-plate
- Category:
- -
- Supplier:
- U-CyTech
- Gene target:
- Chimpanzee TNF_alpha ELISPOT antibody pair
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Related articles to: Chimpanzee TNF_alpha ELISPOT antibody pair
- Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with limited therapeutic options, driven in part by its immunosuppressive tumor microenvironment (TME). Tumor-associated macrophages (TAMs) and neutrophils (TANs) contribute to tumor progression and immune evasion. A Disintegrin and Metalloproteinase 8 (ADAM8), a zinc-dependent protease, is strongly upregulated in PDAC and correlates with poor clinical outcomes, suggesting a regulatory role in tumor progression. - Source: PubMed
Publication date: 2026/08/03
Zandieh KimiaCook LenaZhao KaiNagl ConstanzeGao YutongdiFazio PietroBartsch Detlef KBauer Uta-MariaMeixner MarionYildiz DanielaKeber CorinnaNimsky ChristopherBartsch Jörg W - In vitro osteoarthritis (OA) models are widely used for mechanistic studies. However, inconsistencies in induction protocols limit reproducibility and translational relevance. A systematic comparison of inflammatory inducers based on their temporal dynamics remains elusive. A systematic literature search was conducted across PubMed, Web of Science, and Scopus to identify the most commonly used inflammatory inducers in vitro OA models. The prevalence of each inducer was quantified. In addition, a qualitative mechanistic synthesis was performed by integrating representative studies reporting temporal molecular profiles to construct conceptual kinetic patterns. Based on this synthesis, a kinetic-based framework was developed to compare inducer-specific temporal characteristics. Interleukin-1β (IL-1β) was the most frequently used inducer (62.12%), followed by lipopolysaccharide (LPS, 9.60%) and tumor necrosis factor-α (TNF-α, 7.58%). Temporal synthesis suggested a biphasic enzymatic response characterized by early ADAMTS-5 induction (approximately 6-12 h) and subsequent MMP-13 elevation (24-48 h). IL-1β was associated with sustained signaling activation and pronounced transitions between ferroptosis-related and apoptotic-related markers. In contrast, TNF-α induced rapid but transient early-phase responses, whereas LPS exhibited a delayed yet persistent low-grade inflammatory profile. The selection of inflammatory inducers should be aligned with specific experimental objectives. IL-1β is suitable for modeling sustained catabolic activity and cell death transitions, TNF-α for early-stage inflammatory responses, and LPS for chronic low-grade inflammation. This kinetic-based framework may improve model selection and enhance the translational relevance of in vitro OA studies, although further experimental validation is required. - Source: PubMed
Publication date: 2026/08/03
Cheng GuoyunAtheeqah-Hamzah NurLiu XiaoqianLv FengyangLoh Kwong WengAziz AtiqahTan Han LingTunku Kamarul - This study aimed to assess the effect of Cinnamomum tamala leaf-extract (CTE) on the growth, immune response, antioxidant status, gene expression, and disease resistance of Cyprinus carpio. Over a 70-day period, fish (8.82 ± 0.04 g) were fed diets supplemented with graded levels of CTE (mg/kg): 0 (Control), 200 (CTE2), 300 (CTE3), 400 (CTE4), 500 (CTE5), and 600 (CTE6). Cytokine gene expression was studied 3 days post-challenge with A. hydrophila. CTE at 400-600 mg/kg maximized the growth performance. Key immune parameters, such as total protein, lysozyme, ACH, alkaline phosphatase, skin mucosal protease activity, serum phagocytosis, and peroxidase levels were enhanced (P < 0.05) in CTE4 and/or CTE5 than in the control. Dietary CTE did not influence serum glucose, cortisol, creatinine, urea, total immunoglobulin, or liver metabolic enzyme levels. Intestinal amylase activity, and serum antioxidant levels were higher in CTE4-CTE6; whereas, serum MDA level was decreased in CTE5 (P < 0.05). The 15-day relative post-challenge survival was highest in CTE5 (54.76%). The transcript levels of sod, cat, and nrf2 were strongly upregulated in the liver tissues of CTE4 and CTE5; whereas keap1 transcription was downregulated in CTE5. The expression of tnf-α, il-1β, and hsp70 was down-regulated in CTE4 and CTE5. Conversely, il-10 expression was significantly upregulated in liver tissues of CTE4. The expression of occludin, occludin 7, and zo-1 were significantly upregulated in the intestinal tissues of CTE4 and CTE5. Overall, dietary CTE at appropriate level can enhance growth performance, immunity, and disease resistance in C. carpio. HIGHLIGHTS: C. tamala leaf extract (CTE) at 400-500 mg/kg improved growth performance of Cyprinus carpio. Dietary CTE at 400-500 mg/kg modulated the skin mucosal immunity of fish. CTE enhanced the resistance against Aeromonas hydrophila challenge. CTE at 400-500 mg/kg enhanced serum antioxidant enzymes. - Source: PubMed
