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Biomedical subjects

J Marley

Publications and source records attributed to J Marley.

51 records · Page 3Linked to original sources
PubMed1989

Lifestyle intervention in hypertension.

Patients are often interested in taking some responsibility for treating their own illnesses, especially in a symptom-free condition such as hypertension. Confusing information is available on non-pharmacological measures, which often results in none of these treatments being offered to the patient. This review discusses what is of value, what may be helpful and what is likely to be worthless.

Acupuncture Therapy↗
PubMed1989

Plasma nitrendipine concentrations in elderly normotensive volunteers after single and multiple dosing.

An acute and chronic dosing pharmacokinetic study of the calcium antagonist nitrendipine was carried out in 8 normotensive volunteers (mean age 80.1 +/- 3.4 years) to investigate if drug accumulation occurred in the elderly. Subjects received 10 mg nitrendipine once daily by mouth for 8 days. Plasma nitrendipine concentrations before administration and at 0.5, 1, 2, 4, 6 and 8 hours after dosing were measured after the first and last dose. Comparison of the pharmacokinetic data from Days 1 and 8 failed to show any evidence of nitrendipine accumulation in these elderly subjects.

Aged↗
PubMedDate not supplied

Characterization of a murine model of acute lung injury (ALI): a prominent role for interleukin-1.

This report describes a model developed to study local and systemic events that occur as a result of acute lung injury (ALI). C57BL/6J mice were injected with a single intravenous dose (2, 4, and 6 micrograms) of 12-O-tetradecanoylphorbol-13-acetate (TPA). At 1, 2, 4, 12, 24, and 48 h, after injection, plasma was collected by sinus orbital puncture, bronchoalveolar lavage (BAL) was performed and cells and fluid were collected, lungs were perfused, and pulmonary tissue was isolated and processed for histological, immunochemical, and gene expression studies. The results indicate a dose-dependent increase in animal distress and a decrease in survival. TPA induced an early systemic response, reflected as an initial decrease in numbers of peripheral blood neutrophils at 1 h, followed at 2 h by a sustained increase. There was dose- and time-dependent increase in IL-1 beta mRNA synthesis, detected using RT-PCR, and in immunoreactive IL-1 alpha produced by both tissue-fixed pulmonary cells and cells within alveolar spaces. Infiltration of neutrophils into pulmonary tissue and increased protein content in BAL fluid was detected 2 h after injection of TPA. Disruptions in pulmonary architecture accompanied by the presence of highly vacuolated macrophages within the alveolar spaces and interstitial tissue were evident after IV injection of TPA. The study shows that injection of TPA induces reproducible dose- and time-dependent alterations in cell types, numbers, state of activation, and production of soluble mediators in the peripheral circulation within BAL and pulmonary tissue. Thus, this model offers a means to examine the cellular basis for the local and systemic alterations observed during ALI.

Animals↗
PubMedDate not supplied

Induction and maintenance of T-cell response to a nonimmunogenic murine mesothelioma cell line requires expression of B7-1 and the capacity to upregulate class II major histocompatibility complex expression.

Intratumoral expression of the T-cell costimulator B7-1 has been reported to induce tumor-specific immunity against immunogenic, but not nonimmunogenic, tumors. We transfected the B7-1 gene into a nonimmunogenic murine mesothelioma cell line that constitutively expresses high levels of class I major histocompatibility complex (MHC) and transforming growth factor-beta (TGF-beta). Tumor development by two of the four B7-1 transfectant clones was markedly delayed, although all clones eventually formed tumors. Retardation of tumor growth required both CD4+ and CD8+ T cells. Tumor-specific cytotoxic T-lymphocytes (CTLs) were elicited in response to the least (AC29-B7-6), but not the most (AC29-B7-7), tumorigenic transfectant clone. Tumor-specific CTL activity could be detected at early time points but not at the time of tumor outgrowth. This lack of responsiveness was tumor antigen specific. Differences in immunogenicity of transfectant clones did not relate to the level of expression of MHC class I, vascular cell adhesion molecule-1, or transfected B7-1, or to the level of TGF-beta secreted. Class II MHC expression was most readily inducible in those transfectant clones whose growth in vivo was most delayed. An explant cell line derived from a tumor that developed from AC29-B7-6 had a markedly reduced capacity to upregulate MHC class II expression and produced tumors in vivo at a faster rate than did the parental cell line. Thus, B7-1 expression in this nonimmunogenic tumor cell line can promote the generation of tumor-specific CTLs with consequent retardation of tumor development, and coexpression of MHC class II seems likely to play an important role in this process. This work also illustrates that clonal heterogeneity within a single tumor and the development of immunological nonresponsiveness resulting in tumor outgrowth, even in the presence of continued B7-1 expression, are potential difficulties associated with this therapeutic approach.

Animals↗