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1.
Clin Rheumatol ; 39(4): 1237-1240, 2020 Apr.
Article in English | MEDLINE | ID: mdl-31396836

ABSTRACT

OBJECTIVE: To evaluate the effectiveness of power Doppler ultrasound (US) in assessing the temporomandibular joint (TMJ) involvement in juvenile idiopathic arthritis (JIA) patients using contrast-enhanced magnetic resonance imaging (MRI) as the reference standard. METHODS: We evaluated the US and MRI examinations of the TMJs from 92 JIA patients. These exams were done and scored for inflammatory activity on the same date. RESULTS: There were considerable differences between the US and MRI findings, with MRI detecting more effectively the TMJ involvement. No association was found between synovial inflammation obtained using power Doppler US to assess synovial vascularity determined by US images and synovial enhancement determined by MRI images. US had very poor sensitivity and very low positive predictive value to detect TMJ arthritis in JIA patients compared with MRI as the reference standard. CONCLUSIONS: Power Doppler US cannot replace MRI for the detection of TMJ inflammatory involvement in JIA patients.Key Points• The early diagnosis of TMJ involvement in JIA patients is very important in order to prevent disturbances in the mandibular growth.• Power Doppler US could be a useful diagnostic tool as a screening exam to identify inflammatory activity in this joint.• However, power Doppler US did not show to have this function and cannot replace MRI for the detection of TMJ inflammatory involvement in JIA patients.


Subject(s)
Arthritis, Juvenile/diagnostic imaging , Temporomandibular Joint Disorders/diagnostic imaging , Ultrasonography, Doppler , Adolescent , Arthritis, Juvenile/complications , Child , Child, Preschool , Female , Humans , Magnetic Resonance Imaging , Male , Temporomandibular Joint/anatomy & histology , Temporomandibular Joint/pathology , Temporomandibular Joint Disorders/etiology , Young Adult
3.
Life Sci ; 57(15): PL199-204, 1995.
Article in English | MEDLINE | ID: mdl-7674824

ABSTRACT

Exposure of LLC-PK1 cells to low micromolar concentrations of Cd2+ for 1-4 hours causes the disruption of the adhering and occluding junctions between the cells, whereas exposure to higher concentrations of Cd2+ for longer periods of time causes more severe toxic effects and cell death. The objective of the present studies was to determine whether or not the junctional effects of Cd2+ might be a consequence of apoptotic injury. LLC-PK1 cells on cell culture inserts were exposed to either Cd2+ or tumor necrosis factor (TNF-alpha) plus cycloheximide, a treatment that has recently been shown to cause apoptosis in LLC-PK1 cells. The results showed that at the time the Cd2(+)-induced junctional changes were occurring, there was no increase in the number of apoptotic cells or evidence of DNA fragmentation. By contrast, TNF-alpha plus cycloheximide induced changes that were characteristic of apoptosis. These results indicate that the disruption of intercellular junctions by Cd2+ in the LLC-PK1 cell line occurs independently of apoptosis.


Subject(s)
Apoptosis/drug effects , Cadmium/pharmacology , Intercellular Junctions/drug effects , LLC-PK1 Cells/drug effects , Animals , Cell Line , LLC-PK1 Cells/cytology , Swine , Tumor Necrosis Factor-alpha/pharmacology
4.
Life Sci ; 53(20): PL337-42, 1993.
Article in English | MEDLINE | ID: mdl-8412516

ABSTRACT

Recent studies have shown that ionic cadmium (Cd2+) can selectively damage the tight junctions between LLC-PK1 cells. The objective of the present studies was to determine if cadmium that is bound to metallothionein (Cd-Mt) can also damage the junctions between these cells. Cells on Falcon Cell Culture Inserts were exposed to Cd2+ or Cd-Mt from the apical and basolateral compartments. The integrity of cell junctions was assessed by monitoring the transepithelial electrical resistance, and cell viability was evaluated by monitoring the release of lactate dehydrogenase into the medium. Exposure to Cd2+ for 1-4 hours caused a pronounced decrease in the transepithelial resistance without affecting cell viability. By contrast, exposure to Cd-Mt had little effect on the electrical resistance until the cells began to die, which did not occur until 24-48 hours of exposure. Additional results showed that the cells accumulated Cd2+ more rapidly than Cd-Mt. These results indicate that Cd-Mt does not damage the junctions between LLC-PK1 cells, but that it can kill the cells after prolonged exposure.


Subject(s)
Cadmium/toxicity , Chlorides/toxicity , Kidney/cytology , Kidney/drug effects , Metallothionein/toxicity , Animals , Cadmium/pharmacokinetics , Cadmium Chloride , Cell Line , Cell Survival/drug effects , Chlorides/pharmacokinetics , Epithelial Cells , Epithelium/drug effects , Epithelium/metabolism , Gap Junctions/drug effects , Kidney/metabolism , Membrane Potentials/drug effects , Metallothionein/pharmacokinetics , Rabbits , Swine
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