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Biomedical subjects

T P Bradley

Publications and source records attributed to T P Bradley.

17 recordsLinked to original sources
PubMed1999

Lead poisoning from a retained bullet: a case report and review.

A 47-year-old man with a prior gunshot wound presented with arthritis, constipation, abdominal pain, and weight loss. Arthrocentesis did not reveal the cause of the arthritic complaints, but lead poisoning was suspected and confirmed. We present this case along with a short review of the literature pertaining to this often overlooked and reversible cause of lead poisoning.

Chelating Agents↗
PubMed1998

Adult-onset Still's disease associated with G6PD deficiency: a case report and literature review.

A 37-year-old man presented with symptoms consistent with adult-onset Still's disease. Fever and leukocytosis were prominent, and the patient was started on high-dose aspirin for possible acute rheumatic fever. He developed severe anemia as a result of glucose-6-phosphate dehydrogenase deficiency. His treatment was changed to naproxen, and he recovered with restoration of his hematologic parameters. Although Still's disease is frequently accompanied by mild-to-moderate anemia, the development of severe anemia should raise the possibilities of hemolysis secondary to glucose-6-phosphate dehydrogenase deficiency.

Adult↗
PubMed1992

Elimination of extrachromosomally amplified MYC genes from human tumor cells reduces their tumorigenicity.

Oncogene amplification has been observed in a broad spectrum of human tumors and has been associated with a poor prognosis for patients with several different types of malignancies. Importantly, at biopsy, the amplified genes localize to acentric extrachromosomal elements such as double-minute chromosomes (DMs) in the vast majority of cases. We show here that treatment of several human tumor cell lines with low concentrations of hydroxyurea accelerates the loss of their extrachromosomally amplified oncogenes. The decreases in MYC copy number in a human tumor cell line correlated with a dramatic reduction in cloning efficiency in soft agar and tumorigenicity in nude mice. No effect on gene copy number or tumorigenicity was observed for a closely related cell line containing the same number of chromosomally amplified MYC genes. One step involved in the accelerated loss of extrachromosomal elements is shown to involve their preferential entrapment of DMs within micronuclei. The data suggest that agents that accelerate the loss of extrachromosomally amplified genes could provide valuable tools for moderating the growth of a large number of human neoplasms.

Animals↗
PubMed1987

Radiation effects on cerebral white matter: MR evaluation.

The purpose of this study was to evaluate the white-matter changes associated with cranial radiation by MR imaging. The MR scans of 95 patients receiving conventional external beam radiation for a wide variety of central nervous system tumors were reviewed. Moderately T2-weighted spin-echo images with a 2000-msec repetition time and 56-msec-echo time were analyzed for white-matter abnormalities without knowledge of the patient's history. These were correlated with radiation dose, port, and time interval since completion of therapy, and then compared with an age-matched control group of 180 patients with nonirradiated, space-occupying, intracranial lesions. Radiation-related lesions were characterized as symmetric, high-signal foci in the periventricular white matter. Relative sparing of the posterior fossa, basal ganglia, and internal capsules was noted. In patients older than 20 years, these changes paralleled those seen in ischemia but were more prevalent (p less than .005). In 25 patients with sequential MR scans, these findings remained stable. In those patients with limited treatment fields, for example, pituitary adenomas, no statistical differences were seen between radiation-treated and nontreated groups. Cerebral white-matter changes that mimic deep white-matter infarction are frequently seen in response to therapeutic radiation. There is a variable incidence of radiation effects, becoming more marked in older patients. MR interpretation must consider the neuropathologic consequences of therapeutic radiation, which include demyelination, microvascular occlusion, and blood-brain barrier breakdown.

Adult↗
PubMed1984

Mechanism of cell-mediated cytotoxicity at the single-cell level. VII. Trigger of the lethal hit event is distinct for NK/K and LDCC effector cells as measured in the two-target conjugate assay.

