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The clinical, laboratory, and radiologic improvement due to siltuximab treatment in idiopathic multicentric Castleman's disease.

Idiopathic multicentric Castleman disease (iMCD) comprises approximately 30% of all cases of Castleman disease. It is characterized by constitutional symptoms, enlarged lymph nodes at multiple anatomical sites, and laboratory test abnormalities, which are primarily related to the overproduction of interleukin 6 (IL-6). Siltuximab is a human-mouse chimeric immunoglobulin G1κ monoclonal antibody against human IL-6. In view of the limited treatment options for iMCD, this study aimed to evaluate the efficacy and safety of siltuximab in the management of this condition.

1891 related Products with: The clinical, laboratory, and radiologic improvement due to siltuximab treatment in idiopathic multicentric Castleman's disease.



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A lack of role for antibodies in regulating Helicobacter pylori colonization and associated gastritis.

Helicobacter pylori occupy a unique niche, located within the mucus layer lining the stomach, and attached to the apical surface of the gastric epithelium. As such, antibodies would be expected to play a major role in regulating infection and/or pathogenesis. However, experiments using antibody-deficient mice to study gastric helicobacter infection have yielded inconsistent results, although some pointed toward antibodies increasing colonization levels and decreasing gastritis severity. The variability in these studies is possibly due to their use of nonmatched wild-type controls. This current study presents the first evaluation of the role of antibodies in H pylori infection by comparing antibody-deficient mice with matched wild-type siblings.

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In Vivo Administration of Splice Switching PNAs Using the mdx Mouse as a Model System.

Duchenne muscular dystrophy (DMD) is the most common and severe form of muscular dystrophy and is caused by gene mutations that abolish production of functional dystrophin muscle protein. A promising new treatment exploits specifically targeted RNA-acting drugs that are able to partially restore the dystrophin protein. The mdx mouse model (animal model of DMD) serves as a good in vivo model for testing these antisense drugs. The simplest in vivo test, which circumvents the systemic circulation, is intramuscular administration of the compound. After 7 days it is possible to detect exon skipping by reverse transcriptase PCR, and newly synthesized dystrophin-positive fibers by immunohistochemistry and western blotting. All muscles, including the heart, are affected by the disease and must be treated. Therefore the use of antisense therapy for treatment of DMD requires systemic administration, and the model is also useful for systemic administration.

2643 related Products with: In Vivo Administration of Splice Switching PNAs Using the mdx Mouse as a Model System.

Directed In Vivo Angiogen Mouse Anti-Insulin-Like G Goat Anti-Human, Mouse As Goat Anti-Human, Mouse, R Mouse Anti-Influenza-A HA Mouse anti-human type II Rat monoclonal anti mouse FDA Standard Frozen Tissu Goat Anti-Human, Mouse FH Caspase 8 Inhibitor Drug Mouse Anti-Human Insulin Mouse anti-human type II

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CD82-TRPM7-Numb signaling mediates age-related cognitive impairment.

Aging is a crucial cause of cognitive decline and a major risk factor for Alzheimer's disease (AD); however, AD's underlying molecular mechanisms remain unclear. Recently, tetraspanins have emerged as important modulators of synaptic function and memory. We demonstrate that the level of tetraspanin CD82 is upregulated in the brains of AD patients and middle-aged mice. In young adult mice, injection of AAV-CD82 to the hippocampus induced AD-like cognitive deficits and impairments in neuronal spine density. CD82 overexpression increased TRPM7 α-kinase cleavage via caspase-3 activation and induced Numb phosphorylation at Thr346 and Ser348 residues. CD82 overexpression promoted beta-amyloid peptide (Aβ) secretion which could be reversed by Numb T346S348 mutants. Importantly, hippocampus-related memory functions were improved in Cd82 mice. Taken together, our findings provide the evidence that links the elevated CD82-TRPM7-Numb signaling to age-related cognitive impairment.

2883 related Products with: CD82-TRPM7-Numb signaling mediates age-related cognitive impairment.

GPCR Signaling to MAPK ER 1 Methylindole 3 carboxal 2' Deoxyuridine 5' monoph 1,4 Benzenediboronic acid IHC Related Reagent Citra 1 Phenylsulfonylindole 3 (S) 3 Hydroxybutyric acid 2 Bromo 3 trifluoromethyl Benzeneseleninic anhydrid 1 Ethyl 4 piperidone CAS Cyclopropylamine CAS Numb D Tyrosine CAS Number [55

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