PubMed · 8127378
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
D Pranger. 1994-02-19. [Continuous vegetative state].. https://pubmed.ncbi.nlm.nih.gov/8127378/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Comparative genomic hybridization analysis was used to identify chromosomal imbalances in 20 non-small cell lung carcinoma (NSCLC) biopsies and cell lines. The chromosome arms most often overrepresented were 3q (85%), 5p (70%), 7p (65%), and 8q (65%), which were observed at high copy numbers in many cases. Other common overrepresented sites were 1q, 2p, and 20p. DNA sequence amplification was often observed, with the most frequent site being 3q26 (six cases). Other recurrent sites of amplification included 8q24, 3q13, 3q28-qter, 7q11.2, 8p11-12, 12p12, and 19q13.1-13.2. The most frequent underrepresented segment was 3p21 (50%); other recurrent sites of autosomal loss included 8p21-pter, 15q11.2-13, 5q11.2-15, 9p, 13q12-14, 17p, and 18q21-qter. These regions of copy number decreases are also common sites of allelic loss, further implicating these sites as locations of tumor suppressor genes. Although some of the overrepresented segments harbor known or suspected oncogenes/growth-regulatory genes, we have identified 3q and 5p as new sites that are very frequently overrepresented in NSCLC. These findings could represent entry points for the identification of novel amplified DNA sequences that may contribute to the development or progression of NSCLC.
The purpose of this study was to analyze the role of total prostate-specific-antigen (PSA) and free-PSA levels in the diagnosis and clinical staging of prostate cancer. We determined total-PSA serum concentration and free-PSA percentage in 352 patients, 234 with benign prostatic hyperplasia (BPH) and 118 with prostate cancer. Clinical stage of patients with prostate cancer was T1 N0 M0 in 17, T2 N0 M0 in 27, T3-4 N0 M0 in 34 and T1-4 N0-3 M0-1 in 40. Median total-PSA serum concentration was 3.1 ng/ml in patients with BPH and 26.9 ng/ml in patients with prostate cancer, p < 0.0001. Median free-PSA level was 16.7% in patients with BPH and 8.1% in patients with prostate cancer, p < 0.0001. A cutpoint of 4.0 ng/ml detected 96.6% of the prostate cancer, but the percent rate of negative biopsies was 42.1%. For a free-PSA level of 25% in patients with total PSA greater than 4.0 ng/ml, the sensitivity was 97.4%, and the decrease in negative biopsies was 21%. Median total-PSA serum concentration in patients with prostate cancer according to clinical stage was 8.9 ng/ml for T1 N0 M0, 12.9 ng/ml for T2 N0 M0, 29.9 ng/ml for T3-4 N0 M0 and 317 ng/ml for T1-4 N1-3 M0-1, p < 0.001. Median free-PSA levels were 10.1%, 8.1%, 8.4% and 6.1% respectively, p > 0.05. According to the Gleason score, median total-PSA serum concentration was 10.6 ng/ml in patients between 2 and 4, 22.3 ng/ml between 5 and 7 and 77.0 ng/ml between 8 and 10, p < 0.05. Free PSA levels were 7.7%, 8.7% and 6.6% respectively, p > 0.05. Determination of percentage of free PSA appears to be a helpful method for enhancing the specificity of total PSA. A cutpoint of 25% could detect more than 95% of prostate cancers and avoid 21% of negative biopsies in patients with total PSA above 4.0 ng/ml. However, this parameter does not provide additional information about the clinical staging of prostate cancer.
BACKGROUND: Rejection after pancreas-kidney transplantation may occur isolated or concurrently in both grafts. To get more insight into the cellular mechanisms underlying these rejection episodes, we compared the functional characteristics of pancreas and kidney graft-infiltrating T cells. METHODS: Graft-infiltrating T cell (GIC) lines were cultured from simultaneously taken pancreas and kidney biopsies from eight patients. CD4 to CD8 ratios were determined by fluorescence-activated cell sorter and cytotoxicity toward donor proximal tubular epithelial cells (PTEC) and donor spleen cells (DSC) using a standard cytotoxicity assay. Cytokine production was determined by enzyme-linked immunosorbent assay. RESULTS: CD4 to CD8 ratios were comparable between the pancreas and kidney lines for each patient, but differences were observed in cytotoxicity toward PTEC and DSC. For four of eight patients, the lysis of PTEC by pancreas GIC was less than the lysis induced by kidney GIC. This was also seen in three of five patients for lysis of DSC. The specificity of GIC lines toward mismatched donor antigens was studied for two patients and appeared to be comparable for pancreas and kidney. Most GIC lines produced interferon (IFN)-gamma (75.5+/-22.7 pg/ml), but no IL-10, indicating that the cell lines consisted primarily of Th1 and type 1 CD8+ cells. Mean production of IL-6 was 465.6+/-193.6 pg/ml. No major differences were observed between kidney and pancreas GIC for either cytokine. CONCLUSIONS: We conclude that pancreas and kidney GIC lines have the same phenotype, cytokine production, and allospecificity. Differences were, however, seen for lysis of PTEC and DSC, suggesting that tissue-specific antigens might play a role.