Peptides as substitute osmotic agents for glucose in peritoneal dialysate.
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Biomedical subjects
Publications and source records attributed to E Klein.
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Endotoxins, or fragments thereof, can reach the blood stream of dialysis patients, transported by diffusion and connection across the intact high-flux membrane. This transfer depends upon the phenomenon of back filtration. Back filtration generally occurs under conventional high-flux dialysis conditions with membranes having an ultrafiltration coefficient in blood (UF-C) above 20 ml/hr/m2/mmHg. The clinical consequences of back filtration vary from center to center depending primarily on the quality of dialysate. We therefore surveyed the bacterial and endotoxin levels of purified water and effluent dialysate in a cross section of dialysis centers in the central United States. Using a high recovery medium, we found that 53% of the centers had bacterial counts above the Association for the Advancement of Medical Instruments standard in water (20% cfu/ml) and 35% above the standard in dialysate (2,100 cfu/ml). Endotoxin concentrations higher than 5.0 EU/ml in both water and dialysate were found in 4% and 11.8% of the centers, respectively. Since high-flux membranes are believed to be of benefit for long-term dialysis patients, manufacturers will have to offer dialysate preparation systems with additional safety features. The proper membrane design will be a key to the success of such systems.
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Molecular alterations in the mismatch repair system suggest that this mechanism may be important in the evolution of cutaneous melanoma. Our current study evaluated the expression of two mismatch repair proteins, hMLH1 and hMSH2, in dysplastic nevi (DN) and cutaneous melanoma (CM). Immunohistochemical staining of these proteins was performed on 55 CM and 30 DN specimens. The staining results were divided into three groups: negative, partially positive and strongly positive. Normal adjacent skin cells served as an internal control for positive immunostaining. Altered immunoreactivity of one of the proteins was found in four (13.4%) DN and seven (12.7%) CM. Lack of staining for hMLH1 was observed in two (6.7%) cases of DN and five (9.1%) cases of CM; staining for hMSH2 was absent in two (6.7%) of the DN and two (3.6%) of the CM specimens. Partially positive staining was found in 33.3% and 53.3% for hMLH1 and hMSH2, respectively, in DN, and in 54.5% and 69.1%, respectively, in CMM. Our study shows that complete or partial loss of MMR protein expression occurs in a subset of both DN and CM and may represent a distinct pathway in the development of some DN and CM.
Overinflation of endotraceal-tube cuffs may seriously compromise the patient's airway, due to collapse of the wall of the endotracheal tube. Two case reports describe this complication, with x-ray demonstration of the hyperinflated cuffs.
This is a case report of a three-year-old girl with recurrent ear bleeding which was actually recurrent factitious symptomatology, perpetrated by the mother, which caused the child to undergo many harmful diagnostic procedures. This is a documented case, probably the first case reported in Latin America, and it is also the only one in which there is mention of the mother demonstrating interest in divulging the case. Munchausen's Syndrome by Proxy (MSBP) is a specific modality of child abuse. The mother, often the perpretator, affect concern and affection. The consequences are both psychological and physical and can determine child's death. Diagnosis is rarely considered.
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BACKGROUND: Genetic aberrations observed in the large bowel during the neoplastic progression have a cumulative effect and are responsible for the propagation of the multistep malignant process. In the present study we evaluated the immunoreactivity of c-fos, ras, bcl-2 and p53 in aberrant crypt foci (ACF) and minute polyps of the large bowel obtained from patients with colorectal cancer. METHODS: ACF and minute polyps were collected from macroscopically normal colonic mucosa. Protein immunoreactivity was detected on parafin sections utilizing the biotin-streptavidin method on 25 hyperplastic, 10 dysplastic ACF, 5 hyperplastic and 10 dysplastic adenomas. RESULTS: 41% of the lesions displayed positive ras immunoreactivity. bcl-2 immunoreactivity was positive in six minute polyps of which five were neoplastic. fos immunoreactivity was detected in five ACF and seven minute polyps, mainly in dysplastic lesions. Two neoplastic polyps were positive for p53 immunoreactivity. Coexpression of two or more oncoproteins was found with increasing frequency in dysplastic versus hyperplastic lesions and in polypoid lesions versus ACF. CONCLUSION: Abnormal expression and coexpression in oncoproteins can be identified in the earliest stages of colorectal tumorigenesis and may contribute to the progression of selected lesions during ACF-adenoma-carcinoma sequence.
OBJECTIVES: To understand the mechanism for the refractoriness of B-chronic lymphocyte leukemia (B-CLL) cells for EBV-induced immortalization. STUDY DESIGN/METHODS: Cells from four B-CLL patients were infected with Epstein-Barr virus (EBV). Noninfected and infected aliquots were exposed to CD40L. Five days later, the cultures were analyzed for cell survival, activation, DNA synthesis, and expression of EBV-encoded and of cellular regulatory proteins retinoblastoma (Rb), p53, recombinant sequence binding protein (RBP)Jk, and PU.1. The proteins were detected by immunoblotting and by immunofluorescence. RESULTS: A proportion of the cells were activated and expressed Epstein-Barr nuclear antigens (EBNAs) and elevated Rb level but not latent membrane protein (LMP)-1 and p53. They did not enter the cell cycle. Exposure to CD40L induced DNA synthesis but it did not modify the expression of the EBNAs. CONCLUSIONS: The virus could activate CLL cells, but the full course of the early events that leads to immortalization--as seen in normal B cells--did not proceed beyond a certain point. Compared to B lymphocytes, the critical point is between activation and initiation of the cell cycle.
