Anti-Human CD54 Monoclonal antibody (CABT-L4364) Functional Grade

Mouse Anti-Human CD54 (ICAM-1) Monoclonal antibody for IF

Specifications


Host Species
Mouse
Antibody Isotype
IgG2a
Clone
R6-5-D6
Species Reactivity
Human
Immunogen
EBV transformed lymphoblast cell line
Conjugate
Functional Grade

Target


Alternative Names
ICAM1; intercellular adhesion molecule 1; CD54; ICAM; ICAM-1

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References


Evaluation of the angiogenic potency of a novel exopolysaccharide produced by the MK1 bacterial strain

ARCHIVES OF PHARMACAL RESEARCH

Authors: Park, Ji-Yun; Kim, Beom Su; Lee, Jun

Angiogenesis is an essential physiological step in wound healing and other regenerative processes. Here, we evaluated the angiogenic properties of an exopolysaccharide (EPS) secreted by MK1 (MK1-EPS), a novel bacterial strain isolated from Neungee mushrooms. MK1-EPS significantly increased human umbilical vein endothelial cell (HUVEC) proliferation, migration, and vascular tube formation. MK1-EPS enhanced the phosphorylation of extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and p38, which are mitogen-activated protein kinases. In addition, the expression of p21 and intercellular adhesion molecule 1 (ICAM1), and phosphorylation of signal transducer and activator of transcription 3 (STAT3), but not of protein kinase B (AKT), were increased. Specific inhibitors of p38 (SB203580), ERK (PD98059), and JNK (SP600125) inhibited MK1-EPS-induced HUVEC proliferation, tube formation, and cell migration, and partially attenuated MKI-EPS-induced expression of p21 and ICAM1, and STAT3 phosphorylation. After surgical implantation into rabbit calvarial bone defects, new blood vessel formation was significantly higher with MK1-EPS composite bone granules than with granules alone, and new bone formation increased significantly. Therefore, MK1-EPS induces angiogenesis and may have potential for use as a bone regeneration agent in bone tissue engineering applications.

Risk Factors and Outcomes of Thalidomide-induced Peripheral Neuropathy in a Pediatric Inflammatory Bowel Disease Cohort

INFLAMMATORY BOWEL DISEASES

Authors: Bramuzzo, Matteo; Stocco, Gabriele; Montico, Marcella; Arrigo, Serena; Calvi, Angela; Lanteri, Paola; Costa, Stefano; Pellegrino, Salvatore; Magazzu, Giuseppe; Barp, Jacopo; Ghione, Silvia; Lionetti, Paolo; Zuin, Giovanna; Fontana, Massimo; Di Chio, Teresa; Maggiore, Giuseppe; Lazzerini, Marzia; Lucafo, Marianna; Udina, Chiara; Pellegrin, Maria Chiara; Chicco, Andrea; Carrozzi, Marco; Decorti, Giuliana; Ventura, Alessandro; Martelossi, Stefano

Background: Thalidomide is an effective therapy in children with inflammatory bowel disease refractory to standard treatments, but thalidomide-induced peripheral neuropathy (TiPN) limits its long-term use. We aimed to investigate the risk factors and the outcome of TiPN in children with inflammatory bowel disease. Methods: Within a retrospective multicenter cohort study, we evaluated prevalence and evolution of TiPN. Clinical data and candidate genetic profiles of patients with and without TiPN were compared with detect predisposing factors. Results: One hundred forty-two patients were identified. TiPN was found in 72.5% of patients (38.7% clinical and instrumental alterations, 26.8% exclusive electrophysiological anomalies, and 7.0% exclusive neurological symptoms). Median TiPN-free period of treatment was 16.5 months; percentage of TiPN-free patients was 70.0% and 35.6% at 12 and 24 months of treatment, respectively. The risk of TiPN increased depending on the mean daily dose (50-99 mg/d adjusted hazard ratio 2.62; 95% confidence interval [CI], 1.31-5.21; 100-149 mg/d adjusted hazard ratio 6.16; 95% CI, 20.9-13.06;.150 mg/d adjusted hazard ratio 9.57; 95% CI, 2.6-35.2). Single nucleotide polymorphisms in ICAM1 (rs1799969) and SERPINB2 (rs6103) genes were found to be protective against TiPN (odds ratio 0.15; 95% CI, 0.03-0.82 and 0.36; 95% CI, 0.14-0.88, respectively). TiPN was the cause of drug suspension in 41.8% of patients. Clinical symptoms resolved in 89.2% of cases, whereas instrumental alteration persisted in more than half of the patients during a short follow-up. Conclusions: In children with inflammatory bowel disease, TiPN is common but mild and generally reversible. Cumulative dose seems to be the most relevant risk factor, whereas polymorphisms in genes involved in neuronal inflammation may be protective.

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