Prostate-specific antigen in screening for prostate cancer.
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Biomedical subjects
Publications and source records attributed to F J Mayer.
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Those involved in prostate cancer treatment are often frustrated by the surfeit of careful comparative studies. This frustration is also true in the field of recurrent prostate cancer, where no randomized studies comparing competing treatment methods have been attempted. With an increasing number of men undergoing treatment of localized disease and more sensitive methods of detecting or predicting local failure, a large pool of men suffering failure after attempted cure will soon exist. If any firm conclusions are to be advanced in the management of recurrent prostate cancer, then large randomized comparative trials must be initiated now. New paradigms in thinking about prostate cancer must be developed in order to account for the advancements in prostate sciences in the past 10 years. Serially sectioning of radical prostatectomy specimens with whole-mount evaluation has disclosed an alarming rate of microscopic extraprostatic disease. The sensitivity of serum PSA in detecting microscopic locally recurrent disease has revolutionized the diagnosis of this stage of prostate cancer. Analysis of the DNA ploidy of tumors now provides new prognostic information apart from grade and stage of the primary lesion, and this technique should be used to stratify treatment groups whenever feasible. Carefully designed, multi-institutional studies would prospectively evaluate the benefit of early endocrine therapy versus delayed therapy versus radiation therapy in patients with the earliest stage of advanced prostate cancer--pathologic stage C2 or C3 disease. A prospective study of endocrine therapy versus radical prostatectomy and endocrine therapy should be attempted in patients with pathologic D1 prostate cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
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Laser light energy has been shown in other studies to degrade resins by thermal softening, thermal ablation, or photoablation. If this technology could be successfully applied to bracket debonding, fracturing of both bracket and enamel during debonding might be eliminated. Both polycrystalline alumina and single crystal alumina (sapphire) ceramic orthodontic brackets were bonded to the labial surfaces of lower deciduous bovine incisor teeth with the acid-etch technique as currently practiced in dentistry. Under an externally applied stress of either zero or 0.8 MPa, the brackets were debonded by irradiating the labial surfaces of the brackets with laser light at wavelengths of 248 nm, 308 nm, and 1060 nm, and at light power densities of between about 3 and 33 W/cm2. Debonding times were measured, and the surfaces created by debonding were examined with both light and scanning electron microscopy to determine the extent of bracket and enamel damage. The results showed that under the conditions of this study, no enamel or bracket damage was present in any sample. The polycrystalline brackets debonding times were about 3 seconds, 5 seconds, and 24 seconds for 248 nm, 308 nm, and 1060 nm of radiation, respectively. The debonding of polycrystalline brackets is caused by thermal softening of the bonding resin resulting from heating of the bracket. The hot bracket then slides off the tooth. All sapphire brackets debonded in less than 1 second. At sufficiently high power levels, debonding of sapphire brackets is caused by either thermal ablation or photoablation resulting from direct interaction of the light beam with the resin.(ABSTRACT TRUNCATED AT 250 WORDS)
We measured levels of protein, of complement-derived anaphylatoxins (C3a, C4a, and C5a), and of the lymphokines interleukin-2 and gamma interferon, in vitreous humor from 10 AIDS patients with vitritis and retinitis (group 1). We compared these measurements with levels in vitreous from 7 patients with vitritis but without AIDS (group 2), 10 patients with vitreous hemorrhages (group 3), and 20 patients with retinal detachments or epiretinal membranes without clinical evidence of vitreal inflammation (group 4). Vitreous humor from 10 AIDS patients had measurable levels of interleukin-2 in three of nine samples, gamma interferon in six of nine samples, C3a and C4a in all ten samples, and C5a in only one of ten samples. Vitreous humor from group 1 did not differ significantly from vitreous from group 2. On the other hand, vitreous from group 1 had significantly higher levels of gamma interferon, C3a, and C4a, and higher ratios of these anaphylatoxins to protein, in comparison to vitreous in groups 3 and 4. The results of this study suggest that vitreous humor from AIDS patients with retinitis contains activated complement and may contain interleukin-2 and gamma interferon. Viral retinitis is associated with the presence of lymphokines in vitreous humor. Additionally, anaphylatoxin and gamma interferon levels, but not interleukin-2 levels, correlate with vitreal inflammation. This is the first study to measure interleukin-2, gamma interferon, and C5a levels in human vitreous humor.