Seventeen patients with histologically proven adenocarcinoma of the prostate were selected for evaluation of their immunologic competence and therapy with bacillus Calmette-Guérin (BCG). All patients were in stage D. The immune response was explored in two main aspects: cell-mediated and humoral immunity. Delayed skin hypersensitivity reaction with purified protein derivative (PPD), streptokinase-streptodornase (varidase), Candida, mumps antigen, and Trichophyton were tested. Lymphocyte reactivity was measured by in vitro blastogenesis. Serum immunoglobulin levels and serum protein electrophoresis were also measured. The patients were then divided in two groups according to the skin test response to PPD. Group 1 (PPD-positive) consisted of seven patients. Group 2 (PPD-negative) consisted of ten patients. In group 1, two patients were treated with intraprostatic injection of BCG every week in the following doses: 1 cc the first week, 2 cc the second week, 4 cc the third week, and 6 cc the fourth week. The five remaining patients in this group received only 1 cc every week for 4 weeks. The group 2 patients (PPD-negative) were stimulated by oral intake of BCG in an attempt to convert their skin tests to positive. All patients revealed varying degrees of immunodepression. None of the patients in group 2 (stimulated by oral intake of BCG) converted to positive skin tests. Three patients in group 1 treated with BCG showed necrosis of the tumor. The different aspects of immunodepression in this disease are analyzed and correlated to the clinical staging, histologic grading, and response to therapy. The mechanism of BCG action in advanced prostatic carcinoma is discussed.
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Applying a bonding agent and a resinous adhesive layer before amalgam condensation has become a common clinical procedure. However, interactions between the different interfaces formed, and the extent of sealing obtained, have not been extensively studied. This study characterized the interfaces formed in the bonded amalgam restoration. Specifically, the individual contributions of the bonding agent (One-Step) and the adhesive resin (Resinomer) were examined, along with their mode of application on the prevention of microleakage and the formation of a tight, continuous adhesion to amalgam. To this end, a dye penetration assay and scanning electron microscopy (SEM) were used, including high resolution elemental analysis, for the characterization of the sealing properties and the interface structure obtained following various procedures of applying amalgam adhesives. Results indicated that placing bonding material under the amalgam restoration is essential to preventing microleakage. When condensed against uncured or cured adhesive material, the adhesive resinous glass layer creates a thick interface with protrusions and inclusions in the amalgam, though microleakage studies indicate that condensation over the uncured adhesive results in a better seal than that of the cured adhesive. SEM combined with elemental analysis indicates that the adhesion between amalgam and adhesive material is mainly of mechanical character and is formed by interdigitations of the adhesive material protruding into the amalgam. Gaps formed at the various interfaces in the different modalities could be localized. In addition, resinous glass composite alone, without bonding, was found to provide an unacceptable degree of sealing between the tooth and amalgam. The clinical significance of these findings is further discussed.
OBJECTIVES: To understand the mechanism for the refractoriness of B-chronic lymphocytic leukemia (B-CLL) cells for Epstein-Barr virus (EBV)-induced immortalization. STUDY DESIGN/METHODS: Cultures were initiated with EBV-infected tonsillar B and B-CLL cells. Expression of EBNA-2 and some of the key players regulating G1/S phase transition such as c-myc expression, phosphorylation of Rb protein, expression of G1 cyclins, and the cyclin-dependent kinase inhibitor p27 were followed. RESULTS: In line with earlier studies, EBV infection induced c-myc expression, pRb phosphorylation, D2 and D3 expression, and disappearance of p27 in normal B cells. In contrast, EBV-infected B-CLL cells remained resting and they did not express c-myc; cyclin D2, ppRb and cyclin D3 were seen only in occasional cells. Importantly, p27 expression was maintained. CONCLUSIONS: In B-CLL cells, the expression of the EBV-encoded nuclear proteins EBNAs is not followed by entrance to the cell cycle. Thus, the difference in the interaction of EBV-normal B cells and EBV-B-CLL cells is already apparent early after infection.
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The studies on the T cell response against EBV carrying B cells demonstrated its high power in vivo. Malignancies with phenotypes similar to the in vitro transformed B cells occur only in severely immunosuppressed patients. Presently the goal of the studies is the identification of the antigens recognised by T lymphocytes and their association with the various HLA alleles. The studies on human sarcomas and carcinomas still struggle with the demonstration of specific T cell responses and the characterisation of the target molecules on the tumor cells. The main goals are the possibilities to readminister tumor reactive T cells for therapeutic purposes and the use of in vitro assays for guidance of the design and schedule for immunotherapy protocols.