Normal human peripheral blood lymphocytes (PBL) express several in vitro cytotoxic functions, among which are natural killer (NK), antibody-dependent cellular cytotoxicity (ADCC), and lectin-dependent cellular cytotoxicity (LDCC). The relationship of these various cytotoxic functions and the identity of cells involved has been a subject of controversy. Recently it was reported that NK and K for ADCC can be mediated by the same cell, suggesting that they constitute in large part a single subpopulation with multiple cytotoxic functions. The ability of this NK/K effector cell to mediate LDCC was examined here using the two target conjugate assay. The effector cells were Ficoll-Hypaque PBL or LGL-enriched fractions. The targets used were K562 or MOLT for NK, RAJI coated with antibody for ADCC, and RAJI coated with PHA or Con A or modified by NaIO4 for LDCC. In the two-target conjugate assay, one of the targets is fluorescein labeled for identification. The results show that (a) LDCC copurifies with NK/K and is enriched in the LGL fraction, as measured in both the 51Cr-release assay and the single-cell assay for cytotoxicity; (b) single effector cells simultaneously bind to NK or ADCC and LDCC targets, revealing that single cells bear binding receptors for all targets; and (c) single lymphocytes were not able to kill both bound NK/K and LDCC targets. However, significant two-target killing was obtained when both targets were NK targets, ADCC targets, LDCC targets, or one NK and one ADCC target. These results demonstrate that the NK and LDCC effector cells are distinct subpopulations copurified in the LGL fraction. In addition, the results show that lectin is unable to trigger globally an NK effector cell to mediate cytotoxicity against a bound NK insensitive target. Thus, although both NK and LDCC effector cells are present in the LGL fraction and can bind to both types of targets, the trigger of the lethal hit event is the function of specialized effector cells.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1984

Mechanism of cell-mediated cytotoxicity at the single cell level. VI. Direct assessment of the cytotoxic potential of human peripheral blood non-lytic effector-target cell conjugates.

Single cell cytotoxicity assays reveal that a large percentage of lymphocytes are unable to kill attached targets in a 4- to 18-hr assay. Additional signals (in the form of lectin or anti-target antibody) delivered to target-bound lymphocytes enable these previously non-lytic lymphocytes to kill attached target cells. This finding was obtained by using a modification of the single cell assay, in which lectin or target cell antibody is incorporated into agarose with preformed lymphocyte-target conjugates. Human peripheral blood lymphocytes (PBL) or Percoll density gradient-enriched large granular lymphocytes (LGL) were used as effector cells in natural killer (NK), antibody-dependent cellular cytotoxicity (LDCC) assay systems. The targets used were NK-sensitive K562 and Molt-4 and NK-insensitive Raji. Several findings were made in the modified single cell assay, namely a) the frequency of cytotoxic NK or ADCC effector cells was not augmented, suggesting that the initial trigger was sufficient for lytic expression in these instances. Furthermore, these results showed that the NK-sensitive targets used do not bind nonspecifically to the LDCC effector cells. K562 coated with Con A, however, serve as LDCC targets. b) The frequency of two target conjugate lysis by NK/K effectors was not augmented by Con A. These results suggest that Con A does not potentiate the killing of multiple targets bound to a single cytotoxic lymphocyte. c) Although conjugates formed between LGL or PBL and NK-insensitive Raji are non-lethal, significant lysis was observed when these conjugates were suspended in Con A or antibody agarose. These results demonstrate that Raji bind to cytotoxic NK, K, and LDCC effector cells, but are lysed only when the appropriate trigger is provided. d) The cytotoxic potential of non-lytic conjugates appears to lie within the low density Percoll fraction, although the high density lymphocytes are able to nonlethally bind to targets. Altogether the results demonstrate that target recognition and/or binding by the effector cells is a distinct event from the trigger or lytic process. The implications of these findings are discussed.

Animals↗
PubMed1976

Studies on the induction and expression of T cell-mediated immunity. V. Lectin-induced nonspecific cell-mediated cytotoxicity by alloimmune lymphocytes.

Murine lymphoid cells sensitized against allografts express two types of cytotoxicity measured in vitro in short-term assays of 2 to 3 hr by 51Cr release. One type of cytotoxicity is specific against target cells carrying the sensitizing alloantigens, and the other type is nonspecific against both syngeneic and unrelated target cells and requires the presence of phytohemagglutinin (PHA) or concanavalin A (ConA). Several lines of evidence are presented which demonstrate that both cytotoxic systems are mediated by the same clone of alloimmune effector T lymphocytes and that the lectin-induced cytotoxicity is not attributable to mitogenic polyclonal activation of effector cells. Studies with ConA inhibitor alpha-methyl-D-mannoside suggest a mechanism of interaction that requires the lectin to be present during the reaction. Experiments with other reagents, however, that bring about physical contact of the cells but not lysis, indicate that cytolysis can occur only through specific lectin receptors on the cells. The significance of this lectin-induced cytotoxicity is discussed.

Animals↗
PubMed1971

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Adult↗