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1.
Pediatr Radiol ; 51(13): 2492-2497, 2021 12.
Article in English | MEDLINE | ID: mdl-34435223

ABSTRACT

BACKGROUND: Gastrojejunal tubes are important feeding devices for children with gastro-esophageal reflux, allowing medication and feeding into the small bowel, and allowing gastric venting to prevent reflux. As with many medical devices, there are multiple manufacturers and designs, including balloon-retained tubes and disc-retained tubes. OBJECTIVE: This study evaluated the cost difference between these two types of gastrojejunal tube. MATERIALS AND METHODS: We conducted a 3.5-year retrospective cost evaluation for all pediatric patients undergoing an insertion or change of gastrojejunal tube using a bottom-up micro-costing analysis. We calculated days between encounters and a subsequent cost per day for each patient. RESULTS: A total of 187 children and adolescents were included, with an average age of 9.2 years. They underwent a total of 1,240 encounters, an average of 6.6 encounters per patient during the study period. A total of 82% of these encounters were related to balloon-retained tubes and 18% to disc-retained tubes. The most common reason for an encounter was a routine change (57%), with mechanical complications accounting for 31%. Disc-retained tubes had a longer period between encounters (117.5 days) than balloon-retained tubes (95 days; P=0.038). However, disc-retained tubes cost 6.9 British pound sterling (GBP) per day, which was significantly higher than balloon-retained tubes at 5.2 GBP per day (P<0.0001). CONCLUSION: Despite being more expensive to purchase, balloon-retained tubes were noted to be the least costly device in a cost-per-day analysis.


Subject(s)
Enteral Nutrition , Gastroesophageal Reflux , Adolescent , Child , Gastrostomy , Humans , Intubation, Gastrointestinal , Retrospective Studies , Stomach
2.
J Immunol ; 184(12): 6901-9, 2010 Jun 15.
Article in English | MEDLINE | ID: mdl-20488792

ABSTRACT

The activating receptor NKG2D recognizes proteins that are not normally expressed at the surface of most cells but are expressed during a cellular "stress" response (e.g., upon induction of the DNA damage pathway). This establishes recognition of "induced self" as an important strategy for surveillance of infections or tumor transformation. However, NKG2D ligands can also be induced on human macrophages by TLR stimulation, which has been far less studied. In this paper, we clarify that LPS, which ligates TLR-4, preferentially upregulated MICA and not MICB; CL097, which ligates TLR-7/8, upregulated both MICA and MICB; and polyinosinic-polycytidylic acid, which ligates TLR-3, upregulated neither. To probe how LPS stimulation triggers MICA expression, we determined that the stability of MICA mRNA was much longer than that of MICB mRNA, but neither was changed by LPS stimulation. This finding suggests that increased levels of MICA mRNA following LPS stimulation resulted from increased transcription. However, it was not sufficient for surface protein expression, which was controlled posttranscriptionally via a separate pathway involving the ataxia telangiectasia mutated/ataxia telangiectasia and Rad3 related kinases. Moreover, LPS stimulation decreased expression of microRNAs (miRNA)--miR-17-5, miR-20a, and miR-93--which target MICA, implicating a novel role for miRNAs in NKG2D ligand expression. Thus, TLR stimulation allows expression of NKG2D ligands through multiple pathways, including downmodulation of specific miRNAs.


Subject(s)
Killer Cells, Natural/metabolism , Macrophages/metabolism , NK Cell Lectin-Like Receptor Subfamily K/metabolism , Receptor Cross-Talk/immunology , Toll-Like Receptor 4/metabolism , Cell Separation , Flow Cytometry , Gene Expression , Gene Expression Regulation , Histocompatibility Antigens Class I/biosynthesis , Histocompatibility Antigens Class I/immunology , Humans , Killer Cells, Natural/immunology , Macrophages/immunology , NK Cell Lectin-Like Receptor Subfamily K/immunology , RNA, Messenger/analysis , Reverse Transcriptase Polymerase Chain Reaction , Toll-Like Receptor 4/immunology
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