Lost human capital from early-onset chronic depression.

OBJECTIVE: Chronic depression starts at an early age for many individuals and could affect their accumulation of "human capital" (i.e., education, higher amounts of which can broaden occupational choice and increase earnings potential). The authors examined the impact, by gender, of early- (before age 22) versus late-onset major depressive disorder on educational attainment. They also determined whether the efficacy and sustainability of antidepressant treatments and psychosocial outcomes vary by age at onset and quantified the impact of early- versus late-onset, as well as never-occurring, major depressive disorder on expected lifetime earnings. METHOD: The authors used logistic and multivariate regression methods to analyze data from a three-phase, multicenter, double-blind, randomized trial that compared sertraline and imipramine treatment of 531 patients with chronic depression aged 30 years and older. These data were integrated with U.S. Census Bureau data on 1995 earnings by age, educational attainment, and gender. RESULTS: Early-onset major depressive disorder adversely affected the educational attainment of women but not of men. No significant difference in treatment responsiveness by age at onset was observed after 12 weeks of acute treatment or, for subjects rated as having responded, after 76 weeks of maintenance treatment. A randomly selected 21-year-old woman with early-onset major depressive disorder in 1995 could expect future annual earnings that were 12%-18% lower than those of a randomly selected 21-year-old woman whose onset of major depressive disorder occurred after age 21 or not at all. CONCLUSIONS: Early-onset major depressive disorder causes substantial human capital loss, particularly for women. Detection and effective treatment of early-onset major depressive disorder may have substantial economic benefits.

A reexamination of aluminum in Alzheimer's disease: analysis by energy dispersive X-ray microprobe and flameless atomic absorption spectrophotometry.

We have attempted to verify the presence of increased aluminum (Al) levels in Alzheimer's disease (AD) brains by energy dispersive X-ray microanalysis (EDX) and flameless atomic absorption spectrophotometry (AAS). Tissue from seven AD brains, mounted on carbon polymerized coverslips, were stained with Congo-red or treated immunohistochemically to allow optical localization of AD-associated lesions during EDX. Despite a demonstrated sensitivity of 20-25 ppm, we were unable to detect Al in either plaque cores or neurons containing neurofibrillary tangles. For AAS, wet weight samples (ranging from 48-144 mg) from six of the seven AD brains and four controls were selected from regions similar to those studied under EDX, i.e., Brodmann areas 9, 11, 28, 46, 47, and the hippocampus. The tissue surrounding each sample site was sectioned and stained for thioflavin S. Both controls and AD samples revealed similar levels of Al ranging from undetectable to 1.80 ng/mg wet wt. (mean AD: 0.28 +/- 0.39 (SD), control: 0.54 +/- 0.58 (SD], independent of degree of histopathology or age of the case. We conclude that the combined strengths of these two techniques on similar tissue specimens demonstrate that abnormal Al levels are not required to produce the histologic findings of AD and that this element may not accumulate in the aging brain. It is unlikely, therefore, that Al is essential in the etiology of pathogenesis of plaques and tangles in AD. Al's role as a primary or secondarily associated event, when present, needs further delineation.

Matrix modifiers in graphite furnace atomic absorption analysis of trace lithium in biological fluids.

The use of KH2PO4/NH4NO3 as matrix modifier eliminates severe interference effects on the atomic absorption analysis of lithium in biological fluids. This enables determination of trace lithium in microliter size samples with absolute sensitivity (0.0044 absorbance) of 2 pg. There is no requirement for standard additions experiments to correct for interferences in specific matrices such as serum and saliva. The biological half-life of trace lithium was 16.9 +/- 2.8 h. Saliva lithium is a good estimate of serum level; the two are highly correlated (r = 0.97) and saliva level is about three times serum.

Plasma aluminum is bound to transferrin.

Aluminum ion is bound to at least one of the two specific iron binding sites of serum transferrin and also to serum albumin, as shown by in vivo competition studies with 67-Ga, gel filtration chromatography and ultraviolet difference spectroscopy. Binding of aluminum to transferrin requires CO2 and therefore involves a specific iron site. Samples of commercial transferrin contained large amounts of aluminum. Aluminum may cause anemia by entering pathways of iron distribution and metabolism.

Aluminum levels in brain in Alzheimer's disease.

In both human Alzheimer's disease and aluminum encephalopathy of animals, changes are observed in neurofibrillary structures. We have found that brains from Alzheimer patients contain approximately 1.4 times the aluminum level found in a control series. Some possible methodological problems are discussed. We have proposed a plausible chemical mechanism for the changes of aluminum encephalopathy.

Chronic proliferative arthritis of mice induced by Mycoplasma arthritidis. II. Serological responses of the lost and effect of vaccines.

Complement-fixing antibodies were first detected in mice 7 days after intravenous injection with Mycoplasma arthritidis. Peak titers were observed at 21 days, and high levels of antibody persisted through 293 days. The metabolism-inhibiting antibody response was minimal. On fractionation of mouse sera, only 7S antibody was detected which first appeared at 12 days after injection and persisted throughout the experiment. In contrast, serum taken from rats injected with M. arthritidis contained predominantly 19S antibodies in the early stages of the disease which were gradually replaced with 7S antibodies. The intravenous injection of mice with M. arthritidis culture supernatant fluid had no effect upon their subsequent susceptibility to the arthritogenic effects of M. arthritidis, but this procedure appeared to delay the onset of abscess formation after the subcutaneous injection of M. arthritidis. Formalin-killed cells of M. arthritidis partially protected mice against the arthritis induced by M. arthritidis. Previous infections with M. arthritidis conferred partial immunity against the arthritogenic effects of the organism. Serum taken from convalescent mice at 41 days had a partial protective effect when used to immunize passively normal mice against M. arthritidis. However, rabbit anti-M. arthritidis serum which possessed higher complement-fixing and metabolism-inhibiting antibodies was without significant protective properties.