Epidemic spread of adenovirus type 4-associated acute respiratory disease between U.S. Army installations.

A large outbreak of adenovirus type 4-associated acute respiratory disease (ARD) occurred at Fort Jackson, South Carolina, in 1997. A laboratory-based ARD surveillance program was initiated at Fort Gordon, Georgia, where advanced individual training was heavily populated with Fort Jackson soldiers. Adenovirus type 4 was isolated from 50% of 147 trainees hospitalized with ARD. Most (88%) introduced cases were in trainees from Fort Jackson.

Large, persistent epidemic of adenovirus type 4-associated acute respiratory disease in U.S. army trainees.

In May 1997, a large, persistent epidemic of adenovirus type 4-associated acute respiratory disease began at Fort Jackson, South Carolina, the largest army basic training center. The epidemic lasted until December and declined when vaccine administration resumed. More than 1,000 male and female trainees were hospitalized; 66.1% of those hospitalized had an adenovirus type 4 isolate.

The management of locally advanced carcinoma of the breast by Nolvadex (tamoxifen): a pilot study.

Fifty-one postmenopausal women with locally advanced breast cancer were treated initially by Nolvadex (Tamoxifen, ICI) alone and followed prospectively between 1974 and 1982. Twenty-three patients (40%) showed an objective response to therapy of whom 17 (75%) remain in remission at median follow-up of 36 months. Patients who failed to respond to Nolvadex therapy were treated by radiotherapy which achieved local control in 64%, with 10 months median duration. Nolvadex therapy conveys a good quality lengthy remission to a sizeable minority of patients. The majority of those who fail to respond are satisfactorily managed by radiotherapy.

Autoimmune glomerulotubular nephropathy in mice.

We produced an autoimmune glomerulotubular nephropathy in Swiss-Webster mice using human glomerular antigen in Freund's complete adjuvant. The disease is associated with circulating antibody to both mouse and human glomerular basement membranes (GBM) and tubular basement membranes (TBM). All mouse IgG subgroups are deposited initially in a linear pattern along the GBM and TBM. IgG deposition remains linear, while that of the other subgroups assumes a granular GBM pattern with continued linear TBM deposits. Despite tissue deposition of antibody capable of C-3 fixation, no C-3 is found in vivo along the GMB or TBM, nor is there C-3 fixation in vitro. This appears to be related to spatial limitations of IgG molecule attachment to basement membranes. A unique ultrastructural lesion of the GMB developed, characterized by periodic expansions of the lamina rara externa to form a beaded pattern. Eluate of nephritic kidneys contained all subgroups of IgG, but mainly IgG1 fixed in vitro to mouse kidney and in vivo when injected intravenously into normal mice. Fixation of other IgG subgroups in vivo may have resulted from antibody formation to abnormally formed GBM, thereby accounting for the peculiar ultrastructural findings and tissue fixation characteristics of the eluted immunoglobulin. Abnormal proteinuria without glycosuria or lysozymuria developed in test animals as compared to controls. Our model is similar in certain aspects to previously described models of Stebley nephritis, but differs because of the total involvement of TBMs, unique ultrastructural lesions, and dissimilarity to other reports of this model in mice.

Requirement of functional T-cells in the production of autoimmune glomerulotubular nephropathy in mice.

In order to study T-cell function related to the production of autoimmune nephropathy, we immunized random-bred mice, homozygous athymic nude (nu/nu) mice and heterozygous hairy (nu/+) mice with human glomeruli contained in Freund's complete adjuvant. The random-bred and heterozygous hairy mice developed circulating antibodies to mouse and human kidney and an autoimmune glomerulotubular nephropathy, while the nude mice, even after prolonged immunization, developed neither antibodies nor nephropathy. We therefore concluded that the development of autoimmune glomerulotubular nephropathy in mice requires the presence of functioning T-cells.

Spontaneous glomerular sclerosis in aging Sprague-Dawley rats. I. Lesions associated with mesangial IgM deposits.

The present studies examined the pathogenesis of focal glomerular sclerosis in aging rats. A marked difference in development of the lesion was noted between males and females, and strain variability was an important factor. Increased glomerular basement membrane permeability with loss of selectivity unrelated to changes in glomerular sialoprotein occurred with aging and was accompanied by increasing proteinuria. Noncomplement-fixing mesangial deposits of rat IgM were present after 1 month of age and were also found in lesser amounts in germfree rats. Fluoresceinated eluates of rat kidneys did not have antibody activity against rat serum or tissue antigens. There was no evidence for a pathogenetic role of IgM deposits. Rat IgG, IgA, IgE, C3, and fibrin were occasionally found in sclerotic areas. Analysis of multiple histologic sections revealed a close correlation between aging and glomerular pathology, with a poor correlation between tubular damage and aging. Glomerular damage appeared to be the initial event leading to tubular damage. Indirect evidence suggests that a relative thymic deficiency may play an important role in the pathogenesis of the lesion.