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The H. pylori antibody level was measured in the serum using HM-CAPTM (Enteric Products, Westbury, NY, USA) with an antigen from Japanese (J-HM-CAP).
H. pylori infection was investigated serologically using HM-CAPTM (Enteric Products, Westbury, NY, USA) with antigen from Japanese (J-HM-CAP), and the serum titer of immunoglobulin G antibodies 2.3 or greater was defined as positive infection.
H. pylori infection was evaluated by the presence of serum immunoglobulin G antibody against H. pylori (HM-CAP, Enteric Products, Westbury, NY), a C urea breath test (UBT; with a cut-off value of 2.5‰; Ubit, Otsuka Pharmaceuticals, Tokyo, Japan), and histological examination with toluidine blue staining.
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Despite rapid dissolution in compendial phosphate buffers, gastro resistant (enteric coated) products can take up to 2 h to disintegrate in the human small intestine, which clearly highlights the inadequacy of the in vitro test method to predict in vivo behaviour of these formulations.
For the enteric coated products, exposure to alcohol during the acid stage caused the coating integrity to be compromised and the drug to release earlier than designed.
Formulation selection errors mainly involved enteric coated products.
Not only does this support the use of enteric coated products for treatment of canine EPI, but it emphasises the need to look beyond clinical signs (such as diarrhoea) as evidence of efficacy in this condition.
One such study suggested that enteric-coated products were less effective than uncoated enzyme powders [ 2], although more recent work suggested that there was no difference in response to therapy between dogs on coated and uncoated products [ 3].
The administration of bicarbonate or acid suppressers, preferably proton pomp inhibitors, is often necessary to prevent acid-mediated inactivation of enzymes, although enteric-coated enzyme products are increasingly being used to avoid this problem.
The in vitro drug release behaviour of three enteric coated mesalazine (mesalamine) products is investigated.
Amelioration of these abnormalities by norfloxacin suggests the involvement of enteric bacteria or their products in the triggering of the process.
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