The role of osmic acid in the treatment of immune synovitis

Thirty-seven New Zealand rabbits were observed for up to 1 year after their knee joints were instilled with 1 ml of 1% osmic acid. A selective destruction of synovial lining cells occurred with a concurrent synovitis, but lining cell regenerated by the eighth week. Nonprogressive abnormalities were also present in the cartilage. When an immune synovitis was induced in both knees of 16 rabbits, the osmic acid treated joint demonstrated a significantly greater synovitis and progressive aberrations compared to the untreated knee.     

Physical Examinations and Industrial Productivity

Forty-two workers from a chemical plant producing inorganic mercury compounds were evaluated for neurologic, nephrotic, and ophthalomogic toxicity. Despite elevated blood and urinary mercury levels, routine clinical testing such as physical examination, blood chemistries, and urinalysis were generally normal. These findings from the routine examination are in contrast to the complaints of neuropsychological symptoms, elevated urinary n-acetyl B-D-glucosaminidase (NAG) levels, decreased motor nerve conduction velocities, and the presence of lenticular opacities on slit-lamp examination that were found, when organ systems known to be affected by mercury were targeted. More sensitive but objective indicators of toxicity need to be included in routine medical screening so as to help diagnose the etiology of neuropsychological symptoms and prevent long-term sequelae in workers exposed to mercury.     

Preliminary Evidence for Subdimensions of Geriatric Frailty: The MacArthur Study of Successful Aging

OBJECTIVES: To identify frailty subdimensions. DESIGN: Longitudinal cohort (MacArthur Study). SETTING: Three U.S. urban centers. PARTICIPANTS: One thousand one hundred eighteen high‐functioning subjects aged 70 to 79 in 1988. MEASUREMENTS: Participants with three or more of five Cardiovascular Health Study (CHS) frailty criteria (weight loss, weak grip, exhaustion, slow gait, and low physical activity) in 1991 were classified as having the CHS frailty phenotype. To identify frailty subdimensions, factor analysis was conducted using the CHS variables and an expanded set including the CHS variables, cognitive impairment, interleukin‐6 (IL‐6), C‐reactive protein (CRP), subjective weakness, and anorexia. Participants with four or more of 10 criteria were classified as having an expanded frailty phenotype. Predictive validity of each identified frailty subdimension was assessed using regression models for 4‐year disability and 9‐year mortality. RESULTS: Two subdimensions of the CHS phenotype and four subdimensions of the expanded frailty phenotype were identified. Cognitive function was consistently part of a subdimension including slower gait, weaker grip, and lower physical activity. The CHS subdimension of slower gait, weaker grip, and lower physical activity predicted disability (adjusted odds ratio (AOR)=1.7, 95% confidence interval (CI)=1.3–2.2) and mortality (AOR=1.5, 95% CI=1.3–1.8). Subdimensions of the expanded model with predictive validity were higher IL‐6 and CRP (AOR=1.2 for mortality); slower gait, weaker grip, lower physical activity, and lower cognitive function (AOR=1.8 for disability; AOR=1.5 for mortality), and anorexia and weight loss (AOR=1.2 for disability). CONCLUSION: This study provides preliminary empirical support for subdimensions of geriatric frailty, suggesting that pathways to frailty differ and that subdimension‐adapted care might enhance care of frail seniors.