Technetium Tc-99m albumin aggregated kit

Background and objectives A modified aligner appliance with nickel-titanium springs (MAA) is a relatively new appliance that has not received extensive attention in orthodontics. This study evaluated the patient-reported outcomes when orthodontic treatment was provided using a modified aligner appliance to treat mild lower incisor crowding. Materials and methods This prospective cohort study consisted of 42 patients (11 males and 31 females; mean age 21.69 ± 2.56 years) with mild crowding. Twenty-one patients were treated using a modified aligner with nickel-titanium springs, while the remaining patients were treated with a conventional fixed orthodontic appliance (FA). Patient responses regarding pain, discomfort, and difficulty in chewing, swallowing, and speaking were recorded using a visual analog scale (VAS) at six assessment times: 24 hours (T1), two days (T2), three days (T3), two weeks (T4), one month (T5), and two months (T6) after appliance application. Results The mean perceived pain and discomfort levels were generally lower in the traditional fixed appliance (FA) group than the modified aligner appliance with nickel-titanium springs group at most assessment times. However, no statistically significant differences were found between the two groups. Chewing difficulty levels were similar between the two groups with no substantial differences. Swallowing and speech difficulty were significantly higher in the MAA group compared to the FA group during the first two days of treatment (P < 0.008). Conclusions Patients using both types of orthodontic appliances experienced temporary discomfort, including pain and difficulty chewing. While the modified aligners appliance with nickel-titanium springs caused additional challenges with swallowing and speaking, these issues were resolved over time, allowing patients to adjust to the treatment.

The objective of this study is to determine the associations of protein‐specific anti–malondialdehyde‐acetaldehyde (MAA) antibodies with prevalent and incident rheumatoid arthritis–interstitial lung disease (RA‐ILD).

Within a multicenter, prospective cohort of US veterans with RA, RA‐ILD was validated by medical record review of clinical diagnoses, chest imaging, and pathology. Serum antibodies to MAA‐albumin, MAA‐collagen, MAA‐fibrinogen, and MAA‐vimentin (IgA, IgM, and IgG) were measured by a standardized enzyme‐linked immunosorbent assay. Associations of anti‐MAA antibodies with prevalent and incident RA‐ILD were assessed using multivariable regression models adjusting for established RA‐ILD risk factors.

Among 2,739 participants with RA (88% male, mean age of 64 years), there were 114 with prevalent and 136 with incident RA‐ILD (average time to diagnosis: 6.6 years). Higher IgM anti–MAA‐collagen (per 1 SD: adjusted odds ratio [aOR] 1.28, 95% confidence interval [CI] 1.02–1.61), IgA anti–MAA‐fibrinogen (aOR 1.48, 95% CI 1.14–1.92), and IgA (aOR 1.78, 95% CI 1.34–2.37) and IgG (aOR 1.48, 95% CI 1.14–1.92) anti–MAA‐vimentin antibodies were associated with prevalent RA‐ILD. In incident analyses, higher IgA (per one SD: adjusted hazards ratio [aHR] 1.40, 95% CI 1.11–1.76) and IgM (aHR 1.29, 95% CI 1.04–1.60) anti–MAA‐albumin antibody concentrations were associated with increased ILD risk. Participants with IgA (aHR 2.13, 95% CI 1.16–3.90) or IgM (aHR 1.98, 95% CI 1.08–3.64) anti–MAA‐albumin antibody concentrations in the highest quartile had an approximately two‐fold increased risk of incident RA‐ILD. Across all isotypes, anti–MAA‐fibrinogen, anti–MAA‐collagen, and anti–MAA‐vimentin antibodies were not significantly associated with incident RA‐ILD.

Protein‐specific anti‐MAA antibodies to collagen, fibrinogen, and vimentin were associated with prevalent RA‐ILD. IgA and IgM anti–MAA‐albumin antibodies were associated with a higher risk of incident RA‐ILD. These findings suggest that MAA modifications and resultant immune responses may contribute to RA‐ILD pathogenesis.