Publication date: 2026/08/03
Giri Sib SankarSukumaran VenkatachalamPark Se ChangKim Ji Hyung - Glucagon-like peptide-1 receptor agonists (GLP-1RAs) like semaglutide have transformed type 2 diabetes mellitus (T2DM) management, yet emerging concerns highlight potential risks of accelerated sarcopenia and subsequent metabolic disruptions. This case-driven hypothesis explores a 53-year-old male with T2DM diagnosed in 2014, who experienced progressive glycemic failure despite standard therapies, including metformin, glipizide, sitagliptin, and empagliflozin. Transition to dulaglutide 1.5 mg for 1.5 years followed by semaglutide (titrated from 0.25 to 1 mg weekly starting September 2024) resulted in weight loss from 84 kg to 70 kg by September 2025, accompanied by sarcopenic symptoms (muscle weakness, reduced mobility) and refractory hyperglycemia (fasting glucose 300 mg/dL, HbA1c 9%), persisting post-discontinuation on September 1, 2025, despite metformin and empagliflozin. We posit that semaglutide may precipitate acute sarcopenia via unexpected GLP-1R-mTOR-satellite cells axis crosstalk, disrupting AMPK-mTOR balance to suppress anabolic mTORC1/IGF-1 signaling (potentially by 25-35%) while enhancing catabolic FOXO/ubiquitin-proteasome and excessive autophagy pathways. This could extend to myokine reprogramming (elevated myostatin/GDF15, reduced irisin/IL-15), glucagon/α-cell compensation inducing hyperglucagonemia (15-25% rise), microbiome-bile acid shifts fostering low-grade inflammation (IL-6/TNF-α upregulation by 10-15%), mitochondrial mass reduction (20-25% via AMPK), and NMJ disassembly, collectively impairing muscle as the primary glucose sink (reducing GLUT4-mediated uptake by 35-45%) and initiating a «muscle-glucose feedback loop» with hepatic gluconeogenesis amplification, yielding treatment-resistant hyperglycemia.Supporting evidence from cohorts (e.g., 24-month study showing ASMI/grip strength declines in 432 patients), longitudinal analyses (NMJ degradation with CAF22/NfL elevations in 141 men), secondary trials (9.3% psoas volume loss in 51 MASLD cases), and case reports (fatigue in a 74-year-old, rhabdomyolysis in a 47-year-old) aligns with this framework, as does in vitro data linking GLP-1 excess to kinesin-1/GLUT4 inhibition and ATP depletion (20-30%). This novel hypothesis underscores sarcopenia's role in GLP-1RA-induced metabolic paradoxes, urging prospective studies on muscle-preserving interventions like resistance training or GLP-1R modulators to refine T2DM paradigms and inspire multidisciplinary research into endocrine-muscle interactions. - Source: PubMed
Publication date: 2026/07/22
Ahmed AmrRodini SharifaAlrubyea FahadAkl Maher - Gluconeogenesis, a dual-purpose pathway in type 2 diabetes mellitus (T2DM), not only synthesizes glucose but also clears metabolic waste via the Cori cycle (lactate recycling through LDH, PC, PEPCK) and Alanine cycle (nitrogen disposal via ALT, GDH, urea cycle), preventing acidosis, ROS accumulation, and ammonia toxicity. Metformin, the cornerstone T2DM therapy, inhibits gluconeogenesis by targeting mitochondrial complex I, elevating AMP/ATP ratios, and activating AMPK-PKCι/λ signaling to repress CREB-CRTC2-driven PEPCK/G6Pase expression, disrupting these cycles. This leads to lactate, pyruvate, and ammonia buildup, triggering pro-inflammatory cascades: HIF-1α stabilization induces IL-6/VEGF, ROS from pyruvate excess activates NF-κB for TNF-α, and ammonia primes NLRP3 inflammasome for IL-1β/IL-18 release, fostering chronic inflammation. Multisystem consequences include musculoskeletal fatigue from ATP deficits, cognitive fog via neuroinflammation, atherosclerosis from endothelial dysfunction, hepatic fibrosis from urea cycle stress, and immune inflammaging impairing macrophage function. Clinical evidence reveals short-term anti-inflammatory benefits (reduced IL-6, CRP) via AMPK and microbiota effects, contrasted by long-term risks like lactic acidosis and neurodegeneration in renal-impaired or elderly patients. This review integrates physiological roles, molecular mechanisms, inflammatory pathways, systemic impacts, and clinical findings, highlighting metformin's dual-edged profile glycemic efficacy versus "inflammatory debt." Researchers are urged to explore precision interventions, such as antioxidants or biomarker-guided dosing, to optimize metformin's pleiotropic potential in T2DM and inflammaging-related disorders, redefining therapeutic paradigms. - Source: PubMed
Publication date: 2026/07/22
Akl MaherAhmed Amr