Comparison of prostate specific antigen,prostate specific membrane antigen,and LNCaP-based enzyme-linked immunosorbent assays in prostatic cancer patients and patients with benign prostatic enlargement

Serum assays for prostate specific antigen (PSA; monoclonal), for prostate specific membrane antigen (PSM; Western blot), and a LNCaP/7E11.C5-based competitive enzyme-linked immunosorbent assay (ELISA) were evaluated in a small number of prostate cancer patients with localized or disseminated disease, and judged to be in clinical progression or remission based on National Prostate Cancer Project (NPCP) criteria. PSA values recognized the presence of clinical progression in localized disease (B₁-C) and to a lesser degree disseminated disease (D₁-D₂). In contrast, to a limited degree the ELISA test recognized clinical progression mainly in disseminated disease and chiefly in stage D₂. PSM values were elevated in both D₁ and D₂ but not in a linear fashion as observed with PSA. The ELISA and PSM results may be assessing a different clinical response to prostatic cancer than that recognized by PSA. This could reflect a developing clone of resistant prostatic cells as previously postulated. To further pursue this possibility a secondary generation of monoclonal antibodies to PSM is being developed. The ELISA levels for benign prostatic enlargement were not elevated above normal. In contrast both with PSA and PSM the assays reflected levels significantly above the normal range in benign prostatic hypertrophy (BPH).     

Expression of blood group A antigens in human bone marrow cells

We have studied the appearance of blood group A-activity during hematopoiesis in human bone marrow cells by the use of the blood group A-specific lectin from Vicia cracca. Cells that bound the lectin were identified using antiserum against the lectin followed by rosetting with protein A-containing Staphylococcus aureus cells. Only cells of the erythroid lineage from blood group A individuals formed staphylococcal rosettes. A-activity occurred in basophilic normoblasts and later stages of erythropoiesis, whereas pronormoblasts were negative. The appearance of blood group A-activity coincided roughly with the onset of hemoglobin synthesis and slightly later than the expression of the major sialoglycoprotein of erythrocytes, glycophorin A. Glycophorin A did not, however, contain blood group A-activity when analyzed by immunoprecipitation and gel electrophoresis.     

Sulfatide as a biochemical marker in cerebrospinal fluid of patients with vascular dementia

The myelin-associated glycosphingolipid sulfatide in cerebrospinal fluid (CSF) was investigated in 20 patients with vascular dementia (VAD), 43 with Alzheimer's disease (AD) and 20 age-matched controls. The sulfatide concentration in the VAD group (307 +/- 118 nmol/l) was significantly (p less than 0.0001) higher than that in controls (145 +/- 86 nmol/l) and the AD group (178 +/- 79 nmol/l). Among the VAD patients, 8/20 had a significantly increased concentration of sulfatide (greater than mean + 2 S.D.), as compared with controls, while only 2/43 of the AD patients had a sulfatide concentration above this level. It is suggested that the elevated concentration of sulfatide in CSF from VAD patients reflects demyelination. Furthermore, sulfatide determinations, when combined with clinical findings, may be of diagnostic value, for discriminating between VAD and AD.     

Markedly elevated serum IgE levels following allogeneic and syngeneic bone marrow transplantation

Serum IgE levels were studied in 25 bone marrow transplant recipients (in 12 patients twice weekly and in 13 patients, at random). A 2-748- fold increase in serum IgE was recorded in 20 of the 25 patients after transplantation, the highest IgE value observed being 8,000 kU/liter. The IgE elevation appeared concomitantly with acute graft-versus-host disease (GVHD) in 14 patients. Both events occurred on day 24 +/- 2 (mean +/- SE). When the acute GVHD was diagnosed, there was a significant increase in serum IgE as compared to the first posttransplantation value. In one patient in whom GVHD recurred, a second IgE peak was seen, and in another patient with flaring GVHD, IgE levels increased on several occasions. In 6 patients without clinical signs of GVHD, a rise in IgE occurred on day 35 +/- 12. One of these patients was grafted with marrow from her identical twin. The rise in IgE did not correlate with an elevated proportion of eosinophil granulocytes. In the majority of the patients, no correspondent increases in serum IgG, IgA, or IgM were seen during the period with increased IgE after transplantation.     

参数设置对多层螺旋CT三维重建误差的影响

研究多层螺旋CT三维重建性能与几个主要参数之间的关系。用一台多层螺旋CT对同一个试验物品在不同参数下扫描成像，然后比较和分析不同参数下三维重建结果的误差大小。结果显示层厚、螺距等参数设置对三维成像质量有很大的影响。     

Endometrial carcinoma staging by MR imaging

The potential of magnetic resonance (MR) imaging in the detection of endometrial carcinoma and in the assessment of its extent was evaluated prospectively in 51 patients clinically suspected of having the disease. MR imaging findings were compared with the results of surgical-pathologic staging and lymph node sampling following hysterectomy. Histologic findings showed 45 patients to have endometrial carcinoma, three to have no residual tumor after dilatation and curettage, and three to have adenomatous hyperplasia of the endometrium. MR imaging demonstrated an endometrial abnormality in 43 of the 51 patients (84%). Endometrial carcinoma could not be differentiated from adenomatous hyperplasia or blood clots. Therefore, MR imaging was not specific for tumor detection, and histologic diagnosis remains essential. The overall accuracy of MR imaging in staging endometrial carcinoma was 92%; its overall accuracy in demonstrating the depth of myometrial invasion was 82%. Demonstration of lymphadenopathy and adnexal or peritoneal metastases by MR imaging was suboptimal.     

Insulin antibody production in guinea pigs is accompanied by disturbances in pancreatic islet morphology and glucagon secretion

Long term immunization of seven guniea pigs with crystalline porcine insulin in Freund's adjuvant resulted in the production of high titres of insulin antibodies. With the exception of one guniea pig which became hyperglycaemic by 10 weeks, normoglycaemia was maintained. After 42 weeks, the guinea pigs were killed and examined with regard to islet morphology and glucagon secretion. Immunocytochemical staining revealed an increase in the relative A-cell volume and a decrease in the relative B-cell volume. This was accompanied by a cellular rearrangement with A-cells centrally and B-cells peripherally. The islets of the hyperglycaemic guinea pig were enlarged and contained pyknotic cells with a few well-stained A-cells. Short term culture of normal guinea pig islets in the presence of serum from this animal did not lead to structural change. No evidence of insulitis or islet fibrosis was observed in any of the guinea pigs. Incubation of islets from the immunized animals in vitro revealed that the normal suppression of glucagon secretion by glucose was absent. Despite a degree of cross-reaction between antibodies and guinea pig insulin, as judged from immunocytochemical staining of guinea pig islets, there was no relationship between antibody titre and the degree of the morphological or functional disturbances. Although abnormal glucagon secretion can be partly attributed to disturbances in islet architecture, the exact mechanism remains to be elucidated.