The authors investigated the ability of recombinant human gamma-interferon (rhIFN-gamma) to influence production of complement and expression of human leukocyte antigens (HLA) by human scleral fibroblasts in culture. Cell cultures were established by explanting sclera from normal human donor eyes. To study complement production, fibroblasts were treated with 500 units/ml rhIFN-gamma in cell culture, and media were tested for complement components by hemolytic assay after 0, 1, 3, 6, 9, and 11 days. To induce Class II HLAs, fibroblasts were exposed to rhIFN-gamma at concentrations ranging from 10-500 units/ml and incubated for 1, 3, and 6 days. The HLAs were detected by immunofluorescence in conjunction with flow cytometry. Class I antigen was detected using a monoclonal antibody directed against beta 2-microglobulin. Class II histocompatibility antigens were identified using monoclonal antibodies specific for HLA-DR, -DP, and -DQ. Although complement component C1 was produced constitutively in cell culture, the addition of rhIFN-gamma resulted in an increase in production. Complement components C2 and C4 were detected only after treatment with rhIFN-gamma. Complement production was completely inhibited by cycloheximide, and C3, C5, C6, and C7 were not present in cell culture media with or without rhIFN-gamma. Class I antigen was present on all cells before induction, and an increase in expression was noted after exposure to rhIFN-gamma. Class II antigens were absent before induction with rhIFN-gamma. After treatment with rhIFN-gamma, scleral fibroblasts expressed HLA-DR, -DP, and -DQ in a dose-dependent, time-related fashion. These findings suggest that rhIFN-gamma has multiple effects on scleral fibroblasts: (1) increased production of C1, (2) production of C2 and C4, (3) up-regulation of Class I antigen expression, and (4) expression of Class II antigens. They also suggest that scleral fibroblasts have the potential to participate in immunologic diseases of the eye.
In the present study, we compared hemolytic activities of C1, C4, C2, C3, C5, C6 and C7 in the anterior and posterior sclera. Additionally, we used radial immunodiffusion to measure levels of Factor B, IgG, IgA and albumin in the anterior and posterior sclera. Except for C1, complement levels were significantly higher in the posterior than anterior sclera. Additionally, levels of immunoglobulins as well as albumin were significantly higher in the posterior than anterior sclera. These results suggest that the posterior sclera has a better adjacent vascular supply than the anterior sclera. On the other hand, the results of this study show that the anterior sclera has more C1, the recognition unit of the classical pathway, than the posterior sclera. Because there is nearly twice as much C1 in the anterior sclera, it may be easier for antigen-antibody complexes, whether formed in the sclera itself or derived from the neighboring vessels, to set off the complement cascade in the anterior sclera. This finding may help explain why scleritis associated with immune complex disease is more common in the anterior than posterior sclera.
Sclera from donor globes was eluted in phosphate-buffered saline at 4 degrees C for 24 hr. Hemolytic assays were used to measure functional C1, C4, C2, C3, C5 and C6 in scleral eluates. Radial immunodiffusion was used to measure Factor B, a component of the alternative complement pathway, and albumin in scleral eluates. Molecular weight appeared to be a factor in determining the hemolytic activities of complement components C1-C6 in the sclera, because complement components with higher molecular weights had lower percentages of hemolytic activity in sclera relative to serum, while complement components with lower molecular weights had higher levels of hemolytic activity in sclera relative to serum. The sclera contains complement which could be activated by immune complexes that may be important in the pathogenesis of scleritis.
This is a report on a case of peripheral paralysis of the right side of the larynx. The patient was a 34 year-old male who became completely aphonic following a grippal infection. After 3 weeks of conventional treatment by a well-known specialist, he underwent acupuncture treatment. After 4 months the voice was again normal; however, the laryngoscopy showed a completely normal larynx only 7 months after the illness. The loci used and the reasons for their selection are discussed in detail. The second case was a 62 year-old male with facial paralysis. This patient underwent acupuncture treatment shortly after he was stricken. After 6 days distinct improvement was seen; he was completely healed after 2 months. The loci and the reasons for their selection are discussed. The cases are compared.